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'This is a great resource that reflects the huge expertise of the authors. It will be welcomed by students, researchers and indeed anyone wanting critical but comprehensive coverage of key issues and trends concerning drugs and society - locally and globally, historically and today.' - Nigel South, Professor of Sociology, University of Essex 'Provides informative, balanced and contextualized insights into the relationships between people and drugs. Whatever your background and however knowledgeable you feel you are about contemporary drug issues, I guarantee that you will learn something unexpected and new from this valuable text.' - Joanne Neale, Professor of Public Health, Oxford Brookes University Why do people take drugs? How do we understand moral panics? What is the relationship between drugs and violence? How do people's social positions influence their involvement in drug use? Insightful and illuminating, this book discusses drugs in social contexts. The authors bring together their different theoretical and practical backgrounds, offering a comprehensive and interdisciplinary introduction that opens up a wide scientific understanding moving beyond cultural myths and presuppositions. This is an invaluable reference source for students on criminology, sociology and social sciences programmes, as well as drug service practitioners such as drug workers, social workers and specialist nurses.Top Download:
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Health Drugs, Society and Human Behavior 13th Edition Hart−Ksir−Ray
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ISBN−13: 978−0−39−065732−9
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Contents Hart−Ksir−Ray • Drugs, Society and Human Behavior, 13th Edition Front Matter
1
List of Boxes Preface
1 3
I. Drug Use in Modern Society
7
Introduction 1. Drug Use: An Overview 2. Drug Use as a Social Problem 3. Drug Products and Their Regulations II. How Drugs Work
7 8 31 57 85
Introduction 4. The Nervous System 5. The Actions of Drugs
85 86 107
III. Uppers and Downers
129
Introduction 6. Stimulants 7. Depressants and Inhalants 8. Medication for Mental Disorders
129 130 159 177
IV. Alcohol
197
Introduction 9. Alcohol
197 198
V. Familiar Drugs
237
Introduction 10. Tobacco 11. Caffeine 12. Dietary Supplements and Over−the−Counter Drugs
237 238 262 283
VI. Restricted Drugs
309
Introduction 13. Opioids 14. Hallucinogens 15. Marijuana 16. Performance−Enhancing Drugs
309 310 334 367 393
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VII. Prevention and Treatment
411
Introduction 17. Preventing Substance Abuse 18. Treating Substance Abuse and Dependence
411 412 431
Back Matter
447
Appendix A: Drug Names Appendix B: Resources for Information and Assistance Glossary Credits Index
447 453 457 469 472
iv
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
List of Boxes
© The McGraw−Hill Companies, 2009
1
List of Boxes
Drugs in the Media Reporting on the “Drug du Jour” 4 Pharm Parties? 27 Is Media Coverage of New Prescription Drugs Too Rosy? 53 Brain Teasers: What’s in a Pretty Picture? 82 The Grapefruit-Juice Effect 103 The Drug War in Tulia: Aberration or Representative? 126 The Legacy of Samantha Reid 155 Mental Illness at the Movies 173 Advertising Alcohol on Television 194 Tobacco Use in the Movies 234 Fancy Coffee Drinks and Humor 259 Natural Male Enhancement? 258 The Rise and Fall of Heroin “Epidemics” 308 The Psychedelic 60s—Reflections in Film, Music, and Literature 333 Medical Marijuana in the News 367 Banned Substances and How to Avoid Them 393 Prime-Time Drug-Prevention Programming 412 Celebrity Rehab 431
Should We Be Concerned about Steroid Use by Entertainers? 402 Are “Alternatives to Drugs” Really Alternatives? 416
Drugs in Depth Important Definitions—and a Caution! 6 Methamphetamine Use in Your Community 8 Americans in Prison 68 Drug Interactions 117 Alcohol without Liquid 210 Possible New Painkiller? 248 Caffeine and Panic Attacks 273 The Vioxx Controversy 295 Extrapolating Findings from Animals to Humans: What You Need to Know 351 Nutritional Ergogenic Aids 401 How Much Do You Know About DARE? 419 Effective Prevention Programs 421 The 12 Steps of Alcoholics Anonymous 433
Mind/Body Connection Taking Sides Can We Predict or Control Trends in Drug Use? 7 Are Current Laws Fair? 42 Prescription Marijuana? 71 Animal Toxicity Tests 108 Should Psychologists Be Allowed to Prescribe? 183 Protecting the Unborn from Alcohol 223 Caffeine-Dependence Syndrome? 271 Should There Be a Class of “Pharmacist-Recommended” Drugs? 292 Should Naloxone Be Made Available to Heroin Users? 315 Do You Think the Federal Government Should Fund Hallucinogen Research? 345 Should Medical Patients Have Access to Marijuana? 380
Religion and Drug Use 14 Fear and Decision Making 31 Looking for More Humane Policies 65 How Far Should We Go to Enhance Human Abilities? 146 Learning to Relax 165 Is Alcoholics Anonymous a Religion? 225 The Hidden Costs of Smoking 251 Caffeine and the “Geek” Culture: Buying a Dream 272 Abuse of OTC Dextromethorphan 299 Living in the Flow 359 Baseball: Seeking Alternatives to Amphetamines 396 Integrating Treatment and Prevention with Pregnancy Services 423 The Nature of Dependence 440 xv
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
List of Boxes
List of Boxes Preventing Inhalant Abuse Avoiding Relapse 434
413
Targeting Prevention Preventing What? 18 Clean Needles? 32 Prescribing Practices 57 Avoiding Withdrawal Symptoms 109 Cocaine and Friendship 135 The Drug-Induced Rape Prevention and Punishment Act 160 Falling Asleep Without Pills 163 Estimating Blood Alcohol Concentration 208 The Medicine Chest 290
DSM-IV-TR Psychiatric Diagnosis of Substance-Use Disorders 36 Diagnostic Criteria for Attention-Deficit Hyperactivity Disorder 145 Anxiety Disorders 174 Diagnosis of Schizophrenia 175 Diagnosis of Mood Disorders 176 Psychiatric Diagnosis of Substance Disorders 432
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
3
Preface Today’s media-oriented college students are aware of many issues relating to drug use. Nearly every day we hear new concerns about methamphetamine, club drugs, legal pharmaceuticals, and the effects of tobacco and alcohol, and most of us have had some personal experience with these issues through family, friends, or co-workers. This course is one of the most exciting students will take because it will help them relate the latest information on drugs to their effects on society and human behavior. Students will not only be in a better position to make decisions to enhance their own health and well-being, but they will also have a deeper understanding of the individual problems and social conflicts that arise when others misuse and abuse psychoactive substances. Much has changed in the 38 years since Drugs, Society, and Human Behavior was first published. The 1970s were a period of widespread experimentation with marijuana and hallucinogens, while the 1980s brought increased concern about illegal drugs and conservatism, along with decreased use of alcohol and all illicit drugs. Not only did drugusing behavior change, but so did attitudes and knowledge. And, of course, in each decade the particular drugs of immediate social concern have changed: LSD gave way to angel dust, then to heroin, then to cocaine and crack. In the 1990s, we saw increased use of LSD and marijuana, but not to the levels of the 1970s.
Recent Trends The most alarming trend in recent years has been the increased misuse of prescription opioid pain relievers such as Oxycontin and Vicodin. These pharmaceuticals have now replaced cocaine as the leading cause of drug overdose deaths in the United States (not counting
alcohol overdoses), and they have joined methamphetamine and Ecstasy as leading causes of concern about drug misuse and abuse. Methamphetamine, Esctasy, GHB, and the misuse of prescription painkillers are the big news items. Meanwhile, our old standbys, alcohol and tobacco, remain with us and continue to create serious health and social problems. Regulations undergo frequent changes, new scientific information becomes available, and new approaches to prevention and treatment are being tested, but the reality of substance use and abuse always seems to be with us. This text approaches drugs and drug use from a variety of perspectives—behavioral, pharmacological, historical, social, legal, and clinical—which will help students connect the content to their own interests.
Special Features Updated Content in the Thirteenth Edition Throughout each chapter, we have included the very latest information and statistics, and the Drugs in the Media feature has allowed us to comment on breaking news right up to press time. In addition, we have introduced many timely topics and issues that are sure to pique students’ interest and stimulate class discussion. The following are just some of the updated topics in the thirteenth edition. For a complete, chapter-by-chapter list of changes, please visit the Online Learning Center for the thirteenth edition (www.mhhe.com/hart13e). •
Statistics on drug use trends, new drug treatments, and drug-related mortality statistics from National Survey on Drug Use and Health, Monitoring the Future, DAWN, TEDS, SAMHSA treatment information (Chapter 1 and throughout) xvii
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
Preface
© The McGraw−Hill Companies, 2009
Preface
•
Risk and protective factors for drug use, including the influence of gender, race, level of education, personality, and genetics (Chapters 1 and 2)
•
Cocaine sentencing policy (Chapters 3 and 6)
•
Current research on popular recreational drugs, including methamphetamine (Chapter 6), MDMA (Chapter 14), psilocybin (Chapter 14), and marijuana (Chapter 15)
•
Effectiveness and side effects of antidepressants and antipsychotics (Chapter 8)
•
Self-assessment of alcohol use (Chapter 9)
•
Smoking cessation medications (Chapter 10)
•
Behind-the-counter drugs (Chapter 12)
•
Dietary supplement regulation (Chapter 12)
•
Prescribing naloxone to heroin users as a harm-reduction strategy (Chapter 13)
•
Extrapolating findings of animal studies to humans (Chapter 14)
•
Funding for research on hallucinogens (Chapter 14)
•
medical marijuana (Chapter 15)
•
Use of performance-enhancing drugs by athletes and entertainers (Chapter 16)
•
Medications to treat substance abuse and dependence (Chapter 18)
Taking Sides These boxes discuss a particular drug-related issue or problem and ask students to take a side in the debate. This thought-provoking material will help students apply what they learned in the chapter to real-world situations. Taking Sides topics include potential medical uses of marijuana, current laws relating to drug use, and the issue of government funding for research on hallucinogens. Mind/Body Connections The Mind/Body Connection boxes highlight the interface between the psychological and the physiological aspects of substance use, abuse, and dependence. These boxes help students consider influences on their own attitudes toward drug use. Topics include religion and drug use, the social and emotional costs of smoking, and the nature of dependence. Targeting Prevention The Targeting Prevention boxes offer perspective and provoke thought regarding which drugrelated behaviors we, as a society, want to reduce or prevent. Topics include syringe exchange programs, criminal penalties for use of date rape drugs, and nondrug techniques for overcoming insomnia. These boxes help students better evaluate prevention strategies and messages.
Boxes are used in Drugs, Society, and Human Behavior to explore a wide range of current topics in greater detail than is possible in the text itself. The boxes are organized around key themes.
Drugs in Depth These boxes examine specific, often controversial, drug-related issues such as the extrapolation of animal studies to humans, and the growing number of people in prison for drug-related offenses. Drugs in Depth boxes are a perfect starting point for class or group discussion.
Drugs in the Media Our world revolves around media of all types—TV, films, radio, print media, and the Web. To meet students on familiar ground, we have included Drugs in the Media boxes, which take an informative and critical look at these media sources of drug information. Students can build their critical thinking skills while reading about such topics as alcohol advertising, media coverage of prescription drugs, and the presentation of cigarette smoking in films.
Online Learning Center Resources These boxes, found at the opening of each chapter, direct students toward the useful resources available on the Online Learning Center for Drugs, Society, and Human Behavior. These resources include learning objectives, glossary flashcards, Web activities and links, chapter quizzes, audio chapter summaries, and video clips. Students can use Online Learning Center resources to improve their grades and get the most out of this course.
Focus Boxes
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
www.mhhe.com/hart13e
Preface
Attractive Design and Illustration Package The inviting look, bold colors, and exciting graphics in Drugs, Society, and Human Behavior draw the reader in with every turn of the page. Sharp and appealing photographs, attractive illustrations, and informative tables support and clarify the chapter material.
Pedagogical Aids Although all the features of Drugs, Society, and Human Behavior are designed to facilitate and improve learning, several specific learning aids have been incorporated into the text: •
Chapter Objectives: Chapters begin with a list of objectives that identify the major concepts and help guide students in their reading and review of the text.
xix
of drugs and on drug resources and organizations.
Check Yourself! Activities These self-assessments, found at the end of most chapters, help students put health concepts into practice. Each Check Yourself! activity asks students to answer questions and analyze their own attitudes, habits, and behaviors. Self-assessments are included in such areas as sleep habits, daily mood changes, alcohol use, caffeine consumption, and consideration of consequences.
5
•
Summary Drugs Chart: A helpful chart of drug categories, uses, and effects appears on the back inside cover of the text.
Supplements A comprehensive package of supplementary materials designed to enhance teaching and learning is available with Drugs, Society, and Human Behavior.
Online Learning Center www.mhhe.com/hart13e The following instructor resources are available for download from the Online Learning Center; to obtain a password to download these teaching tools, please contact your local sales representative. •
Instructor’s Manual: Organized by chapter, the Instructor’s Manual includes chapter objectives, key terms, chapter outlines, key points, suggested class discussion questions and activities, and video suggestions.
•
Test Bank: Revised and expanded for the thirteenth edition, the test bank now includes more questions for each chapter. The questions are available as Word files and with the EZ Test computerized testing software. EZ Test provides a powerful, easyto-use test maker to create printed quizzes and exams. For secure online testing, exams created in EZ Test can be exported to WebCT, Blackboard, and EZ Test Online. EZ Test comes with a Quick Start Guide, user’s manual, and Flash tutorials. Additional help is available online at www.mhhe.com/eztest.
•
Definitions of Key Terms: Key terms are set in boldface type and are defined in corresponding boxes. Other important terms in the text are set in italics for emphasis. Both approaches facilitate vocabulary comprehension.
•
Chapter Summaries: Each chapter concludes with a bulleted summary of key concepts. Students can use the chapter summaries to guide their reading and review of the chapters.
•
•
Review Questions: A set of questions appears at the end of each chapter to aid students in their review and analysis of chapter content.
PowerPoint Slides: Updated and expanded for the thirteenth edition, the PowerPoint slides include key lecture points and images from the text and other sources.
•
•
Appendices: The appendices include handy references on brand and generic names
Image Bank: Expanded for the thirteenth edition, the image bank contains over 200 images from the text and other sources.
6
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
Preface
Student resources on the free Online Learning Center include chapter objectives, glossary flashcards, self-correcting quizzes, Web activities, audio chapter summaries, and links. New for the thirteenth edition are online video clips. These clips feature student interviews on topics related to drugs, alcohol, and tobacco; critical thinking and self-reflection questions accompany each clip.
Classroom Performance System (CPS) CPS, a wireless response system, brings interactivity into the classroom or lecture hall. Each student uses a wireless response pad similar to a television remote to instantly respond to polling or quiz questions. Results can be posted for immediate viewing by the instructor and entire class. Contact your local sales representative for more information about using CPS with Drugs, Society, and Human Behavior.
Course Management Systems The Online Learning Center can be customized to work with popular course-management systems such as WebCT and Blackboard. Contact your local sales representative for more information.
Acknowledgments We would like to express our appreciation to the following instructors who reviewed the previous edition and helped lay the groundwork for the improvements and changes needed in the thirteenth edition: Lawrence Anthony University of Cincinnati Rodney Clark Allegheny College Liz Coccia Austin Community College Charles Ellison University of Cincinnati Sandy Festa Rutgers–Camden Marc Gellman University of Miami Janene Grodesky Northern Kentucky University Grace Lartey Western Kentucky University Janet Mason College of Lake County Carl L. Hart
Primis Online www.mhhe.com/primis Primis Online is a database-driven publishing system that allows instructors to create customized textbooks, lab manuals, or readers for their courses directly from the Primis Web site. The custom text can be delivered in print or electronic (eBook) form. A Primis eBook is a digital version of the customized text sold directly to students as a file downloadable to their computer or accessed online by password. Drugs, Society, and Human Behavior can be customized using Primis Online.
Charles Ksir
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
Introduction
© The McGraw−Hill Companies, 2009
7
SECTION
ONE Drug Use in Modern Society The interaction between drugs and behavior can be approached from two general perspectives.
1
Which drugs are being used and why?
2
Certain drugs, the ones we call psychoactive, have profound effects on behavior. Part of what
Drug Use: An Overview Drug Use as a Social Problem Why does our society want to regulate drug use?
3
Drug Products and Their Regulations What are the regulations, and what is their effect?
a book on this topic should do is describe the effects of these drugs on behavior, and later chapters do that in some detail. Another perspective, however, views drug taking as behavior. The psychologist sees drug-taking behaviors as interesting examples of human behavior that are influenced by many psychological, social, and cultural variables. In the first section of this text, we focus on drug taking as behavior that can be studied in the same way that other behaviors, such as aggression, learning, and human sexuality, can be studied.
8
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
1
1. Drug Use: An Overview
© The McGraw−Hill Companies, 2009
Drug Use: An Overview Objectives When you have finished this chapter, you should be able to: • Develop an analytical framework for understanding any specific drug-use issue. • Apply four general principles of psychoactive drug use to any specific drug-use issue. • Explain the differences between misuse, abuse, and dependence. • Describe the general trends of increases and decreases in drug use in the U.S. since 1975.
“The Drug Problem” Talking about Drug Use
• Remember several correlates and antecedents of adolescent drug use. • Describe correlates and antecedents of drug use in the terminology of risk factors and protective factors.
“Drug use on the rise” is a headline that has been seen quite • Discuss motives that people may have for illicit and/or regularly over the years. It gets dangerous drug-using behavior. our attention. At any given time the unwanted use of some kind of drug can be found to be increasing, Journalism students are told that an informaat least in some group of people. How big a tive news story must answer the questions who, problem does the current headline represent? what, when, where, why, and how. Let’s see how Before you can meaningfully evaluate the answering the same questions plus one more extent of such a problem or propose possible question—how much—can help us analyze solutions, it helps to define what you’re talkproblem drug use. ing about. In other words, it helps to be more • Who is taking the drug? We are more conspecific about just what the problem is. Most cerned about a 15-year-old girl drinking a of us don’t really view the problem as drug beer than we are about a 21-year-old woman use, if that includes your Aunt Margie’s takdoing the same thing. We worry more about a ing two aspirins when she has a headache. 10-year-old boy chewing tobacco than we do What we really mean is that some drugs being about a 40-year-old man chewing it (unless we used by some people or in some situations happen to be riding right behind him when constitute problems with which our society he spits out the window). And, although we must deal. 2
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
www.mhhe.com/hart13e
Chapter 1
www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips
• don’t like anyone taking heroin, we undoubtedly get more upset when we hear about the girl next door becoming a user. •
What drug are they taking? This question should be obvious, but often it is overlooked. A simple claim that a high percentage of students are “drug users” doesn’t tell us if there has been an epidemic of methamphetamine use or if the drug referred to is alcohol (more likely). If someone begins to talk about a serious “drug problem” at the local high school, the first question should be “what drug or drugs?”
•
When and where is the drug being used? The situation in which the drug use occurs often makes all the difference. The clearest
Drug Use: An Overview
9
3
example is the drinking of alcohol; if it is confined to appropriate times and places, most people accept drinking as normal behavior. When an individual begins to drink on the job, at school, or in the morning, that behavior may be evidence of a drinking problem. Even subcultures that accept the use of illegal drugs might distinguish between acceptable and unacceptable situations; some college-age groups might accept marijuana smoking at a party but not just before going to a calculus class!
Online Learning Center Resources
• • • • • •
© The McGraw−Hill Companies, 2009
1. Drug Use: An Overview
Why a person takes a drug or does anything else is a tough question to answer. Nevertheless, it is important in some cases. If a person takes Vicodin because her doctor prescribed it for the knee injury she got while skiing, most of us would not be concerned. If, on the other hand, she takes that drug on her own, just because she likes the way it makes her feel, then we should begin to worry about possible abuse of the drug. The motives for drug use, as with motives for other behaviors, can be complex. Even the person taking the drug might not be aware of all the motives involved. One way a psychologist can try to answer why questions is to look for consistency in the situations in which the behavior occurs (when and where). If a person drinks only with other people who
Our concern about the use of a substance often depends on who is using it, how much is being used, and when, where, and why it is being used.
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
1. Drug Use: An Overview
© The McGraw−Hill Companies, 2009
Section One Drug Use in Modern Society
Drugs in the Media Reporting on the “Drug du Jour” At the beginning of this millennium, newspaper and television stories about drugs are dominated by the so-called club drugs, such as Ecstasy and GHB. Before that there was a wave of media reports about crystal meth and other forms of methamphetamine. In the mid-1980s, it was crack cocaine. Of course these waves of media focus are associated with waves of drug use, but the news media all seem to jump on the latest “drug du jour” (drug of the day) at the same time. One question that doesn’t get asked much is this: What role does such media attention play in popularizing the current drug fad, perhaps making it spread farther and faster than would happen without the publicity? About 40 years ago, in a chapter titled “How to Create a Nationwide Drug Epidemic,” journalist E. M. Brecher described a sequence of news stories that he believed were the key factor
are drinking, we may suspect social motives; if a person often drinks alone, we may suspect that the person is trying to deal with personal problems by drinking. •
•
How the drug is taken can often be critical. South American Indians who chew coca leaves absorb cocaine slowly over a long period. The same total amount of cocaine “snorted” into the nose produces a more rapid, more intense effect of shorter duration and probably leads to much stronger dependence. Smoking cocaine in the form of “crack” produces an even more rapid, intense, and brief effect, and dependence occurs very quickly. How much of the drug is being used? This isn’t one of the standard journalism questions, but it is important when describing drug use. Often the difference between what one considers normal use and what one considers abuse of, for example, alcohol or a prescription drug comes down to how much a person takes.
in spreading the practice of sniffing the glues sold to kids for assembling plastic models of cars and airplanes (see volatile solvents in Chapter 7). He argued that, without the well-meant attempts to warn people of the dangers of this practice, it would probably have remained isolated to a small group of youngsters in Pueblo, Colorado. Instead, sales of model glue skyrocketed across America, leading to widespread restrictions on sales to minors. Thinking about the kinds of things such articles often say about the latest drug problem, are there components of those articles that you would include if you were writing an advertisement to promote use of the drug? Do you think such articles actually do more harm than good, as Brecher suggested? If so, does the important principle of a free press mean there is no way to reduce the impact of such journalism?
Four Principles of Psychoactive Drugs Now that we’ve seen how helpful it can be to be specific when talking about drug use, let’s look for some organizing principles. Are there any general statements that can be made about psychoactive drugs—those compounds that alter consciousness and affect mood? Four basic principles seem to apply to all of these drugs. 1.
Drugs, per se, are not good or bad. There are no “bad drugs.” When drug abuse, drug dependence, and deviant drug use are talked about, it is the behavior, the way the drug is being used, that is being referred to. This statement sounds controversial and has angered some prominent political figures and drug educators. It therefore requires some defense. For a pharmacologist, it is difficult to view the drug, the chemical substance itself, as somehow possessing evil intent. It sits there in its bottle and does nothing until we put it into a living system. From the perspective of
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a psychologist who treats drug users, it is difficult to imagine what good there might be in heroin or cocaine. However, heroin is a perfectly good painkiller, at least as effective as morphine, and it is used medically in many countries. Cocaine is a good local anesthetic and is still used for medical procedures, even in the United States. Each of these drugs can also produce bad effects when people abuse them. In the cases of heroin and cocaine, our society has weighed its perception of the risks of bad consequences against the potential benefits and decided that we should severely restrict the availability of these substances. It is wrong, though, to place all of the blame for these bad consequences on the drugs themselves and to conclude that they are simply “bad” drugs. Many people tend to view some of these substances as possessing an almost magical power to produce evil. When we blame the substance itself, our efforts to correct drug-related problems tend to focus exclusively on eliminating the substance, perhaps ignoring all of the factors that led to the abuse of the drug. Every drug has multiple effects. Although a user might focus on a single aspect of a drug’s effect, we do not yet have compounds that alter only one aspect of consciousness. All psychoactive drugs act on more than one place in the brain, so we might expect them to produce complex psychological effects. Also, virtually every drug that acts in the brain also has effects on the rest of the body, influencing blood pressure, intestinal activity, or other functions. Both the size and the quality of a drug’s effect depend on the amount the individual has taken. The relationship between dose and effect works in two ways. By increasing the dose, there is usually an increase in the same effects noticed at lower drug levels. Also, at different dose levels there is often a change in the kind of effect, an alteration in the character of the experience. The effect of any psychoactive drug depends on the individual’s history and expectations.
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The effects of drugs are influenced by the setting and the expectations of the user.
Because these drugs alter consciousness and thought processes, the effect they have on an individual depends on what was there initially. An individual’s attitude can have a major effect on his or her perception of the drug experience. The fact that relatively inexperienced users can experience a high when smoking oregano and dry oak tree leaves— thinking it’s good marijuana—should come as no surprise to anyone who has arrived late at a party and felt a “buzz” after one drink rather than the usual two or three. It is not possible, then, to talk about many of the effects of these drugs independent of the user’s history and attitude and the setting.
How Did We Get Here? Have Things Really Changed? Drug use is not new. Humans have been using alcohol and plant-derived drugs for thousands of years—as far as we know, since Homo sapiens first appeared on the planet. A truly “drug-free society” has probably never existed, and might never exist. Psychoactive drugs were used in rituals that we could today classify as religious psychoactive: having effects on thoughts, emotions, or behavior. marijuana (mare i wan ah): also spelled “marihuana.” Dried leaves of the Cannabis plant.
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Drugs in Depth Important Definitions—and a Caution! Some terms that are commonly used in discussing drugs and drug use are difficult to define with precision, partly because they are so widely used for many different purposes. Therefore, any definition we offer should be viewed with caution because each represents a compromise between leaving out something important versus including so much that the defined term is watered down. The word drug will be defined as “any substance, natural or artificial, other than food, that by its chemical nature alters structure or function in the living organism.” One obvious difficulty is that we haven’t defined food, and how we draw that line can sometimes be arbitrary. Alcoholic beverages, such as wine and beer, may be seen as drug, food, or both. Are we discussing how much sherry wine to include in beef Stroganoff, or are we discussing how many ounces of wine can be consumed before becoming intoxicated? Since this is not a cookbook but, rather, a book on the use of psychoactive chemicals, we will view all alcoholic beverages as drugs. Illicit drug is a term used to refer to a drug that is unlawful to possess or use. Many of these drugs are available by prescription, but when they are manufactured or sold illegally they are illicit. Traditionally, alcohol and tobacco have not been considered illicit substances even when used by minors, probably because of their widespread legal availability to adults. Common household chemicals, such as glues and paints, take on some characteristics of illicit substances when people inhale them to get “high.” Deviant drug use is drug use that is not common within a social group and that is disapproved of by the majority, causing members of the group to take corrective action when it occurs. The corrective action may be informal (making fun of the behavior, criticizing the behavior) or formal (incarceration, treatment). Some examples of drug use might be deviant in the society at large but accepted or even expected in particular subcultures. We still consider this behavior to be deviant, since it makes more sense to apply the perspective of the larger society. Drug misuse generally refers to the use of prescribed drugs in greater amounts than, or for purposes other than, those prescribed by a physician or dentist. For nonprescription drugs or chemicals such as paints, glues, or solvents, misuse might
mean any use other than the use intended by the manufacturer. Abuse consists of the use of a substance in a manner, amounts, or situations such that the drug use causes problems or greatly increases the chances of problems occurring. The problems may be social (including legal), occupational, psychological, or physical. Once again, this definition gives us a good idea of what we’re talking about, but it isn’t precise. For example, some would consider any use of an illicit drug to be abuse because of the possibility of legal problems, but many people who have tried marijuana would argue that they had no problems and therefore didn’t abuse it. Also, the use of almost any drug, even under the orders of a physician, has at least some potential for causing problems. The question might come down to how great the risk is and whether the user is recklessly disregarding the risk. How does cigarette smoking fit this definition? Should all cigarette smoking be considered drug abuse? For someone to receive a diagnosis of having a substance-use disorder (see DSM-IV-TR feature in Chapter 2), the use must be recurrent, and the problems must lead to significant impairment or distress. Addiction is a controversial and complex term that has different meanings for different people. Because the term is so widely used in everyday conversation, it is risky for us to try to give it a precise, scientific definition, and then have our readers use their own long-held perspectives whenever we use the term. Therefore, we have avoided using this term where possible, instead relying on more precisely defined terms such as dependence. Drug dependence refers to a state in which the individual uses the drug so frequently and consistently that it appears that it would be difficult for the person to get along without using the drug. For some drugs and some users, there are clear withdrawal signs when the drug is not taken, implying a physiological dependence. Dependence can take other forms, as shown in the DSM-IV-TR feature in Chapter 2. If a great deal of the individual’s time and effort is devoted to getting and using the drug, if the person often winds up taking more of the substance than he or she intended, and if the person has tried several times without success to cut down or control the use, then the person meets the criteria for dependence.
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Taking Sides Can We Predict or Control Trends in Drug Use? Looking at the overall trends in drug use, it is clear that significant changes have occurred in the number of people using marijuana, cocaine, alcohol, and tobacco. However, while it’s easy to describe the changes once they have happened, it’s much tougher to predict what will come next. Maybe even harder than predicting trends in drug use is knowing what social policies are effective in controlling these trends. The two main kinds of activities that we usually look to as methods to prevent or reduce drug use are legal controls and education (including advertising campaigns). How effective do you think laws have been in helping prevent or reduce
in nature, and Chapter 14 provides several examples of hallucinogenic drugs reported to enhance spiritual experiences. A common belief in many early cultures was that illness results from invasion by evil spirits, so in that context it makes sense that psychoactive drugs were often used as part of a purification ritual to rid the body of those spirits. In these early cultures the use of drugs to treat illness likely was intertwined with spiritual use so that the roles of the “priest” and that of the “shaman” (medicine man) often were not separate. In fact, the earliest uses of many of the drugs that we now consider to be primarily recreational drugs or drugs of abuse (nicotine, caffeine, alcohol, and marijuana) were as treatments for various illnesses. Psychoactive drugs have also played significant roles in the economies of societies in the past. Chapter 10 describes the importance of tobacco in the early days of European exploration and trade around the globe as well as its importance in the establishment of English colonies in America; Chapter 6 discusses the significance of the coca plant (from which cocaine is derived) in the foundation of the Mayan empire in South America; and Chapter 13 points out the importance of the opium trade in opening China’s doors to trade with the West in the 1800s. One area in which enormous change has occurred over the past 100-plus years is in the
drug use? Be sure to consider laws regulating sales of alcohol and tobacco to minors in your analysis. What about the public advertising campaigns you are familiar with? How about school-based prevention programs? As you go through the remainder of this book, these questions will come up again, along with more information about specific laws, drugs, and prevention programs. For now, choose which side you would rather take in a debate on the following proposition: broad changes in drug use reflect shifts in society and are not greatly influenced by drug-control laws, antidrug advertising, or drugprevention programs in schools.
development and marketing of legal pharmaceuticals. The introduction of vaccines to eliminate smallpox, polio, and other communicable diseases, followed by the development of antibiotics that are capable of curing some types of otherwise deadly illnesses, laid the foundation for our current acceptance of medicines as the cornerstone of our health care system. Some of the scientific and medical discoveries, problems, and laws associated with these changes are outlined in Chapter 3. The many kinds of legal pharmaceuticals designed to influence mental and behavioral functioning are discussed in Chapter 8. Another significant development in the past 100 years has been government efforts to limit access to certain kinds of drugs that are deemed too dangerous or too likely to produce dependence to allow them to be used in an unregulated fashion. The enormous growth, both in expenditures and in the breadth of substances now controlled, has led many to refer to this development as a “war on drugs.” These laws are also outlined in Chapter 3, but we will trace their effect throughout the chapters on different drug classes, and the chapters on prevention and treatment of drug abuse and dependence. With both of these developments, the proportion of our economy devoted to psychoactive
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drugs, both legal and illegal, and to their regulation, has also expanded considerably. So drug use would be an important topic for us to understand if only for that fact. In addition, drug use and its regulation are reflective of changes in our society and in how we as individuals interact with that society. Also, drug problems and our attempts to solve them have in turn had major influences on us as individuals and on our perceptions of appropriate roles for government, education, and health care. Therefore, the topic of psychoactive drugs provides a window through which we can study our own current psychology, sociology, and politics.
Drugs and Drug Use Today Extent of Drug Use In trying to get an overall picture of drug use in today’s society, we quickly discover that it’s not easy to get accurate information. It’s not possible to measure with great accuracy the use of, let’s say, cocaine in the United States. We don’t really know how much is imported and sold, because most of it is illegal. We don’t really know how many cocaine users there are in the country, because we have no good way of counting them. For some things, such as prescription drugs, tobacco, and alcohol, we have a wealth of sales information and can make much better estimates of rates of use. Even there, however, our information might not be complete (home-brewed beer would not be counted, for example, and prescription drugs might be bought and then left unused in the medicine cabinet). Let us look at some of the kinds of information we do have. A large number of survey questionnaire studies have been conducted in junior highs, high schools, and colleges, partly because this is one of the easiest ways to get a lot of information with a minimum of fuss. Researchers have always been most interested in drug use by adolescents and young adults, because this age is when drug use usually begins and reaches its highest levels.
This type of research has a couple of drawbacks. The first is that we can use this technique only on the students who are in classrooms. We can’t get this information from high school dropouts. That causes a bias, because those who skip school or have dropped out are more likely to use drugs. A second limitation is that we must assume that most of the self-reports are done honestly. In most cases, we have no way of checking to see if Johnny really did smoke marijuana last week, as he claimed on the questionnaire. Nevertheless, if every effort is made to encourage honesty (including assurances of anonymity), we expect that this factor is minimized. To the extent that tendencies to overreport or underreport drug use are relatively constant from one year to the next, we can use such results to reflect trends in drug use over time and to compare relative reported use of various drugs.
Drugs in Depth Methamphetamine Use in Your Community Assume that you have just been appointed to a community-based committee that is looking into drug problems. A high school student on the committee has just returned from a residential treatment program and reports that methamphetamine use has become “very common” in local high schools. Some members of the committee want to call in some experts immediately to give schoolwide assemblies describing the dangers of methamphetamine. You have asked for a little time to check out the student’s story to find out what you can about the actual extent of use in the community and report back to the group in a month. Make a list of potential information sources and the type of information each might provide. How close do you think you could come to making an estimate of how many current methamphetamine users there are in your community? Do you think it would be above or below the national average?
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Chapter 1
Table 1.1 Percentage of College Students One to Four Years beyond High School Reporting Use of Seven Types of Drugs (2006)
Drug
Used in Used Daily Ever Past for Past Used 30 Days 30 Days
Alcohol
85
65
4.8
Cigarettes
NA
19
9.2
Marijuana/hashish
47
17
4.3
Inhalants
7
0.4
0.0
Amphetamines
11
2.5
0.4
Hallucinogens
11
0.9
0.0
8
1.8
0.1
2.3
0.0
0.0
Cocaine (all) Crack
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Source: Monitoring the Future Project, University of Michigan
Let’s look first at the drugs most commonly reported by young college students in a recent nationwide sample. Table 1.1 presents data from one of the best and most complete research programs of this type, the Monitoring the Future Project at the University of Michigan. Data are collected each year from more than 15,000 high school seniors in schools across the United States, so that nationwide trends can be assessed. Data are also gathered from 8th- and 10th-graders and from college students. Three numbers are presented for each drug: the percentage of college students (one to four years beyond high school) who have ever used the drug, the smaller percentage who report having used it within the past 30 days, and the still smaller percentage who report daily use for the past 30 days.1 Note that most of these college students have tried alcohol at some time in their lives. Half have tried marijuana, and most students report never having tried the rest of the drugs listed. Also note that
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daily use of any of these drugs other than cigarettes can be considered rare.
Trends in Drug Use The Monitoring the Future study, which has now been conducted annually for more than 30 years, allows us to see changes over time in the rates of drug use. Figure 1.1 displays data on marijuana use among 12th-graders. Look first at the line labeled “Use.” In 1975, just under 30 percent of high school seniors reported that they had used marijuana in the past 30 days (an indication of “current use”). This proportion rose each year until 1978, when 37 percent of 12th-graders reported current marijuana use. Over the next 13 years, from 1979 to 1992, marijuana use declined steadily so that by 1992 only 12 percent of 12th-graders reported current use (about one-third as many as in 1978). Then the trend reversed, with rates of current use climbing back to 24 percent of 12th-graders by 1997, followed by a slow decline over the past 10 years to just under 20 percent in 2007. Because marijuana is by far the most commonly used illicit drug, we can use this graph to make a broader statement: Illicit drug use among high school seniors has been slowly declining over the past 10 years. Currently, marijuana use is about half as common among 12th-graders as it was in 1978, but it is more common than it was at its lowest point 15 years ago. This is important because there always seem to be people trying to say that drug use is increasing among young people, or that people are starting to use drugs at younger and younger ages, but the best data we have provide no support for such statements (e.g., data from 8th-graders show the same trends as for 12th-graders). How can we explain these very large changes in rates of marijuana use over time? Maybe marijuana was easier to obtain in 1978, less available in 1992, etc.? Each year the same students were asked their opinion about how easy they thought it would be to get marijuana if they wanted to do so. Looking at the “Availability” line, and using the scale on the right-hand side of Figure 1.1,
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50 Availability
90
40
80 70
30 Use
60 50
20
40
Use
30
Risk and Availability
Risk
20
10
10 0
'76 '78 '80 '82 '84 '86 '88 '90 '92 '94 '96 '98 '00 '02 '04 '06 Use: % using once or more in past 30 days (on left-hand scale)
Risk: % saying great risk of harm in regular use (on right-hand scale)
0
Availability: % saying fairly easy or very easy to get (on right-hand scale)
Figure 1.1 Marijuana: Trends in Perceived Availability, Perceived Risk of Regular Use, and Prevalence of Use in the Past 30 Days for 12th-Graders SOURCE: L. D. Johnston, P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg, “Overall, Illicit Drug Use by American Teens Continues Gradual Decline in 2007.” Ann Arbor, MI: University of Michigan News Service [online], available at www.monitoringthefuture.org; accessed December 11, 2007.
we can see that back in 1975 about 90 percent of the seniors said that it would be fairly easy or very easy for them to get marijuana. The interesting thing is that this perception has not changed much, remaining close to 90 percent for over 30 years. Thus, the perceived availability does NOT appear to explain differences in rates of use over time. This is important because it implies that we can have large changes in rates of drug use even when the supply of the drug does not appear to change much. There is another line on Figure 1.1, labeled “Risk” (and also tied to the right-hand scale). In 1975, about 40 percent of 12th-graders rated the risk of harm from regular marijuana use as “great risk of harm.” The proportion of students reporting great risk declined over the same time that use was increasing (up to 1978). Then, as use dropped from 1979 to 1992, perceived risk increased. Perceived risk declined during the 1990s when use was again increasing, and in re-
cent years perceived risk is slowly rising while rates of use are slowly declining. You should be able to see from Figure 1.1 that as time goes by, the line describing changes in perception of risk from using marijuana is essentially a mirror image of the line describing changes in rates of using marijuana. This is important because it seems to say that the best way to achieve low rates of marijuana use is by convincing students that it is risky to use marijuana, whereas efforts to control the availability of marijuana (“supply reduction”) might have less of an influence. However, we must keep in mind that a cause and effect relationship has not been proven. Changes in both rates of use and perceptions of risk could be caused by something else that we are not directly measuring. In addition to the surveys of students, broad-based self-report information is also gathered through house-to-house surveys. With proper sampling techniques, these studies can
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11
40
Percentage Using in Past Month
35 30 25 20
Ages 18–25
15 10 Ages 12–17
5 0 1970
1975
1980
1985
1990 Year
1995
2000
2005
Figure 1.2 Marijuana Use among Persons Ages 12–25, by Age Group: 1971–2006 Source: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
estimate the drug use in most of the population, not just among students. This technique is much more time-consuming and expensive, it has a greater rate of refusal to participate, and we must suspect that individuals engaged in illegal drug use would be reluctant to reveal that
Marijuana is the most commonly used illicit drug, and major surveys including the Monitoring the Future Project and the National Survey on Drug Use and Health track trends in its usage.
fact to a stranger on their doorstep. The National Survey on Drug Use and Health is a face-to-face, computer-assisted interview done with more than 68,000 individuals in carefully sampled households across the United States. Figure 1.2 displays the trends in reported past month use of marijuana for two different age groups. This study shows the same pattern as the Monitoring the Future study of 12th-graders: Marijuana use apparently grew throughout the 1970s, reaching a peak in about 1980, and then declining until the early 1990s, when it increased again. Again, the past few years have seen a slight decline in rates of marijuana use in both age groups, similar to the declines seen in the Monitoring the Future studies. We have seen fairly dramatic trends over time in marijuana use, but what about other substances? Figure 1.3 shows rates of current use of alcohol and cocaine alongside marijuana use for Americans between 18 and 25 years of age. Many more people are current users of alcohol (about two-thirds of adults), and many
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80 Alcohol
Marijuana
Cocaine
70
Percentage Reporting Use
60
50
40
30
20
10
0 1974 1976 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 2006 Year
Figure 1.3 Trends in Reported Drug Use within the Past 30 Days for Young Adults Ages 18 to 25 SOURCE: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
fewer use cocaine in any given year. But overall, the trends over time are generally similar, with the peak year for all three substances around 1980, lower rates of use in the early 1990s, and less dramatic changes after that. Finding such a similar pattern in two different studies using different sampling techniques gives us additional confidence that these trends have been real and probably reflect broad changes in American society over this time. Political observers will be quick to note that Ronald Reagan was president during most of the 1980s, when use of marijuana and other drugs was declining, while Bill Clinton was in office during most of the 1990s, when these rates rose. Were these changes in drug use the result of more conservative drug-control policies under the Reagan administration and more lib-
eral policies under the Clinton administration? There are two reasons to think that is not the answer. First, the timing is not quite right. President Reagan was elected in 1980, took office in 1981, and didn’t begin focusing on the “Just Say No” antidrug messages until 1983. Most of the important legislation was passed in 1986. All of this was after the downward trend in drug use had already begun. It seems more likely that the Reagan administration recognized the opportunity provided by an underlying change in attitude among the general public. The government’s policies might have helped to amplify the effects of this underlying social change, but they did not create it. The same timing problem is associated with trying to link increased drug use to the Clinton presidency: The election was in 1992, and increased use was already begin-
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ning in 1993, during the first year of the Clinton administration. Also, the Clinton administration can hardly be accused of having liberal drug-control policies—drug-control budgets and arrests for drug violations were both higher than in any previous administration. If we can’t point to government policies as causes of these substantial changes in drug use, how can we explain them? The short answer is that for now, we can’t. We are left with saying that changes in rates of illicit drug use and in alcohol use probably reflect changes over time in a broad range of attitudes and behaviors among Americans—what we can refer to as “social trends.” This isn’t much of an explanation, and that is somewhat frustrating. After all, if we understood why these changes were taking place it might allow us to influence rates of substance use among the general population, or at least to predict what will happen next. Perhaps some of today’s college students will be the ones to develop this understanding over the next few years.
Correlates of Drug Use Once we know that a drug is used by some percentage of a group of people, the next logical step is to ask about the characteristics of those who use the drug, as compared with those who don’t. Often the same questionnaires that ask each person which drugs they have used also include several questions about the persons completing the questionnaires. The researchers might then send their computers “prospecting” through the data to see if certain personal characteristics can be correlated with drug use. But these studies rarely reveal much about either very unusual or very common types or amounts of drug use. For example, if we send a computer combing through the data from 1,000 questionnaires, looking for characteristics correlated with heroin use, only one or two people in that sample might report heroin use, and you can’t correlate much based on one or two people. Likewise, it would be difficult to identify the distinguishing characteris-
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tics of the people who have “ever tried” alcohol, because that group usually represents more than 90 percent of the sample. Much of the research on correlates of drug use has used marijuana smoking as an indicator, partly because marijuana use has been a matter of some concern and partly because enough people have tried it so that meaningful correlations can be done. Other studies focus on early drinking or early cigarette smoking.
Risk and Protective Factors Increasingly, researchers are analyzing the correlates of drug use in terms of risk factors and protective factors. Risk factors are correlated with higher rates of drug use, while protective factors are correlated with lower rates of drug use. A study based on data obtained from the National Survey on Drug Use and Health examined risk and protective factors regarding use of marijuana among adolescents (ages 12–17).2 This largescale study provides some of the best information we have about the correlates of marijuana use among American adolescents. The most significant factors are reported in Table 1.2. In some ways, the results confirm what most people probably assume: the kids who live in rough neighborhoods, whose parents don’t seem to care what they do, who have drugusing friends, who steal and get into fights, who aren’t involved in religious activities, and who don’t do well in school are the most likely to smoke marijuana. The same study analyzed cigarette smoking and alcohol use, with overall similar results. There are some surprising results, however. Those adolescents who reported that their parents frequently monitored their behavior (checking homework, limiting TV watching, and requiring chores, for example) were actually a little more likely to report using marijuana than adolescents who reported less parental correlate (core a let): a variable that is statistically related to some other variable, such as drug use.
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Table 1.2 Risk and Protective Factors Associated with Marijuana Use by Adolescents Risk Factors (in order of importance):
Protective Factors (in order of importance):
1. Having friends who use marijuana or other substances
1. Perceiving that there are strong sanctions against substance use at school
2. Engaging in frequent fighting, stealing, or other antisocial activities 3. Perceiving that substance use is prevalent at your school 4. Knowing adults who use marijuana or other substances 5. Having a positive attitude toward marijuana use
monitoring. This finding points out the main problem with a correlational study: We don’t know if excessive parental monitoring makes adolescents more likely to smoke marijuana, or if adolescents’ smoking marijuana and getting in fights makes their parents more likely to monitor them (the latter seems more likely). Another example of the limitation of correlational studies is the link between marijuana
Mind/Body Connection Religion and Drug Use More than three-fourths of American adolescents report that religion plays an important part in their lives. In study after study, those young people who report more involvement with religion (they attend services regularly and say their religion influences how they make decisions) are less likely to smoke cigarettes, drink alcohol, or use any type of illicit drug. Consider your own feelings about religion and about drug use. Why do you think this relationship between “religiosity” and lower rates of drug use is such a consistent finding? If you have friends from different religious backgrounds, discuss this relationship with them. Some religions have specific teachings against any alcohol use or tobacco use, but the general relationship seems to hold even for those religions that do not forbid these behaviors (at least for adults). What other factors related to religious involvement in general might serve as protective factors against the use of these substances?
2. Having parents as a source of social support 3. Being committed to school 4. Believing that religion is important and frequently attending religious services 5. Participating in two or more extracurricular activities
smoking and poor academic performance. Does smoking marijuana cause the user to get lower grades? Or is it the kids who are getting low grades anyway who are more likely to smoke marijuana? One indication comes from the analysis of risk and protective factors for cigarette smoking in this same study. The association between low academic performance and cigarette smoking was even stronger than the association between low academic performance and marijuana smoking. This leads most people to conclude that it’s the kids who are getting low grades anyway who are more likely to be cigarette smokers, and the same conclusion can probably be reached about marijuana smoking. The overall picture that emerges from studies of risk and protective factors is that the same adolescents who are likely to smoke cigarettes, drink heavily, and smoke marijuana are also likely to engage in other deviant behaviors, such as vandalism, stealing, fighting, and early sexual behavior—what some researchers refer to as problem behaviors. We all can think of individual exceptions to this rule, but correlational studies over many years all come to the same conclusion: If you want to find the greatest number of young people who use illicit drugs, look among the same people who are getting in trouble in other ways.
Race, Gender, and Level of Education Table 1.3 shows how some demographic variables are related to current use of some drugs of interest. The first thing to notice is
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Table 1.3 Drug Use among 18- to 25-year-olds: Percentage Reporting Use in the Past 30 Days
Drug
Male
African Female White American Hispanic
Native American Asian
High School College Graduate Graduate
Alcohol (Age 21+)
66
58
69
47
52
53
50
57
80
Tobacco (all types)
51
37
51
33
31
56
26
48
34
Marijuana
20
13
19
15
10
25
7
17
12
Cocaine
3
2
3
0.5
3
3
0.7
2
1
Source: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
something that has been a consistent finding over many kinds of studies for many years, and that is that males are more likely to drink alcohol, use tobacco, smoke marijuana, and use cocaine than are females. This probably doesn’t surprise most people too much, but it is good to see that in many cases the data do provide support for what most people would expect. Expectations regarding ethnic and racial influences on drug use are more likely to clash with the data from the National Survey on Drug Use and Health. For example, overall, whites are much more likely to drink alcohol, use tobacco, or use cocaine than are African Americans, and whites are slightly more likely to use marijuana as well. These results do not conform to many peoples’ stereotypes, so let’s remind ourselves that we are talking about household surveys that cut across socioeconomic and geographic lines and attempt to examine American society at large. Also, remember that we are getting data simply about recent use of these substances, which for most people means relatively low-level and infrequent use, at least for alcohol, marijuana, and cocaine. If we restricted ourselves to looking at the smaller group of people who can be classified as substance abusers, and if we compared urban neighborhoods with high minority populations to suburban white neighborhoods, we would find higher rates of drug abuse in the
urban “ghetto.” But within the general population, it appears that rates of use are lower among blacks than among whites. We do see from Table 1.3 that the group labeled “Native American” (American Indian and Alaskan Native groups) have somewhat higher rates of tobacco and marijuana use, and across Asian groups there is a generally lower rate of use of all these substances. Education level is powerfully related to two common behaviors: young adults with college degrees (compared to those who only completed high school) are much more likely to drink alcohol and much less likely to use tobacco. Those with more education are also somewhat less likely to use marijuana or cocaine.
Personality Variables The relationships between substance use and various indicators of individual differences in personality variables have been studied extensively over the years. In general, large-scale survey studies of substance use in the general population have yielded weak or inconsistent correlations with most traditional personality traits as measured by questionnaires. So, for example, it has been difficult to find a clear relationship between measures of self-esteem and rates of using marijuana. More recently, several studies have found that various ways of measuring a factor called “impulsivity” can be correlated with rates
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1. Drug Use: An Overview
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Section One Drug Use in Modern Society
of substance use in the general population.3 Impulsivity is turning out to be of much interest to drug researchers, but also hard to pin down in that different laboratories have different ways of measuring it. In general, it seems to relate to a person’s tendency to act quickly and without consideration of the longer-term consequences. We can expect to see more research on this concept over the next few years. Instead of looking at any level of substance use within the general population, we can look for personality differences between those who are dependent on substances and a “normal” group of people. When we do that, we find many personality differences associated with being more heavily involved in substance abuse or dependence. The association with impulsivity, for example, is much stronger in this type of study. Likewise, if we look at groups of people who are diagnosed with personality disorders, such as conduct disorder or antisocial personality disorder, we find high rates of substance use in these groups. Overall, it seems that personality factors may play a small role in whether someone decides to try alcohol or marijuana, but a larger role in whether that use develops into a serious problem. Because the main focus of this first chapter is on rates of drug use in the general population, we will put off further discussion of personality variables to the next chapter.
Genetics There is increasing interest in genetic influences on drug use. Again, studies looking across the general population and asking simply about recent use are less likely to produce significant results than studies that focus on people diagnosed with substance-use disorders. Genetic factors probably play a small role in whether someone tries alcohol or marijuana, but a larger role in whether that use develops into a serious problem. Studies of genetic variability in impulsivity and related traits are beginning to show clear association with substance-use disorders.4 Genetic factors in dependence are discussed further in Chapter 2.
Antecedents of Drug Use Finding characteristics that tend to be associated with drug use doesn’t help us understand causal relationships very well. For example, do adolescents first become involved with a deviant peer group and then use drugs, or do they first use drugs and then begin to hang around with others who do the same? Does drug use cause them to become poor students and to fight and steal? To answer such questions, we might interview the same individuals at different times and look for antecedents, characteristics that predict later initiation of drug use. One such study conducted in Finland found that future initiation of substance use or heavy alcohol use can be predicted by several of the same risk factors we have already discussed: aggressiveness, conduct problems, poor academic performance, “attachment to bad company,” and parent and community norms more supportive of drug use.5 Because these factors were measured before the increase in substance use, we are more likely to conclude that they may be causing substance use. But some other, unmeasured, variables might be causing both the antecedent risk factors and the subsequent substance use to emerge in these adolescents’ lives. A few scientists have been able to follow the same group of people at annual intervals for several years in what is known as a longitudinal study. One such study has tracked more than 1,200 participants from a predominantly African American community in Chicago from ages 6 through 32.6 Males who had shown a high “readiness to learn” in first grade were less likely to be cocaine users as adults, but females with poor academic performance in first grade had lower rates of cocaine use than females with higher first-grade scores. Males who were either “shy” or “aggressive” in first grade were more likely to be adult drug users compared to the students who had been considered neither shy nor aggressive 26 years earlier. It is much more difficult to obtain this type of data, and it is somewhat surprising that any variables measured at age six could reliably predict adult drug use.
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Males who are aggressive in early elementary school are more likely to be drug users as adults.
Gateway Substances One very important study from the 1970s pointed out a typical sequence of involvement with drugs.7 Most of the high school students in that group started their drug involvement with beer or wine. The second stage involved hard liquor, cigarettes, or both; the third stage was marijuana use; and only after going through those stages did they try other illicit substances. Not everyone followed the same pattern, but only 1 percent of the students began their substance use with marijuana or another illicit drug. It is as though they first had to go through the gateway of using alcohol and, in many cases, cigarettes. The students who had not used beer or wine at the beginning of the study were much less likely to be marijuana smokers at the end of the study than the students who had used these substances. The cigarette smokers were about twice as likely as the nonsmokers to move on to smoking marijuana. If the gateway theory can explain something about later drug use, then perhaps looking at
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those people who followed the traditional order of substance use (alcohol/cigarettes, followed by marijuana, followed by other illicit drugs) and comparing them to people who followed different orders of use might tell us something useful about the importance of particular orders of initiation. One recent study examined 375 homeless “street” youth, ages 13–21, in Seattle.8 They were asked at what age they first started using various substances, and then grouped into categories depending on whether they followed the traditional gateway order or some other order of initiation. The order of use did not predict current levels or types of drug use in this population, leading the study’s authors to conclude that knowing which substances people use first might not be very important in helping to prevent future escalation of drug use. One possible interpretation of the gateway phenomenon is that young people are exposed to alcohol and tobacco and that these substances somehow make the person more likely to go on to use other drugs. Because most people who use these gateway substances do not go on to become cocaine users, we should be cautious about jumping to that conclusion. More likely is that early alcohol use and cigarette smoking are common indicators of the general deviance-prone pattern of behavior that also includes an increased likelihood of smoking marijuana or trying cocaine. Because beer and cigarettes are more widely available to a deviance-prone young person than marijuana or cocaine, it is logical that beer and cigarettes would most often be tried first. The socially conforming students are less likely to try even these relatively available substances until they are older, and they are less likely ever to try the illicit substances. Let’s
antecedent (ant eh see dent): a variable that occurs before some event such as the initiation of drug use. longitudinal study (lon jeh too di nul): a study done over a period of time (months or years). gateway: one of the first drugs (e.g., alcohol or tobacco) used by a typical drug user.
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Section One Drug Use in Modern Society
Targeting Prevention Preventing What? Chapter 1 provides an overview of psychoactive drug use, primarily based on data from the United States. As we look forward to the topic of prevention, it’s appropriate to think about what aspects of psychoactive drug use we would most like to reduce. Following are some perspectives: • We should work to prevent any use of tobacco or alcohol by those under age 21, as well as any use of drugs such as marijuana, cocaine, and LSD. These drugs are all illegal, and we know that early use of tobacco and alcohol is associated with a greatly increased risk of illicit drug use in the future. • Focusing only on drug use ignores the fact that illicit drug use is usually part of a larger pattern of deviant or antisocial behavior. Therefore, our efforts would be more effective if we were to target younger people and work to prevent poor
ask the question another way: If we developed a prevention program that stopped all young people from smoking cigarettes, would that cut down on marijuana smoking? Most of us think it might, because people who don’t want to suck tobacco smoke into their lungs probably won’t want to inhale marijuana smoke either. Would such a program keep people from getting D averages or getting into other kinds of trouble? Probably not. In other words, we think of the use of gateway substances not as the cause of later illicit drug use but, instead, as an early indicator of the basic pattern of deviant behavior resulting from a variety of psychosocial risk factors.
Motives for Drug Use To most of us, it doesn’t seem necessary to find explanations for normative behavior; we don’t often ask why someone takes a pain reliever when she has a headache. Our task is to try to explain the drug-taking behavior that frightens and infuriates—the deviant drug use. We
academic performance, fighting, shoplifting, and other early indicators of this lifestyle, in addition to early experimentation with tobacco and alcohol. • Wait a minute! We’re confusing what might be desirable with what might be possible. We can’t prevent everyone from doing things we don’t like. For example, as adults most people will drink alcohol at least once in a while, yet perhaps only 10 percent of drinkers have most of the problems. Trying to prevent all drug use and other undesirable behavior is just too big a job, and it violates our sense of individual freedom. We need to focus our efforts on preventing abuse and the crime that goes with it. That’s a much smaller problem, and we have a better chance of success. With which of these perspectives do you most agree at this point? Are there other perspectives not represented by these three?
should keep one fact about human conduct in mind throughout this book: Despite good, logical evidence telling us we “should” avoid certain things, we all do some of them anyway. We know that we shouldn’t eat that second piece of pie or have that third drink on an empty stomach. Cool-headed logic tells us so. We would be hard pressed to find good, sensible reasons why we should smoke cigarettes, drive faster than the speed limit, go skydiving, sleep late when we have work to do, flirt with someone and risk an established relationship, or use cocaine. Whether one labels these behaviors sinful or just stupid, they don’t seem to be designed to maximize our health or longevity. But humans do not live by logic alone; we are social animals who like to impress each other, and we are pleasure-seeking animals. These factors help explain why people do some of the things they shouldn’t, including using drugs. The research on correlates and antecedents points to a variety of personal and social variables that influence our drug taking, and many psychological and sociological theorists have proposed
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People who use drugs and who identify with a deviant subculture are more likely to engage in a variety of behaviors not condoned by society.
models for explaining illegal or excessive drug use. We have seen evidence for one common reason that some people begin to take certain illegal drugs: usually young, and somewhat more often male than female, they have chosen to identify with a deviant subculture. These groups frequently engage in a variety of behaviors not condoned by the larger society. Within that group, the use of a particular drug might not be deviant at all but might, in fact, be expected. Occasionally the use of a particular drug becomes such a fad among a large number of youth groups that it seems to be a nationwide problem. However, within any given community there will still be people of the same age who don’t use the drug. Rebellious behavior, especially among young people, serves important functions not only for the developing individual but also for the evolving society. Adolescents often try very hard to impress other people and may find it especially difficult to impress their parents. An adolescent who is unable to gain respect from people or who is frustrated in efforts to “go his or her own way” might engage in a particularly dangerous or disgusting behavior as a way of demanding that people be impressed or at least pay attention. One source of excessive drug use may be found within the drugs themselves. Many of these drugs are capable of reinforcing the behavior that gets the drug into the system. Reinforce-
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ment means that, everything else being equal, each time you take the drug you increase slightly the probability that you will take it again. Thus, with many psychoactive drugs there is a constant tendency to increase the frequency or amount of use. Some drugs (such as intravenous heroin or cocaine) appear to be so reinforcing that this process occurs relatively rapidly in a large percentage of those who use them. For other drugs, such as alcohol, the process seems to be slower. In many people, social factors, other reinforcers, or other activities prevent an increase. For some, however, the drug-taking behavior does increase and consumes an increasing share of their lives. Most drug users are seeking an altered state of consciousness, a different perception of the world than is provided by normal, day-to-day activities. Many of the high school students in the nationwide surveys report that they take drugs “to see what it’s like,” or “to get high,” or “because of boredom.” In other words, they are looking for a change, for something new and different in their lives. This aspect of drug use was particularly clear during the 1960s and 1970s, when LSD and other perception-altering drugs were popular. We don’t always recognize the altered states produced by other substances, but they do exist. A man drinking alcohol might have just a bit more of a perception that he’s a tough guy, that he’s influential, that he’s well liked. A cocaine user might get the seductive feeling that everything is great and that she’s doing a great job (even if she isn’t). Many drug-abuse prevention programs have focused on efforts to show young people how to feel good about themselves and how to look for excitement in their lives without using drugs. Another thing seems clear: Although societal, community, and family factors (the outer areas of Figure 1.4) play an important role in determining whether an individual will first try a reinforcement: a procedure in which a behavioral event is followed by a consequent event such that the behavior is then more likely to be repeated. The behavior of taking a drug may be reinforced by the effect of the drug.
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1. Drug Use: An Overview
Section One Drug Use in Modern Society
Societal Laws and Penalties
Availability and Cost
Community and Family Family Political Statements
Peers Antidrug Commercials
Individual
Schools
Alcohol and Tobacco Ads
Personality Knowledge/Attitudes/Beliefs Personal Drug Experience Motives/Needs Biology
Clubs/ Organizations
Church
Statements by Authorities/ Celebrities
Gangs Local Police Portrayal in News Articles/Shows
Portrayal in Movies/Novels
Figure 1.4 Influences on Drug Use drug, with increasing use the individual’s own experiences with the drug become increasingly important. For those who become seriously dependent, the drug and its actions on that individual become central, and social influences, availability, cost, and penalties play a less important role in the continuation of drug use.
•
Deviant drug use includes those forms of drug use not considered either normal or acceptable by the society at large. Drug misuse is using a drug in a way that was not intended by its manufacturer. Drug abuse is drug use that causes problems. (If frequent and serious, then a diagnosis of substance-use disorder is applied.) Drug dependence involves using the substance more often or in greater amounts than the user intended, and having difficulty stopping or cutting down on its use.
•
Among American college students, about 65 percent can be considered current (within the past 30 days) users of alcohol, about 20 percent current smokers of tobacco cigarettes, less than 20 percent current marijuana users, and less than 2 percent current users of cocaine.
Summary •
•
In discussing a drug-use issue, you must consider who is using the drug, what drug is being used, when and where the drug use is occurring, why the person is using the drug, how the person is taking the drug, and how much drug is being used. No drug is either entirely good or bad, and every drug has multiple effects. The size and type of effect depends on the dose of the drug and the user’s history and expectations.
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•
•
•
•
Both alcohol and illicit drug use reached an apparent peak around 1980, then decreased until the early 1990s, with a slower increase after that. Current rates of use are lower than at the peak. Adolescents who use illicit drugs (mostly marijuana) are more likely to know adults who use drugs, less likely to believe that their parents would object to their drug use, less likely to see their parents as a source of social support, more likely to have friends who use drugs, less likely to be religious, and more likely to have academic problems. A typical progression of drug use starts with cigarettes and alcohol, then marijuana, then other drugs such as amphetamines, cocaine, or heroin. However, there is no evidence that using one of the “gateway” substances causes one to escalate to more deviant forms of drug use. People may use illicit or dangerous drugs for a variety of reasons: They may be part of a deviant subculture, they may be signaling their rebellion, they may find the effects of the drugs to be reinforcing, or they may be seeking an altered state of consciousness. The specific types of drugs and the ways they are used will be influenced by the user’s social and physical environment. If dependence develops, then these environmental factors may begin to have less influence.
Chapter 1
4. 5.
6. 7. 8.
Review Questions
2. 3.
Besides asking a person the question directly, what is one way a psychologist can try to determine why a person is taking a drug? What two characteristics of a drug’s effect might change when the dose is increased? In about what year did drug use in the United States peak?
Drug Use: An Overview
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About what percentage of college students use marijuana? What do the results of the National Survey on Drug Use and Health tell us about the overall rates of marijuana and cocaine use among whites compared to African Americans in the United States? How does having a college degree influence rates of drinking alcohol? Using tobacco? Name one risk factor and one protective factor related to the family/parents. How does impulsivity relate to rates of drug use in the general population? How does impulsivity relate to substance dependence?
References 1.
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Johnston, L. D., P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg. Monitoring the Future National Survey Results on Drug Use, 1975–2004. Volume II: College Students and Adults Ages 19–45 (NIH Publication No. 05-5728). Bethesda, MD: National Institute on Drug Abuse, 2005. Wright, D., and M. Pemberton. Risk and Protective Factors for Adolescent Drug Use: Findings from the 1999 National Household Survey on Drug Abuse (DHHS Publication No. SMA 04-3874, Analytic Series A-19). Rockville, MD: Substance Abuse and Mental Health Services Administration, Office of Applied Studies, 2004. Vangsness, L., B. H. Bry, and E. W. LaBouvie. “Impulsivity, Negative Expectancies, and Marijuana Use: A Test of the Acquired Preparedness Model.” Addictive Behaviors 30 (2005), pp. 1071–76. Kreek, M. J., D. A. Nielsen, E. R. Butelman, and K. S. LaForge. “Genetic Influences on Impulsivity, Risk Taking, Stress Responsivity and Vulnerability to Drug Abuse and Addiction.” Nature Neuroscience 8 (2005), pp. 1450–57. Poikolainen, Kari. “Antecedents of Substance Use in Adolescence.” Current Opinion in Psychiatry 15 (2002), pp. 241–45. Ensminger, M. E., H. S. Juon, and K. E. Fothergill. “Childhood and Adolescent Antecedents of Substance Use in Adulthood.” Addiction 97 (2002), pp. 833–44. Kandel, D., and R. Faust. “Sequence and Stages in Patterns of Adolescent Drug Use.” Archives of General Psychiatry 32 (1975), pp. 923–32. Ginzler, J. A., and others. “Sequential Progression of Substance Use among Homeless Youth: An Empirical Investigation of the Gateway Theory.” Substance Use & Misuse 38 (2003), pp. 725–58.
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Check Yourself
Name
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Date
Do Your Goals and Behaviors Match? One interesting thing about young people who get into trouble with drugs or other types of deviant behavior is that they often express fairly conventional long-term goals for themselves. In other words, they want or perhaps even expect to be successful in life, but then do things that interfere with that success. One way to look at this is that their long-term goals don’t match up with their short-term behavior. Everyone does this sort of thing to some extent—you want to get a good grade on the first exam, but then someone talks you into going out instead of studying for the next one. Or perhaps you hope to lose five pounds but just can’t pass up that extra slice of pizza. Make yourself a chart that lists your long-term goals down one side and has a space for short-term behaviors down the other side, like the one below.
Write in your goal under each category as best you can. Then think about some things you do occasionally that tend to interfere with your achieving that goal and put a minus sign next to each of those behaviors. After you have gone through all the goals, write down some short-term behaviors that you could practice to assist you in achieving each goal, and put a plus sign beside each of those behaviors. How does it stack up? Are there some important goals for which you have too many minuses and not enough plusses? If study skills and habits, relationship problems, or substance abuse appear to be serious roadblocks for your success, consider visiting a counselor or therapist to get help in overcoming them.
Goals (Long-Term)
Behaviors (Short-Term)
Educational
Physical health and fitness
Occupational
Spiritual
Personal relationships
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Drug Use as a Social Problem Objectives When you have finished this chapter, you should be able to: • Distinguish between the federal government’s regulatory approach before the early 1900s and now. • Distinguish between acute and chronic toxicity and between physiological and behavioral toxicity. • Describe the two types of data collected in the DAWN system and know the top four drug classes for emergency room visits and for mortality. • Understand why the risks of HIV/AIDS and hepatitis are higher among injection drug users.
As we look into the problems ex• Define tolerance, physical dependence, and behavioral perienced by society as a result of dependence. the use of psychoactive drugs, we need to consider two broad catego• Understand that the scientific perspective on substance ries. The first category is the probdependence has changed in recent years. lems directly related to actually • Differentiate between substance abuse and substance taking the drug, such as the risk dependence using diagnostic criteria. of developing dependence or of overdosing. Second, because the • Debate the various theories on the cause of dependence. use of certain drugs is considered • Describe four ways it has been proposed that drug use a deviant act, the continued use of might cause an increase in crime. those drugs by some individuals represents a different set of social problems, apart from the direct dangers of the drugs themselves. These problems include arrests, fines, jailing, and the expenses associated with efforts to prevent misuse and to Laissez-Faire treat abuse and dependence. We begin by examIn the 1800s, the U.S. government, like the ining the direct drug-related problems that first majority of countries around the world, had raised concerns about cocaine, opium, and other virtually no laws governing the sale or use of drugs. Problems related to law enforcement, premost drugs. The idea seemed to be that, if the vention, and treatment will be examined more seller wanted to sell it and the buyer wanted to thoroughly in Chapters 3, 17, and 18. 25
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Drug Use in Modern Society
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Toxicity
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The word toxic means “poisonous, deadly, or dangerous.” All the drugs we discuss in this text can be toxic if misused or abused. We will use the term to refer to those effects of drugs that interfere with normal functioning in such a way as to produce dangerous or potentially dangerous consequences. Seen in this way, for example, alcohol can be toxic in high doses because it suppresses respiration—this can be dangerous if breathing stops long enough to induce brain damage or death. But we can also consider alcohol to be toxic if it causes a person to be so disoriented that, for them, otherwise normal behaviors, such as driving a car or swimming, become dangerous. This is an example of something we refer to as behavioral toxicity. We make a somewhat arbitrary distinction, then, between behavioral toxicity and “physiological” toxicity—perhaps taking advantage of the widely assumed mind-body distinction, which is more convenient than real. The only reason for making this distinction is that it helps remind us of some important kinds of toxicity that are special to psychoactive drugs and that are sometimes overlooked. Why do we consider physiological toxicity to be a “social” problem? One view might be that if an individual chooses to take a risk and harms his or her own body, that’s the individual’s business. But impacts on hospital emergency rooms, increased health insurance rates, lost productivity, and other consequences of physiological toxicity mean that social systems also are affected when an individual’s health is put at risk, whether by drug use or failure to wear seat belts. Another distinction we make for the purpose of discussion is acute versus chronic. Most of the time when people use the word acute, they mean “sharp” or “intense.” In medicine an acute condition is one that comes on suddenly, as opposed to a chronic or long-lasting condition. When talking about drug effects, we can think of the acute effects as those that result
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buy it, let them do it—laissez-faire, in French. This term has been used to characterize the general nature of the U.S. government of that era. In the 21st century, hundreds of drugs are listed as federally controlled substances, the U.S. government spends more than $12 billion each year trying to control their sale and use, and 1.5 million arrests are made each year for violating controlled substance laws. What happened to cause the leaders of the “land of the free” to believe it was necessary to create especially restrictive regulations for some drugs? Three main concerns aroused public interest: (1) toxicity: some drug sellers were considered to be endangering the public health and victimizing individuals because they were selling dangerous, toxic chemicals, often without labeling them or putting appropriate warnings on them; (2) dependence: some sellers were seen as victimizing individuals and endangering their health by selling them habit-forming drugs, again often without appropriate labels or warnings; and (3) crime: the drug user came to be seen as a threat to public safety—the attitude became widespread that drug-crazed individuals would often commit horrible, violent crimes. In Chapter 3, we will look at the roots of these concerns and how our current legal structures grew from them. For now, let’s look at each issue and develop ground rules for the discussion of toxicity, dependence, and drug-induced criminality.
Categories of Toxicity
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Drugs in the Media Pharm Parties? As evidence from various sources points to an increasing problem with misuse of prescription medications, especially opioids such as Oxycontin and Vicodin, it should not be surprising that sometimes drug “experts” and news organizations will sensationalize the issue. In 2006, USA Today reported that drug counselors across the country were beginning to hear about “pharm” or “pharming” parties, at which young people bring whatever prescription pills they can acquire, put them all into a large bowl, and then just take pills at random from the bowl. The problem with the story was that no actual data on these practices were presented, leading Jack Shafer, a columnist for the online magazine Slate, to respond with an
from a single administration of a drug or are a direct result of the actual presence of the drug in the system at the time. For example, taking an overdose of heroin can lead to acute toxicity. By contrast, the chronic effects of a drug are those that result from long-term exposure and can be present whether or not the substance is actually in the system at a given point. For example, smoking cigarettes can eventually lead to various types of lung disorders. If you have emphysema from years of smoking, that condition is there when you wake up in the morning and when you go to bed at night, and whether your most recent cigarette was five minutes ago or five days ago doesn’t make much difference. Using these definitions, Table 2.1 (p. 28) can help give us an overall picture of the possible toxic consequences of a given type of drug. However, knowing what is possible is different from knowing what is likely. How can we get an idea of which drugs are most likely to produce adverse drug reactions?
Drug Abuse Warning Network In an effort to monitor the toxicity of drugs other than alcohol, the U.S. government set up the Drug Abuse Warning Network (DAWN). This
article, “Phar-fetched Pharm Parties: Real or a Media Invention?” After looking into the origins of these stories, Shafer became even more convinced that this was just a sensationalistic story with little or no basis in fact. It’s not to say that such a party has never happened anywhere—indeed, those of us who have been watching the drug scene for decades recall similar media stories in the early 1970s. But is this really something that has become as frequent as USA Today implied? One concern about such media reports is that they might encourage some young people to try this, because it is reported to be a craze that’s currently sweeping the nation. You can read Shafer’s article online at http://www.slate.com/id/2143982.
system collects data on drug-related emergency room visits from hospital emergency departments in major metropolitan areas around the country. When an individual goes to an emergency room with any sort of problem related to drug misuse or abuse, each drug involved (up to six) is recorded. For each drug or drug type, staff members can add up the number of visits associated with that particular drug. The visit could be for a wide variety of reasons, such as injury due to an accident, accidental overdose, a suicide attempt, or a distressing panic reaction that is not life-threatening to the patient. The emergency
laissez-faire (lay say fair): a hands-off approach to government. toxic: poisonous, dangerous. behavioral toxicity: toxicity resulting from behavioral effects of a drug. acute: referring to drugs, the short-term effects of a single dose. chronic: referring to drugs, the long-term effects from repeated use. DAWN: Drug Abuse Warning Network. System for collecting data on drug-related deaths or emergency room visits.
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Table 2.1 Examples of Four Types of DrugInduced Toxicity Acute (immediate) Behavioral
“Intoxication” from alcohol, marijuana, or other drugs that impair behavior and increase danger to the individual
Physiological
Overdose of heroin or alcohol causing the user to stop breathing
Chronic (long-term) Behavioral
Personality changes reported to occur in alcoholics and suspected by some to occur in marijuana users (a motivational syndrome)
Physiological
Heart disease, lung cancer, and other effects related to smoking; liver damage resulting from chronic alcohol exposure
room personnel who record these incidents do not need to determine that the drug actually caused the visit, only that some type of drug misuse or abuse was involved. This avoids many of the subjective judgments that would vary from place to place and from day to day, especially when (as is often the case) more than one drug is involved. If someone is in an automobile accident after drinking alcohol, smoking marijuana, and using some cocaine, rather than trying to say which one of these substances was responsible for the accident, each of them is counted as being involved in that emergency room visit. Because not every emergency room in the U.S. participates in the DAWN system, for many years the sampled data were used to estimate the overall number of emergency room visits for the entire country. Because of concerns about the accuracy of those estimates, more recent results are not used in that way. The numbers for emergency room visits for
2005 shown on the left side of Table 2.2 (p. 29) are the totals from the sampled hospitals.1 The DAWN system collects another set of data on drug-related deaths, with the reports being completed by medical examiners (coroners) in the same metropolitan areas around the U.S. The agency responsible for the DAWN data (the Office of Applied Studies from the Substance Abuse and Mental Health Services Administration) became so concerned about the accuracy of national estimates that they have stopped providing overall national totals and rankings by drug type. The numbers on the right side of Table 2.2 were derived by adding up the reported number of deaths in 2003 related to each drug type from each of the 32 major metropolitan areas.2 Alcohol is treated somewhat differently than other drugs in the sample. Whenever an emergency room visit or a death is related only to alcohol use by an adult, the DAWN system does not keep track of that. Alcohol-related problems are counted when alcohol and some other drug are involved (alcohol-in-combination); in the latest report alcohol alone is recorded if the individual is under 21 years of age. Notice that alcohol-in-combination is near the top ranking in both types of data, a place it has held for many years. In fact, if alcohol were counted alone its numbers would be large enough to make the other drugs seem much less important beside it. This seems to indicate that alcohol is a fairly
The Drug Abuse Warning Network (DAWN) uses data from hospital emergency rooms to monitor drug toxicity.
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Table 2.2 Toxicity Data from the Drug Abuse Warning Network (DAWN) DRUG-RELATED EMERGENCY ROOM VISITS (2005) Rank
DRUG-RELATED DEATHS (2003)
Drug
Number
Rank
1.
Cocaine
448,481
1.
Opioids (not heroin)
3,667
2.
Alcohol-in-combination
394,224
2.
Cocaine
3,142
3. 4.
Marijuana Prescription opioids
242,200 196,225
3. 4.
Alcohol-in-combination Benzodiazepeines
2,482 1,611
5. 6. 7.
Benzodiazepines Heroin Methamphetamine
172,388 164,572 108,905
5. 6. 7.
1,566 1,171 882
8. 9.
Antidepressants Acetaminophen
61,023 39,494
Antidepressants Methadone Sedative-Hypnotics (non-benzodiazepeine)
8.
Heroin
792
Antipsychotics
37,327
9.
Stimulants (includes methamphetamine) Marijuana
584
10.
10.
Drug
Number
304
Source: Drug Abuse Warning Network, 2005: National Estimates of Drug-Related Emergency Department Visits. DAWN Series D-29, DHHS Publication No. (SMA) 07-4256. Rockville, MD, March 2007; and Drug Abuse Warning Network, 2003: Area Profiles of Drug-Related Mortality. DAWN Series D-27, DHHS Publication No. (SMA) 05-4023. Rockville, MD, 2005.
toxic substance. It can be, but let us also remember that about half of all adult Americans drink alcohol at least once a month, whereas only a small percentage of the adult population uses cocaine, a drug that is also at the top of both lists. The DAWN system does not correct for differences in rates of use, but rather gives us an idea of the relative impact of a substance on medical emergencies and drug-related deaths. Cocaine has vied with alcohol-in-combination for the top spot on these lists since the mid-1980s. Legal drugs are found on both lists, with prescription opioids now at the top of the mortality data. Including the widely prescribed hydrocodone (Vicodin) and oxycodone (Oxycontin), these drugs are increasingly marketed through Internet pharmacies that might be contributing to the increased number of toxic reactions. Other groups of prescription drugs, such as benzodiazepine sedatives (e.g., Xanax) and sleeping pills (e.g., Halcion) and the antidepressants, are relatively
important, especially in the category of drugrelated deaths. The importance of drug combinations, particularly combinations with alcohol, in contributing to these numbers cannot be overstressed. Typically about half of the emergency room visits involve more than one substance, and about three-fourths of the drug-related deaths include multiple drugs. By far the most common “other” drug is alcohol. The most dramatic case is for the benzodiazepines. In 2003, only 16 of the 1,611 benzodiazepine-related deaths were reported as single-drug deaths, implying that the real danger lies in combining sedatives or sleeping pills with alcohol.
How Dangerous Is the Drug? Now that we have some idea of the drugs contributing to the largest numbers of toxic reactions in these two sets of data, let’s see if we can
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use that information to ask some questions about the relative danger to a person taking one drug versus another. We mentioned that the DAWN data do not correct for frequency of use. However, in Chapter 1 we reviewed other sets of data that provide information on the relative rates of use of different drugs, such as the National Survey on Drug Use and Health discussed on pages 10–15. The populations and sampling methods are different, so we’re not going to be able to make fine distinctions with any degree of accuracy. But we know, for example, that roughly eight times as many people report current use of marijuana as report current use of cocaine. The 2003 DAWN mortality report shows roughly six times as many cocaine-related deaths as marijuana-related deaths. If one-eighth as many users experience six times as many deaths, can we say that the risk of death to an individual cocaine user is 48 times the risk of death to an individual marijuana user? That’s too precise an answer, but is seems pretty clear that cocaine is relatively much more toxic than marijuana. We should point out an important difference in the latest DAWN report for 2003 regarding heroin. In past DAWN reports, if a blood sample was positive for morphine, this was recorded under the heroin/morphine category, because it is not possible to distinguish heroin from morphine with the standard toxicology screens. However, morphine is also fairly widely used as a legal prescription pain reliever, so previous reports probably overestimated the number of toxic reactions to heroin itself. In the 2003 data, for the first time heroin is counted separately only if there is specific information that the person actually used heroin. Since that information is not always available, especially after someone has died, the new reports probably underestimate the total number of toxic reactions to heroin. As a result, heroin appears to have dropped from third place in drug-related deaths to eighth place. This change is likely due to changes in the way the records are kept rather than to changes in heroin itself or in its use. We cannot tell precisely from the DAWN data how many total deaths are related to the use of cocaine or heroin, because not all coroners are
included in the system. Data are gathered from metropolitan areas that include about a third of the U.S. population, but they are areas that have higher than average use of illicit drugs. A very rough estimate of the total annual number of deaths related to cocaine, for example, might be three times the reported DAWN figure, or about 9,000 per year. The total for all illicit drugs, including cocaine, heroin, marijuana, and methamphetamine, might be approximately 15,000. Using the same proportions, estimated annual deaths associated with the use of the prescription narcotic analgesics, antidepressants, benzodiazepines, and over-the-counter pain relievers would be roughly 20,000. For comparison, alcohol is estimated to be responsible for 100,000 deaths annually (see Chapter 9), and more than 400,000 annual deaths are attributed to cigarette smoking (see Chapter 10). Of course, many more people use those substances, and in terms of relative danger of toxicity, heroin and cocaine are undoubtedly more dangerous than prescription drugs, alcohol, or cigarettes. However, in looking at the total impact of these drug-related deaths on American society, you might conclude that politicians and the news media have been paying a disproportionate amount of attention to cocaine, heroin, and methamphetamine.
Blood-Borne Diseases One specific toxicity concern for users who inject drugs is the potential for spreading
Needles are collected through an exchange program in an effort to prevent the spread of HIV among needle-using drug users.
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Mind/Body Connection Fear and Decision Making Fear is a useful emotion. Being afraid of something that threatens you helps you to avoid the real dangers that do exist in our world. But, of course, fear also can be irrational, far out of proportion to any real threat. When that happens, as individuals we might be hampered by being unable to use elevators or ride in airliners, or fear of contamination might seriously interfere with our social lives. Fear is also a favorite tool of many politicians. If they can convince us that there is a real threat of some kind and they offer to protect us from it, we are likely to elect them and to give them the power or funding they seek to provide that protection. Again, this is a rational and perfectly appropriate governmental response to the extent that the threat is both real and likely to harm us, but sometimes it is difficult to get it right. Maybe the U.S. government has underestimated the threat of global climate change. Maybe because of the horrible televised images of the World Trade Center attack we overestimate the threat of Al Quaeda. Raising fears about specific types of drugs has been a staple of politics and government in the U.S. for more than 100
blood-borne diseases, such as HIV, AIDS, and the life-threatening liver infections hepatitis B and hepatitis C. These viral diseases can all be transmitted through the sharing of needles. In a recent study of injecting drug users in six U.S. cities, rates of HIV infection ranged from a low of 3 percent to a high of almost 30 percent, representing a serious public health hazard. Rates of hepatitis B infection among injecting drug users were higher, ranging from 50 percent to 80 percent, and rates were even higher for hepatitis C (66 percent to 93 percent). Since rates increased with age, the authors stressed the need for prevention programs targeting younger people who have recently begun injecting drugs.3 This type of drug-associated toxicity is not due to the action of the drug itself, but is incidental to the sharing of needles, no matter which drug is injected or whether the injection is intravenous or intramuscular. An individual drug user may inject 1,000 times a year, and
years, from the age of Demon Rum through heroin, marijuana, LSD, PCP, cocaine, MDMA (Ecstasy), and methamphetamine. How do we get it right? On an individual level, most of us are sufficiently afraid of the possible consequences of using illicit drugs that we avoid using them at all. If those fears are overblown, so what? As long as we avoid using dangerous drugs we can see those fears as being useful. But a politician can easily amplify fears about a drug and use that fear to help get elected, and to pass laws that go too far, compared to the actual magnitude of the threat. Think about frightening things you have heard about specific drugs. For example, there has been a lot of talk about “meth” labs exploding and about the toxic effects of exposure to the harsh chemicals used in making methamphetamine. How can you evaluate such stories other than to go look up statistics on the actual occurrences of such events? Remember to use your common sense. If a story seems to be outrageous, there’s a pretty good chance that someone is overstating the actual risk.
that represents a lot of needles. In several states and cities, drug paraphernalia laws make it illegal to obtain syringes or needles without a prescription, and the resulting shortage of new, clean syringes increases the likelihood that drug users will share needles. One response to this has been the development of syringe exchange programs, in which new, clean syringes are traded for used syringes. Although the U.S. Congress has prohibited the use of federal funds to support these programs, based on the theory that they provide moral encouragement for illegal drug use, exchange programs have been funded by state and local governments, and many other countries support such programs. Evidence shows that given the opportunity, drug
HIV: human immunodeficiency virus. AIDS: acquired immunodeficiency syndrome.
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Targeting Prevention Clean Needles? The spread of the human immunodeficiency virus (HIV) among drug users is associated primarily with the sharing of the needles used for injecting heroin and other drugs. Evidence from several studies indicates that HIV transmission can be reduced if clean syringes and needles are made readily available to injecting drug users. Do you know whether a user of illicit drugs in your community can get access to clean syringes and needles? You might start learning about this by asking a local pharmacist to see what the rules are for purchasing these items, as well as how expensive they are. It will also be interesting to see how the pharmacist reacts to your questions about this topic. How do you react to the idea of possibly being
injectors increase their use of clean syringes, rates of infection are lowered, and the programs more than pay for themselves in the long run.4 Despite political opposition, syringe exchange currently represents one of the most practical ways to prevent the spread of these blood-borne diseases among drug users and from them to the non-drug-using population.
Substance Dependence: What Is It? All our lives we have heard people talk about “alcoholics” and “addicts,” and we’re sure we know what we’re talking about when one of these terms is used. Years ago when people first became concerned about some people being frequent, heavy users of cocaine or morphine, the term habituation was often used. If we try to develop scientific definitions, terms such as alcoholic or addict are actually hard to pin down. For example, not everyone who is considered an alcoholic drinks every day—some drink in binges, with brief periods of sobriety in between. Not everyone who drinks every day is considered an alcoholic—a glass of wine with
looked at as a user of illegal drugs? You might take this book along to show that you do have an academic reason for asking! Once you find out what the situation is with direct purchasing, see if you can discover if there is a needle exchange program in your community. This will be a little harder, but you can start by looking up “public health” in the phone book and calling that office. Are there steps your community could take to make clean needles more readily available to users of illicit drugs? Do you believe that such programs encourage or condone drug use? Would the program help prevent the spread of HIV in your community? Visit the Online Learning Center for links to more information on needle exchange programs.
dinner every night doesn’t match most people’s idea of alcoholism. The most extreme examples are easy to spot: the homeless man dressed in rags, drinking from a bottle of cheap wine, or the heroin user who needs a fix three or four times a day to avoid withdrawal symptoms. No hard-and-fast rule for quantity or frequency of use can help us draw a clear line between what we want to think of as a “normal drinker” or a “recreational user” and someone who has developed a dependence on the substance, who is compelled to use it, or who has lost control over use of the substance. It would be nice if we could separate substance use into two distinct categories: In one case, the individual controls the use of the substance; in the other case, the substance seems to take control of the individual. However, the real world of substance use, misuse, abuse, and dependence does not come wrapped in such convenient packages.
Three Basic Processes The extreme examples mentioned above, of the homeless wine drinker or the frequent heroin user, typically exhibit three characteristics of their substance use that distinguish
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them from first-time or occasional users. These appear to represent three processes that may occur with repeated drug use, and each of these processes can be defined and studied by researchers interested in understanding drug dependence. Tolerance Tolerance refers to a phenomenon seen with many drugs, in which repeated exposure to the same dose of the drug results in a lesser effect. There are many ways this diminished effect can occur, and some examples are given in Chapter 5. For now, it is enough for us to think of the body as developing ways to compensate for the chemical imbalance caused by introducing a drug into the system. As the individual experiences less and less of the desired effect, often the tolerance can be overcome by increasing the dose of the drug. Some regular drug users might eventually build up to taking much more of the drug than it would take to kill a nontolerant individual. Physical Dependence Physical dependence is defined by the occurrence of a withdrawal syndrome. Suppose a person has begun to take a drug and a tolerance has developed. The person increases the amount of drug and continues to take these higher doses so regularly that the body is continuously exposed to the drug for days or weeks. With some drugs, when the person stops taking the drug abruptly, a set of symptoms begins to appear as the drug level in the system drops. For example, as the level of heroin drops in a regular user, that person’s nose might run and he or she might begin to experience chills and fever, diarrhea, and other symptoms. When we have a drug that produces a consistent set of these symptoms in different individuals, we refer to the collection of symptoms as a withdrawal syndrome. These withdrawal syndromes vary from one class of drugs to another. Our model for why withdrawal symptoms appear is that the drug initially disrupts the body’s normal physiological balances. These imbalances are detected by the nervous system, and over a period of re-
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peated drug use the body’s normal regulatory mechanisms compensate for the presence of the drug. When the drug is suddenly removed, these compensating mechanisms produce an imbalance. Tolerance typically precedes physical dependence. To continue with the heroin example, when it is first used it slows intestinal movement and produces constipation. After several days of constant heroin use, other mechanisms in the body counteract this effect and get the intestines moving again (tolerance). If the heroin use is suddenly stopped, the compensating mechanisms produce too much intestinal motility. Diarrhea is one of the most reliable and dramatic heroin withdrawal symptoms. Because of the presumed involvement of these compensating mechanisms, the presence of a withdrawal syndrome is said to reflect physical (or physiological) dependence on the drug. In other words, the individual has come to depend on the presence of some amount of that drug to function normally; removing the drug leads to an imbalance, which is slowly corrected over a few days. Psychological Dependence Psychological dependence (also called behavioral dependence) can be defined in terms of observable behavior. It is indicated by the frequency of using a drug or by the amount of time or effort an individual spends in drug-seeking behavior. Often it is accompanied by reports of craving the drug or its effects. A major contribution of behavioral psychology has been to point out the scientific
tolerance: reduced effect of a drug after repeated use. withdrawal syndrome: a consistent set of symptoms that appears after discontinuing use of a drug. physical dependence: drug dependence defined by the presence of a withdrawal syndrome, implying that the body has become adapted to the drug’s presence. psychological dependence: behavioral dependence; indicated by high rate of drug use, craving for the drug, and a tendency to relapse after stopping use.
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weak-willed, lazy, or immoral (the “moral model”). Then medical and scientific studies began of users of alcohol and opioids. It seemed as if something more powerful than mere selfindulgence was at work, and the predominant view began to be that dependence is a druginduced illness.
Frequent drug use, craving for the drug, and a high rate of relapse after quitting indicate psychological dependence.
value of the concept of reinforcement for understanding psychological dependence. The term reinforcement is used in psychology to describe a process: A behavioral act is followed by a consequence, resulting in an increased tendency to repeat that behavioral act. The consequence may be described as pleasurable or as a “reward” in some cases (e.g., providing a tasty piece of food to someone who has not eaten for a while). In other cases, the consequence may be described in terms of escape from pain or discomfort. The behavior itself is said to be strengthened, or reinforced, by its consequences. The administration of certain drugs can reinforce the behaviors that led to the drug’s administration. Laboratory rats and monkeys have been trained to press levers when the only consequence of lever pressing is a small intravenous injection of heroin, cocaine, or another drug. Because some drugs but not others are capable of serving this function, it is possible to refer to some drugs as having “reinforcing properties” and to note that there is a general correlation between those drugs and the ones to which people often develop psychological dependence.
Changing Views of Dependence Until the 20th century, the most common view was probably that dependent individuals were
Early Medical Models If heroin dependence is induced by heroin, or alcohol dependence by alcohol, then why do some users develop dependence and others not? An early guess was simply that some people, for whatever reasons, were exposed to large amounts of the substance for a long time. This could happen through medical treatment or self-indulgence. The most obvious changes resulting from long exposure to large doses are the withdrawal symptoms that occur when the drug is stopped. Both alcohol and the opioids can produce rather dramatic withdrawal syndromes. Thus, the problem came to be associated with the presence of physical dependence (a withdrawal syndrome), and enlightened medically oriented researchers went looking for treatments based on reducing or eliminating withdrawal symptoms. According to the most narrow interpretation of this model, the dependence itself was cured when the person had successfully completed withdrawal and the symptoms disappeared. Pharmacologists and medical authorities continued into the 1970s to define “addiction” as occurring only when physical dependence was seen. Based on this view, public policy decisions, medical treatment, and individual drug-use decisions could be influenced by the question “Is this an addicting drug?” If some drugs produce dependence but others do not, then legal restrictions on specific drugs, care in the medical use of those drugs, and education in avoiding the recreational use of those drugs are appropriate. The determination of whether a drug is or is not “addicting” was therefore crucial. In the 1960s, some drugs, particularly marijuana and amphetamines, were not considered to have well-defined, dramatic, physical withdrawal syndromes. The growing group of interested scientists began to refer to drugs
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such as marijuana, amphetamines, and cocaine as “merely” producing psychological dependence, whereas heroin produced a “true addiction,” which includes physical dependence. The idea seemed to be that psychological dependence was “all in the head,” whereas with physical dependence actual bodily processes were involved, subject to physiological and biochemical analysis and possibly to improved medical treatments. This was the view held by most drug-abuse experts in the 1960s.
the basis of what had been called psychological dependence. Drugs such as amphetamines and cocaine could easily be used as reinforcers in these experiments, and they were known to produce strong psychological dependence in humans. Animal experiments using drug selfadministration are now of central importance in determining which drugs are likely to be used repeatedly by people, as well as in exploring the basic behavioral and biological features associated with drug dependence.5
Positive Reinforcement Model In the 1960s, a remarkable series of experiments began to appear in the scientific literature—experiments in which laboratory monkeys and rats were given intravenous catheters connected to motorized syringes and controlling equipment so that pressing a lever would produce a single brief injection of morphine, an opioid very similar to heroin. In the initial experiments, monkeys were exposed for several days to large doses of morphine, allowed to experience the initial stages of withdrawal, and then connected to the apparatus to see if they would learn to press the lever, thereby avoiding the withdrawal symptoms. These experiments were based on the predominant view of drug use as being driven by physical dependence. The monkeys did learn to press the levers. As these scientists began to publish their results and as more experiments like this were done, interesting facts became apparent. First, monkeys would begin pressing and maintain pressing without first being made physically dependent. Second, monkeys who had given themselves only fairly small doses and who had never experienced withdrawal symptoms could be trained to work very hard for their morphine. A history of physical dependence and withdrawal didn’t seem to have much influence on response rates in the long run. Clearly, the small drug injections themselves were working as positive reinforcers of the lever-pressing behavior, just as food can be a positive reinforcer to a hungry rat or monkey. Thus, the idea spread that drugs can act as reinforcers of behavior and that this might be
Which Is More Important, Physical Dependence or Psychological Dependence? The animal research that led to the positive reinforcement model implies that psychological dependence is more important than physical dependence in explaining repeated drug use, and this has led people to examine the lives of heroin users from a different perspective. Stories were told of users who occasionally stopped taking heroin, voluntarily going through withdrawal so as to reduce their tolerance level and get back to the lower doses of drug they could more easily afford. When we examine the total daily heroin intake of many users, we see that they do not need a large amount and that the agonies of withdrawal they experience are no worse than a case of intestinal flu. We have known for a long time that heroin users who have already gone through withdrawal in treatment programs or in jail have a high probability of returning to active heroin use. In other words, if all we had to worry about was users’ avoiding withdrawal symptoms, the problem would be much smaller than it actually is.
reinforcement: a procedure in which a behavioral event is followed by a consequent event such that the behavior is then more likely to be repeated. The behavior of taking a drug may be reinforced by the effect-of the drug. catheters (cath a ters): plastic or other tubing implanted into the body.
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DSM-IV-TR Psychiatric Diagnosis of Substance-Use Disorders Diagnostic Criteria for Substance Dependence A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of the substance to achieve intoxication or desired effect b. Markedly diminished effect with continued use of the same amount of the substance 2. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the substance b. The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms 3. The substance is often taken in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful efforts to cut down or control substance use. 5. A great deal of time is spent in activities necessary to obtain the substance. 6. Important social, occupational, or recreational activities are given up or reduced because of substance use. 7. The substance use is continued despite knowledge of having a persistent or recurrent physical or
Psychological dependence, based on reinforcement, is increasingly accepted as the real driving force behind repeated drug use, and tolerance and physical dependence are now seen as related phenomena that sometimes occur but probably are not critical to the development of frequent patterns of drug-using behavior. Researchers and treatment providers rely heavily on the definitions of substance dependence and substance abuse developed by the American Psychiatric Association and presented in their Diagnostic and Statistical Manual (DSM-IV-TR).6 These are presented in
psychological problem that is likely to have been caused or exacerbated by the substance. • With physiological dependence: evidence of tolerance or withdrawal (i.e., either Item 1 or 2 is present) • Without physiological dependence: no evidence of tolerance or withdrawal (i.e., neither Item 1 nor 2 is present) Diagnostic Criteria for Substance Abuse A. A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: 1. Recurrent substance use resulting in failure to fulfill major role obligations at work, school, or home 2. Recurrent substance use in situations in which it is physically hazardous 3. Recurrent substance-related legal problems 4. Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance B. The symptoms have never met the criteria for substance dependence for this class of substance.
outline form above. Notice that both substance dependence and substance abuse are complex behavioral definitions, and the exact set of behaviors seen may vary from person to person. Also, please note that three of the seven criteria must be met for substance dependence, and that five of the seven describe behaviors, such as taking more of the substance than was intended or giving up other important activities because of substance use. This again points out that these substance-use disorders are primarily seen as behavioral in nature, with tolerance and physical dependence being less important.
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Broad Views of Substance Dependence If we define drug dependence not in terms of withdrawal but in more behavioral or psychological terms, as an overwhelming involvement with getting and using the drug, then might this model also be used to describe other kinds of behavior? What about a man who visits prostitutes several times a day; someone who eats large amounts of food throughout the day; or someone who places bets on every football and basketball game, every horse race or automobile race, and who spends hours each day planning these bets and finding money to bet again? Shouldn’t these also be considered examples of dependence? Do the experiences of overeating, gambling, sex, and drugs have something in common—a common change in physiology or brain chemistry or a common personality trait that leads to any or many of these compulsive behaviors? Are all of these filling an unmet social or spiritual need? More and more, researchers are looking for these common threads and discussing “dependencies” as a varied set of behavioral manifestations of a common dependence process or disorder.
Is Dependence Caused by the Substance? Especially with chemical dependence, many people speak as though the substance itself is the cause of the dependence. Certainly some drugs are more likely than others to result in dependence. For example, it is widely believed that heroin and crack cocaine are both extremely likely to lead to compulsive use. In contrast, most users of marijuana report occasional use and little difficulty in deciding when to use it and when not to. We also know that some methods of taking a drug (e.g., intravenous injection) are more likely to result in repeated use than other methods of taking the same drug (by mouth, for instance). We can determine which drugs, or which methods of using those drugs, pose the greatest risk for dependence. One major study reviewed 350 published articles to come up with relative ratings, then had the prelimi-
Alcohol causes serious dependence in perhaps 1 of 10 drinkers.
nary tables reviewed by a panel of psychopharmacologists for suggested changes.7 Based on that report, we can classify psychoactive drugs into seven categories of “dependence potential.” Smoked or injected methamphetamine would probably be in one of the top two categories in such a ranking (see Table 2.3). The range of risk of dependence depends to some extent upon the drug itself, but also depends upon its method of use (as well as a variety of other biological, psychological, and social factors). Thus, the substance itself cannot be seen as the entire cause of the problem, even though some people would like to put all the blame on “demon rum” or on heroin or crack cocaine. When we extend the concept of dependence to other activities, such as gambling, sex, or overeating, it seems harder to place the entire blame on the activity, again because many people do not exhibit compulsive patterns of such behaviors. Some activities might be more of a problem than others—few people become dependent on filling out income tax forms, whereas a higher proportion of all those who gamble become overwhelmingly involved. Still, it is wrong to conclude that any activity is by its nature always “habit forming.” When a chemical is seen as causing the dependence, there is a tendency to give that substance a personality and to ascribe motives to it. When we listen either to a practicing user’s loving description of his interaction with the drug
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Table 2.3 Dependence Potential of Psychoactive Drugs Very high:
Heroin (IV) Crack cocaine
High:
Morphine (injected) Opium (smoked)
Moderate/high:
Cocaine powder (snorted) Tobacco cigarettes PCP (smoked)
Moderate:
Diazepam (Valium) Alcohol Amphetamines (oral)
Moderate/low:
Caffeine MDMA* (Ecstasy) Marijuana
Low:
Ketamine (see Chapter 14)
Very low:
LSD† Mescaline Psilocybin
*MDMA, methylenedioxy methamphetamine †
LSD, lysergic acid diethylamide
or to a recovering alcoholic describe her struggle against the bottle’s attempts to destroy her, the substance seems to take on almost human characteristics. We all realize that is going too far, yet the analogy is so powerful that it pervades our thinking. Alcoholics Anonymous (AA) members often describe alcohol as being “cunning, baffling, and powerful” and admit that they are powerless against such a foe. And those seeking the prohibition of alcohol, cocaine, marijuana, heroin, and other drugs have over the years tended to demonize those substances, making them into powerful forces of evil. The concept of a “war on drugs” reflects in part such a perspective—that some drugs are evil and war must be waged against the substances themselves.
Is Dependence Biological? In recent years, interest has increased in the possibility that all compulsive behaviors might
have some common physiological or biochemical action in the brain. For example, many theorists have recently focused on dopamine, one of the brain’s important neurotransmitters, which some believe to play a large role in positive reinforcement. The idea is that any drug use or other activity that has pleasurable or rewarding properties spurs dopamine activity in a particular part of the brain. This idea is discussed more fully in Chapter 4. Although this theory has been widely tested in animal models and much evidence is consistent with it, considerable evidence also shows that this model is too simple and that other neurotransmitters and other brain regions are also important. A great deal of attention has been given to reports from various brain-scanning experiments done on drug users. For example, cues that stimulate craving for cocaine activate many areas that are widely separated in the brain, including some that are known to be dopamine-rich areas and some that are not.8 Although these studies show some of the physiological consequences produced by cocaine or by even thinking about cocaine, they have not yet been useful in examining the possible biological causes of dependence. One important question that remains is whether the brains of people who have used cocaine intermittently show different responses, compared with the brains of dependent cocaine users. Ultimately, the strongest demonstration of the power of such techniques would be if it were possible to know, based on looking at a brain scan, whether a person had developed dependence. Many previous biological theories of dependence have failed this test: so far, no genetic, physiological or biochemical marker has been found that strongly predicts drug dependence.
Is There an “Addictive Personality”? Perhaps the explanation for why some people become dependent but others do not lies in the personality—that complex set of attributes and attitudes that develops over time, partly as a result of particular experiences. Is there a common
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personality factor that is seen in compulsive drug users but not in others? We’ve known for some time that people who are diagnosed with certain types of personality disorders, such as antisocial personality or conduct disorder, are more likely to also have one of the substanceuse disorder diagnoses (substance abuse or substance dependence). We’ve also known that people who have a long history of alcohol dependence or heroin dependence will demonstrate a variety of differences from the normal population on personality tests. But neither of these findings tells us anything about what caused these relationships. Conduct disorder and antisocial personality disorder reflect a general tendency for a person to violate social norms. Perhaps drug use is just one of many ways this person might choose to break the rules? And someone who has been drinking heavily for many years, has had health problems, perhaps lost a job and family, might well have developed personality differences due to the consequences of years of substance abuse. So we have not had much good information until fairly recently about personality differences that might predispose individuals to develop a substance-use disorder. One personality trait that has frequently been associated with greater risk for abuse of stimulants such as amphetamine or cocaine is called “sensation-seeking.” The sensation-seeking scale, which is discussed further in Chapter 6 and is printed on page 151, measures the person’s preference for variety, risk, and various physical sensations. People who score higher on this scale tend to report a greater “high” and a greater “liking” for the drug when given amphetamine in a laboratory setting.9. Another, possibly related, personality factor is often referred to as impulsivity—the tendency to act quickly without as much regard to long-term consequences. The relationships between impulsivity and drug use are complex, and researchers are becoming more sophisticated in trying to understand the relationships among impulsivity, specific types of drug use, and the setting in which the drug is used. In
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other words, being impulsive might have more to do with whether a person drinks heavily when away from home on a weekend night than it does with whether a person has a glass of wine with dinner.10
Is Dependence a Family Disorder? Although few scientific studies have been done, examination of the lives of alcohol-dependent individuals reveals some typical patterns of family adaptation to the problem. A common example in a home with an alcohol-dependent father is that the mother enables this behavior, by calling her husband’s boss to say he is ill or by making excuses to family and friends for failures to appear at dinners or parties and generally by caring for her incapacitated husband. The children might also compensate in various ways, and all conspire to keep the family secret. Thus, it is said that alcohol dependence often exists within a dysfunctional family—the functions of individual members adjust to the needs created by the presence of excessive drinking. This new arrangement can make it difficult for the drinker alone to change his or her behavior, because doing so would disrupt the family system. Some people suspect that certain family structures actually enhance the likelihood of alcohol abuse or dependence developing. For example, the “codependent” needs of other family members to take care of someone who is dependent on them might facilitate drunkenness. Much has been written about the effects on children who grow up in an “alcoholic family,” and there is some indication that even as adults these individuals tend to exhibit certain personality characteristics. The “adult children of alcoholics” are then perhaps more likely to become involved in dysfunctional relation-
Alcoholics Anonymous (AA): a worldwide organization of self-help groups based on alcoholics helping each other achieve and maintain sobriety.
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ships that increase the likelihood of alcohol abuse, either in themselves or in another family member. Again, the evidence indicates that such influences are statistical tendencies and are not all-powerful. It is perhaps unfortunate that some people with alcoholic parents have adopted the role of “adult children” and try to explain their entire personalities and all their difficulties in terms of that status.
Is Substance Dependence a Disease? The most important reason for adopting a disease model for dependence is based on the experiences of the founders of AA and is discussed in Chapter 9. Psychiatrists had commonly assumed that alcohol dependence was secondary to another disorder, such as anxiety or depression, and often attempted to treat the presumed underlying disorder while encouraging the drinker to try to “cut down.” The founders of AA believed that alcohol dependence itself was the primary problem and needed to be recognized as such and treated directly. This is the reason for the continued insistence that alcohol dependence is a disease—that it is often the primary disturbance and deserves to stand in its own right as a recognized disorder requiring treatment. On the other hand, Peele11 and others have argued that substance dependence does not have many of the characteristics of some classic medical diseases, such as tuberculosis or syphilis: We can’t use an X-ray or blood test to reveal the underlying cause, and we don’t have a way to treat the underlying cause and cure the symptoms—we don’t really know that there is an underlying cause, because all we have are the symptoms of excessive involvement. Furthermore, if substance dependence itself is a disease, then gambling, excessive sexual involvement, and overeating should also be seen as diseases. This in turn weakens our normal understanding of the concept of disease. The disease model is perhaps best seen as an analogy—substance dependence is like a disease in many ways, but that is different from insisting
that it is a disease. One reason for the conflict over the disease model of dependence may be differences in how we think of the term disease. For example, many would agree that high blood pressure is considered a disease—it’s certainly viewed as a medical disorder. We know that high blood pressure can be produced by genetic factors, cigarette smoking, diet, lack of exercise, or by other medical conditions. In that context, the idea that alcohol or drug dependence is like a disease doesn’t seem so far-fetched. This is taking a broad, biopsychosocial perspective that dependence might be related to dysfunctions of biology, personality, social interactions, or a combination of these factors.
Crime and Violence: Does Drug Use Cause Crime? It might seem obvious to a reader of today’s newspapers or to a viewer of today’s television that drugs and crime are linked. There are frequent reports of killings attributed to warring gangs of
There are more than 1.5 million drug arrests every year.
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drug dealers. Our prisons house a large population of people convicted of drug-related crimes, and several reports have revealed that a large fraction of arrestees for nondrug felonies have positive results from urine tests for illicit substances. The belief that there is a causal relationship between many forms of drug use and criminality probably forms the basis for many of our laws concerning drug use and drug users. The relationship between crime and illegal drug use is complex, and only recently have, 5' dimethoxy –4' – methylamphetamine (DOM)
3, 4 methylenedioxy amphetamine (MDA) 3, 4, 5 trimethoxyphenylethylamine (mescaline)
Carbon Oxygen Hydrogen Nitrogen
3,4 methylenedioxy methamphetamine (MDMA)
Figure 14.2 Catechol Hallucinogens known as “mescal buttons,” remain psychoactive indefinitely and are the source of the drug between the yearly harvests. The indigenous peoples’ journey in November and December to harvest the peyote is an elaborate ceremony, sometimes taking almost a month and a half. When the mescal buttons are to be used, they are soaked in the mouth until soft, then formed by hand into a bolus and swallowed. Mescal buttons should not be confused with mescal beans—or with mescal liquor,
which is distilled from the fermentation of the agave cactus and is the starting point for making tequila. Mescal buttons are slices of the peyote cactus and contain mescaline as the primary active agent. Mescal beans, however,
peyote (pay oh tee): a type of hallucinogenic cactus. mescaline (mess ka lin): the active chemical in the peyote cactus.
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are dark red seeds from the shrub Sophora secundiflora. These seeds, formerly the basis of a vision-seeking cult, contain a highly toxic alkaloid, cytisine, the effects of which resemble those of nicotine, causing nausea, convulsions, hallucinations, and occasionally death from respiratory failure. The mescal bean has a long history, and there is some evidence that use of the bean diminished when the safer peyote became available in the southwestern United States. In the transition from a mescal bean to a mescal button cult, some tribes experienced a period in which a mixture of peyote and mescal seeds was concocted and drunk. These factors contributed to considerable confusion in the early (and some recent) literature.28 Although there was evidence that the use of peyote had moved north into the United States as early as 1760, it was not until the late 19th century that a peyote cult was widely established among the Native Americans of the plains. From that time to the present, Native American missionaries have spread the peyote religion to almost a quarter of a million Native Americans, some as far north as Canada. The Native American Church of the United States was first chartered in Oklahoma in 1918 and is an amalgamation of Christianity and traditional beliefs and practices of the Native Americans, with peyote use incorporated into its ceremonies. Peyotism continues to be an important religious practice among the Indians of the United States between the Rocky Mountains and the Mississippi. Peyote is also used in other ways because the Native Americans attribute spiritual power to the peyote plant. As such, peyote is believed to be helpful, along with prayers and modern medicines, in curing illnesses. It is also worn as an amulet, much as some Christians wear a Saint Christopher’s medal, to protect the wearer from harm. For many years the use of peyote as a sacrament by the Native American Church was protected by the constitutional guarantee of freedom of religion. That protection had inspired Timothy Leary to attempt a similar exclusion for LSD in his newly founded 1960s
Peyotism remains an important religious practice among Native Americans in certain areas of the United States. This painting from the early 20th century includes scenes of peyote cult practices.
League of Spiritual Discovery. However, in 1990 the Supreme Court ruled that the State of Oregon could prosecute its citizens for using peyote, and the freedom of religion argument was not allowed. A large group of religious and civil liberties organizations asked the court to reconsider its decision, but it declined to do so. The two defendants in the case were Native Americans and members of the Native American Church. Federal law and many state laws specifically exclude sacramental peyote use, and the court pointed out that Oregon could exclude such use, too. Other states have not moved to outlaw religious use of peyote. San Pedro Cactus Another mescaline-containing cactus, Trichocereus pachanoi, whose common name is the San Pedro cactus, is native to the Andes Mountains of Peru and Ecuador and has been used for thousands of years as a religious sacrament.32 The San Pedro is a large, multibranched cactus, often growing to heights of 10 to 15 feet. Its mescaline content is less than that of peyote, and its recreational use more often results in adverse side effects than in the desired hallucinogenic experience. Discovery and Early Research on Mescaline Near the end of the 19th century, Arthur Heffter isolated several alkaloids from peyote and showed that
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mescaline was the primary agent for the visual effect induced by peyote. Mescaline was synthesized in 1918, and most experiments on the psychoactive and/or behavioral effects since then have used synthesized mescaline. More than 30 psychoactive alkaloids have now been identified in peyote, but mescaline does seem to be the agent responsible for the vivid colors and other visual effects. The fact that mescaline is not equivalent to peyote is not always made clear in the literature. One of the early investigators of the effects of peyote was Dr. Weir Mitchell, who used an extract of peyote and reported, in part: The display which for an enchanted two hours followed was such as I find it hopeless to describe in language which shall convey to others the beauty and splendor of what I saw. Stars, delicate floating films of color, then an abrupt rush of countless points of white light swept across the field of view, as if the unseen millions of the Milky Way were to flow in a sparkling river before my eyes . . . zigzag lines of very bright colors . . . the wonderful loveliness of swelling clouds of more vivid colors gone before I could name them.33
Another early experimenter was Havelock Ellis. Interestingly, he took his peyote on Good Friday in 1897, 65 years before the Good Friday experiment with psilocybin. His experience is described in detail in a 1902 article titled “Mescal: A Study of a Divine Plant” in Popular Science Monthly, but a brief quotation gives the essence of the experience: On the whole, if I had to describe the visions in one word, I should say that they were living arabesques. There was generally a certain incomplete tendency to symmetry, the effect being somewhat as if the underlying mechanism consisted of a large number of polished facets acting as mirrors. It constantly happened that the same image was repeated over a large part of the field, though this holds good mainly of the forms, for in the colors there would still remain all sorts of delicious varieties. Thus at a moment when uniformly jewelled flowers seemed to be springing up and extending all over the field of vision,
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the flowers still showed every variety of delicate tone and tint.34
Not every individual wants every educational opportunity. William James, surprisingly, was one who did not. He wrote to his brother Henry: “I ate one but three days ago, was violently sick for twenty-four hours, and had no other symptoms whatever except that and the Katzenjammer the following day. I will take the visions on trust.” Even Dr. Weir Mitchell, who had the effect previously recorded, said, “These shows are expensive. . . . The experience, however, was worth one such headache and indigestion but was not worth a second.” Even if you get by without too much nausea and physical discomfort, which the Native Americans also report, all might not go well. Huxley, whose 1954 The Doors of Perception35 made him a guru in this area, admitted, “Along with the happily transfigured majority of mescaline takers there is a minority that finds in the drug only hell and purgatory.” It is reported that natives sometimes wished for bad trips when taking this or other plants. By meeting their personal demons, they hoped to conquer them and remove problems from their lives. Pharmacology of Mescaline Mescaline is readily absorbed if taken orally, but it poorly passes the blood-brain barrier (which explains the high doses required). There is a maximal concentration of the drug in the brain after 30 to 120 minutes. About half of it is removed from the body in six hours, and there is evidence that some mescaline persists in the brain for up to 10 hours. Similar to the indole hallucinogens, the effects obtained with low doses, about 3 mg/kg body weight, are primarily euphoric, whereas doses in the range of 5 mg/kg give rise to a full set of hallucinations. Most of the mescaline is excreted unchanged in the urine, and the metabolites identified thus far are not psychoactive. A dose that is psychoactive in humans causes pupil dilation, pulse rate and blood pressure increases, and an elevation in body
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temperature. All of these effects are similar to those induced by LSD, psilocybin, and most other alkaloid hallucinogens. There are other signs of central stimulation, such as EEG arousal, after mescaline intake. In rats the LD50 is about 370 mg/kg body weight, 10 to 30 times the dose that causes behavioral effects. Death results from convulsions and respiratory arrest. Tolerance develops more slowly to mescaline than to LSD, and there is cross-tolerance between them. As with LSD, mescaline intoxication can be blocked with chlorpromazine. Although mescaline and the other catechol hallucinogens have a structure that resembles the catecholamine neurotransmitters, they act indirectly on the serotonin 2A receptor. Amphetamine Derivatives A large group of synthetic hallucinogens is chemically related to the amphetamines. However, most of these drugs have little amphetamine-like stimulant activity. Thanks to certain chemical substitutions on the ring part of the catechol nucleus, these drugs are more mescaline-like (Figure 14.2). DOM (STP) DOM is 2,5-dimethoxy-4-methylamphetamine. In the 1960s and 1970s, DOM was called STP, and street talk was that the initials stood for serenity, tranquility, and peace. Its actions and effects are similar to those of mescaline and LSD, with a total dose of 1 to 3 mg yielding euphoria and 3 to 5 mg a six- to eighthour hallucinogenic period. This makes DOM about a hundred times as potent as mescaline but only one-thirtieth as potent as LSD. MDA and Others In addition to DOM, many other amphetamine derivatives have been synthesized and shown to have hallucinogenic properties. Most of these have effects very similar to those of DOM and mescaline, as well as LSD and the indole types. There is some indication that one type of derivative, MDA (Figure 14.2), has effects that are subjectively somewhat different. MDA, which is somewhat more potent than mescaline, has seen some recreational use through illicit manufacture. Because of the variety of possible
Some evidence suggests that Ecstasy may be neurotoxic, affecting serotonin neurons in the brain.
hallucinogenic amphetamine derivatives and because most of these chemicals are not specifically listed as controlled substances, illicit drug makers were drawn to this group of chemicals in the production of various designer drugs to be sold on the street as hallucinogens. MDMA One of the amphetamine derivatives— MDMA—received special attention in July 1984 when the DEA first proposed scheduling it. Although there had been some recreational use of MDMA (it is called “Ecstasy” or “XTC”), a number of psychiatrists testified against the scheduling of MDMA. They insisted that it was not a true hallucinogen and that it had a special ability to promote empathy, thus aiding the psychoanalytic process.36 There is some evidence supporting this claim of increased empathy: In one study, 100 people completed detailed questionnaires describing the effects of their previous use of MDMA.37 Although such retrospective reports are less reliable than reports obtained during or immediately after the experience, a remarkably common report (90 percent of the individuals) was that they experienced a heightened sense of “closeness” with other people. And like other amphetamines, MDMA increases euphoria, sociability, blood pressure, and heart rate. Although several people reported that objects seemed more “luminescent,” very few reported actual visual hallucinations.
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Drugs in Depth Extrapolating Findings from Animals to Humans: What You Need to Know “The amount of the drug Ecstasy that some recreational users take in a single night may cause permanent brain damage and lead to symptoms like those of Parkinson’s disease,” read an article published in The New York Times on September 27, 2002. This and similar statements were based on assertions made in a scientific paper that had just appeared in the highly respected and influential journal Science.38 George Ricaurte and his team of researchers gave nonhuman primates three doses of MDMA (also known as Ecstasy) over the course of six hours and, then, a couple of weeks later evaluated neuroanatomical and neurochemical alterations. They found extensive damage to dopamine and serotonin neurons as well as reduced levels of these neurotransmitters in the brain. The finding that MDMA damaged brain cells was not new. Several studies documented the neurotoxic effects of MDMA in laboratory animals.39 The majority of these studies, however, had used dosing regimens that were much larger and longer than those used by recreational MDMA users. Studies using laboratory animals, for instance, typically administer MDMA via routes other than oral, and in doses greater than 5 mg/kg twice a day for four or more consecutive days. By contrast, human recreational drug users almost always administer the drug orally and typically do not exceed 2–4 mg/kg in only one evening. What made Ricaurte and colleagues’ results intriguing was that the doses of MDMA used and the pattern of drug administration were claimed to be comparable to those used by recreational human users. The researchers injected MDMA at a dosage of 2 mg/kg, three times, at three-hour intervals, for a total dose of 6 mg/kg. As noted above, even this dosing regimen does not exactly correspond with those typically used by humans. Importantly, the route of drug administration is a critical determinant of neurochemical consequences (e.g., toxicity) because these effects depend on the rate of rise of drug concentrations and the maximum brain concentrations achieved. Recall from Chapter 5 that drugs administered by injection result in a more rapid onset of effects and greater brain concentrations. Furthermore, potential toxicity is decreased when a drug is self-administered compared to experimenteradministered.40 Thus, these two factors increased
the likelihood of observing toxicity in the Ricaurte study. Nevertheless, the study findings generated a wave of controversy. Critics argued that the total dose given to the animals far exceeded doses taken by humans and that the kind of brain damage observed has never been found in humans. They also noted that 20 percent of the animals died following MDMA administrations, whereas human mortality is rare. Supporters, in contrast, took the findings as evidence that MDMA is a highly toxic drug that should not be taken even once. But in an embarrassing turn of events, Ricaurte and colleagues were forced to retract their paper one year after its publication because they discovered that methamphetamine had been mistakenly given, rather than MDMA.41 This was deduced after several unsuccessful attempts by the researchers to replicate their original findings. It is noteworthy that those negative data were never published. This suggests that there is a bias toward publishing positive results (i.e., demonstration of MDMA-induced neurotoxicity). A similar situation has been noted regarding antidepressant medications (see Chapter 8). Even so, these events raise important questions about drug-induced neurotoxicity observed in laboratory animals and the relevancy of such findings for the human drug users. Unfortunately, uneven (and sometimes sensationalized) reports about drug-induced toxicity can be discouraging to students. As a result, some may reject all related information from scientific sources. Who should you believe? How do you determine which dataset is more compelling? In your attempt to understand research investigating drug-induced toxicity, you should ask a few simple questions: (1) What was the drug dosing regimen used and is it similar to regimens used by humans? (2) what was the route of drug administration used and do humans use the drug in this manner? (3) Was the drug self-administered or administered by the experimenter? (4) Because the development of tolerance can be protective against some types of toxicity, like human drug-taking behavior, were the animals administered escalating doses prior to receiving a larger dose? All of these factors potentially impact neurochemical findings and should be considered when making extrapolations about data collected in laboratory animals to humans.
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Anecdotal reports suggest that MDMA users report substantially more negative or depressed mood states in the days immediately following MDMA administration. Colloquially, this phenomenon is frequently referred to as “Suicide Tuesday.” Some have speculated that initially MDMA administration causes a substantial release of serotonin, followed by a marked reduction of the neurotransmitter, lasting several hours to days after the last dose. Because serotonin plays a major role in mood regulation, this produces the depressed mood state reported by MDMA users in the days following drug use. But there is no hard evidence. In fact, preliminary data collected in our laboratory at Columbia University do not indicate the emergence of depressed mood states in the days after MDMA use, even when the drug is given repeatedly. Another frequently mentioned potential negative consequence of MDMA is damage to brain cells. Several investigators have shown that large doses of MDMA given to laboratory animals can destroy serotonin neurons, but the relevance of this and related findings for human recreational use is unclear (see the Drugs in Depth box). Recreational users of the drug perform similar to their education- and agematched counterparts on cognitive tests and do not typically use doses as large as those used in animal experiments. However, this does not suggest that the drug should be used recreationally. MDMA remains listed as a Schedule I controlled substance, which means its recreational use is prohibited. 2-CB and 2-C-T 7 It’s happened before and it will happen again: As federal and state agencies work to limit access to one drug, another arrives to fill the gap. In this case, two drugs have arrived to share the rave scene with MDMA: 4-bromo-2,5-dimethoxyphenethylamine (known as 2-CB) and 4-propylthio-2, 5-dimethoxyphenethylamine (2-C-T7). As phenylethylamines, both are chemical cousins to the amphetamine series of hallucinogens. Along with the recently popularized tryptamine deriv-
atives MTA and “foxy methoxy” (see page 346), a confusing array of chemicals is being made available to “ravers,” who may find themselves trying unknown amounts of unfamiliar drugs more often than they’d like.
Deliriants If the indole and catechol hallucinogens are grouped together as “phantastica” with all having similar effects, and acting primarily through the serotonin 2A receptor, then how do we classify all the remaining hallucinogens? We have chosen the term deliriants, implying that the drugs to follow have somewhat more of a tendency to produce mental confusion and a loss of touch with reality. The drugs we describe next represent a variety of effects and act through different brain mechanisms, so it is perhaps better to think of each type by itself rather than as belonging to a group with common effects.
PCP In the 1950s, Parke, Davis & Company investigated a series of drugs in the search for an efficient intravenous anesthetic. On the basis of animal studies, the company selected 1-(1phenylcyclohexyl) piperidine hydrochloride (PCP, generic name phencyclidine) for testing in humans. The studies on monkeys had indicated that PCP was a good analgesic but did not produce good muscle relaxation or sleep. Instead, the animals showed a sort of “dissociation” from what was happening: “During the operation the animal had its eyes open and looked about unconcernedly.” In 1958, the first report was published on the use of PCP (Sernyl) for surgical anesthesia in humans. Sernyl produced good analgesia without depressing blood circulation or respiration and did not produce irregularities in heartbeat. Loss of sensation occurred within two or three minutes of beginning the intravenous infusion, after about 10 mg of the drug had been delivered. The patients later had no memory of the procedure, did not
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remember being spoken to, and remembered no pain. Compared with existing anesthetics, which tend to depress both respiration and circulation through general depression of the CNS, this type of “dissociative” anesthetic seemed to be quite safe. However, the psychological reactions to the drug were unpredictable. During administration of the drug a few patients became very excited, and a different anesthetic had to be used. Several patients were “unmanageable” as they emerged from the anesthetic, exhibiting severely manic behavior. This and later reports indicated that many people given anesthetic doses of Sernyl reported changes in body perception and hallucinations, and about 15 percent of the patients experienced a “prolonged confusional psychosis,” lasting up to four days after the drug was given. This period of confusion was characterized by feelings of unreality, depersonalization, persecution, depression, and intense anxiety. News of this new hallucinogen soon reached Dr. Luby, a psychiatrist, who began testing it in both normal and schizophrenic subjects.42 All the subjects reported changes in perception of their own bodies, with one normal subject saying, “my arm feels like a twenty-mile pole with a pin at the end.” Another said, “I am a small . . . not human . . . just a block of something in a great big laboratory.” There were a number of reports of floating, flying, dizziness, and alternate contraction and expansion of body size. All subjects also showed a thought disorder. Some made up new words, uttered strings of unrelated words, or repeated words or simple phrases. Also, all became increasingly drowsy and apathetic. At times a subject would appear to be asleep but when asked a direct question would respond. When asked, “Can you hear me?” subjects often responded, “No.” The majority became either angry or uncooperative. Many of the normal subjects said they felt as if they were drunk from alcohol. All subjects displayed diminished pain, touch, and position sense, and all showed nystagmus (rapid oscillations of the eyes) and a slapping, ataxic walk. Luby and his colleagues felt that PCP was dif-
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ferent from LSD or mescaline in that there were few reports of intense visual experiences and many more reports of body image changes. The disorganized thinking, suspiciousness, and lack of cooperation made the PCP state resemble schizophrenia much more than the LSD state. Thus, by 1960, PCP had been characterized as an excellent anesthetic for monkeys, a medically safe but psychologically troublesome anesthetic for humans, and a hallucinogen different from LSD and mescaline, with profound effects on body perception. Parke, Davis withdrew Sernyl as an investigational drug for humans in 1965 and in 1967 licensed another company to sell Sernylan as an animal anesthetic. It was primarily used with primates, in both research laboratories and zoos. Also, because of its rapid action and wide safety margin, Sernylan was used in syringe bullets to immobilize stray, wild, or dangerous zoo animals. Because of the popular term tranquilizer gun for this use, PCP became popularly, and inaccurately, known as an animal “tranquilizer.” Other PCP-like Drugs: Ketamine, Dextromethorphan, and Nitrous Oxide Even though Sernyl was never marketed for human use, a related chemical from the same series was marketed as a dissociative anesthetic. Ketamine hydrochloride (Ketalar) has been in continued human use for more than 30 years. Although ketamine has more depressant effects than PCP and fewer prolonged reactions, clinical reports indicate that emergence reactions occur in about 12 percent of patients. These reactions include hallucinations and delirium, sometimes accompanied by confusion and irrational behavior. In 1999, widespread reports of ketamine abuse and its notoriety as a party drug (called Special K, or K) caused the Department of Health and Human Services to recommend adding ketamine to the list of Schedule III controlled substances.
PCP: phencyclidine; originally developed as an anesthetic; has hallucinogenic properties.
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Like PCP and ketamine, two more common substances are also capable of causing dissociative effects, perhaps by blocking NMDA-type glutamate receptors in the brain. Nitrous oxide (laughing gas, Chapter 7) and dextromethorphan, an over-the-counter cough suppressant (Chapter 12) can, at very high doses, produce dissociative-type hallucinations similar to those produced by PCP. Unfortunately, at these doses there is also evidence of pathological changes to neurons in the cerebral cortex of animals. It was reported that the combination of nitrous oxide and ketamine, sometimes used for general anesthesia, produces synergistic neurotoxic effects in animals.43 Recreational Use of PCP In late 1967, workers at the Haight-Ashbury Medical Clinic obtained samples of a substance being distributed as the “Peace Pill.” The drug was analyzed and determined to be PCP, and its identity and dangers were publicized in the community in December 1967. By the next year, it was reported that this drug had enjoyed only brief popularity and then disappeared. It appeared briefly in New York in 1968 as “hog” and at other times as “trank.” Into the early 1970s, PCP was apparently regarded as pretty much a “garbage” drug by street people. In the early 1970s, PCP crystals were sometimes sprinkled onto oregano, parsley, or alfalfa and sold to unsuspecting youngsters as marijuana. In this form, it became known as angel dust. Because PCP can be made inexpensively and relatively easily by amateur chemists, when it is available it usually doesn’t cost much. Eventually, the rapid and potent effects of angel dust made it a desired substance in its own right. Joints made with PCP sometimes contained marijuana, sometimes another plant substance, and were known as “killer joints” or “sherms” (because they hit the user like a Sherman tank). In the late 1970s, PCP use was the most common cause of drug-induced visits to hospital emergency rooms in many communities, and in some neighborhoods young users could be seen “moonwalking” down the street (taking
very high, careful, and slow steps) on any Saturday night. The dependence-producing properties of PCP have also been studied in monkeys, which will press a lever to obtain access to the drug.44 This is in contrast to LSD and other hallucinogens, which do not support animal self-administration and do not produce psychological dependence in most users. Because some PCP users have been reported to behave violently, there is a question as to whether PCP tends to promote violence directly or whether violence is a side effect of the suspicion and anesthesia produced by the drug. Most users do not report feeling violent and feel so uncoordinated that they can’t imagine starting a fight. However, police who have tried to arrest PCP users have had trouble subduing them because many of the commonly used arrest techniques rely on restraining holds that result in pain if the arrestee resists. Because the PCP user is anesthetized, these restraint techniques are less effective. Manual restraint by more than one officer might be required to arrest some PCP users, although one might question how different this is from the problem of arresting a greatly alcohol intoxicated person who is “feeling no pain.” That PCP users might not feel pain has resulted in some gruesome legends about users biting or cutting off their own fingers and so forth. Like earlier stories about LSD users blinding themselves by staring at the sun, these legends cannot be substantiated and most likely have not really occurred. One oft-repeated story probably falls into the category of police folklore. Every cop knows for a fact the story about the PCP user who was so violent, had such superhuman strength, and was so insensitive to pain that he was shot 28 times (or a similar large number of times) before he fell. Although everyone “knows” that this happened, no one can tell you exactly when or where. One might dismiss such folklore as harmless, unless it contributes to events such as the shooting, six times at close range, of an unarmed, naked, 35year-old biochemist who was trying to climb the
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street sign outside his laboratory. This story really did happen, on August 4, 1977, during the height of PCP use in the U.S. The lethal shots were fired by a Los Angeles police officer. The coroner’s office reported that the victim’s blood did contain traces of a drug similar to PCP.45 Several years later, Los Angeles police officers involved in the widely publicized videotaped beating of Rodney King said during their trial that they used such force because they believed King might have been “dusted”—under the influence of PCP. The mechanism of PCP’s action on the brain was a mystery for several years, because PCP alters many neurotransmitter systems but does not appear to act directly on any of them. In 1979, it was reported that a specific receptor for PCP was present in the brain, and in 1981 the identity between the receptor and another that had previously been considered a subtype of opiate receptor was reported. The drug cyclazocine, which has some opiate activity and has also been reported to produce hallucinations, binds well to this “sigma” receptor, but morphine, naloxone, and other opiates do not. Thus, the sigma receptor is probably better characterized as being selective for PCP, ketamine, and other similar drugs rather than as a type of opiate receptor. The presence of the sigma receptor implies that some endogenous substance should bind to it, but more than 20 years of research has not yet determined what that might be or what the normal functions are for this receptor. Several drugs have been developed that bind to the sigma receptor, but none has reached the market.46
The family of plants in which all these genera are found is Solanaceae, “herbs of consolation,” and three pharmacologically active alkaloids are responsible for the effects of these plants. Atropine, which is dl-hyoscyamine, scopolamine, or l-hyoscine, and l-hyoscyamine are all potent central and peripheral cholinergic blocking agents. These drugs occupy the acetylcholine receptor site but do not activate it; thus, their effect is primarily to block muscarinic cholinergic neurons, including the parasympathetic system. These agents have potent peripheral and central effects, and some of the psychological responses to these drugs are probably a reaction to peripheral changes. These alkaloids block the production of mucus in the nose and throat. They also prevent salivation, so the mouth becomes uncommonly dry, and perspiration stops. Temperature can increase to fever levels (109°F has been reported in infants with atropine poisoning), and heart rate can show a 50-beat-per-minute increase with atropine. Even at moderate doses these chemicals cause considerable dilation of the pupils of the eyes, with a resulting inability to focus on nearby objects. With large enough doses, a behavioral pattern develops that resembles toxic psychosis; there is delirium, mental confusion, loss of attention, drowsiness, and loss of memory for recent events. These two characteristics—a clouding of consciousness and no memory for the period of intoxication—plus the absence of vivid sensory effects separate these drugs from the indole and catechol hallucinogens. The anticholinergics are the original deliriants.
Anticholinergic Hallucinogens
Belladonna Atropine, which was isolated in 1831, is the active ingredient in the deadly nightshade, Atropa belladonna. The name of the plant reflects two of its major uses in the Middle Ages and before. The genus name
The potato family contains all the naturally occurring agents to be discussed in this section. Three of the genera—Atropa, Hyoscyamus, and Mandragora—have a single species of importance and were primarily restricted to Europe. The fourth genus, Datura, is worldwide and has many species containing the active agents.
angel dust: the street name for PCP sprinkled on plant material.
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Belladonna, or deadly nightshade, is a poisonous plant that contains an anticholinergic hallucinogen.
reflects its use as a poison. Deadly nightshade was one of the plants used extensively by both professional and amateur poisoners; 14 of its berries contain enough of the alkaloid to cause death. Belladonna, the species name, meaning “beautiful woman,” comes from the use of the extract of this plant to dilate the pupils of the eyes. Interestingly, ancient Roman and Egyptian women knew something that science did not learn until more recently. In the 1950s, it was demonstrated, by using pairs of photographs identical except for the amount of pupil dilation, that most people judge the girl with the more dilated eyes to be prettier. Of more interest here than pretty girls or poisoned men is the sensation of flying reported by some users of belladonna. The origin of this story goes back at least to the Middle Ages in Europe, and in particular to descriptions of witches and witchcraft. Every early society for which we have any history has a tradition of people with special knowledge of useful plants. In Europe, the people who were consulted for their special arcane knowledge of plant potions were most often women, and their traditions are kept alive in our modern concept of “witches.” Among the rich folklore about witches are several
accounts from the 1400s describing “flying ointments” (e.g., The Book of the Sacred Magic of Abremelin the Mage, 1458), and one ingredient often included in these ointments was deadly nightshade. The notion is that this ointment was spread upon the body and/or on a stick, or “staffe,” which was straddled. This is certainly the origin of our notion that witches flew about on broomsticks, though in many accounts it seems that the sticks were used more as phallic symbols and were perhaps ridden in a different manner. What is actually known about witches and witchcraft of this era is confused considerably by what was written about witches by Catholic priests during the Inquisition. During the Middle Ages, all such pagan rituals were considered to be heresy, and practitioners were tortured and killed. Admissions by witches that they “flew” long distances to celebrate Black Mass were extracted during torture and were likely to have reflected the beliefs of the inquisitors more than the history of the person being tortured. Some incredibly lurid accounts of the practices of witches associated drugs, sex, and human sacrifice. Similar lurid accounts linking other drugs (marijuana, LSD, cocaine) to sexual abandon and criminal violence have appeared during more recent years, also promoted by those protecting the established order. The facts are usually not so exciting. Anticholinergics can make people feel lightheaded, and in conjunction with the power of suggestion one might get the sensation of floating, or flying, but it’s not a realistic way to get from New York to Chicago. Mandrake The mandrake plant (Mandragora officinarum) contains all three alkaloids. Although many drugs can be traced to the Bible, it is particularly important to do so with mandrake because its close association with love and lovemaking has persisted from Genesis to recent times: In the time of wheat-harvest Reuben went out and found some mandrakes in the open country
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www.mhhe.com/hart13e and brought them to his mother Leah. Then Rachel asked Leah for some of her son’s mandrakes, but Leah said, “Is it so small a thing to have taken away my husband, that you should take my son’s mandrakes as well?” But Rachel said, “Very well, let him sleep with you tonight in exchange for your son’s mandrakes.” So when Jacob came in from the country in the evening, Leah went out to meet him and said, “You are to sleep with me tonight; I have hired you with my son’s mandrakes.” That night he slept with her.47
The mandrake root is forked and, if you have a vivid imagination, resembles a human body. The root contains the psychoactive agents and was endowed with all sorts of magical and medical properties. The association with the human form is alluded to in Shakespeare’s Juliet’s farewell speech: “And shrieks like mandrakes torn out of the earth, That living mortals hearing them run mad.” Henbane Compared with deadly nightshade and mandrake, Hyoscyamus niger has had a most uninteresting life. This is strange, because it is pharmacologically quite active and contains both scopolamine and l-hyoscyamine. Other plants of this genus contain effective levels of the alkaloids, but it is Hyoscyamus niger that appears throughout history as henbane, a highly poisonous substance and truly the bane of hens, as well as other animals. Pliny in AD 60 said, “For this is certainly known, that, if one takes it in drink more than four leaves, it will put him beside himself.” Shakespeare’s Hamlet’s father must have had more than four leaves because it was henbane that was used to poison him. Datura The distribution of the many Datura species is worldwide, but they all contain the three alkaloids under discussion—atropine, scopolamine, and hyoscyamine—in varying amounts. Almost as extensive as the distribution are its uses and its history. Although it is not clear when the Chinese first used Datura metel as a medicine to treat colds and nervous
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disorders, the plant was important enough to become associated with Buddha: The Chinese valued this drug far back into ancient times. A comparatively recent Chinese medical text, published in 1590, reported that “when Buddha preaches a sermon, the heavens bedew the petals of this plant with rain drops.”48
Halfway around the world 2,500 years before the Chinese text, virgins sat in the temple to Apollo in Delphi and, probably under the influence of Datura, mumbled sounds that holy men interpreted as predictions that always came true. Engraved on the temple at Delphi were the words “Know thyself.” Datura is associated with the worship of Shiva in India, where it has long been recognized as an ingredient in love potions and has been known as “deceiver” and “foolmaker.” In Asia the practice of mixing the crushed seeds of Datura metel in tobacco, cannabis, and food persists even today. One interesting use of Datura stramonium, which is native and grows wild in the eastern United States, was devised by the Algonquin Indians. They used the plant to solve the problem of the adolescent search for identity: The youths are confined for long periods, given “ . . . no other substance but the infusion or decoction of some poisonous, intoxicating roots . . . ” and “they became stark, staring mad, in which raving condition they were kept eighteen or twenty days.” These poor creatures drink so much of that water of Lethe that they perfectly lose the remembrance of all former things, even of their parents, their treasure, and their language. When the doctors find that they have drunk sufficiently of the wysoccan . . . they gradually restore them to their senses again. . . . Thus they unlive their former lives and commence men by forgetting that they ever have been boys.48
The same plant is now called Jamestown weed, or jimsonweed, as a result of an incident in the 17th century. This was recorded for history in the book The History and Present State
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of Virginia, published first in 1705 by Robert Beverly.49 The James-Town Weed (which resembles the Thorny Apple of Peru, and I take to be the Plant so call’d) is supposed to be one of the greatest Coolers in the World. This being an early Plant, was gather’d very young for a boil’d Salad, by some of the Soldiers sent thither, to pacifie the Troubles of Bacon; and some of them eat plentifully of it, the Effect of which was a very pleasant Comedy; for they turn’d natural Fools upon it for several Days.
Although there has been some recent abuse of jimsonweed, the unpleasant and dangerous side effects of this plant limit its recreational use. Synthetic Anticholinergics Anticholinergic drugs were once used to treat Parkinson’s disease (before the introduction of L-dopa) and are still widely used to treat the pseudoparkinsonism produced by antipsychotic drugs (see Chapter 8). Particularly in older people there is concern about inadvertently producing an “anticholinergic syndrome,” characterized by excessive dry mouth, elevated temperature, delusions, and hallucinations. Anticholinergic drugs such as trihexyphenidyl (Artane) and benztropine (Cogentin) have only rarely been abused for their delirium-producing properties.
Amanita Muscaria The Amanita muscaria mushroom is also called “fly agaric,” probably because of what it does to flies. It doesn’t kill them, but when they suck its juice, it puts them into a stupor for two to three hours. It is one of the common poisonous mushrooms found in forests in many parts of the world. The older literature suggests that eating 5 to 10 Amanita mushrooms results in severe effects of intoxication, such as muscular twitching, leading to twitches of limbs and raving drunkenness, with agitation and vivid hallucinations. Later follow many hours of partial paralysis with sleep and dreams.
The red- and white-speckled mushroom Amanita muscaria played a major role in the early history of Indo-European and Central American religions.
When the ancient Aryan invaders swept down from the north into India 3,500 years ago, they took soma, itself considered a deity. The cult of Soma ruled India’s religion and culture for many years—the poems of the Rig Veda celebrate the sacramental use of this substance. It has only been within the past 30 years that scholars have discovered and agreed on the identity of soma as Amanita.1 The suggestion has been made that the ambrosia (“food of the gods”) mentioned in the secret rites of the god Dionysius in Greece was a solution of the Amanita mushroom. And based on paintings representing the “tree of life” found in ancient European cave paintings, it has been suggested that Amanita muscaria use formed a basis for the cult that originated about 2,000 years ago and today calls itself Christianity.50 Until the Russians introduced them to alcohol, many of the isolated nomadic tribes of Siberia had no intoxicant but Amanita: Use of the Amanita mushroom by Siberian tribes continues today largely free from social control of any sort. Use of the drug has a Shamanist aspect, and forms the basis for orgiastic communal
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Mind/Body Connection Living in the Flow During the 1960s, the spirit of kinship with a peer group helped fuel the spread of LSD. More recently, the feeling of making intense emotional connections seems to have helped spread a “rave” subculture in the United States and elsewhere. This scene, known for its all-night dance parties featuring techno tunes and the drug Ecstasy, has had a dedicated following since the early 1990s. It’s not, however, just about the music or the drugs, according to those in the rave community. It’s about being in the moment, having a brief conversation with a stranger who affects you, having an emotional internal experience. What really makes people glad to be alive? What are the inner experiences that make life worthwhile? It’s easier to talk about dancing than it is to describe a moment of mystical union with the universe. Joy can find us and lift us in moments of ordinary connection, though, and the opening we feel to life is not unlike that experienced through a spiritual quest or mystical practice. The elation comes when we know we belong—to another, to ourselves, to the mystery that is larger than ourselves. In our society, celebrations and relaxation often involve moving away from the emotion, numbing ourselves with alcohol or drugs. Dance and music are exceptions to this, but too often we are simply spectators in our lives. Sometimes we discount the small joys in daily living. Sometimes we spoil the good by focusing on the less than perfect or seemingly
indulgences. Since the drug can induce murderous rages in addition to more moderate hallucinogenic experiences, serious injuries frequently result.51
In the frozen northland, these mushrooms are expensive; sometimes several reindeer are exchanged for an effective number of the mushrooms. During the long winter months they might be worth the price. While the mushrooms themselves are not reusable (once eaten, they’re gone), the hallucinogen is excreted unchanged in the urine. When the effect begins to wear off, “midway in the party the cry of ‘pass
incompatible. Perhaps we don’t want to be let down, so we anticipate disappointment rather than expect success and happiness. Can you think of a time when joy came unexpectedly and caught you off guard? Maybe it was a sudden realization that made you smile. Perhaps it was something you didn’t even know you were looking for. Chances are it was a moment when you felt so alive that, ironically, you forgot yourself. Mihaly Csikszentmihalyi, a University of Chicago psychology professor who has devoted his life’s work to studying what makes people happy, satisfied, and fulfilled, describes “flow” as a state of consciousness so focused that you are totally absorbed in an activity and lose track of time. It is a state of complete engagement with life in which you feel strong, alert, in effortless control, unself-conscious, and at the peak of your abilities. Examples of when you might experience flow include after completing a hard task, when feeling the wind in your hair during a walk on the beach, during yoga or sex, and when seeing your child respond to your smile for the first time. What activities usually make you feel happy and completely engaged? During the next week, be aware of and record what activities give you this feeling of deep enjoyment. Then try to build some of these activities into your daily routine to improve the spiritual and emotional quality of your life.
the pot’ goes out.”52 The active ingredient can be reused four or five times in this way. There is evidence that Amanita was also used as a holy plant by several tribal groups in the Americas, ranging from Alaska and the Great Lakes to Mexico and Central America. In several of the legends, its origin is associated with thunder and lightning.1 For many years the active agent in this mushroom was thought to be muscarine (for which the muscarinic cholinergic receptors were named). This substance activates the same type of acetylcholine receptor that
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is blocked by the anticholinergics. However, pharmacological studies with other cholinergic agonists did not produce similar psychoactive effects. Next, attention focused on bufotenin, an indole that is found in high concentrations in the skins of toads. However, the hallucinogenic properties of bufotenin have been in doubt, and Amanita species contain only small amounts of it. In the mid-1960s, meaningful amounts of two chemicals were found: ibotenic acid and muscimol. The effects of Amanita ingestion are not similar to those of other hallucinogens, and that helped confuse the picture with regard to the mechanism. Muscimol can act as an agonist at GABA receptors, which are inhibitory and found throughout the CNS. Muscimol is more potent than ibotenic acid, and drying of the mushroom, which is usually done by those who use it, promotes the transformation of ibotenic acid to muscimol. Muscimol has been given to humans, resulting in confusion, disorientation in time and place, sensory disturbances, muscle twitching, weariness, fatigue, and sleep.28 Amanita muscaria and other related poisonous mushrooms are found in North America, and they are a particularly dangerous type of plant with which to experiment.
Salvia Divinorum This member of the mint family is known by its botanical name, which is translated as “diviner’s sage.” It has been used for centuries by the Mazatec people of Oaxaca, Mexico, in religious ceremonies, and more recently some young people in Mexico have smoked it as a substitute for marijuana. The traditional methods of using the plant include chewing the leaves, drinking a tea made from the crushed leaves, or smoking the dried leaves. The resulting hallucinatory effect is reported to last for up to an hour.53 People in the United States and in Europe have cultivated the plant for the past several years and use it as a legal hallucinogen. Salvia is not currently listed as a controlled substance in the United States.
The plant was identified in 1962 by Wasson and Hoffman, and the active agent, salvinorin A, was identified in 1982. Salvinorin A is nearly as potent as LSD, in that an effective human dose may be as little as 200 μg (micrograms) when smoked. It was reported in 1994 that salvinorin A binds selectively to the kappa opioid receptor, where it acts as an agonist. Thus, this drug represents a newly discovered type of chemical structure and a unique pharmacological effect, which is stimulating research to develop new, related compounds.53 Meanwhile, it will be interesting to see what happens to the legal status of Salvia and of salvinorin A. That will no doubt be influenced by whether there are highly publicized examples of abuse.
Summary •
Hallucinogenic plants have been used for many centuries, not only as medicines but for spiritual and recreational purposes as well.
•
LSD, a synthetic hallucinogen, alters perceptual processes and enhances emotionality, so that the real world is seen differently and is responded to with great emotion.
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Other chemicals that contain the indole nucleus, such as psilocybin (from the Mexican mushroom), have effects similar to those of LSD.
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Mescaline, from the peyote cactus, and synthetic derivatives of the amphetamines represent the catechol hallucinogens. They have psychological effects quite similar to those of the indole types.
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PCP, or angel dust, produces more changes in body perception and fewer visual effects than LSD.
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Anticholinergics are found in many plants throughout the world and have been used not only recreationally, medically, and spiritually but also as poisons.
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Review Questions 1. What are the distinctions among phantastica, deliriants, psychedelics, psychotomimetics, entheogens, and hallucinogens? 2. What is the precise relationship between ergotism and LSD? 3. Why was LSD used in psychoanalysis in the 1950s and 1960s? How does this relate to its proposed use by the Army and the CIA? 4. Describe the dependence potential of LSD in terms of tolerance, physical dependence, and psychological dependence. 5. What is the diagnostic term for flashbacks? 6. What is the active agent in the “magic mushrooms” of Mexico, and is it an indole or a catechol? 7. Besides the psychological effects, what other effects are reliably produced by peyote? 8. Contrast MDMA and PCP in terms of how they appear to make people feel about being close to others. 9. Which of the hallucinogenic plants was most associated with witchcraft? 10. What can be concluded from the evidence regarding the neurotoxic effects of MDMA? 11. Which hallucinogen acts as an agonist at kappa opiate receptors?
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10. 11. 12. 13.
14. 15.
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Schultes, R. E., and A. Hofmann. Plants of the Gods. New York: McGraw-Hill, 1979. Caporael, L. R. “Ergotism: The Satan Loosed in Salem.” Science 192 (1976), pp. 21–26. Gottlieb, J., and N. P. Spanos. “Ergotism and the Salem Village Witch Trials.” Science 194 (1976), pp. 1390–94. Hofmann, A. “Psychotomimetic Agents.” In A. Burger, ed. Drugs affecting the central nervous system (Vol. 2). New York: Marcel Dekker, 1968. Segal, J., ed. Research in the Service of Mental Health, Research on Drug Abuse. National Institute on Mental Health, Pub. No. (ADM) 75-236, U.S. Department of Health, Education, and Welfare. Washington, DC: U.S. Government Printing Office, 1975. Johnston, L. “Ford Signs Grant of $750,000 in LSD Death in CIA Test.” The New York Times, October 14, 1976, p. C43. Treaster, J. B. “Mind-Drug Test a Federal Project for Almost 25 Years.” The New York Times, August 11, 1975, p. M42.
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“CIA Considered Big LSD Purchase.” Washington Star, August 4, 1975. See also Knight, M. “LSD Creator Says Army Sought Drug.” The New York Times, August 1, 1975. Taylor, J. R., and W. N. Johnson. Use of Volunteers in Chemical Agent Research. Inspector General Report No. DAIGIN 21-75, Washington, DC: U.S. Department of Army, March 10, 1976. Weil, A. T. “The Strange Case of the Harvard Drug Scandal.” Look, November 5, 1963, pp. 38–48. Blumenthal, R. “Leary Drug Cult Stirs Millbrook.” The New York Times, June 14, 1967, p. 49. “Celebration #1.” New Yorker 42 (1966), p. 43. Council on Mental Health and Committee on Alcoholism and Drug Dependence. “Dependence on LSD and Other Hallucinogenic Drugs.” Journal of the American Medical Association 202 (1967), pp. 141–44. Leary and Liddy, Debating Specialists. The New York Times, September 3, 1981, p. B26. Appel, J. B., and J.A. Rosecrans. “Behavioral Pharmacology of Hallucinogens in Animals: Conditioning Studies.” In B. L. Jacobs, ed. Hallucinogens: Neurochemical, Behavioral and Clinical Perspectives. New York: Raven Press, 1984. Julien, R. M. A Primer of Drug Action, 10th ed. New York: Worth, 2005. Siegel, R. K. “The Natural History of Hallucinogens.” In B. L. Jacobs, ed. Hallucinogens: Neurochemical, Behavioral and Clinical Perspectives. New York: Raven Press, 1984. Krippner, S. “Psychedelic Experience and the Language Process.” Journal of Psychedelic Drugs 3, no. 1 (1970), pp. 41–51. Levine, J., and A. M. Ludwig. “The LSD Controversy.” Comprehensive Psychiatry 5, no. 5 (1964), pp. 318–19. Forsch, W. A., E. S. Robbins, and M. Stern. “Untoward Reactions to Lysergic Acid Diethylamide (LSD) Resulting in Hospitalization.” New England Journal of Medicine 273 (1965), pp. 1235–39. Halpern, J. H., and others. “Hallucinogen Persisting Perceptual Disorder: What Do We Know after 50 Years?” Drug & Alcohol Dependence 69 (2003), pp. 109–19. Zegans, L. S., J. C. Pollard, and D. Brown. “The Effects of LSD-25 on Creativity and Tolerance to Regression.” Archives of General Psychiatry 16 (1967), pp. 740–49. Spitzer, M., and others. “Increased Activation of Indirect Semantic Associations Under Psilocybin.” Biological Psychiatry 39 (1996), pp. 1055–57. Hollister, L. E., J. Shelton, and G. Krieger. “A Controlled Comparison of Lysergic Acid Diethylamide (LSD) and Dextroamphetamine in Alcoholics.” American Journal of Psychiatry 125 (1969), pp. 1352–57. NIMH Research on LSD. “Extramural Programs Fiscal Year 1948 to Present.” Prepared September 1, 1975. Pahnke, W. “Drugs and Mysticism: An Analysis of the Relationship Between Psychedelic Drugs and the Mystical Consciousness.” Ph.D. thesis, Harvard University, 1963. Griffiths R. R., W. A. Richards, U. McCann, and R. Jesse. “Psilocybin Can Occasion Mystical-type Experiences Having Substantial and Sustained Personal Meaning and Spiritual Significance.” Psychopharmacology 187 (2006), pp. 268–83. Schultes, R. E., and A. Hofmann. The Botany and Chemistry of Hallucinogens. Springfield, IL: Charles C. Thomas, 1980.
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Al-Assmar, S. E. “The Seeds of the Hawaiian Baby Woodrose Are a Powerful Hallucinogen [letter].” Archives of Internal Medicine 159 (1999), p. 2090. Strassman, R. J., and others. “Differential Tolerance to Biological and Subjective Effects of Four Closely-Spaced Doses of N,N-dimethyltryptamine in Humans.” Biological Psychiatry 39 (1996), pp. 784–95. Grob, C. S., and others. “Human Psychopharmacology of Hoasca, a Plant Hallucinogen Used in Ritual Context in Brazil.” Journal of Nervous and Mental Disease 184 (1996), pp. 86–94. Dobkin de Rios, M., and M. Cardenas. “Plant Hallucinogens, Shamanism, and Nazca Ceramics.” Journal of Ethnopharmacology 2 (1980), pp. 233–46. De Ropp, R. S. Drugs and the Mind. New York: Grove Press, 1957. Ellis, H. “Mescal: A Study of a Divine Plant.” Popular Science Monthly 61 (1902), pp. 59, 65. Huxley, A. The Doors of Perception. New York: Harper & Row, 1954. MDMA. “Compound Raises Medical, Legal Issues.” Brain/ Mind Bulletin, April 15, 1985. Peroutka, S. J., and others. “Subjective Effects of 3,4-methylenedioxymethamphetamine in Recreational Users.” Neuropsychopharmacology 1 (1988), pp. 273–77. Ricaurte, G. A., J. Yuan, G. Hatzidimitriou, B. J. Cord, and U. D. McCann. “Severe Dopaminergic Neurotoxicity in Primates after a Common Recreational Dose Regimen of MDMA (Ecstasy).” Science 297 (2002), pp. 2260–3. Ricaurte, G. A., J. Yuan, and U. D. McCann. “(⫹/⫺)3,4-Methylenedioxymethamphetamine (‘Ecstasy’)-induced Serotonin Neurotoxicity: Studies in Animals.” Neuropsychobiology 42 (2000), pp. 5–10. Dworkin, S. I., S. Mirkis, and J. E. Smith. “Responsedependent versus Response-independent Presentation of Cocaine: Differences in the Lethal Effects of the Drug.” Psychopharmacology 117 (1995), pp. 262–6. Ricaurte, G. A. , J. Yuan, G. Hatzidimitriou, B. J. Cord, and U. D. McCann. “Retraction.” Science 301(2003), p. 1479.
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Luby, E., and others. “Study of a New Schizophrenomimetic Drug—Sernyl.” American Medical Association Archive of Neurological Psychiatry 81 (1959), pp. 113–19. Jevtovic-Todorovic, V., and others. “Ketamine Potentiates Cerebrocortical Damage Induced by the Common Anaesthetic Agent Nitrous Oxide in Adult Rats.” British Journal of Pharmacology 130 (2000), pp. 1692–98. Cosgrove, K. P., and M. E. Carroll. “Differential Effects of Bremazocine on Oral Phencyclidine (PCP) Self-Administration in Male and Female Rhesus Monkeys.” Experimental & Clinical Psychopharmacology 12 (2004), pp. 111–17. Overend, W. “PCP: Death in the ‘Dust.’ ” Los Angeles Times, September 26, 1977. Guitart, X., and others. “Sigma Receptors: Biology and Therapeutic Potential.” Psychopharmacology 174 (2004), pp. 301–19. Genesis 30:14–16. The New English Bible. Oxford University Press and Cambridge University Press, 1970. Schultes, R. E. “The Plant Kingdom and Hallucinogens (Part III).” Bulletin on Narcotics 22, no. 1 (1970), pp. 43–46. Beverly, R. The History and Present State of Virginia, 1705. Chapel Hill: University of North Carolina Press, 1947. Allegro, J. M. The Sacred Mushroom and the Cross. New York: Doubleday, 1970. Wasson, R. G. “Fly Agaric and Man.” In D.H. Efron, ed. Ethnopharmacologic Search for Psychoactive Drugs. Washington, DC: National Institute of Mental Health, 1967. See also Wasson, R. G. Soma, Divine Mushroom of Immortality. New York: Harcourt Brace Jovanovich, 1971. “Hallucinogens.” Columbia Law Review 68, no. 3 (1968), pp. 521–60. Sheffler, D. J., B. L. Roth, and A. Salvinorin. “The ‘Magic Mint’ Hallucinogen Finds a Molecular Target in the Kappa Opioid Receptor.” Trends in Pharmacological Sciences 24 (2003), pp. 107–09.
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14. Hallucinogens
Check Yourself
Name
Date
Hallucinogens from Plants Match the plants on the left with the appropriate hallucinogenic chemical on the right:
ayahuasca
mescaline
peyote
muscimol
sacred mushrooms (from Mexico)
d-lysergic acid amide
morning glories
atropine
belladonna
DMT and harmaline
Amanita
psilocybin
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Marijuana Objectives When you have finished this chapter, you should be able to: • Describe the relationship among marijuana, cannabis, and THC and discuss different preparations of cannabis. • Describe how Europeans became exposed to the psychological effects of cannabis. • Explain how marijuana was described in the years leading up to the 1937 Marijuana Tax Act. • Discuss the legal status of marijuana in the U.S. since 1937, including current debates. • Draw parallels among the various scientific and medical
Marijuana has meant so many studies on marijuana. things to so many people over • Describe the type of receptor THC acts on in the brain the years that it is hard to deand compare the time course of smoked vs. oral THC. scribe it from a single perspective. The matter of classifying • List the two most consistent physiological effects of marijuana among the other psymarijuana. choactive drugs is so complex • Discuss evidence for the abuse potential of marijuana that we, like most authors, avoid and influences on the psychological effects of marijuana. the issue by setting it off by itself. Marijuana can produce some • Describe the effects of marijuana use on driving ability, sedative-like effects, some pain the lungs, sperm motility, and the immune system. relief, and, in large doses, hal• Describe the range of evidence relating to whether lucinogenic effects. Thus, many marijuana smoking leads to brain damage in humans. of its users treat it as a depressant; it has been called a narcotic (for both pharmacological, as well as political, reasons); and it is often included among descriptions of hallucinogenic plants. Cannabis, the Plant However, the effects it produces when used as most people use it are sufficiently different Marijuana (or marihuana; either spelling is corfrom those of other psychoactive drugs to jusrect) is a preparation of leafy material from the tify its consideration as a unique substance. Cannabis plant that is smoked. The question is 365
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Online Learning Center Resources www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. • • • • • •
Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips
which Cannabis plant, because there is still botanical debate over whether there is one, three, or more species of Cannabis. In previous years, this issue spurred legal arguments because the laws mentioned only Cannabis sativa. Does that include all marijuana or not? The evidence is strong that there are three separate species. Cannabis sativa originated in Asia but now grows worldwide and primarily has been used for its fibers, from which hemp rope is made. This is the species that grows as a weed in the United States and Canada. Cannabis indica is grown for its psychoactive resins and is cultivated in many areas of the world, including selected planters and backyards of the United States. The third species, Cannabis ruderalis, grows primarily in Russia and not at all in America. The plant Linnaeus named C. sativa in 1753 is what is still known as C. sativa.1 C. sativa that is cultivated for use as hemp grows as a lanky plant up to 18 feet high. C. indica plants cultivated for their psychoactive effects are more compact and usually only two or three feet tall. The psychoactive potency results from an interaction between genetics and environmental conditions. Plants of different species grown under identical conditions produce different amounts of psychoactive material, and the same plants vary in potency from year to year, depending on the amount of sunshine, warm weather, and moisture.
A leaf of the Cannabis (marijuana) plant.
Preparations from Cannabis The primary psychoactive agent, delta-9tetrahydrocannabinol (THC), is concentrated in the resin of Cannabis; most of the resin is in the flowering tops, less is in the leaves, and there is little in the fibrous stalks. The psychoactive potency of a Cannabis preparation depends on the amount of resin present and therefore varies, depending on the part of the plant used.1 India has produced three traditional Cannabis preparations, each of which corresponds roughly to preparations available in the United States. The most potent of these is called charas in India, and it consists of pure resin that has been carefully removed from the surface of leaves and stems. Hashish, or hasheesh, is a substance widely known around the world and in its purest form is pure resin, like charas. It may be less pure, depending on how carefully the resin has been separated from the plant material. Hashish is rare in the United States, constituting less than 1 percent of all confiscated marijuana samples in the past 10 years. The average THC content of hashish has ranged from 3 to 7 percent with rare samples as high as about 20 percent.
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Drugs in the Media Medical Marijuana in the News Probably no single psychoactive drug topic has received more publicity in the past few years than the issue of medical marijuana, which has been placed as a referendum on the ballot in several states. Each time, there are stories about the plight of people with AIDS who say they need marijuana to stimulate their appetites. And each time there are stories reflecting the views of local police and federal drug-control officials who say that medical marijuana is just an excuse for people who want to grow and use an illegal substance. Here is a sampling of a few days’ headlines that reveal the complexity of the issues raised when these laws are considered and then passed: “Medical cannabis may be legalized in Illinois,” by Kate Stickelmaier, Daily Vidette, March 18, 2008. NORMAL, IL—In a decision on March 5, the Senate Public Health Committee voted 6–4 in favor of allowing the medical use of marijuana to become legal for those with debilitating diseases. “Pot for medical use on ballot: Supporters gather signatures to ensure the initiative will go before public in November,” by Mark Hornbeck, Detroit News, March 4, 2008. LANSING, MI—An initiative to legalize marijuana for medical use likely is headed for the November ballot in Michigan, following certification Monday of supporters’ petitions by a state elections panel. “Medical marijuana may go on Ohio ballot,” by Alan Johnson, The Columbus Dispatch, August 18, 2007. COLUMBUS, OH—A statewide issue to legalize medical marijuana is headed for the ballot in Michigan next year—and could swing south to Ohio shortly thereafter. “Doctors group backs marijuana for medical uses,” by Will Dunham, Reuters, February 15, 2008.
The second most potent preparation is traditionally called ganja in India, and it consists of the dried flowering tops of plants with pistillate flowers (female plants). The male plants are removed from the fields before the female plants can become pollinated and put their energy into seed production. This increases the potency of the female plants and produces high-grade
WASHINGTON, DC—A leading U.S. doctors’ group has endorsed using marijuana for medical purposes, urging the government to roll back a prohibition on using it to treat patients and supporting studies into its medical applications. “Calif. Firms Can Fire Medical Marijuana Users: State’s High Court Finds Compassionate Use Act Does Not Affect Employers’ Rights, by Karl Vick, Washington Post, January 25, 2008. LOS ANGELES, CA—The California Supreme Court ruled Thursday that employers can fire workers who test positive for marijuana even if they have a note from a doctor recommending its use for medical reasons. Judging from the small but increasing number of states that permit seriously ill patients to grow and use marijuana under medical supervision (California took the lead in 1996), the issue isn’t going away anytime soon. And this is separate from the issue of general legalization. Currently, marijuana maintains a slot alongside heroin and methamphetamine as a “drug of concern” in its listing on the federal Drug Enforcement Administration’s Web site. The average American so far seems uninterested in a serious national debate on the use of marijuana. The mere mention of legalizing any illegal drug means political suicide for any politician willing to broach the subject. A notable exception is former New Mexico Governor Gary Johnson, a Republican. An outspoken advocate for legalizing pot while in office, Johnson is also a triathlete who maintained steady popularity ratings in his state. Although most U.S. citizens may not be ready to embrace his stance, we will certainly be seeing more arguments in the media for legalizing medical marijuana use.
Cannabis (can a biss): the genus of plant known as marijuana. THC: delta-9-tetrahydrocannabinol, the most active chemical in marijuana. hashish (hash eesh or hash eesh): concentrated resin from the Cannabis plant.
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Hashish, concentrated resin from the Cannabis plant, is relatively rare in the United States.
marijuana known as sinsemilla (from the Spanish sin semilla, “without seeds”). The average THC content of sinsemilla samples from the United States also varies widely, ranging from 7 to 12 percent. The weakest form in India is bhang, which is made by using the entire remainder of the plant after the top has been picked, then drying it and grinding it into a powder. The powder can then be mixed into drinks or candies.1 This type of preparation is rare in the United States, but it is similar to low-grade marijuana, which consists of the leaves of a plant, perhaps even a sativa plant found growing as a weed. Some of this low-grade marijuana contains less than 1 percent THC. Manually scraping exuded resin off the plant to make hashish is a tedious process, and a more efficient method of separating the resin from plants has been known for many years. The plants are boiled in alcohol, then the solids filtered out and the liquid evaporated down to a thick, dark substance once known medically as “red oil of cannabis” and now referred to as hash oil. Again, this product varies widely in its potency but can contain more than 50 percent THC. Until fairly recently, both the medical and the psychological effects of Cannabis preparations were variable. All the traditional methods could do was produce relatively pure
plant resin, but that resin could vary considerably in its THC content. If we consider only the marijuana available for smoking in the United States, we can see that it can vary widely in potency from a low-grade product containing less than 1 percent THC to a high-grade sinsemilla containing 9 percent or more THC. The usual range of potency for marijuana seems to be 2 to 8 percent, however. Since the early 1980s, repeated reports have stated that the marijuana available on the streets today is “10 times” more potent than the marijuana of the 1960s. The political message behind this is that the marijuana of the 1960s may have been relatively harmless, but the current marijuana is more dangerous. In fact, the entire range of these traditional preparations has been known, and scientific, literary, and medical descriptions of the wide range of effects have been based on this entire range of potencies, for 150 years. But it is true that U.S. marijuana growers are becoming more sophisticated and producing more sinsemilla.
History Early History The earliest reference to Cannabis is in a pharmacy book written in 2737 BC by Chinese emperor Shen Nung. Referring to the euphoriant effects of Cannabis, he called it the “Liberator of Sin.” He recommended it for some medical uses, including “female weakness, gout, rheumatism, malaria, beriberi, constipation and absent-mindedness.” Social use of the plant had spread to the Muslim world and North Africa by AD 1000. In this period in the eastern Mediterranean area, a legend developed around a religious cult that committed murder for political reasons. The cult was called “hashishiyya,” from which our word assassin developed. In 1299, Marco Polo told the story he had heard of this group and its leader. It was a marvelous tale and had all the ingredients necessary for a tale to survive through the
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ages: intrigue, murder, sex, the use of drugs, and mysterious lands. The story of this group and its activities was told in many ways over the years, and Boccaccio’s Decameron contained one story based on it. Stories of this cult, combined with the frequent reference to the power and wonderment of hashish in The Arabian Nights, were widely circulated in Europe over the years.
The 19th Century: Romantic Literature and the New Science of Psychology At the start of the 19th century, world commerce was expanding. New and exciting reports from the world travelers of the 17th and 18th centuries introduced new cultures and new ideas to Europe. Asia and the Middle East had yielded exotic spices, as well as the stimulants coffee and tea. Europe was ready for another new sensation, and got it. The returning veteran, as usual, gets part of the blame for introducing what Europe was ready to receive: Napoleon’s campaign to Egypt at the beginning of the nineteenth century increased the Romantic’s acquaintance with hashish and caused them to associate it with the Near East. . . . Napoleon was forced to give an order forbidding all French soldiers to indulge in hashish. Some of the soldiers brought the habit to France, however, as did many other Frenchmen who worked for the government or traveled in the Near East.2
By the 1830s and 1840s, everyone who was anyone was using, thinking about using, or decrying the use of mind-tickling agents such as opium and hashish. One of the earliest (1844) popular accounts of the use of hashish is in The Count of Monte Cristo by Alexander Dumas. The story includes a reference to the Assassins tale and contains statements about the characteristics of the drug that still sound contemporary. During the 1840s, a group of artists and writers gathered monthly at the Hotel Pimodan in Paris’s Latin Quarter to use drugs. This group became famous because one of the participants, Gautier, wrote a book, Le Club de Hachischins, that described their activities. From this group
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have come some of the best literary descriptions of hashish intoxication. These French Romantics, like the Impressionist painters of a later period, were searching for new experiences, new sources of creativity from within, and new ways of seeing the world outside. A few of the regulars were well-known writers, including Baudelaire, Gautier, and Dumas. Baudelaire used hashish and was an astute observer of its effects in himself and in others. In his book Artificial Paradises, he echoed what Dumas had written about the kind of effect to expect from hashish: The intoxication will be nothing but one immense dream, thanks to intensity of color and the rapidity of conceptions; but it will always preserve the particular tonality of the individual. . . . The dream will certainly reflect its dreamer. He is only the same man grown larger . . . sophisticate and ingenu . . . will find nothing miraculous, absolutely nothing but the natural to an extreme.3
As the end of the 19th century approached, the use of psychoactive drugs increased, but the hashish experience held little interest for the dweller in middle America.
“Marijuana, Assassin of Youth” At the beginning of the 20th century, public interest in Cannabis and its use was not widespread. In the early 1920s, a few references in the mass media reported the use by Mexican Americans of something the newspapers called marijuana, but public concern was not aroused. In 1926, however, a series of articles associating marijuana and crime appeared in a New Orleans newspaper. As a result, the public began to take an interest in this “new” drug. The U.S. commissioner of narcotics, Harry Anslinger, said that in 1931 the Bureau of Narcotics’ file on marijuana was less than two
sinsemilla (sin se mee ya): “without seeds”; a method of growing more potent marijuana.
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inches thick. The same year, the Treasury Department stated: A great deal of public interest has been aroused by the newspaper articles appearing from time to time on the evils of the abuse of marijuana, or Indian hemp. This publicity tends to magnify the extent of the evil and lends color to an inference that there is an alarming spread of the improper use of the drug, whereas the actual increase in such use may not have been inordinately large.4
Even so, by 1935, 36 states had laws regulating the use, sale, and/or possession of marijuana. By the end of 1936, all 48 states had similar laws. The Federal Bureau of Narcotics also changed its tune. In 1937, at congressional hearings, Anslinger stated, “Traffic in marihuana is increasing to such an extent that it has come to be the cause for the greatest national concern.”5 From 1931 to 1937, the use of marijuana had spread throughout the country, but there is no evidence that there was extensive use in most communities. The primary motivation for the congressional hearings on marijuana came not because of the use of marijuana as an inebriant or a euphoriant but because of reports by police and in the popular literature stating, “Most crimes of violence are laid to users of marihuana.”6 Scientific American reported in March 1936: Marijuana produces a wide variety of symptoms in the user, including hilarity, swooning, and sexual excitement. Combined with intoxicants, it often makes the smoker vicious, with a desire to fight and kill.7
And Popular Science Monthly in May 1936 contained a lengthy article with such statements as this: The Chief of Philadelphia County detectives declared that whenever any particularly horrible crime was committed—and especially one pointing to perversion—his officers searched first in marijuana dens and questioned marijuana smokers for suspects.8
It hardly seemed necessary for readers to be told that marijuana had arrived as “the foremost menace to life, health, and morals in the list of drugs used in America.”8 In this period the association was repeatedly made between crime, particularly violent and/or perverted crime, and marijuana use. A typical report follows: In Los Angeles, Calif., a youth was walking along a downtown street after inhaling a marijuana cigarette. For many addicts, merely a portion of a “reefer” is enough to induce intoxication. Suddenly, for no reason, he decided that someone had threatened to kill him and that his life at that very moment was in danger. Wildly he looked about him. The only person in sight was an aged boot-black. Drug-crazed nerve centers conjured the innocent old shoe-shiner into a destroying monster. Mad with fright, the addict hurried to his room and got a gun. He killed the old man, and then, later, babbled his grief over what had been wanton, uncontrolled murder. “I thought someone was after me,” he said. “That’s the only reason I did it. I had never seen the old fellow before. Something just told me to kill him!” That’s marijuana!9
However, not all articles condemned marijuana as the precipitator of violent crimes. An article in The Literary Digest reported that the chief psychiatrist at Bellevue Hospital in New York City had reviewed the cases of more than 2,200 criminals convicted of felonies. Referring to marijuana, he said, “None of the assault cases could be said to have been committed under the drug’s influence. Of the sexual crimes, there was none due to marihuana intoxication. It is quite probable that alcohol is more responsible as an agent for crime than is marihuana.”10 There was very poor documentation of the relationship between marijuana and crime, which in the 1930s was stated as if it had been proved. A thorough review of Commissioner Anslinger’s writings on marijuana concluded: In the works of Mr. Anslinger, there are either no references or references to volumes which my
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www.mhhe.com/hart13e assistants and I have checked and which, in our checking, we find to be based upon much hearsay and little or no experimentation. We found a mythology in which later writers cite the authority of earlier writers, who also had little evidence. We have found, by and large, what can most charitably be described as a pyramid of prejudice, with each level of the structure built upon the shaky foundations of earlier distortions.11
Examples of this “pyramid of prejudice” abound, but here’s one way it worked: One of Mr. Anslinger’s Treasury agents would testify before Congress and relate one of the outrageous stories of marijuana-induced violence. Next, the testimony would be referred to in an editorial in a medical journal, such as the Journal of the American Medical Association (JAMA). Then Anslinger or one of his people would write a magazine article, citing the prestigious JAMA as the source of the information. With such poor evidence supporting the relationship between marijuana use and crime, it seems strange that the true story was never told. There are probably several reasons. One was the Great Depression, which made everyone acutely sensitive to, and wary of, any new and particularly foreign influences. The fact that it was lower-class Mexican Americans and African Americans who were associated with use of the drug made the drug doubly dangerous to the white middle class. Another contributing factor probably was the regular reference in associating marijuana and crime to the murdering cult of Assassins as suggestive of the characteristics of the drug. The 1936 Popular Science Monthly reference to the Assassins is the most concise: The origin of the word “assassin” has two explanations, but either demonstrates the menace of Indian hemp. According to one version, members of a band of Persian terrorists committed their worst atrocities while under the influence of hashish. In the other version, Saracens who opposed the Crusaders were said to employ the services of hashish addicts to secure secret murderers of the leaders of the Crusades. In both
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versions, the murderers were known as “haschischin,” “hashshash” or “hashishi” and from those terms comes the modern and ominous “assassin.”8
In none of the original stories and legends were the murders committed by individuals under the influence of hashish; rather, hashish may have been part of the reward for carrying out various crimes. No matter. As the 1930s rolled on, fear of marijuana users and of marijuana itself increased, as did state marijuanacontrol laws. In the mid-1930s, the Narcotics Bureau acted to support federal legislation, and in the spring of 1937 congressional hearings were held.
The Marijuana Tax Act of 1937 Passage of the Marijuana Tax Act was a foregone conclusion. Few witnesses testified other than law enforcement officers. People dealing in birdseed had the act modified so they could import sterilized Cannabis seed for use in their product. An official of the American Medical Association (AMA) testified on his own behalf, not representing the AMA, against the bill. His reasons for opposing the bill were multiple. Primarily, he thought the state antimarijuana laws were adequate and that the social-menace case against Cannabis had not been proved. It might be that most other medical doctors didn’t associate the old remedies based on Cannabis with this new, foreign-sounding drug marijuana. The bill was passed in August and became effective on October 1, 1937. The general characteristics of the law followed the regulation-by-taxation theme of the Harrison Act of 1914. The federal law did not outlaw Cannabis or its preparations; it just taxed the grower, distributor, seller, and buyer and made it, administratively, almost impossible for anyone to have anything to do with Cannabis. In addition, the Bureau of Narcotics prepared a uniform law that many states adopted. The uniform law on marijuana specifically named C. sativa as the species of plant whose leafy material is illegal.
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In later years, the defense in some court cases argued that the material confiscated by the police had come from C. indica and thus was not illegal. In the usual specimens obtained by police or presented in court, all distinguishing characteristics between species are either not present or are obliterated by drying and crushing. Because the cannabinoids are present in all species, there is no way of telling what species most confiscated marijuana belongs to. The current federal and uniform laws refer only to Cannabis. The state laws made possession and use of Cannabis illegal per se. In May 1969, 32 years later, the U.S. Supreme Court declared the Marijuana Tax Act unconstitutional and overturned the conviction of Timothy Leary because there was in the Federal anti-marijuana law—a section that requires the suspect to pay a tax on the drug, thus incriminating himself, in violation of the Fifth Amendment: and a section that assumes (rather than requiring proof) that a person with foreign-grown marijuana in his possession knows it is smuggled.12
After the Marijuana Tax Act Passage of the Marijuana Tax Act had an amazing effect. Almost immediately there was a sharp reduction in the reports of heinous crimes committed under the influence of marijuana. The price of the merchandise increased rapidly (the war came along, too), so that five years after passage of the act the cost of a marijuana cigarette—a reefer—had increased 6 to 12 times and cost about a dollar. The year after the law was enacted, 1938, Mayor Fiorello LaGuardia of New York City remembered what no one else wanted to recall. What he recalled were two army studies on marijuana use by soldiers in the Panama Canal Zone around 1930. Both reports had found marijuana to be innocuous and had said that its reputation as a troublemaker “was due to its association with alcohol which was always found the prime agent.”13 Mayor LaGuardia asked the New York Academy of Medicine to study marijuana, its
use, its effects, and the necessity for control. The report, issued in 1944, was intensive and extensive and a very good study for its time. Following is only a part of the report’s summary:14 It was found that marihuana in an effective dose impairs intellectual functioning in general. . . . Marihuana does not change the basic personality structure of the individual. It induces a feeling of self-confidence, but this expressed in thought rather than in performance. There is, in fact, evidence of a diminution in physical activity. . . . Those who have been smoking marihuana for a period of years showed no mental or physical deterioration which may be attributed to the drug.14
This 1944 report, which was completed by a reputable committee of the New York Academy of Medicine, brought a violent reaction. The AMA stated in a 1945 editorial: For many years medical scientists have considered cannabis a dangerous drug. Nevertheless, a book called “Marihuana Problems” by New York City Mayor’s Committee on Marihuana submits an analysis of seventeen doctors of tests on 77 prisoners and, on this narrow and thoroughly unscientific foundation, draws sweeping and inadequate conclusions which minimize the harmfulness of marijuana. Already the book has done harm. One investigator has described some tearful parents who brought their 16 year old son to a physician after he had been detected in the act of smoking marihuana. A noticeable mental deterioration had been evident for some time even to their lay minds. The boy said he had read an account of the LaGuardia Committee report and that this was his justification for using marihuana.15
As in all such reports and reactions to reports, there is little dispute over the facts, only over the interpretation. The LaGuardia Report is consistent with the Indian Hemp Commission Report of the 1890s, the Panama Canal Zone reports of the 1930s, and the comprehensive reports in the 1970s by the governments of New Zealand, Canada, Great Britain, and the United States, in addition to the 1981 report to the World Health Organization and the 1982 report
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Anandamide Carbon
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Figure 15.1 Delta-9 THC, The Most Active Substance Found in Cannabis, and Anandamide, Isolated from Brain Tissue by the National Academy of Science to the Congress of the United States, so it is likely that the conclusions of the LaGuardia Report were and are for the most part valid. The 1950s and 1960s were a unique period in the history of marijuana. There was a hiatus in scientific research on Cannabis, but experimentation in the streets increased. With the arrival of the “psychedelic ’60s,” the popular press emphasized the more sensational hallucinogens. Marijuana, however, became the most common symbol of youthful rejection of authority and identification with a new era of personal freedom. According to the annual high school senior survey and the NIDA household survey (see Chapter 1), marijuana apparently peaked in popularity in the United States in the late 1970s. During the mid-1980s and early 1990s, marijuana use became much less popular than it had been in the 1970s, but the mid-1990s saw the beginning of a significant rise in the number of young people using marijuana.
Pharmacology Cannabinoid Chemicals The chemistry of Cannabis is quite complex, and the isolation and extraction of the active ingredient are difficult even today. The active
agent in Cannabis is unique among psychoactive plant materials in that it contains no nitrogen and thus is not an alkaloid. There are more than 400 chemicals in marijuana, but only 66 of them are unique to the Cannabis plant—these are called cannabinoids. One of them, delta-9-tetrahydrocannabinol (THC), was isolated and synthesized in 1964 and is clearly the most pharmacologically active. Structures of some of these chemicals are shown in Figure 15.1. The major active metabolite in the body of THC is 11-hydroxy-delta-9-THC. The relationship of THC to Cannabis is probably more similar to the relationship of nicotine to tobacco than of alcohol to beer, wine, or distilled spirits. Alcohol is the only behaviorally active agent in alcoholic beverages, but there might be several active agents in Cannabis.
Absorption, Distribution, and Elimination When smoked, THC is rapidly absorbed into the blood and distributed first to the brain, then redistributed to the rest of the body, so that within 30 minutes much is gone from the brain. The peak psychological and cardiovascular effects occur together, usually within 5 to 10 minutes. The THC remaining in the blood has a half-life of about 19 hours, but metabolites (of
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which there are at least 45), primarily 11hydroxy-delta-9-THC, are formed in the liver and have a half-life of 50 hours. After one week, 25 to 30 percent of the THC and its metabolites might still remain in the body. Complete elimination of a large dose of THC and its metabolites might take two or three weeks. THC taken orally is slowly absorbed, and the liver transforms it to 11-hydroxy-delta-9-THC; therefore, much less THC reaches the brain after oral ingestion, and it takes much longer for it to have psychological and cardiovascular effects. The peak effects following oral ingestion usually occur at about 90 minutes. The high lipid solubility of THC means that it (like its metabolites) is selectively taken up and stored in fatty tissue to be released slowly. Excretion is primarily through the feces. All of this has two important implications: (1) there is no easy way to monitor (in urine or blood) THC/metabolite levels and relate them to behavioral and/or physiological effects, as can be done with alcohol, and (2) the long-lasting, steady, low concentration of THC and its metabolites on the brain and other organs might have effects not yet determined.
Mechanism of Action Scientists searched for years for a key to help them unlock the mystery of marijuana’s action on the central nervous system. The identification and purification of THC was a necessary step. A significant breakthrough was made by researchers in 1988 who developed a technique to identify and measure highly specific and selective binding sites for THC and related compounds in rat brains. One result was the development and testing of more potent marijuana analogues. Another result was the 1992 discovery of a natural substance produced in the body that has marijuana-like effects when administered to animals. This endogenous substance (see Figure 15.1) is called anandamide (ananda is sanskrit for “bliss”).16 THC and other cannabinoids are known to bind to two receptors, designated CB1 and
CB2.17 There are substantial differences in the structures of these two receptors and their anatomical distribution in the body. CB2 receptors are found mainly outside the brain in immune cells, suggesting that cannabinoids may play a role in the modulation of the immune response. CB1 receptors are found throughout the body, but primarily in the brain. These receptors are much more abundant than receptors for morphine and heroin,17 suggesting that the potential actions of cannabinoids are widespread. The locations of CB1 receptors in the brain also may provide some clues about their functions. For example, the highest density of CB1 receptors has been found in cells of the basal ganglia; its primary components include the caudate nucleus, putamen, and globus pallidus. Cells of the basal ganglia are involved in coordinating body movements. Other regions that also contain a larger number of CB1 receptors include the cerebellum, which coordinates fine body movements; hippocampus, which is involved in aspects of memory storage; cerebral cortex, which regulates the integration of higher cognitive functions; and nucleus accumbens, which is involved in reward. A number of drugs have been developed in an effort to more selectively act on these receptors. Rimonabant, a selective CB1 receptor antagonist, is currently available in several countries as an anti-obesity agent. The U.S. Food and Drug Administration, however, declined to approve it for use because of concerns about side effects such as depression and anxiety.
Physiological Effects One of the most consistent acute physiological effects of both smoked marijuana and oral THC is an increase in heart rate. Figure 15.2 shows that both smoked marijuana and oral THC increased the heart rate of marijuana smokers in a dose-dependent fashion (i.e., larger THC doses produced larger heart rate elevations).18,19 While the peak effects produced by smoking marijuana containing 4 percent THC are similar to 20 mg oral THC, the drug’s time course of action is
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Figure 15.2 The Time Course for Heart Rate after Smoking Marijuana (left) and Ingesting Oral THC (right) different. Peak heart-rate elevations produced by smoked marijuana occurred within 10 minutes and returned to baseline levels after about 90 minutes, whereas peak heart-rate elevations produced by oral THC did not occur until 90 minutes following ingestion and remained elevated for at least four hours after drug administration. The effect of cannabis-based drugs on blood pressure is more variable, with some studies reporting slight increases and others reporting no effect. Concern has been raised that smoking marijuana might have permanent deleterious effects on the cardiovascular system, but there is no evidence to indicate that marijuana-related cardiovascular effects are associated with serious health problems for most young, healthy users.20 Patients with hypertension, cerebrovascular disease, and coronary atherosclerosis, however, should probably avoid smoking marijuana or ingesting THC because of the drug’s effects on heart rate. Other consistent acute effects of smoked marijuana are reddening of the eyes and dryness of the mouth and throat. Except for bronchodilation, acute exposure to marijuana has little effect on breathing as measured by conventional pulmonary tests. Heavy marijuana smoking over a much longer period could lead to clinically signifi-
cant and less readily reversible impairment of pulmonary function.
Behavioral Effects While physiological effects produced by cannabis-based drugs provide important information, the behavior of most interest for the assessment of abuse potential is drug taking. Until recently, cannabinoids were not shown to maintain self-administration in laboratory animals, suggesting that the abuse potential of cannabis-based drugs was minimal. This seemed inconsistent with epidemiological data showing that marijuana is the most widely used illicit drug in the world21 and that a substantial proportion of Americans seek treatment for marijuana abuse and dependence each year.22 Findings from recent studies, however, demonstrate clearly that rats and squirrel monkeys will consistently self-administer cannabinoids.23 The success of recent attempts to obtain reliable selfadministration in laboratory animals has been
anandamide (an and a mide): a chemical isolated from brain tissue that has marijuana-like properties.
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attributed to intravenously injecting THC doses more rapidly than had been previously tried. Several laboratory studies have shown that marijuana produces robust self-administration by human marijuana smokers, and that marijuana self-administration is related to the THC content of the cigarettes. That is, marijuana cigarettes containing a higher concentration of THC are preferred to those containing a lower THC concentration.24 These findings not only confirm the abuse potential of smoked marijuana, but they also suggest that THC administered alone (e.g., oral administration of THC capsules) might have abuse potential. In a recent study, experienced marijuana smokers were given repeated opportunities to self-administer oral THC capsules or to receive $2. Several important findings from that study are worth mentioning. Participants selected: (1) money on more occasions than the capsules; (2) more drugcontaining capsules than placebo; and (3) more THC capsules during social/recreational periods compared to non–social/recreational periods. These observations indicate that oral THC’s abuse potential is modest at best, experienced marijuana smokers can readily distinguish THCrelated effects, and cannabis self-administration is influenced by social factors.19 Some have argued that before novice marijuana smokers are able to experience marijuanaassociated positive subjective effects (e.g., euphoria, stoned), they must go through a process by which they learn to recognize and interpret the psychoactive effects produced by smoked marijuana.25 While this position remains open for debate, the subjective effects on experienced marijuana smokers have been well characterized. In general, experienced smokers report increased ratings of euphoria, “high,” mellowness, hunger, and stimulation after smoking marijuana. These effects peak within 5 to 10 minutes and last for about two hours; they are usually THC concentration-dependent (i.e., the magnitude of effects is increased with increasing THC concentrations). Subjective effects reported by infrequent smokers are similar but more intense because these individuals are
Experienced marijuana smokers report euphoria, “high,” hunger, and mellowness after smoking; the magnitude of the effects depends on the THC concentration.
less tolerant to marijuana-associated effects. Also, at higher THC concentrations some infrequent smokers may report negative effects such as mild paranoia and hallucination. As seen with heart rate, peak subjective effects of oral THC are similar to those produced by smoked marijuana except that the time course of the effects is different. Peak subjective effects occur about 90 minutes following oral ingestion and can last for several hours. An important factor in determining whether a drug is likely to be abused is the rapidity of the onset of its effects. The more rapidly a drug’s effects are experienced, the more likely it will be abused. This might be why the abuse potential of oral THC is limited.
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While an earlier study demonstrated that relatively less-experienced marijuana smokers reported being intoxicated after smoking a placebo cigarette, more recent studies demonstrate that regular marijuana smokers are not so readily duped. Placebo cigarettes were made by extracting the THC and other cannabinoids from marijuana—the cigarettes looked and smelled like regular marijuana cigarettes. In these studies, participants “sampled” marijuana cigarettes (containing placebo or different THC concentrations) and alternative reinforcers (e.g., money or snack food), and subsequently were given an option to choose. Participants selected cigarettes containing THC on more than 75 percent of choice opportunities compared to only about 40 percent when placebo cigarettes were available.26 Furthermore, subjective effects produced by the placebo cigarette were identical to baseline levels, whereas subjective effects produced by cigarettes containing THC were significantly elevated. The effect of marijuana on cognitive performance has received a great deal of attention in the popular press and the scientific literature for many years with little resolution. Unfortunately, many discussions on this topic add to the confusion because they fail to differentiate between the direct (acute) effects and long-term (chronic) effects of marijuana. They also fail to consider the marijuana use history of the user. Following acute administration of smoked marijuana to infrequent marijuana smokers, cognitive performance is disrupted temporarily in several domains: The amount of time that is required to complete cognitive tasks is increased (slowed cognitive processing); performance on immediate recall tasks is decreased (impaired short-term memory); premature responding is increased (impaired inhibitory control); performance on tracking tasks is decreased (loss of sustained concentration or vigilance); and performance on tasks requiring participants to reproduce computer-generated patterns is disrupted (impaired visuospatial processing). The acute effects of marijuana on the performance of frequent smokers are less dramatic, leading
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some to hypothesize that regular marijuana smokers are tolerant to many marijuana-related cognitive effects.18 Some negative cognitive effects, however, have been reported. For example, slowing of cognitive performance is a consistent finding, even in regular users. This effect may have significant behavioral consequences under circumstances requiring complex operations that must be accomplished in a limited time frame, such as certain workplace tasks and the operation of machinery and automobiles. It is also difficult to make definitive statements about long-term cognitive effects of marijuana use because of divergent findings and interpretations. More general conclusions, however, are possible. Based on the available evidence, it appears that following a sufficient period of abstinence (greater than one month), regular marijuana use produces minimal effects on cognition as measured by standard neuropsychological tests.27 The reader is cautioned, though, because as the number of better controlled studies increase, the current conclusions about the long-term effects of marijuana on cognition may change. We’ve all heard about someone smoking marijuana and then getting a case of the “munchies,” a marked increase in food intake. Data from a large number of studies clearly demonstrate that marijuana and oral THC significantly increase food intake. These findings provided the basis for at least one clinical use of cannabisbased drugs—appetite stimulation (see “Medical Uses of Cannabis”). A related question that has received less scientific attention is: Why aren’t most chronic marijuana users overweight? Some have speculated that tolerance develops to the food intake-enhancing effect of cannabis-based drugs, but no empirical data support this view. The bottom line is that the average weight of chronic marijuana users is not known because there have been no studies addressing this issue. So, the average chronic marijuana user may indeed be overweight. Or it could be that most marijuana use occurs during youth (this is certainly supported by data from national surveys), when people and their metabolism are most active.
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Another consistent behavioral effect of marijuana is on verbal behavior (talking). Stimulant drugs such as amphetamines have been shown to increase verbal interactions, as have moderate doses of alcohol. Marijuana appears to be different. Several researchers have reported that while nonverbal social interactions are increased following marijuana smoking, verbal exchanges are dramatically decreased.28
Medical Uses of Cannabis Cannabis has never attained the medical status of opium, but the first report of medical use was by Shen Nung in 2737 BC. About 2,900 years after the Shen Nung report, another Chinese physician, Hoa-tho (AD 200) recommended Cannabis resin mixed with wine as a surgical anesthetic. Although Cannabis preparations were used extensively in medicine in India and after about AD 900 in the Near East, almost nothing about it appeared in European medical journals until the 1800s. Early reports in Europe, such as de Sacy’s 1809 article titled “Intoxicating Preparations Made with Cannabis,” awakened more interest among the writers and artists of the period than among physicians. In 1839, however, a lengthy article, “On the Preparations of the Indian Hemp, or Gunjah,” was published by a British physician working in India.29 He reviewed the use of Cannabis in Indian medicine and reported on his own work with animals, which suggested that Cannabis preparations were quite safe. Having shown Cannabis to be nontoxic, he used it clinically and found it to be an effective anticonvulsant and muscle relaxant, as well as a valuable drug for the relief of the pain of rheumatism. In 1860, the Ohio State Medical Society’s Committee on C. indica reported its successful use in the treatment of stomach pain, chronic cough, and gonorrhea. One physician felt he had to “assign to the Indian hemp a place among the so-called hypnotic medicines next to opium.”30 One difficulty that has always plagued the scientific, medical, and social use of Cannabis is
the variability of the product. An 1898 brochure reviewed the assay and standardization techniques used with many of the common plant drugs and stated: “In Cannabis Indica we have a drug of great importance and one which of all materia medica is undoubtedly the most variable.”31 Four years later, Parke, Davis,32 using new standardization procedures, claimed that “each lot sent out upon the market by us is of full potency and to be relied upon.” The company listed a variety of Cannabis products available for medical use, including “a Chocolate Coated Tablet Extract Indian Cannabis 1/4 grain.” Passage of the Marijuana Tax Act of 1937 resulted in all 28 of the legal Cannabis preparations being withdrawn from the market, and in 1941 Cannabis was dropped from The National Formulary and The U.S. Pharmacopoeia. The decline in the medical use of Cannabis occurred long before 1937, and the law did not eliminate an actively used therapeutic agent. Four factors, however, contributed to the declining prescription rate of this plant. One was the development of new and better drugs for most illnesses. Second was the variability of the available medicinal preparations of Cannabis, which was repeatedly mentioned in the 1937 hearings.5 Third, the active ingredient is very insoluble in water and thus not amenable to injectable preparations. Last, taken orally it has an unusually long (oneto two-hour) latency to onset of action. With the recent renewed interest in marijuana as a social drug has come some reevaluation of the implications of some of the older therapeutic reports. Scientists have looked again at some of the most interesting reported therapeutic effects of Cannabis. One is its anticonvulsant activity. A 1949 report found it effective in some cases in which phenytoin (Dilantin), the anticonvulsant of choice both then and now, was ineffective.33 The fact that both Queen Victoria’s physician and Sir William Osler, as well as others, found Cannabis to be very effective against tension and migraine headaches also caused some interest. A 1971 report showed that marijuana smoking was effective in reducing the fluid pressure
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evidence is most impressive in glaucoma . . . ; in asthma . . . ; and in the nausea and vomiting of cancer chemotherapy . . . and might also be useful in seizures, spasticity, and other nervous system disorders.36
The potential medical benefits of marijuana is an issue with a long and controversial history.
of the eye in a glaucoma patient.34 That report became a cause célèbre in 1975, when Robert Randall, a glaucoma patient, was arrested for growing marijuana plants on his back porch for medical purposes. Fifteen months later, he (1) saw the charges against him dropped, (2) had his physician certify that the only way for him to avoid blindness was to smoke five joints a day, and (3) had these marijuana joints legally supplied to him by the United States government.35 This began a limited program in which the National Institute on Drug Abuse (NIDA) provided marijuana cigarettes to patients with the FDA’s approval of a “compassionate use” protocol. A second possible important medical use was reported in 1975. Medication containing THC was found to be effective in reducing the severe nausea caused by certain drugs used to treat cancer. A 1982 report from the National Academy of Sciences stated: Cannabis and its derivatives have shown promise in the treatment of a variety of disorders. The
In 1985, the FDA licensed a small drug company, Unimed, Inc., to begin producing a capsule containing THC for sale to cancer chemotherapy patients who are experiencing nausea. The drug is referred to by the generic name dronabinol and the brand name Marinol. Dronabinol has helped cancer chemotherapy patients gain weight, and in 1993 the FDA also approved its use for stimulating appetite in AIDS patients. Proponents of medical marijuana argue that the smoked version of the drug should be made legally available as well. They contend that smoked marijuana has several advantages relative to oral THC, including a more rapid onset of effects and greater ability of the patient to control medication effects. It is also possible that marijuana plant constituents other than THC may contribute to the drug’s therapeutic effects, that is the combination and/or balance of the chemicals contained in the plant may be an important factor for beneficial effects. Such arguments, however, have not been successful in terms of reclassifying marijuana under the U.S. Controlled Substance Act. Marijuana remains a Schedule I drug, which means, from a federal government perspective, it cannot be legally prescribed because it has no acceptable medical use. Of course, many citizens and medical professionals disagree with the U.S. government’s position regarding the medical utility of marijuana. This has become more apparent in recent years as citizens have attempted to take action at the state level. In November 1996, both Arizona and California voters passed ballot initiatives allowing physicians to recommend marijuana
dronabinol (dro nab i noll): the generic name for prescription THC in oil in a gelatin capsule. Marinol (mare i noll): the brand name for dronabinol.
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Taking Sides Should Medical Patients Have Access to Marijuana? At least 12 states have passed ballot initiatives allowing patients to use marijuana on the advice of their physicians. Passage of these initiatives has fueled public interest in this topic. The bestdemonstrated effects of marijuana (and of THC) are the reduction of the nausea caused by chemotherapy for cancer and the stimulation of appetite, which might benefit AIDS patients. With such serious illnesses involved, many feel that the compassionate thing is to allow marijuana to be used if it might help, since the risk of dependence seems to be a rather small issue in such cases. In fact, “Cannabis buyers clubs” sprang up in many large cities—most notably, San Francisco—and patients who had notes from the physicians could purchase from them. These clubs were illegal, but local law enforcement agencies for the most part left them alone, not wanting to arrest seriously ill patients. Of course, because the clubs were illegal and informally operated, there was no guarantee that everyone purchasing marijuana was, in fact, seriously ill. Following the passage of the first ballot initiatives, the U.S. government in December 1996 announced that it would move to revoke the DEA registration of any physician who advised a patient to use illegal drugs. This caused some to wonder about violations of the tradition of privileged communications between doctors and patients, and so far the legality of all of this is open to question. In early 1998, the U.S. Justice Department announced plans to shut down all Cannabis buyers clubs in California. In September 2000, the U.S. District Court in San Francisco issued an injunction permanently barring the government from revoking a physician’s
for serious illnesses and allowing patients to possess and use marijuana if their physicians recommend it. There was still no legal way for patients to purchase marijuana, of course, and no legal growers or distributors. More than half the states had previously passed laws allowing medicinal use of marijuana, so in a sense this was not new. However, those previous laws had passed in the 1970s, when
license to prescribe medicine “merely because the doctor recommends medical marijuana to a patient based on a sincere medical judgement.” The court also prevented the government from initiating an investigation of a doctor’s other prescribing practices solely because he or she had recommended marijuana. In November 2000, at the White House’s request, the U.S. Supreme Court issued an emergency ban (by a vote of 7–1) on the distribution of marijuana for medical purposes. The court struck down the U.S. Court of Appeals ruling in San Francisco, which would have made “medical necessity” a defense against violation of federal drug statutes. The court voted 8–0 against such defenses in May 2001. In November 2004, the Supreme Court heard arguments in Raich v Ashcroft, a case brought on behalf of Angel Raich, a California patient, and others. They asserted that because the marijuana was provided to Ms. Raich free, the transactions did not constitute “commerce.” And, since the growing, transfer, and use of the marijuana were all done within California, the federal government could not assert jurisdiction based on its ability to regulate interstate commerce. In June 2005, the U.S. Supreme Court disagreed ruling that federal law enforcement personnel could prosecute patients for possessing marijuana even if their physicians recommended marijuana use for a serious illness. Despite this ruling, the medical marijuana issue is far from being resolved. In fact, in July 2007, New Mexico became the twelfth state to legalize the medical use of marijuana. Do you think medical necessity is a compelling argument for the use of marijuana? Why or why not?
decriminalization and even legalization of marijuana were being debated openly. Also, many of those older laws allowed marijuana to be used only as part of an approved research effort, not for individual patients. As of early 2008, 12 states had some form of legislation allowing a patient, with a physician’s authorization (or prescription), to use marijuana for medical purposes (see Taking Sides).
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In 1997, in response to public pressure to allow the medical use of marijuana, the White House Office of National Drug Control Policy funded another study by the Institute of Medicine (IOM) of the National Academy of Sciences to perform a comprehensive review of the scientific evidence for potential benefits and risks of using marijuana as a medicine. The resulting 1999 report has been pointed to by proponents of medical marijuana as supporting the idea that marijuana is a relatively safe and effective medicine for patients suffering from chronic conditions, such as AIDS wasting syndrome or chronic pain. However, the report also recommends more research on cannabinoid biology, additional clinical studies on marijuana and synthetic cannabinoids, and the development of an effective inhaler to solve the problem of poor oral absorption of THC. In the meantime, the panel recommended that the compassionate use of smoked marijuana cigarettes be allowed for no more than six months for patients with debilitating, intractable pain or vomiting, when the following conditions are met: •
The failure of approved medications to provide relief has been documented.
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The symptoms can reasonably be expected to be relieved by rapid-onset cannabinoid drugs.
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Such treatment is administered under medical supervision in a manner that allows for the assessment of treatment effectiveness.
•
An oversight strategy is in place to approve or reject requests within 24 hours after a physician seeks permission to provide marijuana to a patient for a specified use.
The entire report can be found on the Internet at books.nap.edu/catalog/9586.html.
Causes for Concern Abuse and Dependence The evidence now suggests that if high levels of marijuana are used regularly over a sustained
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period, tolerance can develop to many marijuanarelated effects, including the cognitive- impairing, physiological, and subjective effects. However, tolerance may not develop uniformly across each of these variables. For example, it has been demonstrated that heavy marijuana smokers exhibit minimal cognitive impairment following acute marijuana smoking, while showing dramatic heart rate increases and reporting significant levels of euphoria. These findings suggest that tolerance may develop more readily to marijuana-related cognitive effects than to heart rate responses and subjective effects.18 Relative to other drugs of abuse, many people perceive marijuana to be an innocuous drug with limited abuse potential. People have made comparisons between marijuana abuse and abuse of other drugs such as crack cocaine. However, the social consequences associated with marijuana use and those associated with crack cocaine use are dissimilar, making oneto-one comparisons imperfect. Research showing that THC and marijuana produce robust self-administration in laboratory animals and in human research participants clearly demonstrates that the drug has some abuse potential. In addition, of the 7 million Americans classified with dependence on or abuse of illicit drugs in 2006, 4.2 million were dependent on or abused marijuana.37 Although this number represents a relatively small fraction of current marijuana users (less than 30 percent), it shows that a significant number of marijuana smokers do suffer ill effects from using the drug. Can regular marijuana use produce a withdrawal syndrome? According to the DSM-IV-TR (the standard diagnostic instrument), the answer is no. The DSM-IV-TR does not recognize a diagnosis of cannabis withdrawal. Data from a variety of human laboratory and clinical studies, however, demonstrate that an abstinence syndrome can be observed following abrupt cessation of several days of smoked marijuana administration or oral ⌬9-THC administration. Cannabinoid withdrawal is not life threatening, but symptoms can be unpleasant. Marijuana
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withdrawal syndrome in humans may include negative mood states (e.g., anxiety, restlessness, depression, and irritability), disrupted sleep, decreased food intake, and in some cases, aggressive behavior. These symptoms have been reported to begin 1 day after cannabinoid cessation and persist from 4 to 12 days, depending on an individual’s level of marijuana dependence. Clearly, the majority of marijuana users do not experience withdrawal symptoms nor do they meet DSM-IV-TR criteria for cannabis-use disorders. But these findings indicate that regular marijuana use may not be as innocuous as previously perceived.38
Toxicity Potential Acute Physiological Effects The acute physiological effects of marijuana, primarily an increase in heart rate, have not been thought to be a threat to health. However, as the marijuanausing population ages, there is concern that individuals with high blood pressure, heart disease, or hardening of the arteries might be harmed by smoking marijuana.39 The lethal dose of THC has not been extensively studied in animals, and no human deaths have been reported from “overdoses” of Cannabis. Driving Ability A large number of studies have investigated the effects of marijuana on driving performance, but the findings have been inconsistent. Some studies have reported marijuanarelated driving impairments, while others have not. Traditionally, two types of studies have been conducted: (1) epidemiological: These studies determine whether marijuana use is over-represented among drivers involved in automobile accidents; and (2) laboratory: These studies determine the direct effects of marijuana on skills related to driving performance. Findings from the majority of the epidemiological studies show little evidence that drivers who use marijuana alone are more likely to be involved in an accident than nondrug-using drivers. But data from laboratory studies of computer-controlled driving simula-
Inhaling marijuana smoke.
tors indicate that marijuana produces significant impairments.40 Most of the laboratory studies have employed relatively infrequent marijuana users as participants, a group that would be expected to show marked impairments. Because tolerance can develop to many of the cognitive-impairing effects of marijuana, further laboratory studies should include heavy marijuana smokers. Panic Reactions The other major behavioral problem associated with acute marijuana intoxication is the panic reaction. Much like many of the bad trips with hallucinogens, the reaction is usually fear of loss of control and fear that things will not return to normal. This reaction is more common among less-experienced marijuana users. Even Baudelaire understood this and advised his readers to surround themselves with friends and a pleasant environment before using hashish. Although many people do seek emergency medical treatment for marijuana-induced panic and are sometimes given sedatives or tranquilizers, the best treatment is probably “talking down,” or reminding the person of who and where they are, that the reaction is temporary, and that everything will be all right. Chronic Lung Exposure There has been a great deal of concern about the possible long-term effects of chronic marijuana use. A couple of
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physiological concerns merit attention. One is the effect on lung function and the concern about lung cancer. Experiments have shown that chronic, daily smoking of marijuana impairs air flow in and out of the lungs.41 It is hard to tell yet whether years of such an effect results in permanent, major obstructive lung disease in the same way that smoking tobacco cigarettes does. Also, no direct evidence links marijuana smoking to lung cancer in humans. Remember that it took many years of cigarette smoking by millions of Americans before the links between tobacco and lung cancer and other lung diseases were shown. Marijuana smoke has been compared with tobacco smoke.42 Some of the constituents differ (there is no nicotine in marijuana smoke and no THC in tobacco), but many of the dangerous components are found in both. Total tar levels, carbon monoxide, hydrogen cyanide, and nitrosamines are found in similar amounts (except for tobacco-specific nitrosamines, which are carcinogens). Another potent carcinogen, benzopyrene, is found in greater amounts in marijuana than in tobacco. Everyone suspects that marijuana smoking will eventually be shown to cause cancer, but how much of a problem this will be compared with tobacco is hard to say. On the one hand, few marijuana smokers smoke 20 marijuana cigarettes every day, whereas tobacco smokers regularly smoke this much. On the other hand, the marijuana cigarette is not filtered and the user generally gets as much concentrated smoke as possible as far down in the lungs as possible and holds it there. So, while some wait and see when the data will come out, others are participating in the experiment. Reproductive Effects Another area of concern is reproductive effects in both men and women. Heavy marijuana smoking can decrease testosterone levels in men, although the levels are still within the normal range and the significance of those decreases is not known. Diminished sperm counts and abnormal sperm structure in heavy marijuana users has been
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reported, perhaps because anandamide plays a role in normal sperm function.43 A number of studies have reported either lower birth weight or shorter length at birth for infants whose mothers smoked marijuana during pregnancy, but because so many of the women also smoked tobacco or drank alcohol, it is not possible to determine the exact contribution of marijuana to these effects. It is, of course, wise to avoid the use of all drugs during pregnancy. The Immune System Effects There have also been reports that marijuana smoking impairs some measures of the functioning of the immune system.44 Animal studies have found that THC injections can reduce immunity to infection, but at doses well above those obtainable by smoking marijuana. Some human studies of marijuana smokers have suggested reduced immunity, but most have not. If the effect were real, it could result in marijuana smokers’ being more susceptible to infections, cancer, and other diseases, such as genital herpes. One might suspect that such problems would eventually be reflected in the overall death rate of marijuana users. However, a report examining 10 years of mortality data for more than 65,000 people found no relationship between marijuana use and overall death rates.45 Amotivational Syndrome Since 1971, when some psychiatric case reports were published identifying an amotivational syndrome in marijuana smokers, concern has been expressed about the effect of regular marijuana use on behavior and motivation. A number of experiments and correlational studies have been aimed at answering this question. There does seem to be evidence for this diminished motivation, impaired ability to learn, and school and family problems in some adolescents who are chronic, heavy marijuana smokers. If they stop smoking and remain in counseling, the condition improves.46 This probably implies a constant state of intoxication rather than a long-lasting change in brain function or personality.
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Insanity The connection between marijuana use and insanity was one of the main arguments for outlawing the drug in the 1930s, and the notion still remains that marijuana can cause a type of psychosis. There have been reports of psychotic “breakdowns” occurring with rare frequency after marijuana has been smoked, but the causal relationship is in question. The psychotic episodes are generally self-limiting and seem to occur in individuals with a history of psychiatric problems.46 Brain Damage For about 30 years, it has been speculated that amotivational or prolonged psychotic reactions could reflect an underlying damage to brain tissue produced by marijuana. For example, a 1972 report from England indicated that two individuals who demonstrated cerebral atrophy had a history of smoking marijuana. They also had a history of using many other illicit drugs, plus other medical problems, but it was suggested that the brain damage might have been caused by the marijuana. Several experiments have since been done, and all have failed to find a relationship between marijuana smoking and cerebral atrophy. Ironically, some of the nonpsychoactive ingredients in marijuana, including cannabidiol, have been shown to have powerful antioxidant properties that protect brain cells from the toxic effects of other chemicals.47 This effect was strong enough that the NIMH filed a patent in 1988 entitled “Cannabinoids as Antioxidants and Neuroprotectants.” Emotion has played an obvious and influential role. Scientists on both sides have become crusaders for their cause. Some individuals seem to think it is their professional duty to seek out and publicize every potential evil associated with marijuana, even if no strong scientific evidence supports their views. Others seem to automatically question the negative reports and look for ways to discredit them. We can predict that the emotion, the premature announcements of new scary findings, the repeating of long discredited stories, and the conflicting reports will continue.
Marijuana and American Society Our patterns of drug use are but one facet of our evolving society. Drug use affects and is affected by other social trends, including a couple of significant themes from the 1980s. One trend was the increased emphasis on physical health. Jogging, working out, dieting, drinking less alcohol and caffeine, and smoking less all were reflections of our national concern over shaping up. The health trend obviously worked against marijuana use: How many people who wouldn’t smoke tobacco felt good about inhaling marijuana smoke? Second, the 1980s saw a move toward social and political conservatism, which worked against such counterculture behavior as marijuana smoking. And, of course, drug use tends to be faddish. If marijuana was the fashionable drug of the 1970s, then it couldn’t be the fashionable drug of the 1980s. However, in the 1990s the drug came back into fashion, at least somewhat.
Federal and state laws and penalties related to marijuana possession tend to reflect other social trends, becoming more severe in periods of social and political conservatism.
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Data from the yearly survey of high school seniors shows the trends most clearly. After peaking in 1978–1979, the number of high school seniors who had ever smoked marijuana dropped from just over 60 percent to 32 percent in 1992, then rebounded to 45 percent by the class of 2005. Equally dramatic were the trends in daily use, which went from 11 percent in 1978 to 2 percent in 1992 and back to 6 percent by 2005.48 The earlier decreases in marijuana use went along with a steady increase in the belief among these students that “people risk harming themselves if they smoke marijuana regularly.” Whereas just over one-third of the high school seniors agreed with that statement in 1978, more than three-fourths agreed in 1992. Fads being what they are, this downward trend in marijuana use had to end sometime, and the turnaround was seen in the high school senior class of 1992. Significant increases in marijuana use in the 1992–2005 period were accompanied by decreased estimates of risk (see Chapter 1). Although marijuana is not used by most Americans, it is still remarkable how many people have used and continue to use a substance that shouldn’t exist at all in our society, according to the Controlled Substances Act and the DEA. That a large fraction of the society continues to violate the laws regarding marijuana is a matter for concern. It is easy to look back and wish that the 1937 Marijuana Tax Act had never happened. Marijuana use was spreading slowly across the United States and, with any luck, it might have become acculturated. Society would have adapted to marijuana and adapted marijuana to society. Soon it would have become part of society: Perhaps most people would never have used it regularly; of those who did use it, most would have known how to use it; some, of course, would have abused it. It has happened before with coffee, tea, tobacco, and alcohol. The 1937 law prevented all that. It didn’t affect most Americans a great deal until the 1960s, when a large number of young people began experimenting with drugs. Marijuana,
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more than anything else, convinced many young people that the government had been lying to them about drugs. They had been told that marijuana would make them insane, enslave them in drug dependence, and lead to violence and perverted sexual acts. Their experience told them that marijuana was pretty innocuous, compared with those stories, and it became an important symbol: Smoking marijuana struck a blow for truth and freedom. The problem was that laws existed that allowed young people to be sent to jail for 20 years for striking this blow, and that didn’t sit well with some people. Voice was given to the millions of marijuana users in 1970 when a young Washington lawyer established the National Organization for the Reform of Marijuana Laws (NORML) with a grant from the Playboy Foundation. As the founder of NORML put it, “The only people working for reform then were freaks who wanted to turn on the world, an approach that was obviously doomed to failure. I wanted an effective, middle-class approach, not pro-grass but antijail.” Also, in 1970 the Comprehensive Drug Abuse Prevention and Control Act of 1970 established the Commission on Marijuana and Drug Abuse. Its 1972 report recommended that federal and state laws be changed so that private possession of small amounts of marijuana for personal use, and casual distribution of small amounts without monetary profit, would no longer be offenses. The year 1972 was a turning point in the fight to decriminalize marijuana. In June the American Medical Association came out in favor of dropping penalties for possession of “insignificant amounts” of marijuana and noted that “there is no evidence supporting the idea that marijuana leads to violence, aggressive behavior, or crime.” In August the American Bar Association called for the reduction of criminal penalties for possession, and a year later the organization recommended decriminalization. Both traditional liberals and conservatives could support the idea, not to declare marijuana legal but to make possession of marijuana a civil offense, punishable only by a fine.
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In October 1973, Oregon abolished criminal penalties for marijuana use, substituting civil fines of up to $100. Marijuana offenders were given citations that are processed similar to traffic tickets. Did marijuana use increase in Oregon as a result of the decriminalization? Yes. By leaps and bounds? No. From the fall of 1974, a year after decriminalization, to the fall of 1977, the percentage of adults over 18 who had ever used marijuana went from 19 percent to 25 percent. Current users went from 9 percent to 10 percent over the same period. However, marijuana use was increasing toward its 1978 to 1979 peak all over the country at the same time. Possession of a small amount of marijuana was made only a civil offense by eight other states: Maine, Colorado, California, Ohio, Minnesota, Mississippi, New York, and North Carolina. In Alaska, private possession of up to four ounces of marijuana was not illegal. Changing marijuana possession from a felony to a misdemeanor saved money on court costs, juries, and jails. The state of California enjoyed an estimated average annual savings of more than $95 million between 1976 and 1985 as a result of its citation plan for marijuana possession.49 At the federal level, action picked up in 1977. In January, Rosalynn Carter joined her husband, the president, in calling for the decriminalization of marijuana and revealed that their oldest son had been discharged from the Navy for smoking marijuana. Bills to decriminalize marijuana possession were introduced into both houses of Congress, and in August President Carter sent a message to Congress in which he asked them to abolish all federal criminal penalties for the possession of small amounts of marijuana. In the late 1970s, de facto decriminalization had already occurred in many areas of the country. Law enforcement agencies in many of the larger U.S. cities had stopped arresting marijuana users and did not search out those with small amounts for personal use. When the Reagan administration came into office in 1981, any hope of federal decriminal-
ization was gone, replaced by a “get tough” attitude toward all illegal drugs. Marijuana was no exception. In addition to increased efforts to intercept marijuana shipments from abroad, a nationwide effort was launched to combat the cultivation of marijuana plants. More than 100 million plants were tugged out of the ground in 1987 by state, local, and federal law enforcement teams.50 Add to that the zero tolerance seizures of boats, cars, and planes containing even traces of marijuana and the 1988 legislation putting extra pressure on the user (e.g., $10,000 fines at the federal level; see Chapter 3), and we can see that the pendulum had definitely swung back. The states began to follow suit: In 1989, Oregon raised its civil penalty for possession from a $100 maximum to a $500 minimum. In 1990, Alaska voters approved the recriminalization of marijuana possession, making it a misdemeanor punishable by a jail term and up to a $1,000 fine. In 1993, an Alaska Court of Appeals ruled that individuals did have the right to possess up to four ounces of marijuana for personal use. An initiative in 2004 that would have removed criminal penalties for marijuana possession and allowed its regulated (and taxed) sale in Alaska failed to pass.
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Cannabis has a rich history relating both to its medicinal use and to its recreational uses.
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Marijuana became famous as the “Assassin of Youth” in the 1930s and was outlawed in 1937.
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Cannabis contains many active chemicals, but the most active is delta-9-THC.
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THC is absorbed rapidly by smoking but slowly and incompletely when taken by mouth.
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THC has a long half-life of elimination, and its metabolites can be found in the body for up to several weeks after THC enters the body.
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Selective THC receptors exist in brain tissue, leading to the discovery of a naturally occurring brain cannabinoid, anandamide.
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Marijuana causes an increase in the heart rate and reddening of the eyes as its main physiological effects.
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Psychologically, THC has some sedative properties, produces some analgesia, and at high doses can produce hallucinations.
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Marijuana is useful in the treatment of glaucoma, the reduction of nausea in patients undergoing cancer chemotherapy, and the increase of appetite in AIDS patients. A legal form of THC is available by prescription.
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Although strong dependence is not common, it does occur in some individuals.
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Marijuana can impair driving skills, but it is not clear that smoking marijuana leads to an increased frequency of accidents.
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Most experts agree that chronic smoking of marijuana impairs lung function somewhat and probably increases the risk of lung cancer.
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1. What are the major differences between C. sativa and C. indica? 2. How are hashish and sinsemilla produced? 3. When and where was the earliest recorded medical use of cannabis? 4. Why were Harry Anslinger’s writings on marijuana referred to as a “pyramid of prejudice”? 5. What were the general conclusions of the 1944 LaGuardia Commission? 6. What is meant by “cannabinoid,” and about how many are there in Cannabis? What is the cannabinoid found in brain tissue? 7. How is the action of THC in the brain terminated after about 30 minutes, when the halflife of metabolism is much longer than that? 8. What are the two most consistent physiological effects of smoking marijuana?
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9. What two medical uses have been approved by the FDA for dronabinol? 10. What evidence suggests that marijuana use might interfere with reproduction?
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Schultes, R. E., and A. Hofmann. The Botany and Chemistry of Hallucinogens. Springfield, IL: Charles C Thomas, 1980. Mickel, E. J. The Artificial Paradises in French Literature. Chapel Hill: University of North Carolina Press, 1969. Baudelaire, C. P. Artificial Paradises; on Hashish and Wine as Means of Expanding Individuality. Translated by Ellen Fox. New York: Herder & Herder, 1971. Musto, D. F. The American Disease: Origins of Narcotic Control, 3rd ed. New York: Oxford, 1999, p. 221. Taxation of Marihuana, Hearings before the Committee on Ways and Means, House of Representatives, Seventy-fifth Congress, First Session, on HR 6385, April 27–30 and May 4, 1937. Washington, DC: U.S. Government Printing Office. Parry, A. “The Menace of Marihuana.” American Mercury 36 (1935), pp. 487–88. “Marihuana Menaces Youth.” Scientific American 154 (1936), p. 151. Wolf, W. “Uncle Sam Fights a New Drug Menace . . . Marijuana.” Popular Science Monthly 128 (1936), p. 14. Anslinger, H. J., and C. R. Cooper. “Marijuana: Assassin of Youth.” The American Magazine 124 (1937), pp. 19, 153. “Facts and Fancies about Marihuana.” Literary Digest 122 (1936), pp. 7–8. Whitlock, L. “Review: Marijuana.” Crime and Delinquency Literature 2, no. 3 (1970), p. 367. Fort, J. “Pot: A Rational Approach.” Playboy, October 1969, pp. 131, 154. “The Marihuana Bugaboo.” Military Surgeon 93 (1943), p. 95. “Mayor LaGuardia’s Committee on Marijuana.” In D. Solomon, ed. The Marihuana Papers. New York: New American Library, 1966. “Marijuana Problems.” Journal of the American Medical Association 127 (1945), p. 1129. DiMarzo, V., and others. “Formation and Inactivation of Endogenous Cannabinoid Anandamide in Central Neurons.” Nature 372 (1994), p. 686. Sim, L. I., and others. “Differences in G-protein Activation by Mu- and Delta-opioid, and Cannabinoid, Receptors in Rat Striatum.” European Journal of Pharmacology 307 (1996), pp. 97–105. Hart, C. L., and others. “Effects of Acute Smoked Marijuana on Complex Cognitive Performance.” Neuropsychopharmacology 25 (2001), pp. 757–65. Hart, C. L., and others. “Reinforcing Effects of Oral ⌬9-THC in Male Marijuanna Smokers in a Laboratory Choice Procedure.” Psychopharmacology, 181 (2005) pp. 237–243. Jones, R. T. “Cardiovascular System Effects of Marijuana.” Journal of Clinical Pharmacology 42, no. 11 (2002), pp. 585–635. Anthony, J. C., and J. Helzer. “Epidemiology of Drug Dependence.” In M.T. Tsuang and others, eds. Textbook in
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Psychiatric Epidemiology. New York: John Wiley & Sons, 1995, pp. 361–406. Substance Abuse and Mental Health Services Administration. Treatment Episode Data Set (TEDS): 1995–2005. National Admissions to Substance Abuse Treatment Services. DASIS Series: S-37, DHHS Publication No. SMA 074234. Rockville, MD: Office of Applied Studies, 2007. Justinova, Z., and others. “Self-Administration of Delta9tetrahydrocannabinol (THC) by Drug Naive Squirrel Monkeys.” Psychopharmacology 169 (2003), pp. 135–40. Kelly, T. H., and others. “Effects of D9-THC on Marijuana Smoking, Dose Choice, and Verbal Report of Drug Liking.” Journal of the Experimental Analysis of Behavior 61 (1994), pp. 203–11. Becker, H. S. “Becoming a Marijuana User.” American Journal of Sociology 59 (1953), pp. 235–43. Ward, A. S., and others. “The Effects of a Monetary Alternative on Marijuana Self-administration.” Behavioural Pharmacology 8 (1997), pp. 275–86. Pope, H. G., and others. “Neuropsychological Performance in Long-Term Cannabis Users.” Archives of General Psychiatry 58 (2001), pp. 909–15. Foltin, R. W., and M. W. Fischman. “Effects of Smoked Marijuana on Human Social Behavior in Small Groups.” Pharmacology, Biochemistry, and Behavior 30 (1988), pp. 539–41. O’Shaughnessy, W. B. “On the Preparations of the Indian Hemp, or Gunja.” Transactions of the Physical and Medical Society of Bengal, 1838–1840, pp. 71–102, 1842, pp. 421–61. Mikuriya, T. H. “Marijuana in Medicine: Past, Present and Future.” California Medicine 110 (1969), pp. 34–40. Standardization of Drug Extracts, promotional brochure. Detroit: Parke, Davis & Co., 1898. Letter to EP Delabarre, 9 Arlington Ave., Providence, RI, from Parke, Davis & Co., Manufacturing Department, Main Laboratories, Detroit, Superintendent’s Office, Control Department, March 10, 1902. Davis, J. P., and H. H. Ramsey. “Antiepileptic Action of Marihuana-active Substances.” Federation Proceedings 8 (1949), pp. 284–85. Hepler, R. S., and I. R. Frank “Marijuana Smoking and Intraocular Pressure.” Journal of the American Medical Association 217 (1971), pp. 1392. “Medical Therapy, Legalization Issues Debated at Marijuana Reform Conference.” National Drug Reporter 7, no. 1 (1977), pp. 3–5. Institute of Medicine, National Academy of Sciences. Marijuana and Health. Washington, DC: National Academy Press, 1982. Substance Abuse and Mental Health Services Administration. Results from the 2006 National Survey on Drug
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Use and Health: National Findings. NSDUH Series H-32, DHHS Publication No. SMA 07-4293. Rockville, MD: Office of Applied Studies, 2007. Hart, C. L. “Increasing Treatment Options for Cannabis Dependence: A Review of Potential Pharmacotherapies.” Drug and Alcohol Dependence 80 (2005), pp. 147–59. Aryana, A., and M. A. Williams. “Marijuana as a Trigger of Cardiovascular Events: Speculation or Scientific Certainty?” International Journal of Cardiology 118 (2007), pp. 141–44. Ramaekers, J. G., and others. “Dose-related Risk of Motor Vehicle Crashes after Cannabis Use.” Drug and Alcohol Dependence 73 (2004), pp. 109–19. Tashkin, D. P. “Airway Effects of Marijuana, Cocaine and Other Inhaled Illicit Agents.” Current Opinion in Pulmonary Medicine 7 (2001), pp. 43–61. Moir, D., and others. “A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions.” Chemical Research and Toxicology 21 (2008), pp. 494–502. Schuel, H., and others. “Evidence That Anandamidesignalling Regulates Human Sperm Functions Required for Fertilization.” Molecular Reproduction and Development 63 (2002), pp. 376–87. Shay, A. H., and others. “Impairment of Antimicrobial Activity and Nitric Oxide Production in Alveolar Macrophages from Smokers of Marijuana and Cocaine.” Journal of Infectious Diseases 187 (2003), pp. 700–04. Sidney, S., J. E. Beck, and G. D. Friedman. “Marijuana Use and Mortality.” American Journal of Public Health 87 (1997), pp. 585–90. Smith, D. E., R. B. Seymour. “Clinical Perspectives on the Toxicology of Marijuana: 1967–1981.” In Marijuana and Youth: Clinical Observations on Motivation and Learning. Washington, DC: U.S. Department of Health and Human Services, U.S. Government Printing Office, 1982. Hampson, A. J., and others. “Neuroprotective Antioxidants from Marijuana.” Annals of the New York Academy of Sciences 899 (2000), pp. 274–82. Johnston, L. D., P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg. “Monitoring the Future National Results on Adolescent Drug Use: Overview of Key Findings, 2005.” NIH Publication No. 06-5882. Bethesda, MD: National Institute on Drug Abuse, 2006. Aldrich, M. R., and T. Mikuriya. “Savings in California Marijuana Law Enforcement Costs Attributable to the Moscone Act of 1976—a Summary.” Journal of Psychoactive Drugs 20 (1988), pp. 75–81. Drug Enforcement Administration, 1987 Domestic Cannabis Eradication/Suppression Program Final Report. Washington, DC: U.S. Department of Justice, 1987.
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Short-term Memory One of the most consistent findings about the effects of marijuana is that it impairs short-term memory. To learn more about short-term memory and get an idea of the types of tests that are used to measure it, go
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to the following Web site, which has an interactive test for short-term memory: faculty.washington.edu/ chudler/stm0.html. You can use this chart to record your responses.
The letters I remember are
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PerformanceEnhancing Drugs Objectives When you have finished this chapter, you should be able to: • Relate historical uses of performance-enhancing drugs by athletes. • Describe the history of use of stimulants to enhance performance. • Describe the development and current state of drug testing in sports. • Explain why the BALCO scandal received so much publicity. • Describe the performance-enhancing effects and primary dangers of stimulant drugs.
Why is there so much concern • Distinguish between androgenic and anabolic effects of over drug use by athletes? Why testosterone and other related steroid hormones. not focus on drug use by clarinet • Describe the desired effects and undesirable side-effects players or muffler repair people? of steroids in men, women, and adolescents. There are several answers to this question, and together they dem• Explain the effects of human growth hormone as well as onstrate the special reasons to its dangers. be concerned about drug use in • Explain the effects of creatine. sports. First, well-known athletes are seen as role models for young • Discuss the usefulness of dietary supplements in relation people, portraying youth, strength, to their label claims. and health. When a famous athlete is reported to be using steroids or some other illicit substance, there our tradition of fair play in sports, and wideis concern that impressionable young people will spread cheating of any kind tends to diminish a see drug use in a more positive light. Corporate sport and public interest in it. Professional wressponsors pay these athletes to endorse their prodtling, which is widely viewed as being rigged ucts, from shoes to breakfast cereal, based on this or staged, is enjoyed more as a form of comic presumed influence over young consumers. entertainment than as an athletic contest. Most Second, some of the drugs used by athletes professional and amateur athletes guard their are intended to give the user an advantage over honor carefully, and the use of performancethe competition, an advantage that is clearly enhancing drugs is seen as a threat to that honor. viewed as being unfair. This is inconsistent with 391
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Online Learning Center Resources www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. • • • • • •
Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips One of the major concerns over the use of performance-enhancing drugs is that they violate the tradition of fair play in sports.
Third, there is a concern that both the famous and the not-so-famous athletes who use drugs are endangering their health and perhaps their lives for the sake of a temporary burst of power or speed. Athletes should be aware of the risks associated with the use of these drugs. Because these drugs are often obtained illicitly, we can assume that the providers of the drugs do not present a balanced cost/benefit analysis to the potential user but, instead, probably maximize any possible benefit and minimize the dangers.
Historical Use of Drugs in Athletics Ancient Times Although we tend to think of drug use by athletes as a recent phenomenon, the use of chemicals to enhance performance might be as old as sport itself. As with many early drugs, some of these concoctions seemed to make sense at the time but probably had only placebo value. We no longer think that the powdered hooves of an ass will make our feet fly as fast as that animal’s, but perhaps it was a belief in that powder that helped the ancient Egyptian competitor’s self-confidence. Also, if all the others are using it, why take chances? The early Greek Olympians used various herbs and mushrooms that might have had
some pharmacological actions as stimulants, and Aztec athletes used a cactus-based stimulant resembling strychnine. Athletic competitions probably developed in tribal societies as a means of training and preparing for war or for hunting, and various psychoactive plants were used by tribal peoples during battles and hunts, so it is not surprising that the drugs were also used in athletic contests from the beginning.
Early Use of Stimulants During the 1800s and early 1900s, three types of stimulants were reported to be in use by athletes. Strychnine, which became famous as a rat poison, can at low doses act as a central nervous system stimulant. However, if the dose is too high, seizure activity will be produced in the brain. The resulting convulsions can paralyze respiration, leading to death. At least some boxers were reported to have used strychnine tablets. This might have made them more aggressive and kept them from tiring very quickly, but it was a dangerous way to do it. We’ll never know how many of those rugged heroes were killed in this way, but there must have been a few. Thomas Hicks won the marathon in the 1904 St. Louis Olympics, then collapsed and had to be revived. His race was partly fueled by
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Drugs in the Media Banned Substances and How to Avoid Them Television and other news from the past several Olympic games reported multiple instances of athletes being disqualified for using banned substances. In some cases, the disqualification was not contested, but in others the athletes thought they had been disqualified unfairly because they had taken something prescribed for them or something that they were not aware had been banned. The following list, from an article in Technique magazine by Jack Swarbick, lawyer for USA Gymnastics, includes tips for athletes on how to avoid the problem. Even if you aren’t an Olympic competitor, these tips should give you an idea of how complex and difficult this problem can be. 1. Be familiar with the banned substances list of the governing body (International Olympic Committee or NCAA). This means knowing not only what drugs are on the list but also the types of medications or even foods in which those drugs are often found. 2. Make certain that others who ought to know, such as your parents, physician, and school nurse, are also familiar with the banned substances list. 3. Know what medications you are using. Athletes should consult with the governing body regarding the potential for any medications to contain elements of banned substances and should be careful to list
a mixture of brandy and strychnine.1 Although the availability of amphetamines later made highly dangerous drugs such as strychnine less attractive, some evidence indicates the occasional use of strychnine continued at the level of world competition into the 1960s. Cocaine was also available in the 1800s, at first in the form of Mariani’s Coca Wine (used by the French cycling team), which was referred to in some advertisements as “wine for athletes.”2 When pure cocaine became available, athletes quickly adopted this more potent form. Many athletes used coffee as a mild stimulant, and some added pure caffeine to their coffee or took caffeine tablets. There were numerous reports
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all medications when completing the screening form as part of the drug-testing program. At competitions, drink only out of containers that were sealed when you got them, and once you have begun drinking out of a container do not leave it unattended. Several sports have implemented fairly rigorous security measures for the handling of coolers and water bottles. When you are required to produce a urine sample as part of the drug-testing procedures, never surrender possession of the sample or leave it unattended until after you have sealed it inside the shipping canister provided by the officials. If there are any irregularities in the process by which you give a urine sample and place that sample in the sealed container (e.g., a cracked beaker, a spilled sample, or unauthorized individuals on-site), immediately bring those irregularities to the attention of the drug-control administrator on-site. If you are informed that you have tested positive for a banned substance (and you dispute that result), you will be invited to witness the testing of the second half (i.e., the “B sample”) of your urine sample. Attend the test of the B sample, take with you an individual qualified to evaluate the process, and consider videotaping the test.
of the suspected doping of swimmers, cyclists, boxers, runners, and other athletes during this period. Then, as now, some of the suspicions were raised by the losers, who might or might not have had any evidence of doping. Our use of the word dope for illicit drugs is derived from a Dutch word used in South Africa to refer to a cheap brandy, which was sometimes given to racing dogs or horses to slow them down. From this came the term for doping horses and then people, more often in an effort to improve rather than impair performance. Dogs and horses received all the substances used by humans, including coca wine and cocaine, before the days of testing for drugs.
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Amphetamines It isn’t clear when athletes first started using amphetamines for their stimulant effects, but it was probably not long after the drugs were introduced in the 1930s. Amphetamines were widely used throughout the world during World War II, and in the 1940s and 1950s there were reports of the use of these pep pills by professional soccer players in England and Italy. Boxers and cyclists also relied on this new synthetic energy source. More potent than caffeine, longer-lasting than cocaine, and safer than strychnine, it seemed for a while to be the ideal ergogenic (energy-producing) drug for both training and competition. In 1952, the presence of syringes and broken ampules in the speed-skating locker room at the Oslo Winter Olympics was an indication of amphetamines’ presence in international competition. There were other reports from the 1952 summer games in Helsinki and the 1956 Melbourne Olympics. Several deaths during this period were attributed to overdoses of amphetamines or other drugs. By the time of the 1960 Rome games, amphetamine use had spread around the world and to most sports. On opening day a Danish cyclist died during time trials. An autopsy revealed that his death resulting from “sunstroke” was aided by the presence of amphetamines, which reduce blood flow to the skin, making it more difficult for the body to cool itself. Three other cyclists collapsed that day, and two were hospitalized.1 This and other examples of amphetamine abuse led to investigations and to antidoping laws in France and Belgium. Other nations, including the United States, seemed less concerned.
International Drug Testing Some sports, especially cycling, began to test competitors for drugs on a sporadic basis. Throughout the 1960s, some athletes refused to submit to tests or failed tests and were disqualified. These early testing efforts were not enough to prevent the death of cyclist Tommy Simpson, an ex-world champion, who died during the
1967 Tour de France. His death was seen on television, and weeks later it was reported that his body contained two types of amphetamines and that drugs had been found in his luggage. This caused the International Olympic Committee in 1968 to establish rules requiring the disqualification of any competitor who refuses to take a drug test or who is found guilty of using banned drugs. Beginning with fewer than 700 urine tests at the 1968 Mexico City Olympics, each subsequent international competition has had more testing, more disqualifications, and more controversy.
American Football Most Americans did not seem to be very concerned about drug use by athletes until reports surfaced in the late 1960s and early 1970s that professional football players were using amphetamines during games. Before that, people might not have been very concerned about it even if they had known. Remember from Chapter 6 that the amphetamines underwent a major status change in the United States during the 1960s. For years an increasing number of Americans had used amphetamines to keep them awake, to provide extra energy, or to lose weight. They were seen by most people as legal, harmless pep pills. It was in that context that the physicians for professional football teams ordered large quantities of the drugs as a routine part of their supplies, and trainers dispensed them liberally. At the end of the 1960s, amphetamines were widely considered to be drugs of abuse, dangerous drugs that could lead to violent behavior. In this context, revelations that many professionals were playing high made for sensational headlines. Several National Football League (NFL) players sued their teams for injuries received while playing under the influence of drugs, and the NFL officially banned the distribution of amphetamines by team physicians and trainers in 1971. Although the drugs were no longer condoned by the league, the NFL did little at that time to enforce the ban, except to request
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copies of each team’s orders for medical supplies. Athletes who wanted amphetamines still obtained and used them, often through a legal prescription from their own physicians. The attitude seemed to be that, if the players wanted to use pep pills and obtained them on their own, that was their business, but team physicians and trainers shouldn’t be using medications to push the athletes beyond their normal endurance. The current NFL policy, of course, restricts all use of amphetamines, as well as many other drugs, no matter where they are obtained.
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were a Bulgarian discus thrower, a Romanian shotputter, a Polish discus thrower, and weight lifters from several countries. By that time, individual Western athletes might have chosen to use steroids, but some of the eastern European countries seemed to have adopted their use almost as a matter of official policy. When the East German swimming coach was asked during the 1976 Olympics why so many of their women swimmers had deep voices, the answer was, “We have come here to swim, not sing.”4
The BALCO Scandal Steroids During and after World War II, it was found that malnourished people could gain weight and build themselves up more rapidly if they were given the male hormone testosterone. The Soviets were the first to put this hormone to use on a wide scale to build up their athletes. An American team physician at the 1956 Olympics reported that the Soviet athletes were using straight testosterone, sometimes in excessive doses and with unfortunate side effects. Testosterone helps both men and women become more muscular, but its masculinizing effects on women and enlargement of the prostate gland in men are definite drawbacks. The American physician at the 1956 Olympics returned to the United States and helped develop and test anabolic steroids, which were quickly adopted by American weight lifters and bodybuilders.3 American and British athletes in events such as discus and shotput were the first to acknowledge publicly that they had used steroids, and there was evidence that steroid use was widespread during the 1960s in most track and field events. These drugs were not officially banned, nor were they tested for in international competition until the early 1970s, mainly because a sensitive urine test was not available until then. Of the 2,000 urine samples taken during the 1976 Olympics, fewer than 300 were tested for the presence of steroids, and 8 of those were positive.1 The first international athletes to be found guilty of taking steroids
For years, rumors had circulated around professional baseball that certain players were using steroids, but Major League Baseball did not test for them. When Barry Bonds came into the 2001 season looking bigger and stronger, and went on to hit a record 79 home runs, some speculated that he might have used steroids, but the rumors were always denied. In 2002, former player Ken Caminiti admitted to using steroids and claimed that “half” the Major League players were doing so. Major League Baseball did institute a limited testing program that was generally considered to be too weak to have much effect. In June 2003, an unidentified track coach delivered to the U.S. Anti-Doping Agency a syringe containing an “undetectable” steroid, naming the source as Victor Conte, founder of BALCO Laboratories. Analysis determined that the syringe contained tetrahydrogestrinone (THG), a steroid previously unknown to the agency that did not show up in agency tests. The BALCO investigation led to a raid on the laboratory and the discovery of other steroids and human-growth hormone.5 Conte testified before a grand jury in San Francisco after being given immunity from prosecution and named a long list of Olympic and professional athletes who ergogenic (er go gen ic): producing work or energy; a general term for performance enhancement. anabolic (an a ball ick): promoting constructive metabolism; building tissue.
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Mind / Body Connection Baseball: Seeking Alternatives to Amphetamines Psychologically, amphetamine increases feelings of alertness and well-being and improves attention, focus, reaction time, and vigilance. The drug also reverses psychological decrements caused by fatigue and sleep deprivation. Physically, it increases motor and cardiovascular activity. Undoubtedly, these features have contributed to the use of this drug in Major League Baseball for at least a half of a century. It is important to note that amphetamine use in baseball has continued, despite the fact that it has been available only by prescription in the U.S. since 1970. According to investigations of drug use in baseball, this legal technicality did not seem to interfere with the widespread use of amphetamine. However, under baseball’s new drug policy, which took effect at the start of the 2006 season, amphetamine is now banned. While penalties associated with amphetamine infractions are not as severe as steroid violations, players consistently testing positive for the substance run the risk of being banned from the game. The Major League Baseball season is a grueling endurance test, comprised of seven weeks of spring training followed by 162 games in six months. There are also double-headers (two games in one day), rain delays, cross-country flights, and the expectation that players perform at their peak each game. Given this situation, it is not difficult to see why amphetamine use was common. One frequently asked question is what impact will the ban have on the players and game? Some observers have speculated that ultimately it will be
had been his clients, including Barry Bonds and many other professional baseball players. As a result of this and other developments, at the start of the 2006 season, Major League Baseball instituted more frequent testing and toughened penalties for drug policy violations. In addition, testing for amphetamines was included as part of the new policy for the first time (see the Mind/Body Connection box). Under the current policy, each player is tested at least twice: once during the preseason and
a positive development, prompting players to seek healthier and natural alternatives. For example, some players might adapt strategies to improve their physical conditioning. Others may seek out sport psychologists to learn mental skills necessary to perform consistently in training and competition. Some may alter their lifestyles such that they decrease their alcohol intake and attend more carefully to their diet and sleep habits. Another view is that players will continue to use pharmacological tools to aid them through marathon seasons. It has been suggested that high caffeinecontaining energy drink consumption will increase as well as the use of over-the-counter stimulants. Although it is difficult to track this type of stimulant use, information is available regarding the number of players granted therapeutic-use exemptions for Attention-Deficit Hyperactivity Disorder (ADHD). As discussed in Chapter 6, stimulants, including amphetamine, are used to treat this disorder, and its diagnosis could provide a legal avenue through which a player could obtain amphetamine. In 2006, for example, of the 1,354 Major League Baseball players, 28 were granted therapeutic-use exemptions for ADHD. In 2007, this number dramatically increased to 103.6 It is worth noting that the U.S. adult prevalent rate for ADHD is substantially lower than baseball’s 2007 exemptions. It is too early to know for certain the impact of baseball’s ban on amphetamine. But, judging from these early indications, a significant number of individuals will employ strategies, both pharmacological and nonpharmacological, to circumvent the ban.
once during the regular season. All players are also subjected to additional random tests throughout the season. Table 16.1 summarizes the penalties associated with violations.
The Battle over Testing During the 1980s, public revelations of drug use by athletes became common and cocaine was often mentioned. Professional basketball, baseball, and football players in the United States
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Table 16.1 Penalties for Violating Major League Baseball Drug Policy Penalty Steroid First positive test Second positive test
50-game suspension 100-game suspension
Third positive test
Lifetime suspension— may seek reinstatement after two years
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Mandatory follow-up testing 25-game suspension
Third positive test
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Fourth positive test
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were being sent into treatment centers for cocaine dependence, and several either dropped out or were kicked out of professional sports. Most amateur and professional sports organizations adopted longer and more complicated lists of banned substances and rules providing for more and more participants to be tested. For example, in 1986, the National Collegiate Athletic Association (NCAA) adopted a list of more than 3,000 brand-name drugs containing banned substances. All participants are to be tested during the championship contest and after all postseason football games. In many events around the world, all contestants must now be subjected to urine tests as a matter of routine. Because of both the expense and the inconvenience, some have questioned the wisdom of trying to test every athlete for everything. Despite the enormous expense to which sports organizations have gone, the use of steroids, stimulants, and other performance-enhancing substances seems to be as great as ever. Both the extent of testing and the ingenuity of athletes trying to beat the tests continue to escalate. The BALCO scandal demonstrates that chemists will keep coming up with new ways to help the athletes avoid detection.
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Stimulants as Performance Enhancers The first question to be answered about the use of a drug to increase energy or otherwise enhance athletic performance is, Does it work? We might not worry so much about unfair competition if we didn’t feel that the use of a drug would really help the person using it. Also, if we could prove that these drugs were ineffective, then we could presumably convince young people not to take the risk of using drugs because there would be no gain to be had. But experiments can never prove that a drug has no effect—you might have done a hundred experiments and not used the right dose or the right test (peak output? endurance? accuracy?). The possibility always exists that someone will come along later with the right combination to demonstrate a beneficial effect. Therefore, be wary when someone tries to use scientific evidence to argue that a drug doesn’t work, has no effect, is not toxic, or is otherwise inactive. We’ve had a pretty good idea of the effectiveness of the amphetamines since 1959, when Smith and Beecher published the results of a double-blind study comparing amphetamines and placebos in runners, swimmers, and weight throwers.7 They concluded that most of the athletes performed better under amphetamines, but the improvement was small (a few percentage points’ improvement). Several studies have reported no differences or very small differences
Stimulants have been shown to improve endurance.
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in performance, and some medical experts in the 1960s wanted to argue that amphetamines were essentially ineffective and there was no reason for people to use them. An excellent 1981 review of the existing literature put it all into perspective. Pointing out that it had been taking athletes an average of about seven years for each 1 percent improvement in the world record speed for the mile run, if amphetamines produced even a 1 percent improvement they could make an important difference at that level of competition. The study concluded that there is an amphetamine margin. It is usually small, amounting to a few percent under most circumstances. But even when that tiny, it can spell the difference between a gold medal and sixth place.8 Whether amphetamines or other stimulants increase physical ability (provide pep or energy) or produce their actions only through effects on the brain is an interesting question, which might not be answerable. Surely a person who feels more confident will train harder, compete with a winning attitude, try harder, and keep trying longer. With amphetamines, improvements have been seen both in events requiring brief, explosive power (shotput) and in events requiring endurance, such as distance running. In laboratory studies, increases have been found in isometric strength and in work output during endurance testing on a stationary bicycle (the subjects rode longer under amphetamine conditions). This endurance improvement could be due to the masking of fatigue effects, allowing a person to compete to utter exhaustion. Caffeine has also been shown to improve endurance performance under laboratory conditions. In one experiment, 330 mg of caffeine (approximately equivalent to three cups of brewed coffee) increased the length of a stationary bicycle ride by almost 20 percent. In another experiment, when subjects rode for two hours, their total energy output was 7 percent higher after 500 mg caffeine than in the control condition.9 The effectiveness of caffeine might depend on other factors: For example, one study reported no benefit from caffeine when athletes ran long
distances (12 miles) in hot, humid conditions.10 Small amounts of caffeine are acceptable in most sports, but a urine level above 12 μg/mL will lead to disqualification in many competitions. The doses needed to produce large performance increases produce much higher levels than that, but there could still be a slight improvement even at legal levels. Apparently no controlled laboratory or field experiments have tested the performanceenhancing capabilities of cocaine, but especially during the 1980s many athletes believed in its power. Cocaine’s stimulant properties are generally similar to those of the amphetamines, so we can assume that cocaine would be effective under some circumstances. Given cocaine’s shorter duration of action, it would not be expected to improve endurance over a several-hour period as well as either amphetamines or caffeine. For years, athletes had another readily available stimulant in the form of ephedrine, either as a drug or in the form of ephedra extract. Ephedra (ma huang) was introduced in Chapter 6 as the herbal source of ephedrine, and it was the ephedrine molecule that was modified in the 1920s to produce amphetamine. When Olympic and NCAA officials developed lists of banned substances, ephedrine soon made its way onto the lists (except for people whose physicians said they suffered from asthma—ephedrine relaxes bronchial passages and is an ingredient in asthma medications). Professional sports organizations were at first less concerned about ephedrine, but eventually the National Football League also banned it. Major League Baseball did not, and baseball players used it to provide extra energy, or in some cases to reduce weight, since ephedra was also found in many weight-control dietary supplements (Chapter 12). In 2003, Baltimore Orioles pitcher Steve Bechler died after collapsing during practice—his temperature rose to 108 degrees in the hospital before his death, which was attributed to heat stroke due to the ingestion of “significant amounts” of ephedrine from a dietary supplement.11 This widely publicized death finally gave the FDA enough political backing to go along with the years of
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evidence it had been accumulating, leading to the 2004 ban on ephedra and ephedrine in dietary supplements. With all these and several other CNS stimulants banned by most sports associations, some athletes have continued to use them during training, to allow them to run, ride, or swim harder. They then do not use the drug for several days before the competition or during the competition, hoping that traces of the substance will not appear in the urine test. This might make sense, but no one knows whether training under one drug condition has an effect on competition under another condition. Also, overexertion under the influence of a fatigue-masking drug might be most dangerous during training, leading to muscle injury, a fall or another accident, or heat exhaustion. Athletes and others who use amphetamines or cocaine regularly run the risk of developing a dependence on the drug, developing paranoid or violent behavior patterns, and suffering from the loss of energy and psychological depression that occur as the drugs wear off (see Chapter 6).
Steroids The male sex hormone testosterone has two major types of effects on the developing man. Androgenic effects are masculinizing actions: Initial growth of the penis and other male sex glands, deepening of the voice, and increased facial hair are examples. This steroid hormone also has anabolic effects. These include increased muscle mass, increases in the size of various internal organs, control of the distribution of body fat, increased protein synthesis, and increased calcium in the bones. In the 1950s, drug companies began to synthesize various steroids that have fewer of the androgenic effects and more of the anabolic effects than testosterone. These are referred to as anabolic steroids, although none of them is entirely free of some masculinizing effect. Whether these drugs are effective in improving athletic performance has been controversial:
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For many years the medical position was that they were not, whereas the lore around the locker room was that they would make anyone bigger, stronger, and more masculine-looking. A lot of people must have had more faith in the locker-room lore than in the official word. The 1989 Physician’s Desk Reference contained the following statement in boldface type: “Anabolic Steroids Have Not Been Shown to Enhance Athletic Ability.” Try telling that to any current major league baseball player, sports writer, or fan. That disclaimer is no longer required by the FDA. There is no doubt that testosterone has a tremendous effect on muscle mass and strength during puberty, and experiments on castrated animals clearly show the muscle-developing ability of the synthetic anabolics.12 What is not so clear is the effect of adding additional anabolic stimulation to adolescent or adult males who already have normal circulating levels of testosterone. Laboratory research on healthy men who are engaged in weight training and are maintained on a proper diet has often found that anabolic steroids produce small increases in lean muscle mass and sometimes small increases in muscular strength. There is no evidence for an overall increase in aerobic capacity or endurance in those studies. However, it might never be possible to conduct experiments demonstrating the effectiveness of the high doses used by some athletes. Many athletes report that they take 10 or more times the dose of a steroid that has been tested and recommended for treatment of a deficiency disorder.13 It is also common for athletes to take more than one steroid at a time (both an oral and an injectable form, for example). This practice is known as “stacking.” To expose research subjects to such massive doses would clearly be unethical. Another impediment to doing careful research on this topic is that these steroids produce detectable psychological effects. When double-blind experiments have been attempted,
androgenic (an drow gen ick): masculinizing.
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almost always the subjects have known when they were on steroids, thus destroying the blind control.14 This is important because steroid users report that they feel they can lift more or work harder when they are on the steroids. This may be due to CNS effects of the steroids leading to a stimulant-like feeling of energy and loss of fatigue or to increased aggressiveness expressed as more aggressive training. There is a further possibility of what is known as an active placebo effect, with a belief in the power of steroids, enhanced by the clear sensation that the drug is doing something because one can “feel” it. Until recently, many of the scientists studying steroid hormones believed that their main effects were psychological, combined with a “bloating” effect on the muscle, in which the muscle retains more fluids, is larger, weighs more, but has no more physical strength.1
Psychological Effects of Steroids The reported psychological effects of steroids, including a stimulant-like high and increased aggressiveness, might be beneficial for increasing the amount of work done during training and for increasing the intensity of effort during competition. However, there are also concerns that these psychological effects might produce great problems, especially at high doses. One concern is that a psychological dependence seems to develop in some users, who feel great when they are on the steroids but become depressed when they are off them. Many users take the drugs in cycles, and their mood swings can interfere with their social relationships and other life functions. There has been a great deal of discussion about “roid rage,” a kind of manic rage that has been reported by some steroid users.15 We should be careful about attributing instances of violence to a drug on the basis of uncontrolled retrospective reports, especially when the perpetrator of a violent crime might be looking for an excuse.16 However, there are a suffi-
cient number of reports of violent feelings and actions among steroid users for us to be concerned and to await further research. Says Dr. William Taylor, a leading authority on anabolic steroids, “I’ve seen total personality changes. A passive, low-key guy goes on steroids for muscle enhancement, and the next thing you know, he’s being arrested for assault or disorderly conduct.”17
Adverse Effects on the Body There are many concerns about the effects of steroid use on the body. In young users who have not attained their full height, steroids can cause premature closing of the growth plates of the long bones, thus limiting their adult height. For all users the risk of peliosis hepatitis (bloody cysts in the liver) and the changes in blood lipids possibly leading to atherosclerosis, high blood pressure, and heart disease are potentially serious concerns. Acne and baldness are reported, as are atrophy of the testes and breast enlargement in men using anabolic steroids. There are also considerations for women who use anabolic steroids. Because women usually have only trace amounts of testosterone produced by the adrenals, the addition of even relatively small doses of anabolic steroids can have dramatic effects, in terms of both muscle growth and masculinization. Some of the side effects, such as mild acne, decreased breast size, and fluid retention, are reversible. The enlargement of the clitoris might be reversible if steroid use is stopped soon after it is noticed. Other effects, such as increased facial hair and deepening of the voice, might be irreversible.14
Regulation As we found in Chapter 2, when a drug produces dependence, violent behavior, and toxic side effects, society may feel justified in trying to restrict the drug’s availability. In 1988, congressional hearings were held on the notion
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Drugs in Depth Nutritional Ergogenic Aids If athletes can’t get or refuse to use pharmacological aids in athletic competition, most believe that certain foods or nutritional supplements are a “natural” way to enhance their performance. Following is a very abbreviated description of a more complete review of this topic.18 Amino acids are the natural building blocks of the protein required to build muscle, and one certainly requires a basic minimum intake. There is some evidence that very active people can benefit from a somewhat increased intake of dietary protein, slightly above the recommended daily allowances, but there is no demonstrated need to purchase expensive amino acid supplements to achieve this. Marketers of these “muscle-building” dietary supplements walk a fine line by avoiding making specific claims on the product labels, so they do not fall under the FDA’s rules for demonstrating effectiveness. Usually nearby posters or pamphlets link amino acids to the idea of muscle growth. These supplements are probably of little or no value to an athlete who is receiving proper nutrition. Carbohydrates are burned as fuels, especially during prolonged aerobic exercise. Carbohydrates taken two to four hours before an endurance performance lasting for more than an hour may enhance the performance by maintaining blood glucose levels and preventing the depletion of muscle stores of glycogen. Carbohydrate loading before marathon runs consists of resting for the last day or two while ingesting extra carbohydrates, increasing both muscle and liver stores of carbohydrates. In either case, there is not much evidence to support the value of carbohydrate supplements for athletic performances lasting less than an hour. Fats, in experiments with fat supplements, have not been found to be a useful ergogenic aid. Vitamins, especially the water-soluble B vitamins, are necessary for normal utilization of food energy.
of placing anabolic steroids on the list of controlled substances. Evidence was presented that a large black market had developed for these drugs, amounting to perhaps $100 million per
Deficiencies in these vitamins, such as might result when a wrestler is dieting to meet a weight limit, can clearly impair physical performance. However, once the necessary minimum amount is available for metabolic purposes, further supplements are of no value. Many experiments have been done with supplements of C, E, and B-complex vitamins or with multivitamin supplements, the so-called vitamin B15, and with bee pollen, and there is no evidence for enhanced performance or faster recovery after workouts. Again, these supplements are probably of no value to an athlete who is receiving proper nutrition. Minerals, in the form of various mineral supplements, are widely used by athletes. Once again, most are probably not needed or useful, but there may be some exceptions. Electrolyte drinks are designed to replace both fluids and electrolytes, such as sodium and chloride that are lost in sweat. Actually, sweat contains a lower concentration of these electrolytes than does blood, so it is more important to replace the fluids than the electrolytes under most circumstances. Sodium supplementation may be useful for those engaged in ultraendurance events, such as 100-mile runs. Iron supplements are helpful in athletes who are iron-deficient, as may occur especially in female distance runners. However, if iron status is normal, there is probably no value in iron supplements. The jury is still out on whether “buffering” the blood pH with sodium bicarbonate (baking soda) enhances performance in anaerobic events, such as 400- to 800-meter runs. Some studies indicate improvements, whereas others do not. Water is needed by endurance athletes to keep their body temperatures down, especially in a warm environment. Drinking water both before and during prolonged exercise can deter dehydration and improve performance. Visit the Online Learning Center for links to more information on supplements.
year. In addition, there was concern that adolescent boys, many of whom were not athletic at all, had begun to use steroids in the belief that they would quickly become more muscular
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Taking Sides Should We Be Concerned about Steroid Use by Entertainers? In recent years, the U.S. Congress has focused much attention on Major League Baseball players’ alleged use of performance-enhancing drugs. However, some are warning that steroids and human growth hormone are being illegally prescribed throughout the country at an alarming rate under the belief they will aid healing, enhance physical attractiveness, and/or slow aging. The list of people accused of using these drugs is extensive and ranges from ordinary citizens to prominent entertainers. For example, in March 2007, Sylvester Stallone was required to pay a fine of nearly $3,000 to Australian officials after they discovered in his luggage several vials of human growth hormone. The use of antiaging, anti-obesity, and anti-fatigue agents in the entertainment industry has been known and accepted for decades. But recent claims that some members of the industry are using steroids and related compounds raise similar questions to those mentioned
and “macho” looking. As part of the Omnibus Crime Control Act of 1990, anabolic steroids became listed as a Schedule III controlled substance, requiring more record-keeping and limited prescription refills.19
Other Hormonal Manipulations Whereas the anabolic steroids have been in wide use, other treatments have been experimented with on a more limited basis. Female sex hormones have been used to feminize men, so that they could compete in women’s events. The women’s gold medal sprinter in the 1964 Olympics was shown by chromosome testing to have been a man, and he had to return the medal. Hormone receptor–blocking drugs have probably been used to delay puberty in female gymnasts. In women, puberty shifts the center of gravity lower in the body and changes body proportions in ways that adversely affect performance in some gymnastic events. Smaller
regarding the use of these drugs by athletes. Entertainers are role models for young people. Will their steroid use suggest to impressionable youngsters that this type of drug use is acceptable? Performance-enhancing drugs are usually taken to create an advantage over the competition. For example, professional models may take amphetamines in an effort to decrease body weight and enhance their chances of landing the “supermodel” contract. This is clearly viewed as being unfair to models not taking antiobesity drugs. And of course, there are healthrelated risks associated with these drugs, especially when taken illicitly. As a result of these issues, should we increase our monitoring of performance-enhancing drug use by members of the entertainment industry? Should Congress also conduct investigations of drug use in the entertainment industry? Or should Congress refrain from such drug-use investigations altogether?
women appear to be more graceful, spin faster on the uneven bars, and generally have the advantage, which is why top female gymnasts are usually in their teens. However, the Soviets were suspected of tampering with nature: Their top three international gymnasts in 1978 were all 17 or 18 years old, but the following were their heights and weights: 53 inches, 63 pounds; 60 inches, 90 pounds; and 57 inches, 79 pounds. We have certainly not seen the end of growth-promoting hormonal treatments. Human growth hormone, which is released from the pituitary gland, can potentially increase the height and weight of an individual to gigantic proportions, especially if administered during childhood and adolescence. In rare instances, the excessive production of this hormone creates giants well over 7 feet tall. These giants usually die at an early age because their internal organs continue to grow. However, administration of a few doses of this hormone at the right time might produce a more controlled increase
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in body size. Likewise, the growth-hormonereleasing hormone, and some of the cellular intermediary hormones by which growth hormone exerts its effects, might work to enhance growth. It is difficult to test for the presence of these substances. Despite the possible dangers, the lure of an otherwise capable basketball player growing a couple of inches taller or of a football player being 30 pounds heavier has no doubt caused many young athletes to experiment with these substances. Studies have shown that growth hormone increases lean body mass but may not improve strength.20 The 1990 legislation that placed anabolic steroids on the list of controlled substances also made it a crime to distribute human growth hormone for nonmedical purposes.
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is no evidence that beta-2 agonists improve athletic performance.21
Creatine One widely used substance among bodybuilders has been creatine, a natural substance found in meat and fish. This legal product is sold as a food supplement. There is clear evidence that creatine helps regenerate ATP, which provides the energy for muscle contractions. Users of creatine tend to gain some weight, some of which is water weight. There is considerable evidence that the use of creatine can improve strength and short-term speed in sprinting. However, studies of longer-distance running, cycling, and swimming often find no effect, and in one case a significant slowing was reported, probably due to weight gain.4
Beta-2 Agonists At the beginning of the 1992 Olympics, the leader of the British team was disqualified because of the detection of a new drug. Clenbuterol was developed as a treatment for asthma and is a relative of several other bronchodilators that are found in prescription inhalers. These drugs have sympathomimetic effects on the bronchi of the lungs but are designed to be more specific than older sympathomimetics, such as ephedrine or the amphetamines (see Chapter 6). Their specificity comes from a selective stimulation of the beta-2 subtype of adrenergic receptors. Research with cows had revealed an increase in muscle mass, and speculation was beginning that this might represent a new type of nonsteroidal anabolic agent. Apparently someone in Great Britain was keeping an eye on the animal research literature and decided to try the anabolic actions on at least one Olympic athlete. Presumably it was hoped that such a new drug would not be tested for, but the Olympic officials were also well informed and ready, at least for clenbuterol. Human studies have shown some increases in strength of selected muscle types with clenbuterol or a similar drug, but there
Getting “Cut” If getting “cut,” “ripped,” and “shredded” sounds like something you’d want to avoid, then you’re probably not into bodybuilding. These terms refer to the appearance of someone who is both muscular and lean. Because amateur wrestlers compete in weight classes and they need to be strong, they have always had the problem of eating well to build strength and train hard, but then needing to “cut” weight before the weigh-ins for matches. Jockeys have had a similar problem. Over the years, some of these athletes have engaged in fairly extreme methods to achieve short-term weight reduction, such as purging, taking diuretic drugs to lose water weight, and exercising in a heated environment or wearing nonporous clothing to maximize sweating. The entire list of weight-control drugs mentioned in Chapters 6 and 12 have been used as
human growth hormone: a pituitary hormone responsible for some types of giantism.
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Bodybuilders and other athletes have used steroids or other supplements to develop a lean, strong, muscular body—to become “cut” or “ripped.”
well, ranging from amphetamine to ephedrine to caffeine. Increasingly, bodybuilders are seeking the look of someone who is both strong and lean, with lots of muscle definition. That appearance is referred to as looking “cut,” probably derived from the idea of cutting weight or cutting fat, but perhaps also carrying the connotation of “sculpted.” A more extreme version of looking cut is looking “ripped,” or sometimes “shredded.” These are the men and women whose every muscle fiber and vein can be seen through the skin, perhaps with a body fat percentage down to an unhealthy 6 to 9 percent (14 to 20 percent is considered ideal for a healthy male). They also are using drugs and nutritional supplements to help achieve this appearance. Steroids increase muscle mass, but they don’t produce this kind of lean definition. A brisk market has developed in dietary supplements containing the word ripped in their name, such as “Ripped Fuel” and “Ripped Fast.” For many years these products relied mainly on ephedra as the main active ingredient. Once ephedra was banned, these
profitable products did not go away, they simply changed their formulas and kept making the same claims about being “fat burners” and promising incredible results. They contain a bewildering variety of plant extracts, many of which contain caffeine in unknown amounts (e.g., guarana extract, green tea extract, and coffee bean extract). Remember that these dietary supplements do not have to be demonstrated to be effective, and the beneficial claims have not been evaluated by the FDA (or anyone else). If an included ingredient should turn out to be dangerous, it might take a long time for this to come to the attention of the FDA, and it would then take a long time for the agency to build a case to remove the ingredient from the market (it took 10 years for ephedra). No such product has ever been shown to actually be a “fat burner,” so it’s unlikely that these are either. If you buy them, the closest you’ll get to being “ripped” as a result is probably feeling “ripped off” when the magic pill doesn’t deliver what you hoped.
Summary •
Performance-enhancing drugs have been used by athletes throughout history.
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Athletic use of stimulants appears to have increased and spread to most sports with the use of amphetamines during the 1950s and 1960s.
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Amphetamines and caffeine have both been shown to increase work output and to mask the effects of fatigue.
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Some athletes continue to use stimulants for training, despite the dangers of injury and overexertion.
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Anabolic steroids are capable of increasing muscle mass and probably strength, although it has been difficult to separate the psychological stimulant-like effect of these drugs from the physical effects on the muscles themselves.
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Anabolic steroids can also produce a variety of dangerous and sometimes irreversible side effects.
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It is difficult to do ethical and well-controlled research on the effects of steroids.
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Misuse of human growth hormone and related substances might be the next problem to arise.
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Creatine is a legally available nutritional supplement that can increase strength but might slow distance runners because of resultant weight gain.
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Review Questions 1. What was the first type of stimulant drug reported to be used by boxers and other athletes in the 1800s? 2. What was the first type of drug known to be widely used in international competition and that led to the first Olympic urine-testing programs? 3. When and in what country were the selective anabolic steroids first developed? 4. Do amphetamines and caffeine actually enhance athletic performance? If so, how much? 5. How was ephedrine used by athletes, and what happened to it? 6. What muscle effect do we know for certain that anabolic steroids can produce in healthy men? 7. What is meant by “roid rage,” and what double-blind studies have been done on this phenomenon? 8. What specific effect of anabolic steroids might be of concern to young users? to females? 9. Why do “pituitary giants” often die at an early age? 10. How does creatine increase strength?
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8. 9. 10.
11. 12. 13. 14. 15.
16.
17. 18.
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20.
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Donohue, T., and N. Johnson. Foul Play: Drug Abuse in Sports. Oxford, England: Basil Blackwell, 1986. Asken, M. J. Dying to Win: The Athlete’s Guide to Safe and Unsafe Drugs in Sports. Washington, DC: Acropolis, 1988. Eichner, E. R. “Ergogenic Aids: What Athletes Are Using— and Why.” Physician and Sportsmedicine 25 (1997), pp. 70–83. Goldman, B. Death in the Locker Room. South Bend, IN: Icarus Press, 1984. Fainaru-Wada, M., and L. Williams. “Sports and Drugs: How the Doping Scandal Unfolded. Fallout from BALCO Probe Could Taint Olympics, Pro Sports.” San Francisco Chronicle, December 21, 2003. Schmidt, M. S., and A. Schwarz. “Baseball Is Challenged on Rise in Stimulant Use.” The New York Times, January 16, 2008. Smith, G. M., and H. K. Beecher. “Amphetamine Sulfate and Athletic Performance.” Journal of the American Medical Association 170 (1959), pp. 542–57. Laties, V. G., and B. Weiss. “The Amphetamine Margin in Sports.” Federation Proceedings 40 (1981), pp. 2689–92. Noble, B. J. Physiology of Exercise and Sport. St Louis: Mosby, 1986. Cohen, B. S., and others. “Effects of Caffeine Ingestion on Endurance Racing in Heat and Humidity.” European Journal of Applied Physiology 73 (1996), pp. 358–63. Bodley, H. “Medical Examiner: Ephedra a Factor in Bechler Death.” USA Today, March 13, 2003. Williams, M. H. Ergogenic Aids in Sports. Champaign, IL: Human Kinetics, 1983. Marshall, E. “The Drug of Champions.” Science 242 (1983), pp. 183–84. Taylor, W. N. Hormonal Manipulation: a New Era of Monstrous Athletes. Jefferson, NC: McFarland & Co., 1985. Pope, H. G., and D. L. Katz. “Affective and Psychotic Symptoms Associated with Anabolic Steroid Use.” American Journal of Psychiatry 145 (1988), pp. 487–90. Lubell, A. “Does Steroid Abuse Cause— or Excuse— Violence? Physician and Sportsmedicine 17 (1989), pp. 176–85. Fultz, O. “’Roid Rage.” American Health 10 (1991), p. 60. Burke, L., and others. “Supplements and Sports Foods.” Clinical Sports Nutrition, 3rd ed. Edited by L. Burke and V. Deakin. Sydney: McGraw-Hill, 2006, pp. 485–579. Available at http://www.ais.org.au/nutrition/documents/ 16Complete.pdf Nightingale, S. L. “Anabolic Steroids as Controlled Substances.” Journal of the American Medical Association 265 (1991), p. 1229. Liu, H., and others. “Systematic Review: The Effects of Growth Hormone on Athletic Performance.” Annals of Internal Medicine (2008) [March 17 Epub ahead of print] Spann, S. “Effect of Clenbuterol on Athletic Performance.” Annals of Pharmacotherapy 29 (1995), p. 75.
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How Would You Run the Race? Imagine that you have gone out for the track team. You compete in the 3,000-meter races and have been training hard for the past two years. It seems as though you have worked as hard as you could every day, yet it’s clear that your times have gotten as fast as they’re going to get. The conference championships are tomorrow. Your parents have traveled 300 miles to see you run, and lots of your friends will be there, cheering you on. You know your own times, and you know the competition, and, although you expect a close race for the top three spots, you figure to come in fourth. You yourself have never used any type of stimulant drug, but you have heard rumors that several of the fastest runners take amphetamines before the race, and you suspect that it is true. Your conference has not yet adopted a drug-screening program for track, however, so there’s no way to know for sure.
Under these circumstances, what would you do if 1. Someone you don’t know very well but who you heard is a drug dealer offers you some “speed” just for the race? 2. A friend of yours has some prescription diet pills that contain amphetamines, and the friend offers you one? 3. You are offered some cocaine to snort right before the race? 4. You are offered coffee or tea? Or would you rather not take artificial stimulants at all, come in fourth, and know you did your best and ran a clean race?
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SEVEN Prevention and Treatment This final section on prevention and treatment comes at the end of the book for a reason. Now
17 Preventing Substance Abuse What kinds of prevention programs have been tested in the schools, and which ones seem to be effective? What can parents and communities do?
that you’re more familiar with the wide spectrum of substances that people can abuse, and also
18 Treating Substance Abuse and Dependence What are the differences among the various approaches to treating alcohol, opioid, cocaine dependence, and others? How well do these programs work?
with the wide variety of forms of substance abuse and dependence, we are better able to talk about what we’re trying to prevent, and what we’re trying to treat. Because many of the medication-based treatments depend on specific interactions with the targeted substances of abuse, you now should understand how those medications have been developed and used.
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Preventing Substance Abuse Objectives After you have studied this chapter, you should be able to: • Distinguish between education and propaganda programs based on their goals and approaches. • Describe two systems for classifying prevention programs: one based on stages of involvement, the other based on target populations defined by risk for drug use. • Describe the historical shifts in substance abuse prevention programs from the knowledge-attitudes-behavior model to affective education to anti-drug norms. • Explain how the social influence model for smoking prevention led to the development of DARE and similar programs.
Why can’t we do something to keep young people from ruining their lives with drugs? As • Describe the outcome of research on DARE’s effectiveness our society seeks to prevent drug and how DARE America has responded. abuse by limiting the availabil• List some examples of effective prevention programs that ity of such drugs as heroin and have been adopted as model programs by SAMHSA. cocaine, we are forced to recognize several other facts. First, as • Give some examples of peer, family, and community long as there is a sizable market approaches to prevention. for these substances, there will • Describe the most consistent feature of workplace prevenbe people to supply them. Thus, tion programs. only if we can teach people not to want the drugs can we attack the source of the problem. Second, these substances will never disappear, so we should try to teach people to Defining Goals and live in a world that includes them. Third, our Evaluating Outcomes society has accepted the continued existence Think about the process you are engaged in of tobacco and alcohol, yet some people are while reading and studying this book. The text harmed by them. Can we teach people to coexis aimed at teaching its readers about drugs: ist with both legal and illegal substances and their effects, how they are used, and how they to live in such a way that their lives and health relate to society. The goal of the authors is are not impaired by them? 410
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education. A person who understands all this information about all these drugs will perhaps be better prepared to make decisions about personal drug use, more able to understand drug use by others, and better prepared to participate in social decisions about drug use and abuse. We hope that a person who knew all this would be in a position to act more rationally, neither glorifying a drug and expecting miraculous changes from using it nor condemning it as the essence of evil. But our ultimate goal is not to change the readers’ behavior in a particular direction. For example, the chapter on alcohol, although pointing out the dangers of its use and the problems it can cause, does not attempt to influence readers to avoid all alcohol use. The success of this book is measured by how much a person knows about alcohol, tobacco, or marijuana, not by whether he or she is convinced never to drink or smoke. On the other hand, a tradition exists, going back to the “demon rum” programs of the late 1800s, of presenting negative information about alcohol and other drugs in the public schools with the clear goal of prevention of use. Some of these early programs presented information that was so clearly one-sided that they could have been classified as propaganda rather than education. We would not measure the success of such a program by how much objective information the students gained about the pharmacology of cocaine, for example. A more appropriate index might be how many of the
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students did subsequently experiment with the drugs against which the program was aimed. Until the early 1970s, it was simply assumed that these programs would have the desired effect, and few attempts were made to evaluate them.
Types of Prevention The goals and methods of a prevention program also depend on the drug-using status of those served by the program. The programs designed to prevent young people from starting smoking might be different from those used to try to prevent relapse in smokers who have quit, for example. Until recently, drug-abuse prevention programs have been classified according to a public health model: •
Primary prevention programs are those aimed mainly at young people who have not yet tried the substances in question or who may have tried tobacco or alcohol a few times. As discussed in the section “Defining Goals and Evaluating Outcomes,” such programs might encourage abstinence from specific drugs or might have the broader goal of teaching people how to view drugs and the potential influences of drugs on their lives, emotions, and social relationships. Because those programs are presented to people with little personal experience with drugs, they might be expected to be especially effective. But, there is the danger of introducing large numbers of children to information about drugs that they might otherwise never have heard of, thus arousing their curiosity.
•
Secondary prevention programs can be thought of as designed for people who have tried the drug in question or a variety of other substances. The goals of such programs are usually the prevention of the use of other, more dangerous substances and the prevention of the development of more dangerous forms of use of the substances they are already experimenting with. We
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Drugs in the Media Prime-Time Drug-Prevention Programming In late 1997, the U.S. Congress approved the expenditure of $1 billion over a five-year period for anti-drug advertising on television networks. This was a lot of revenue for the networks, but the catch was that they had to broadcast the messages at half the normal market price. After industry protests, the White House Office of National Drug Control Policy struck deals to discharge networks from the halfcost advertising time requirements if they would incorporate drug-abuse prevention messages into the content of television shows. For example, the program “E.R.,” about a hospital emergency room,
might describe the clientele here as more “sophisticated” substance users who have not suffered seriously from their drug experiences and who are not obvious candidates for treatment. Many college students fall into this category, and programs aimed at encouraging responsible use of alcohol among college students are good examples of this stage of prevention. •
Tertiary prevention, in our scheme, is relapse prevention, or follow-up programs. For alcohol-or heroin-dependent individuals, treatment programs are the first order of priority. However, once a person has been treated or has stopped the substance use without assistance, we enter another stage of prevention.
The Institute of Medicine has proposed a new classification of the “continuum of care,” which includes prevention, treatment, and maintenance.1 Prevention efforts are categorized according to the intended target population, but the targets are not defined only by prior drug use: •
Universal prevention programs are designed for delivery to an entire population—for example, all schoolchildren or an entire community.
has included several episodes dramatizing the consequences of illicit drug use. The agreement was brought to light in early 2000 by the online newsmagazine salon.com, which raised concerns about hidden government “propaganda.” See if you can get a few people to keep an eye out for such integrated anti-drug content for one week. Did you find some obvious examples? Have you been aware of this type of integrated content before? What is the danger involved in having the federal government influence the content of television programming in this subtle way?
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Selective prevention strategies are designed for groups within the general population that are deemed to be at high risk—for example, students who are not doing well academically or the poorest neighborhoods in a community.
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Indicated prevention strategies are targeted at individuals who show signs of developing problems, such as a child who began smoking cigarettes at a young age or an adult arrested for a first offense of driving under the influence of alcohol.
Prevention Programs in the Schools The Knowledge-Attitudes-Behavior Model After the increase in the use of illicit drugs by young middle-class people in the 1960s, there was a general sense that society was not doing an adequate job of drug education, and most school systems increased their efforts. However, there was confusion over the methods to be used. Traditional anti-drug programs had relied heavily on representatives of the local police, who went into schools and told a few horror stories, describing the legal trouble due anyone who got caught with illicit drugs. Sometimes
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Targeting Prevention Preventing Inhalant Abuse The abuse by children of spray paints and other products containing solvents appears to have increased somewhat in recent years (see Chapter 7). Several characteristics of this type of abuse make it an interesting problem for prevention workers. First, the variety of available products and their ready availability in stores, the home, and even in schools make preventing access to the inhalants an impossibility. Second, most of the kids who use these substances probably know it’s unhealthy and dangerous to do so, so further information of that sort may not add much in the way of preventing their use. Third, this use is very “faddish”—a group of eighthgraders in one school might start inhaling cleaning fluid; a group of sixth-graders in another neighborhood might be into gold paint (in distinct preference to black, yellow, or white). Given these characteristics, where does a school-based prevention education program begin
the officers showed what the drugs looked like or demonstrated the smell of burning marijuana, so that the kids would know what to avoid. Sometimes, especially in larger cities, a former user described how easy it was to get “hooked,” the horrible life of the junkie, and the horror of withdrawal symptoms. The 1960s saw more of that, plus the production of a large number of scary anti-drug films. Teachers and counselors knew little about these substances, and many teachers attended courses taught by experts. Some of the experts were enforcement-oriented and presented the traditional scare-tactics information, whereas others were pharmacologists who presented the “dry facts” about the classification and effects of various drugs. The teachers then brought many of these facts into their classrooms. It was later pointed out that the programs of this era were based on an assumed model: that providing information about drugs would increase the students’ knowledge of drugs and their effects, that this increased knowledge would lead to
to attack the problem? Does it focus on a particular product and try to talk kids out of using gold paint? Does it talk about a whole variety of products and thereby perhaps introduce the kids to new things they hadn’t thought of? One videotape (Inhalants: Kids in Danger, Adults in the Dark) took the approach of attempting to inform parents and teachers of the varieties of paints, perfumes, solvents, and other spray products used by abusers and to inform them of some of the subterfuges used by some of the kids (carrying a small cologne vial to school, spraying paint into empty soft drink cans, etc.). However, this video is not meant to be shown to children, because it describes exactly what to do and how to do it. Probably the best idea in prevention classes is to reinforce to children in general terms the dangers of inhalants without describing a particular substance or method of use.
changes in attitudes about drug use, and that these changed attitudes would be reflected in decreased drug-using behavior.2 In the early 1970s, this model began to be questioned. A 1971 study indicated that students who had more knowledge about drugs tended to have a more positive attitude toward drug use.3 Of course, it may have been that prodrug students were more interested in learning about drugs, so this was not an actual assessment of the value of drug education programs. A 1973 report by the same group indicated that four different types of drug education programs were equally effective in producing increased knowledge about drugs and equally ineffective in altering attitudes or behavior.4 Nationwide, drug use had increased even with the greater emphasis on drug education. Concern arose about the possibility that drug education may even have contributed to increased drug use. Before the 1960s, the use of marijuana and LSD was rare among school-age youngsters. Most of them didn’t know much about these things, had
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given them little thought, and had probably never considered using them. Telling them over and over not to use drugs was a bit like telling a young boy not to put beans in his nose. He probably hadn’t thought of it before, and your warning gives him the idea. These concerns led the federal government in 1973 to stop supporting the production of drug-abuse films and educational materials until it could determine what kinds of approaches would be effective. The question of effectiveness depended greatly on the goals of the program. Did we want all students never to experiment with cigarettes, alcohol, marijuana, or other drugs? Or did we want students to be prepared to make rational decisions about drugs? For example, a 1976 report indicated that students in drug education programs did increase their use of drugs over the two years after the program, but they were less likely to show drastic escalation of the amount or type of drug use over that period, when compared with a control group.5 Perhaps by giving the students information about drugs, we make them more likely to try them, but we also make them more aware of the dangers of excessive use. For a time in the 1970s, it seemed as though teaching students to make rational decisions about their own drug use with the goal of reducing the overall harm produced by misuse and abuse could be a possible goal of prevention programs.
Affective Education Educators have been talking for several years about education as including both a “cognitive domain” and an “affective domain,” the domain of emotions and attitudes. One reason that young people might use psychoactive drugs is to produce certain feelings: of excitement, of relaxation, of power, of being in control. Or perhaps a child might not really want to take drugs but does so after being influenced by others. Helping children know their own feelings and express them, helping them achieve altered emotional states without drugs, and teaching them to feel valued,
Helping young people learn to deal with emotions in healthy ways and giving them successful experiences may reduce their rates of smoking, drinking, and drug use.
accepted, and wanted are all presumed to be ways of reducing drug use. Values Clarification The values clarification approach makes the assumption that what is lacking in drug-using adolescents is not factual information about drugs but, rather, the ability to make appropriate decisions based on that information.6 Perhaps drug use should not be “flagged” for the students by having special curricula designed just for drugs but, instead, emphasis should be placed on teaching generic decision-making skills. Teaching students to analyze and clarify their own values in life is accomplished by having them discuss their reactions to various situations that pose moral and ethical dilemmas. Groups of parents or other citizens who are concerned about drug abuse sometimes have great difficulty understanding and accepting these approaches because they do not take a direct anti-drug approach. In the 1970s, when these programs were developed, it seemed important that the schools not try to impose a particular set of values but, rather, allow for differences in religion, family background, and so on. For this reason, the programs were often said to be value-free. To many parents, the purpose of values clarification training is not
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immediately clear, and teaching young children to decide moral issues for themselves may run contrary to the particular set of values the parents want their children to learn. Alternatives to Drugs Along with values clarification, another aspect of affective education involves the teaching of alternatives to drug use. Under the assumption that students might take drugs for the experience, for the altered states of consciousness that a drug might produce, students are taught so-called natural highs, or altered states, that can be produced through relaxation exercises, meditation, vigorous exercise, or an exciting sport. Students are encouraged to try these things and to focus on the psychological changes that occur. These alternatives should be discussed with some degree of sensitivity to the audience; for example, it would make little sense to suggest to many inner-city 13-year-olds that expensive activities such as scuba diving and snow skiing would be good alternatives to drugs. Personal and Social Skills Several studies indicate that adolescents who smoke, drink, or use marijuana also get lower grades and are less involved in organized sports or school clubs. One view of this is that students might take up substance use in response to personal or social failure. Therefore, teaching students how to communicate with others and giving them success experiences is another component of affective education approaches. For example, one exercise that has been used is having the students operate a school store. This is done as a group effort with frequent group meetings. The involved students are expected to develop a sense of social and personal competence without using drugs. Another approach is to have older students tutor younger students, which is designed to give the older students a sense of competence. An experiment carried out in Napa, California, combined these approaches with a drug education course, small-group discussions led by teachers, and classroom management techniques designed to teach
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discipline and communication skills and to enhance the students’ self-concepts.7 Although a small effect on alcohol, marijuana, and cigarette use was found among the girls, the effects were gone by the one-year follow-up.
Anti-drug Norms A 1984 review of prevention studies concluded that (1) most substance abuse prevention programs have not contained adequate evaluation components; (2) increased knowledge has virtually no impact on substance abuse or on intentions to smoke, drink, or use drugs; (3) affective education approaches appear to be experiential in their orientation and to place too little emphasis on the acquisition of skills necessary to increase personal and social competence, particularly those skills needed to enable students to resist the various interpersonal pressures to begin using drugs; and (4) few studies have demonstrated any degree of success in terms of actual substance abuse prevention.8
This last point is not entirely a criticism of the programs themselves but reflects the difficulty of demonstrating statistically significant changes in behavior over a period of time after the programs. Refusal Skills In response to the third point, that affective education approaches were too general and experiential, the next efforts at preventing drug use focused on teaching students to recognize peer pressure to use drugs and on teaching specific ways to respond to such pressures without using drugs. This is sometimes referred to as psychological inoculation. In addition to the focus on substance use, “refusal skills” and “pressure resistance” strategies are
values clarification: teaching students to recognize and express their own feelings and beliefs. alternatives: alternative nondrug activities, such as relaxation or dancing.
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Taking Sides Are “Alternatives to Drugs” Really Alternatives? As one part of many drug education programs, students are taught that they can produce natural highs—that is, altered states of consciousness similar to those produced by drugs, but without using drugs. One such alternative that has been mentioned in these programs is skydiving. Obviously an activity of that sort has all the glamour, danger, and excitement most of us would want. Maybe if the kids could do this whenever they wanted, they wouldn’t want to try cocaine or marijuana. But let’s examine this as an alternative for a bunch of junior high school kids. First, there’s the matter of cost and availability. How realistic is it to think that most of these kids would have access to skydiving? Second, there’s the issue of convenience. Even if you were a rich kid, with your own airplane, parachute, and pilot, it’s unlikely that you’d be able to go skydiving every afternoon after school. Drugs and alcohol may not provide the best
taught in a broader context of self-assertion and social skills training. The first successful application of this technique was a film in which young actors acted out situations in which one person was being pressured to smoke cigarettes. The film then demonstrated effective ways of responding to the pressure gracefully without smoking. After the film, students discuss alternative strategies and practice the coping techniques presented in the film. This approach has been demonstrated to be successful in reducing cigarette smoking in adolescent populations. It has been adapted for use with groups of various ages and for a wider variety of drugs and other behaviors, and students are taught from kindergarten on to “just say no” when someone is trying to get them to do something they know is wrong. Drug-Free Schools In 1986 the federal government launched a massive program to support “drug-free schools and communities.” Among other things, the government provided mil-
highs in the world, but often they are easy to get and use, compared with activities such as skydiving. Maybe skydiving isn’t a practical alternative to drugs for a lot of people. Still, it seems more wholesome and desirable. Let’s become social philosophers and ask ourselves why the image of a person skydiving is more positive than the image of a person snorting cocaine. After all, skydiving doesn’t make any obvious contributions to society. Let’s play devil’s advocate and propose that skydiving is not preferable to taking cocaine. Either way, the person is engaged in dangerous, expensive, self-indulgent activity. Contrast skydiving with cocaine, and see if you can answer for yourself why skydiving has a more positive image than cocaine use. You may have to talk about this with several people before you get a consistent feeling for why our society respects one of these activities so much more than the other. What about skiing? bungee-cord jumping?
lions of dollars’ worth of direct aid to local school districts to implement or enhance drugprevention activities. Along with this, the Department of Education produced a small book called What Works: Schools Without Drugs,9 which made specific recommendations for schools to follow. This book did not recommend a specific curriculum; its most significant feature was the emphasis on factors other than curriculum, such as school policies on drug and alcohol use. It suggested policies regarding locker searches, suspension, and expulsion of students. The purpose was not so much to take a punitive approach to alcohol or drug use as to point out through example and official policy that the school and community were opposed to drug and alcohol use by minors. Following this general drug-free lead, schools adopted “tobacco-free” policies, stating that not only the students but also teachers and other staff people were not to use tobacco products at school or on school-sponsored trips or activities.
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According to this approach, the curriculum should include teaching about the laws against drugs, as well as about the school policies. In other words, as opposed to the 1970s values clarification approach of teaching students how to make responsible decisions for themselves, this approach wants to make it clear to the students that the society at large, the community in which they live, and the school in which they study have already made the decision not to condone drug use or underage alcohol use. This seems to be part of a more general educational trend away from “value-free” schools toward teaching values that are generally accepted in our society. For schools to be eligible for federal Drug-Free Schools funding, they must certify that their program teaches that “illicit drug use is wrong and harmful.”
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the social influence model.10 Out of all this research, certain consistencies appear. The most important of these is that it is possible to design smoking prevention programs that are effective in reducing the number of adolescents who begin smoking. Some practical lessons about the components of those programs have also emerged.11 For example, presenting information about the delayed consequences of smoking (possible lung cancer many years later) is relatively ineffective. Information about the immediate physiological effects (increased heart rate, shortness of breath) is included instead. Some of the most important key elements that were shown to be effective were the following:. •
Training refusal skills (for example, eight ways to say no). This was originally based on films demonstrating the kinds of social pressures that peers might use to encourage smoking and modeling a variety of appropriate responses. Then the students engage in role-playing exercises in which they practice these refusal skills. By using such techniques as changing the subject or having a good excuse handy, students learn to refuse to “cooperate” without being negative. When all else fails, however, they are taught to be assertive and insist on their right to refuse.
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Public commitment. Researchers found that having each child stand before his or her peers and promise not to start smoking and sign a pledge not to smoke are effective prevention techniques. Countering advertising. Students are shown examples of cigarette advertising, and then the “hidden messages” are discussed (young, attractive, healthy, active models are typically used; cigarette smoking might be associated with dating or with sports). Then the logical inconsistencies
Development of the Social Influence Model Some of the most sophisticated prevention research in recent years has been focused directly on cigarette smoking in adolescents. This problem has two major advantages over other types of drug use, as far as prevention research is concerned. First, a large enough fraction of adolescents do smoke cigarettes so that measurable behavior change is possible in a group of reasonable size. In contrast, one would have to perform an intervention with tens of thousands of people before significant alterations in the proportion of heroin users would be statistically evident. Second, the health consequences of smoking are so clear with respect to cancer and heart disease that there is a fairly good consensus over goals: We’d like to prevent adolescents from becoming smokers. One research advantage is the relatively simple verification available for self-reported use of tobacco: Saliva samples can be measured for cotinine, a nicotine metabolite. Virtually all the various approaches to drug-abuse prevention have been tried with smoking behavior; in fact, Evans’s 1976 smoking prevention paper introduced the use of the psychological inoculation approach based on
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social influence model: a prevention model adopted from successful smoking programs
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Training in refusal skills, including role-playing exercises, is a key component of the social influence model.
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between these hidden messages and the actual effects of cigarette smoking (e.g., bad breath, yellow teeth, shortness of breath) are pointed out. The purpose of this is to “inoculate” the children against cigarette advertising by teaching them to question its messages. Normative education. Adolescents tend to overestimate the proportion of their peers who smoke. Presenting factual information about the smoking practices of adolescents provides students with a more realistic picture of the true social norms regarding smoking and reduces the “everybody is doing it” attitude. When possible, statistics on smoking from the specific school or community should be used in presenting this information.
Use of teen leaders. Presenting dry facts about the actual proportion of smokers should ideally be reinforced by example. If you’re presenting the program to junior high students, it’s one thing to say that fewer than one-fifth of the high school students in that community smoke, but it’s another to bring a few high school students into the room and have them discuss the fact that neither they nor their friends smoke, their attitudes about smokers, and ways they have dealt with others’ attempts to get them to smoke.
Possible improvements to those approaches are offered by the cognitive developmental approach to smoking behavior. McCarthy criticized the social influence/social skills training model for assuming that all students should be taught social skills or refusal skills without regard to whether they need such training.12 The model “is that of a defenseless teenager who, for lack of general social skills or refusal skills, passively accedes to social pressures to smoke.” Alternative models have been proposed in which the individual makes active, conscious decisions in preparation for trying cigarettes, trying smoking and becoming an occasional or regular user. The decision-making processes, and thus the appropriate prevention strategy, might be different at each of these “stages of cognitive development” as a smoker. Furthermore, smokers who begin smoking very young behave differently than smokers who begin as older adolescents (e.g., those who start young show more unanimity in selecting the most popular brand). Unfortunately, adolescents continue to initiate smoking every year, and the risk and protective factors reviewed in Chapter 1 have more influence on smoking behavior (and on alcohol and other drug use) than any information or education programs yet devised.13
DARE Perhaps the most amazing educational phenomenon in a long time had fairly modest beginnings in 1983 as a joint project of the Los
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Angeles police department and school district. Those who are familiar with the Drug Abuse Resistance Education (DARE) program will have recognized its components described under the social influence model of smoking cessation. The difference here is that the educational program with DARE is delivered by police officers, originally in fifth- and sixth-grade classrooms. By basing the curriculum on sound educational research, by maintaining strict training standards for the officers who were to present the curriculum, and by encouraging the classroom teacher to participate, some of the old barriers to having nonteachers responsible for curriculum were overcome. The officers are in uniform, and they use interactive techniques as described for the social influence model. Most of the components are there: refusal skills, teen leaders, and a public commitment not to use illicit drugs. In addition, some of the affective education components are included: self-esteem building, alternatives to drug use, and decision making. The component on consequences of drug abuse is, no doubt, enhanced by the presence of a uniformed officer who can serve as an information source and symbol for concerns over gang activity and violence and can discuss arrest and incarceration. The 17-week program is capped by a commencement assembly at which certificates are awarded. This program happened to be in place at just the right time, both financially and politically. With the assistance of drug-free schools money and with nationwide enthusiasm for new drug-prevention activities in the 1980s, the program spread rapidly across the United States. By the early 1990s, DARE programs were found in every state. This program was accepted quickly by many schools, and endorsed enthusiastically by educators, students, parents, and police participants, even though its effectiveness in preventing drug use was not evaluated extensively until 1994. In 1994, two important, large-scale studies of the effects of DARE were reported. One was based on a longitudinal study in rural, suburban,
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Drugs in Depth How Much Do You Know about DARE? 1. Almost everyone in the United State has heard of DARE. What do the letters stand for? 2. One component of DARE is practicing how to refuse using drugs. Do you know the origin of DARE’s eight ways to say no? 3. DARE has been implemented in more schools than any other substance-abuse prevention program. Does research on its effectiveness show that it’s one of the best at preventing drug abuse? 4. Besides school-based programs, what other kinds of substance-abuse prevention programs have been developed? 5. The Institute of Medicine has a relatively new way of categorizing prevention programs into various types. Do you know what factor is used to differentiate among the types? Answers 1. Drug Abuse Resistance Education 2. This and most components of DARE were adopted from smoking prevention programs developed in the 1970s. 3. Research on the effectiveness of DARE has not demonstrated a strong impact on preventing drug use. Other programs described in this chapter appear to be more effective. 4. Parent, family, and community programs and public media campaigns have also been developed to prevent drug abuse. 5. The target population (the entire population, at-risk populations, and individuals with early signs of problems).
and urban schools in Illinois, comparing students exposed to DARE with students who were not.14 Although the program had some effects on reported self-esteem, there was no evidence DARE: Drug Abuse Resistance Education, the most popular prevention program in schools.
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for long-term reductions in self-reported use of drugs. The other report was based on a review of eight smaller outcome evaluations of DARE, selected from 18 evaluations based on whether the reports had a control group, a pretest-posttest design, and reliable outcome measures.15 The overall impact of these eight programs was to increase drug knowledge and knowledge about social skills, but the effects on drug use were marginal at best. There was a very small but statistically significant reduction of tobacco use and no reliable effect on alcohol or marijuana use. A more recent review of all the experimental studies on DARE published in peer-reviewed journals found an average effect size that was small and not statistically significant. The authors reported that their results supported previous conclusions about the ineffectiveness of DARE.16 The repeated failures to demonstrate a significant impact of the DARE program on drug use remain a dilemma in light of its widespread popularity. Communities have not abandoned the program. Instead, DARE America has developed additional programs, including DARE + PLUS (Play and Learn Under Supervision) as an extension to the elementary program, and curriculum for middle school and high school DARE programs designed to follow up with these older adolescents. We cannot yet evaluate the effectiveness of these additional programs.
Programs That Work Several school-based drug-use prevention programs have been modeled after the successful social influence model and have components similar to those of DARE. A few of these programs have been demonstrated to have beneficial effects on actual drug use: Project ALERT was first tested in 30 junior high schools in California and Oregon.17 The program targeted cigarette smoking, alcohol use, and marijuana use. Before the program, each student was surveyed and classified as a nonuser, an experimenter, or a user for each of the three substances. The curriculum was taught either by health educators or by educa-
School-based drug-use prevention programs have been shown to reduce initiation and levels of drug use.
tors with the assistance of trained teen leaders. Control schools simply continued whatever health or drug curriculum they had been using. The program was delivered in the seventh grade, and follow-up surveys were done 3, 12, and 15 months later. Three “booster” lessons were given in the eighth grade. The program surprisingly had no measurable effect on initiation of smoking by nonusers. However, those who were cigarette experimenters before the program began were more likely to quit or to maintain low rates of smoking than the control group. The group with teen leader support showed the largest reduction: 50 percent fewer students were weekly smokers at the 15-month follow-up. The experimental groups drank less alcohol soon after the program was presented, for previous alcohol nonusers, experimenters, and users. However, this effect diminished over time and disappeared by the end of the study. The most consistent results were in reducing initiation of marijuana smoking and reducing levels of marijuana smoking. For example, among those who were not marijuana users at the beginning, about 12 percent of the controlgroup students had begun using marijuana
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Drugs in Depth Effective Prevention Programs The Center for Substance Abuse Prevention (CSAP), a branch of the Substance Abuse and Mental Health Administration in the U.S. Department of Health and Human Services, has been studying research on effective prevention programs. It has developed a list of model programs. Some of the programs on this partial list are described within this chapter, and more information on the others can be obtained from the SAMHSA Web site. Also, as new programs are approved, they are being added to the list, so for the most current list, check on the Web at prevention.samhsa.gov. Model Programs • Across Ages • Athletes Training and Learning to Avoid Steroids (ATLAS)
by the 15-month follow-up. In the treatment groups, only 8 percent began using during that time period, representing a one-third decrease in initiation to marijuana use. Another program, the Life Skills Training program, has been subjected to several tests and has shown long-term positive results. This three-year program is based on the social influence model and teaches resistance skills, normative education, and media influences. Self-management skills and general social skills are also included. One study of this program found significantly lower use of marijuana, alcohol, and tobacco after six years. A subsequent application of this program among ethnic minority youth (Latino and African American) in New York City found reduced use on a two-year follow-up.18
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that is why most efforts at drug-abuse prevention have been carried out there. However, peers, parents, and the community at large also exert powerful social influences on young people. Because these groups are less accessible than the schools, fewer prevention programs have been based on using parent and community influences. Nevertheless, important efforts have been made in all these areas.
Peer Programs Most peer programs have occurred in the school setting, but some have used youth-oriented community service programs (such as YMCA, YWCA, and recreation centers) or have focused on “street” youth by using them in group community service projects. •
Peers, Parents, and the Community Our nation’s public schools clearly are the most convenient conduit for attempts to achieve widespread social changes among young people, and
Child Development Project Communities Mobilizing for Change on Alcohol Creating Lasting Family Connections Dare to Be You Families and Schools Together Keep a Clear Mind Life Skills Training Project ALERT Project Northland Project Towards No Tobacco Use Reconnecting Youth Residential Student Assistance Program Safe Dates SMART Team Strengthening Families Program Too Good for Drugs
Peer influence approaches start with the assumption that the opinions of an adolescent’s peers are significant influences on the adolescent’s behavior. Often using an adult group facilitator/coordinator, the program’s emphasis is on open discussion among a group of children or adolescents.
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These discussions might focus on drugs, with the peer group discussing dangers and alternatives, or they might simply have the more general goal of building positive group cohesiveness, a sense of belonging, and communication skills. •
Peer participation programs often focus on groups of youth in high-risk areas. The idea here is that young people participate in making important decisions and in doing significant work, either as “peers” with cooperating adults or in programs managed almost entirely by the youth themselves. Sometimes participants are paid for community service work, in other cases they engage in money-making businesses, and sometimes they provide youth-oriented information services. These groups almost never focus on drug use in any significant way; rather, the idea is to help people become participating members of society.
The benefits of these “extracurricular” peer approaches are measurable in terms of acquired skills, improved academic success, higher selfesteem, and a more positive attitude toward peers and school. As to whether they alter drug use significantly, the data either are not available or are inconclusive for the most part.
Parent and Family Programs The various programs that have worked with parents have been described as taking at least one of four approaches.19 Most of the programs include more than one of these approaches. •
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Informational programs provide parents with basic information about alcohol and drugs, as well as information about their use and effects. Although the parents often want to know simply what to look for, how to tell if their child is using drugs, and what the consequences of drug abuse are, the best programs provide additional information. One important piece of information is the actual extent of the use of various types of drugs among young people. Another goal
might be to make parents aware of their own alcohol and drug use to gain a broader perspective of the issue. A basic rationale is that well-informed parents will be able to teach appropriate attitudes about drugs, beginning when their child is young, and will be better able to recognize potential problems relating to drug or alcohol use. •
Parenting skills might be taught through practical training programs. Communication with children, decision-making skills, how to set goals and limits, and when and how to say no to your child can be learned in the abstract and then practiced in role-playing exercises. One risk factor for adolescent drug and alcohol use is poor family relationships, and improving family interaction and strengthening communication can help prevent alcohol and drug abuse.
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Parent support groups can be important adjuncts to skills training or in planning community efforts. Groups of parents meet regularly to discuss problem solving, parenting skills, their perceptions of the problem, actions to be taken, and so on.
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Family interaction approaches call for families to work as a unit to examine, discuss, and confront issues relating to alcohol and drug use. Other exercises might include more general problem solving or response to emergencies. Not only do these programs attempt to improve family communication, but also the parents are placed in the roles of teacher of drug facts and coordinator of family action, thus strengthening their knowledge and skills.
One selective prevention program, called the Strengthening Families program, targets children of parents who are substance abusers. This program has been successfully implemented several times within diverse populations. It has three major goals: improving parenting skills, increasing children’s skills (such as communication skills, refusal skills, awareness of feelings, and emotion expression
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skills), and improving family relationships (decreasing conflict, improving communication, increasing parent-child time together, and increasing the planning and organizational skills of the family). Children and parents attend evening sessions weekly for 14 weeks to learn and practice these skills. Evaluations of this program indicate that it reduces tobacco and alcohol use in the children as well as reduces substance abuse and other problems in the parents.20
Community Programs Two basic reasons exist for organizing prevention programs at the community level. The first is that a coordinated approach using schools, parent and peer groups, civic organizations, police, newspapers, radio, and television can have a much greater impact than an isolated program that occurs only in the school, for example. Another reason is that drug-abuse prevention and drug education are controversial and emotional topics. Parents might question the need for or the methods used in drug education programs in the schools. Jealousy and mistrust about approaches can separate schools, police, church, and parent groups. A program that starts by involving all these groups in the planning stages is more likely to receive widespread community support. Clearly, the spread of the DARE program in the schools is based partly on the fact that it demonstrates and encourages cooperation between the police and the schools, as well as encourages parental involvement. Community-based programs can bring other resources to bear. For example, the city council and local businesses can be involved in sponsoring alcohol-free parties, developing recreational facilities, and arranging field trips so that, when the school-based program talks about alternatives, the alternatives are available. The public media can be enlisted not only to publicize public meetings and programs but also to present drug- and alcohol-related information that reinforces what is learned in the other programs.
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Mind / Body Connection Integrating Treatment and Prevention with Pregnancy Services Does your community provide needed services and compassionate support for pregnant women who use alcohol and drugs? An emerging consensus views alcohol, tobacco, and other drug use during pregnancy as a community problem. During this period when women anticipate major life change, prevention initiatives can enhance their motivation to have a healthy baby. And, for women with substance-abuse problems, pregnancy provides a similarly strong motivation to seek help. Fear of blame, legal intervention, and loss of child custody prevent many women from getting help. To counteract these barriers to services, prevention initiatives should promote services that are safe and confidential. Services should be not only physically accessible but also culturally accessible. Efforts that recognize the importance of relationships to women can call on the support of family members and others for alcohol-free and other drug-free pregnancies. Prevention strategies that combine information with options for change have shown promising results in reducing drug use during pregnancy. Find out if women in your area have access to an integrated system of alcohol, tobacco, and other drug treatment and maternal and child health care.
Communities Mobilizing for Change on Alcohol is one of SAMHSA’s model prevention programs (see page 421). The program works for change in alcohol ordinances in the community and alcohol policies of schools, universities, and civic organizations. It encourages parents, faith organizations, the police, city government, and all businesses and organizations within the community to promote the idea of limiting alcohol availability for 13- to 18year-olds. The program was studied in 15 communities over a five-year period and resulted in decreased alcohol sales to minors, decreases in friends providing alcohol to minors, and
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and to notify employees of the consequences of violating company policy regarding drug use. The ultimate goal is not to catch drug users and fire them but to prevent drug use by making it clear that it is not condoned.
What Should We Be Doing?
Community-based programs work best when they have widespread community support. This anti-tobacco mural is tied to the values of a local community and focuses on the traditional sacred origins of tobacco use among Native Americans.
decreases in self-reported drinking in the targeted age group.
Prevention in the Workplace As a part of its efforts to reduce the demand for drugs, the federal government has encouraged private employers, especially those who do business with the government, to adopt policies to prevent drug use by their employees. The most consistent feature of these programs is random urine screens. In 1989, rules went into effect requiring all companies and organizations that obtain grants or contracts from the federal government to adopt a “drug-free workplace” plan. The exact nature of the plan is up to the company, but guidelines were produced by the Department of Labor. Modeled after the Education Department’s What Works book, the Labor Department’s is called What Works: Workplaces Without Drugs.21 At a minimum, the Labor Department expects employers to state clearly that drug use on the job is unacceptable
By now you have picked up some ideas for things to do to reduce drug use, as well as some things to avoid doing. But the answer as to what needs to be done in a particular situation depends on the motivations for doing it. Most states require drug- and alcohol-abuse prevention education as part of a health curriculum, for example. If that is the primary motive for doing something, and if there doesn’t seem to be a particular problem with substance abuse in the schools, then the best thing would be to adopt one of the modern school-based programs that have been developed for this purpose, to make sure the teachers and other participants are properly trained in it, and to go ahead. In selecting from among the curricula, a sensible, balanced approach that combines some factual information with social skills training, perhaps integrated into the more general themes of health, personal values, and decision making, would be appropriate. The ones mentioned in the section “Programs That Work” fit this general description, and each deserves a careful look. Above all, avoid sensational scare stories, preachy approaches from the teacher to the student, and untrained personnel developing their own curricula. Another good thing to avoid is the inadvertent demonstration of how to do things you don’t want students to do. If, on the other hand, there is a public outcry about the “epidemic” of drugs and alcohol abuse in the community, speakers have inflamed passions, and there is a widespread fervor to do something about it, this presents both a danger and an opportunity. The danger is that this passionate group might attack and undermine the efforts already being made in the schools, substituting scary, preachy,
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negative approaches, which can have negative consequences. The opportunity lies in the possibility that this energy can be organized into a community planning effort, out of which could develop cooperation, increased parent understanding, a focus on family communication, interest in the lives of the community’s young people, and increased recreational and creative opportunities. The key to making this happen is convincing the aroused citizenry of the possibly negative consequences of doing what seems obvious and selling them on the idea of studying what needs to be done. A good place to start is by visiting the Web site of the Center for Substance Abuse Prevention (www.samhsa.gov/ csap). This agency produces updated materials for groups interested in developing drug- and alcohol-abuse prevention programs, provides technical assistance and training to communities interested in developing programs, and offers Community Partnership Grants. (A list of CSAP model programs is shown in the Drugs in Depth box on page 421.)
Summary •
We can distinguish between education programs with the goal of imparting knowledge and prevention programs aimed at modifying drug-using behavior.
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Most of the research over the past 30 years has failed to demonstrate that prevention programs can produce clear, meaningful, long-lasting effects on drug-using behavior.
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The affective education programs of the 1970s have been criticized for being too value-free.
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Based on the success of the social influence model in reducing cigarette smoking, a variety of school-based prevention programs have used the same techniques with illicit drugs.
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The DARE program has been adopted rapidly and widely, despite research showing limited impact on drug-using behavior.
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Current school-based approaches use refusal skills, countering advertising, public commitments, and teen leaders. Several of these programs have been demonstrated to be effective.
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Other nonschool programs are peer-based through after-school groups or activities, parent-based through parent and family training, or community-based.
Review Questions 1. What is the distinction between secondary and tertiary prevention? 2. What is the knowledge-attitudes-behavior model, and what information first called it into question? 3. Explain what is meant by “value-free” values clarification programs, and why they fell out of favor in the 1980s. 4. When the Drug-Free Schools programs began in 1986, the emphasis shifted away from curriculum to what? 5. What were the five successful components of the social influence model for smoking prevention? 6. In Project ALERT, what was the impact of using teen leaders to assist the instructors? 7. What distinguishes DARE from other similar programs based on the social influence model? 8. What do ALERT and Life Skills Training have in common, besides their effectiveness? 9. What are some of the “parenting” skills that might be taught and practiced in a prevention program? 10. What is the most common component of “drug-free workplace” plans?
References 1.
2.
National Institute on Drug Abuse. Drug Abuse Prevention for the General Population. Washington, DC: U.S. Department of Health and Human Services, 1997. Goodstadt, M. S. “School-based Drug Education in North America: What Is Wrong? What Can Be Done?” Journal of School Health 56 (1986), pp. 278–81.
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Swisher, J. D., and others. “Drug Education: Pushing or Preventing?” Peabody Journal of Education 49 (1971), pp. 68–75. Swisher, J. D., and others. “A Comparison of Four Approaches to Drug Abuse Prevention at the College Level.” Journal of College Student Personnel 14 (1973), pp. 231–35. Blum, R. H., E. Blum, and E. Garfield. Drug Education: Results and Recommendations. Lexington, MA: D.C. Heath, 1976. Swisher, J. D. “Prevention Issues.” In R. I. DuPont, A. Goldstein, J. O’Donnell, eds. Handbook on Drug Abuse. Washington, DC: NIDA, U.S. Government Printing Office, 1979. Schaps, E., and others. The Napa Drug Abuse Prevention Project: Research Findings. Washington, DC: DHHS Publication No. (ADM) 84-1339, U.S. Government Printing Office, 1984. “Prevention Research.” In Drug Abuse and Drug Abuse Research. Washington, DC: DHHS Publication No. (ADM) 85-1372, U.S. Government Printing Office, 1984. U.S. Department of Education. What Works: Schools without Drugs. Washington, DC: 1987. Evans, R. I. “Smoking in Children: Developing a Social Psychological Strategy of Deterrence.” Preventive Medicine 5 (1976), pp. 122–27. Flay, B. R. “What We Know About the Social Influences Approach to Smoking Prevention: Review and Recommendations.” In C. S. Bell and R. Battjes, eds. Prevention Research: Deterring Drug Abuse Among Children and Adolescents. Washington, DC: NIDA Research Monograph 63, DHHS Publication No. (ADM) 85-1334, U.S. Government Printing Office, 1985. McCarthy, W. J. “The Cognitive Developmental Model and Other Alternatives to the Social Skills Deficit Model of Smoking Onset.” In C. S. Bell and R. Battjes, eds. Preven-
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tion Research: Deterring Drug Abuse Among Children and Adolescents. Washington, DC: NIDA Research Monograph 63, DHHS Publication No. (ADM) 85-1334, U.S. Government Printing Office, 1985. Albaum, G., and others. “Smoking Behavior, Information Sources, and Consumption Value of Teenagers: Implications for Public Policy and Other Intervention Failures.” Journal of Consumer Affairs 36 (2002), pp. 50–76. Ennett, S. T., and others. “Long-term Evaluation of Drug Abuse Resistance Education.” Addictive Behaviors 19 (1994), p. 113. Ennett, S. T., and others. “How Effective Is Drug Abuse Resistance Education? A Meta-analysis of Project DARE Outcome Evaluations.” American Journal of Public Health 84 (1994), p. 1394. West, S. L., and K. K. O’Neal. “Project D.A.R.E. Outcome Effectiveness Revisited.” American Journal of Public Health 94 (2004), pp. 1027–30. Ellickson, P. L., and R. M. Bell. “Drug Prevention in Junior High: A Multi-site Longitudinal Test.” Science 247 (1990), pp. 1299–1305. Botvin, G. J., and S. P. Schinke. “Effectiveness of Culturally Focused and Generic Skills Training Approaches to Alcohol and Drug Abuse Prevention Among Minority Adolescents: Two-Year Follow-up Results.” Psychology of Addictive Behaviors 9 (1995), p. 183. “Parent Education.” In Prevention Plus: Involving Schools, Parents, and the Community in Alcohol and Drug Education. Washington, DC: DHHS Publication No. (ADM) 84-1256, U.S. Government Printing Office, 1984. National Institute on Drug Abuse. Drug Abuse Prevention for At-risk Groups. Washington, DC: U.S. Department of Health and Human Services, 1997. U.S. Department of Labor. What Works: Workplaces Without Drugs. Washington, DC: 1989.
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Do Your Goals and Behaviors Match? If you are a parent, think about your own family for a moment. Several of the risk and protective factors mentioned in Chapter 2 are related to family, and some of the effective prevention strategies target family activities. Consider the following questions (they can be answered either from the perspective of a child or a parent). 1. Is the interaction between the parent(s) and child generally positive? 2. Do the parents provide attention and praise to the child? 3. Is discipline consistent and usually effective and never involves physical punishment? 4. Is the child able to communicate his or her feelings to the parent(s)?
5. Does the child feel comfortable discussing rules and consequences, especially when it comes to the use of substances or other inappropriate behavior? 6. Does the family spend time together doing things every week? 7. Is the family capable of planning and organizing family activities? If the answer to most of these questions is yes, then your family is probably functioning pretty well. If the answer to most of them is no, then think about what steps you can take to change this situation. That might include scheduling some time with a family therapist or counselor.
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Treating Substance Abuse and Dependence Objectives After you have studied this chapter, you should be able to: • Discuss different types of treatment goals for substance abuse and how those goals relate to one’s belief about the nature of substance abuse. • Describe the influence of Alcoholics Anonymous on substance abuse treatment programs for alcohol and for other substances. • Explain how motivational interviewing is used in conjunction with the notion of stages of change to better prepare people for treatment.
Every year, hundreds of thousands of Americans undergo treatment for substance abuse and dependence. The word treatment conjures up images of hospitals, nurses, and physicians, but traditional medical approaches form only a small part of the overall treatment picture. As we will see, the variety of treatment approaches reflects the variety of substance abuse problems, as well as the variety of theories about substance abuse. The various treatment approaches are often used in combination.
Behavioral/ Psychosocial Treatments
• List the benefits and limitations of using contingency management to maintain abstinence. • Explain why drugs are sometimes used during the initial detoxification phase of treatment. • Discuss the three drugs that are available for use in treating alcohol dependence. • Describe the various forms of nicotine-replacement therapies and the use of Zyban in nicotine dependence treatment. • Explain both antagonist and substitution treatment for opioid dependence and list the most commonly used medication for substitution. • Describe the status of development of medications for treating cocaine dependence and cannabis dependence. • Explain why, despite the well-known failure rates in substance abuse treatment, the book still concludes that these treatments are effective.
Many early theories of substance dependence were based primarily on studying alcoholdependent individuals, so it should come
as no surprise that the history of behavioral/ psychosocial treatment approaches also began with the treatment of alcohol dependence. 429
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However, most behavioral/psychosocial treatment programs today are not designed for a particular substance, but treat a variety of types of substance dependence. Below, we present some behavioral/psychosocial treatment approaches often used in helping individuals deal with their substance abuse problems.
Defining Treatment Goals The particular theoretical view one has of substance abuse influences not only the treatment approaches one is likely to take but also the goals of treatment. For example, if one accepts the increasingly predominant view of alcohol dependence as a biological disease, which someone either “has” or does not have and which has an inevitable progression to more and more drinking, then the only acceptable treatment goal is total abstinence. Other experts view alcohol dependence as representing one end of a continuum of drinking, with no clear dividing line. For some of these theorists, a possible beneficial outcome of treatment is controlled social drinking. Likewise, if one views opioid dependence as inherently evil, undermining the physical and mental health of its victims (a common view until fairly recently), then abstinence from opioids is the only acceptable goal. Americans seem to have accepted dependence on the legal opioid methadone as preferable to heroin dependence, so the goal has changed from eliminating opioid use to eliminating
heroin use. The case with cigarette smoking is similar; some programs have focused on cutting down on smoking, whereas most programs aim for complete abstinence. When we look for indicators of a treatment program’s success, if we find that some people are still using, but using less, should we claim any benefit? Or should we assume, as some do, that any decreases will be temporary and that, unless the person quits entirely, there has been no real improvement? Although the answer depends on your goals, the DSM-IV-TR can provide a useful guide for answering this question. Researchers have begun to estimate the cost savings resulting from increased employment and decreased crime after treatment, and to compare these savings with the cost of treatment itself, to develop a cost/benefit analysis of the effectiveness of treatment.
Alcoholics Anonymous The formation of Alcoholics Anonymous (AA) in 1935 can now be seen as an important milestone in treatment. This group, which has total abstinence as a goal, has given support to the disease model of alcohol dependence. One of the basic tenets of this group is that the “alcoholic” is biologically different from others and therefore can never safely drink any alcohol. Central to this disease model is the idea that the disease takes away the person’s control of his or her own drinking behavior and therefore removes the blame for the problem. AA members are quick to point out that removing blame for the disease does not remove responsibility for dealing with it. By analogy, we would not blame diabetics for being diabetic, but we do expect diabetics to control their diets, take their medication, and so on. Thus, the alcohol-dependent person is seen as having the responsibility for managing the disease on a day-by-day basis but need not feel guilty about being different. The major approach used by AA has been group support and a buddy system. The members of AA help each other through difficult periods and encourage each other in their sobriety.
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Drugs in the Media Celebrity Rehab It seems that every few weeks another well-known celebrity is caught in some kind of public misbehavior, followed by the explanation that the famous person is suffering from a substance-use disorder and will be entering a treatment program. Mel Gibson, Amy Winehouse, Drew Barrymore, Gary Busey, Britney Spears, Lindsay Lohan, Paris Hilton, and other film actors and music stars have made public confessions of their substance abuse and have gone to expensive residential treatment programs. This has become such a part of our culture that the cable channel VH1 began a reality TV series in 2008 called “Celebrity Rehab with Dr. Drew.” Eight somewhat less well known celebrities checked in for treatment with Dr. Drew Pinsky and his staff and were followed for 10 episodes until they “graduated.” Whether or not
Although AA has been described as a loose affiliation of local groups, each with its own character, they have in common adherence to a method. Nevertheless, formal evaluations of the success of AA have been few and have not been very positive. For example, studies of court-ordered referrals to AA or to other types
The major approach of Alcoholics Anonymous, founded in 1935, is group support and a buddy system.
these individuals will be successful in abstaining from future substance use, the series itself was apparently successful enough that a second season is planned. One question that most people raise when they hear about these famous people going into “rehab” is whether they are trying to blame their misbehavior on a substance rather than taking responsibility for their actions. Do you think that being under the influence of a drug or alcohol excuses people’s misconduct, or in some way diminishes their guilt? Do you suspect that sometimes a person who goes away to an expensive and sometimes luxurious “rehab” facility is just taking the easy way out? Finally, do those famous repeat offenders who keep going back to rehab give substance-abuse treatment itself a worse reputation than it deserves?
of interventions have not shown AA to be more effective. However, AA was developed by and for people who have made a personal decision to stop drinking and who want to affiliate with others who have made that decision, and it might not be the most appropriate approach for individuals who are coerced into attending meetings as an alternative to jail. More appropriate (and more difficult and expensive) evaluations of AA should be done to determine which types of drinkers are most likely to benefit from this organization’s program. This point is particularly important because many treatment programs, such as the Betty Ford Center, Hazelden, and Phoenix House, rely mostly on the 12-step model of AA (see Drugs in Depth). Moreover, a wide variety
abstinence: no alcohol or drug use at all. controlled drinking: the idea that alcohol abusers may be able to drink under control. Alcoholics Anonymous: a worldwide organization of self-help groups based on alcohol abusers helping each other achieve and maintain sobriety.
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DSM-IV-TR Psychiatric Diagnosis of Substance Disorders Diagnostic Criteria for Substance Dependence A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of the substance to achieve intoxication or desired effect b. Markedly diminished effect with continued use of the same amount of the substance 2. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the substance b. The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms 3. The substance is often taken in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful efforts to cut down or control substance use. 5. A great deal of time is spent in activities necessary to obtain the substance.
of other self-help groups, including Cocaine Anonymous (CA), Narcotics Anonymous (NA), and Gamblers Anonymous (GA), have modeled the AA treatment approach.
Motivational Enhancement Therapy For many years, the predominant theories on why people seek treatment for substance abuse were based on the anecdotal experiences of alcohol-dependent individuals. According to the conventional wisdom, most substance abusers use the defense mechanism of denial and are obstinately unwilling to admit either that their substance use is unusual or that it has serious consequences for themselves or others. In this context,
6. Important social, occupational, or recreational activities are given up or reduced because of substance use. 7. The substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance. Diagnostic Criteria for Substance Abuse A. A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: 1. Recurrent substance use resulting in failure to fulfill major role obligations at work, school, or home. 2. Recurrent substance use in situations in which it is physically hazardous. 3. Recurrent substance-related legal problems. 4. Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance. B. The symptoms have never met the criteria for substance dependence for this class of substance.
only when the abuser “hits bottom”—that is, suffers sufficient consequences that the reality of the problem finally sinks in—will he or she be ready to seek help. The obvious problem with this perspective is that grave consequences (e.g., death) may occur before the abuser’s perception of “hitting bottom.” One relatively new treatment approach, motivational enhancement therapy, attempts to shift the focus away from denial and toward motivation to change.1 The idea is that targeting the abuser’s degree of motivation to quit substance use could enhance the effectiveness of treatment. Hence, ambivalent or less ready substance abusers should first receive motivational interviewing. During this nonconfrontational process, an assessment of the substance-using
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Drugs in the Media The 12 Steps of Alcoholics Anonymous 1. 2. 3. 4. 5. 6. 7. 8. 9.
We admitted we were powerless over alcohol— that our lives had become unmanageable. Came to believe that a Power greater than ourselves could restore us to sanity. Made a decision to turn our will and our lives over to the care of God as we understood Him. Made a searching and fearless moral inventory of ourselves. Admitted to God, to ourselves, and to another human being the exact nature of our wrongs. Were entirely ready to have God remove all these defects of character. Humbly asked Him to remove our shortcomings. Made a list of all persons we had harmed and became willing to make amends to them all. Made direct amends to such people wherever possible, except when to do so would injure them or others.
behavior and its consequences is completed to determine the abuser’s current stage of change because, according to this view, to help someone move from one stage to another through motivational interviewing, you need to know where he or she is in the decision-making process. In the precontemplation stage, the individual does not recognize that a problem exists. In the contemplation stage, the individual believes that a problem might exist and gives some consideration to the possibility of changing her or his behavior. In the preparation stage, the individual decides to change and makes plans to do so. In the action stage, the individual takes active steps toward change, such as entering treatment. Finally, the maintenance stage involves activities intended to maintain the change. The motivational interviewer attempts to help the client focus on the concerns and problem behavior but does not directly tell the client what to do. Ideally, if the therapist knows which stage of change the client is in, the discussion can be guided appropriately to help move the client to the next stage. Although this approach has been demonstrated
10. Continued to take moral inventory and when we were wrong promptly admitted it. 11. Sought through prayer and meditation to improve our conscious contact with God as we understood Him, praying only for knowledge of His will for us and the power to carry that out. 12. Having had a spiritual awakening as the result of these steps, we tried to carry this message to alcoholics, and to practice these principles in all our affairs. Source: The Twelve Steps are reprinted with permission of Alcoholics Anonymous World Services, Inc. Permission to reprint the Twelve Steps does not mean that AA has reviewed or approved the contents of this publication, nor that AA agrees with the views expressed herein. AA is a program of recovery from alcoholism only— use of the Twelve Steps in connection with programs and activities which are patterned after AA, but which address other problems, or in any other non-AA context, does not imply otherwise.
to decrease substance use,2 it is probably best conceptualized as a preparation for other therapies rather than as a stand-alone treatment.
Contingency Management A behavioral approach to treating substance abuse that has received substantial attention in recent years is contingency management. This approach has produced consistent reductions in substance-using behaviors among diverse substance-abusing populations.3 In this approach, individuals receive immediate rewards (e.g., vouchers redeemable for goods or services) for providing drug-free urine samples, and the value of the rewards is increased with consecutive drug-free urine samples. However, rewards are withheld if the client’s
stages of change: a model for decision making consisting of precontemplation, contemplation, preparation, action, and maintenance.
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Targeting Prevention Avoiding Relapse Relapse Avoiding One important type of substance-abuse prevention involves those who have been in treatment and are trying to avoid relapsing, or going back to their previously abusive behavior. Think about the messages these people receive each day from public media (such as television, movies, newspapers, and the Web) and from other individuals. Which of these messages support relapse prevention and which tend to encourage relapse? Have a conversation with a friend, relative, or classmate who has been in treatment for substance abuse and has had to deal with the problem of relapse prevention. Ask what was helpful for him or her and what made it more difficult to avoid substance abuse.
urine sample is positive for an illicit drug. In addition to receiving rewards, clients participate in counseling sessions weekly, where they learn a variety of skills to help them minimize substance use. A weakness of contingency management is the cost of the rewards, which could preclude the use of this procedure by small, less well-funded treatment programs.
Relapse Prevention Another behavioral strategy is called relapse prevention, an approach that uses cognitivetherapy techniques with behavioral-skills training. Individuals learn to identify and change behaviors that may lead to continued drug use, such as going out to bars or associating with users. Relapse prevention has been shown to be more effective at decreasing substance use than most standard psychotherapies, and the beneficial effects persist for as long as a year following treatment.4 This approach is criticized for placing greater demands on the patients compared to other substance-abuse treatments, and it may be particularly challenging for individuals who have cognitive limitations.5
Pharmacotherapies (Medication Treatments) Substance abuse and dependence are increasingly viewed as “brain diseases,” much like, for example, Parkinson’s disease. But the overwhelming majority of individuals who use substances do not become dependent, whereas virtually all of the individuals who lose greater than 80 percent of nigrostriatal dopamine neurons will exhibit symptoms of Parkinson’s disease. Nevertheless, an intense amount of research efforts have focused on developing medications to treat substance abuse and dependence. The rationale is that as we increase our understanding of brain mechanisms mediating substance abuse, we should be better able to use medications to target these mechanisms, thereby blocking the reinforcing effects of drugs of abuse (i.e., the “magic bullet approach”). Despite the enthusiasm accompanying medication development efforts, most experts do not believe that pharmacotherapies alone will cure a chronic, relapsing disorder such as substance abuse, in part, because the problem of substance abuse is expressed behaviorally. Thus, a major hope is that pharmacotherapies will provide a window of opportunity by relieving withdrawal symptoms, for example, so that behavioral/ psychosocial treatments can be used. Below we describe some medications that have been used to help substance abusers deal with withdrawal symptoms and maintain abstinence. The focus of our discussion will be limited to alcohol, nicotine, the opioids, cocaine, and cannabis. These substances were selected for their public health importance and because a large amount of research has been conducted regarding their use.
Detoxification and Maintenance Phase Pharmacological interventions are typically initiated at two different phases of the dependence cycle: detoxification and maintenance. Detoxification can be viewed as an initial and immediate goal during which medications are administered to alleviate unpleasant
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withdrawal symptoms that may appear following abrupt cessation of drug use (e.g., the nicotine patch and nicotine gum have been used to treat individuals experiencing cigarette smoking abstinence symptoms). Medications used in the detoxification phase are also sometimes used in the maintenance phase (e.g., nicotine replacement medications). Thus, the distinction between a detoxification medication and a maintenance medication is sometimes less clear. Maintenance on pharmacological agents can be viewed as a longer-term strategy used to help the dependent individual avoid relapsing to the abused drug. Three major maintenance strategies are used. First, agonist or substitution therapy is used to induce cross-tolerance to the abused drug. Methadone, a long-acting μ-opioid agonist, for heroin dependence, and nicotine replacement medications for tobacco dependence have been used as agonist maintenance treatments to prevent relapse and cravings in individuals attempting to maintain abstinence. Agonist maintenance agents typically have safer routes of administration and/ or diminished psychoactive effects. Second, antagonist therapy is used to produce extinction by preventing the user from experiencing the reinforcing effects of the abused drug (e.g., the opioid antagonist naltrexone, which selectively blocks opioid effects). Finally, punishment therapy is used to produce an aversive reaction following ingestion of the abused drug. Disulfiram (Antabuse) for the treatment of alcohol dependence is an example of punishment therapy. Disulfiram inhibits aldehyde dehydrogenase, a major enzyme involved in alcohol metabolism, which, in the presence of alcohol, can produce unpleasant symptoms including headache, vomiting, and breathing difficulties.
Alcohol Pharmacotherapies have become increasingly important in the treatment of alcohol dependence, in part, because of the serious nature of
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the acute alcohol withdrawal syndrome. This syndrome is typically characterized by tremors, tachycardia (rapid heartbeat), hypertension, perfuse sweating, insomnia, hallucinations, and seizures. Medical risks associated with the alcohol withdrawal process often require an inpatient medical setting. During detoxification, two of the central tasks for the clinician are to reduce autonomic hyperactivity and to prevent the development of seizures. For several reasons, administration of a benzodiazepine during alcohol detoxification is the standard treatment approach. There is a high degree of cross-tolerance between alcohol and the benzodiazepines. Because benzodiazepines can serve as substitutes for alcohol and generally have longer half-lives than alcohol, the withdrawal process can be safely completed. Benzodiazepines, by potentiating the inhibitory actions of GABA on the central nervous system, significantly decrease the risk of seizures during detoxification. In addition, the increased autonomic arousal that occurs during alcohol withdrawal is similar to the initiation of the “stress response” (i.e., increased heart rate, blood pressure, respiration, and anxiety). This suggests the mechanisms that mediate the stress response may also play a role in alcohol withdrawal symptoms. Because it is well documented that increased GABAergic transmission markedly diminishes the stress response,6 it is not surprising that benzodiazepines are also effective in attenuating the autonomic hyperactivity that accompanies alcohol withdrawal symptoms. Some clinicians might be wary about the potential for abuse associated with the use of some rapid-acting benzodiazepines (e.g., alprazolam), particularly in alcohol-abusing populations.7 Thus, benzodiazepines with a slower onset of action such as clonazepam or oxazepam may be more suitable in this population. Three medications have received Food and Drug Administration (FDA) approval for the treatment of alcohol abuse and dependence: disulfiram (Antabuse), naltrexone, and acamprosate (calcium acetylhomotaurinate). All of these medications are used during the main-
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tenance phase. Typically, these medications are used for weeks or months, but indefinite maintenance for years is unusual with these approaches. Nearly a half century ago it was discovered that ingestion of disulfiram in the presence of alcohol resulted in an unpleasant reaction, including facial flushing, accelerated pulse, throbbing headache, nausea, and vomiting.8 As stated above, these symptoms occur as a result of the increased amount of acetaldehyde in the body following inhibition of aldehyde dehydrogenase by disulfiram. Since this initial observation, several studies have assessed disulfiram as a pharmacotherapeutic option in treating alcohol-use disorders. In general, disulfiram has not been shown to be effective in achieving abstinence or delaying relapse; most individuals simply do not take the medication. Naltrexone was developed as an opioid antagonist and has been used in the treatment of opioid dependence. In the early 1990s, data from two large studies of naltrexone for the treatment of alcohol dependence showed that the medication substantially reduced days of alcohol drinking per week, the rate of relapse among those who drank, and alcohol craving.9 The precise mechanism of action for naltrexone-related reductions in alcohol drinking is not fully understood, but it has been suggested that the medication blocks opioid receptors, thereby preventing the release of alcohol-induced dopamine, which in turn blocks the reinforcing effects of alcohol.10 Although great fanfare accompanied the approval of naltrexone and many alcoholdependent individuals were treated with this medication, it has not had a big impact on overall treatment success. The latest medication to receive approval for the treatment of alcohol-use disorders is acamprosate, a compound that bears a structural resemblance to GABA. Acamprosate exerts at least two actions that have been proposed to be important for its clinical utility in treating alcohol dependence: normalizing basal GABA concentrations, which are proposed to
be disrupted in alcohol-dependent individuals, and blocking the glutamate increases observed during alcohol withdrawal.11 In several studies, acamprosate has been shown to be effective in decreasing alcohol relapse. But, because the medication only recently received FDA approval, the impact of its availability on treating alcohol-use disorder in broader clinical populations has yet to be determined.
Nicotine More than 98 percent of tobacco users are cigarette smokers. Despite the declining social acceptability and rates of cigarette smoking, a substantial proportion of individuals remains dependent. Tobacco smoke contains as many as 4,000 chemical constituents, but nicotine is thought to be the primary component responsible for the maintenance of continued use. When most smokers attempt to quit, they experience withdrawal symptoms, such as anxiety, depression, dysphoria, irritability, decreased concentration, insomnia, increased food intake, and cigarette craving. Pharmacotherapies have been used primarily to attenuate these symptoms. Five nicotine-replacement therapies have received FDA-approval for treating nicotine dependence: transdermal nicotine patch, nicotine gum, nicotine nasal spray, nicotine vapor inhaler, and nicotine lozenge. Before initiating nicotine-replacement treatments, smokers are advised to discontinue the use of other nicotine-containing products because of concerns about nicotine toxicity that might result from concurrent use of nicotine-containing products (e.g., cigarettes in combination with the nicotine patch). All of these treatments have been demonstrated to increase quit rates in controlled clinical studies.12 These studies have been conducted under fairly strict conditions, with a prescribed quitting period, several visits to the clinic to assess progress, and the usual trappings of a clinical research study, often including the collection of saliva or other samples to detect tobacco use. That’s a far cry from buying nicotine gum at the corner store, with
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no plan for quitting, no follow-up interviews, and no monitoring. Thus, it is not surprising that the average person might have great difficulties quitting even with the aid of nicotinereplacement medications. In 1997, the FDA approved bupropion (Zyban), the first non-nicotine pharmacotherapy for smoking cessation. Bupropion is also used in the treatment of depression, where it is referred to as Wellbutrin. Although the neurochemical mechanisms that underlie bupropion’s therapeutic effects have yet to be definitively determined, the mechanism of action most commonly attributed to bupropion is inhibition of dopamine and norepinephrine reuptake and, to a lesser extent, blockade of acetylcholine receptors.13 Unlike nicotine-replacement therapies, there is no absolute requirement for the smoker to abstain from the
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use of nicotine-containing products. Bupropion has been shown to gradually decrease cigarette craving and use in some clinical trials. Because nicotine-replacement medications and bupropion have been demonstrated to decrease cigarette smoking when administered alone, it has been suggested that greater treatment success might be achieved if the two strategies were combined. Unfortunately, data from a recent investigation indicated that the addition of bupropion treatment to nicotine-replacement therapy did not significantly increase smoking cessation rates.14 In May 2006, the FDA approved the latest smoking cessation medication. Varenicline is a partial nicotinic-receptor agonist, meaning that, even at large doses, it does not produce the full response of nicotine. As a result of its properties, it should be able to reduce symptoms of withdrawal and craving, while blocking the effects of nicotine should the smoker relapse. Varenicline was found to be more effective than placebo or bupropion and is a viable option for smoking cessation therapy.15
Opioids
Zyban (bupropion) was the first non-nicotine pharmacotherapy for smoking cessation. The drug, also used to treat depression, appears to gradually reduce cravings for cigarettes.
Historically, anticholinergic drugs, such as belladonna, were used in the treatment of opioid dependence.16 The idea was that anticholinergics would produce a state of delirium for several days, after which the dependent person would emerge cured of dependence without remembering the dreadful experience of the withdrawal process. A more recent version of this approach is “rapid opioid detoxification.” Opioid-dependent individuals are anesthetized and, while unconscious, are given an opioid antagonist, so that withdrawal will occur while they are unconscious. After 24 hours the patient is released and enters a period of counseling, combined with continued opioid antagonist treatment. This procedure has been vehemently criticized because it increases the risk of problems during the withdrawal process and because aftercare (behavioral/psychosocial treatment) is often deemphasized.
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Drug withdrawal can have unpleasant and potentially dangerous symptoms. Drugs may be administered to reduce withdrawal symptoms.
Although opioid withdrawal is not life threatening, symptoms such as nausea, vomiting, diarrhea, aches, and pain can be unpleasant. Medications are administered to minimize discomfort. Methadone (Dolophine), an opioid analgesic developed in Germany during World War II, is commonly used
in this capacity. It has a long duration of action, which means that it needs to be taken less frequently to prevent withdrawal symptoms. Another medication that has been shown to decrease opioid withdrawal symptoms is buprenorphine, a partial opioid agonist. Buprenorphine has a relatively large margin of safety and a low overdose potential. In addition, it has a long duration of action and blocks the effects of other opioid agonists such as heroin. As a result of these features, both methadone and buprenorphine are FDA-approved opioid-dependence medications. These medications are used not only during detoxification, but during maintenance as well. Methadone maintenance, the most common form of treatment for opioid dependence, may continue for months or years. The duration of buprenorphine maintenance might be similar, but because the medication has only recently received approval, this is not yet known. One major concern in the treatment of opioid dependence is opioid-induced overdose,
Table 18.1 Medications Used to Treat Substance Abuse and Dependence Substance
Treatment Medication
Proposed Mechanism(s) of Action
Alcohol
Benzodiazepines Disulfiram Naltrexone Acamprosate
Increase the activity of GABA Inhibits aldehyde dehydrogenase Opioid receptor antagonist Normalizes basal GABA concentrations; blocks alcohol-withdrawal-induced glutamate increases
Nicotine
Nicotine replacements Bupropion Varenicline
Full agonists at nicotine receptors Inhibits the reuptake of dopamine and norepinephrine; acetylcholine receptors antagonist Partial nicotine-receptor agonist
Opioids
Methadone Buprenorphine Naltrexone
Full agonist at opioid receptors Partial agonist at opioid receptors Opioid receptor antagonist
Cocaine
Modafinil*
Increases the activity of dopamine, norepinephrine, and glutamate; decreases the release of GABA
Cannabis
Dronabinol*
Full agonist at cannabinoid receptors
*Not FDA approved to treat substance abuse or dependence.
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which could lead to a coma and eventual death via respiratory depression. Because the shortacting opioid antagonist naloxone has a greater affinity for brain opioid receptors than do most opioid agonists, including heroin, it is often used for treating opioid overdose. Following its administration, naloxone displaces the opioid agonist from the receptors, and thereby rapidly reverses the overdose. This observation led to speculations about the use of opioid antagonists in treating opioid dependence. That is, if a user takes heroin, for example, while being maintained on an opioid antagonist, the effects of heroin would not be felt. This rationale provided the basis for the approval of the longacting opioid antagonist naltrexone for treating opioid dependence. Although naltrexone therapy has been shown to be effective in the treatment of opioid dependence, this therapy appears to be appropriate for only highly motivated individuals because most opioid abusers enrolled in naltrexone therapy prematurely discontinue treatment. To circumvent compliance problems, a new depot formulation of naltrexone, which requires one administration per month, is being studied as a potential opioiddependence treatment medication. Initial findings are encouraging, as depot naltrexone has been demonstrated to block heroin-related effects for up to six weeks.17 An interesting problem arises if a patient on naltrexone is involved in an accident and requires some pain relief. Current practice is to give high doses of hydromorphone (Dilaudid) to overcome the antagonism. This should be done only in a hospital and with extreme caution.
Cocaine Although a cocaine withdrawal syndrome does not appear to be a major feature of cocaine dependence,18 some investigators have documented symptoms of depression, nervousness, dysphoria, anhedonia, fatigue, irritability, sleep and activity disturbances, and craving for cocaine.19 Behavioral and mood changes that accompany cocaine withdrawal might be related
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to a decrease in the activity of monoamine neurotransmitters, which play an important role in movement and mood regulation. Accordingly, medications that increase monoaminergic activity may be useful in treating withdrawal symptoms and thereby prevent relapse. A plethora of medications, ranging from selective agonists of monoamine neurotransmitters to agents that simultaneously enhance the activity of multiple neurotransmitters, have been evaluated according to this theory. Unfortunately, to date, the vast majority of medications assessed have not been effective at treating cocaine withdrawal symptoms or dependence.20 The situation is not completely bleak, however, as recent data from investigations of modafinil (Chapter 6) suggest that the medication is useful in treating cocaine dependence.21 In these studies, cocaine use and cocaine-related subjective effects (e.g., euphoria and craving) were markedly reduced when cocaine abusers were taking modafinil compared with placebo. While the mechanisms underlying modafinil’s therapeutic actions are unknown, the drug appears to increase the activity of several neurotransmitters (e.g., dopamine, norepinephrine, and glutamate) and decrease the release of GABA.22 Although modafinil is not FDA approved for the treatment of cocaine abuse or dependence, some physicians may use the medication for this purpose off-label. There are no medications approved to treat cocaine abuse or dependence.
Cannabis Most users of cannabis consume the drug infrequently without apparent negative consequences. A small proportion, however, experience problems related to frequent cannabis use.
anhedonia [an hee doeⴕ nee ya]: lack of emotional response; especially an inability to experience joy or pleasure. off-label: use of prescription drug to treat a condition for which the drug has not received U.S. FDA approval.
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Mind/Body Connection The Nature of Dependence Is drug dependence strictly a matter of neurotransmitters and neural adaptation, as seems increasingly to be the accepted viewpoint, or will it ultimately be impossible to understand such a complex set of behaviors by reducing the problem to its biochemical correlates? This has been a huge and ongoing debate among proponents of the various views of drug dependence, but currently the research funding and most of the information seen in the popular media favor biological approaches to understanding these problems. This chapter’s focus on drug treatments for substance dependence seems to be based on an implied acceptance that some biochemical imbalance is at the heart of people who are seemingly unable to exert control over their own drug-using behavior. However, many, including proponents of the Alcoholics Anonymous philosophy, believe that substance dependence is a “spiritual” disorder— essentially that an individual human is not recognizing the need to draw upon either God or
An estimated 1 in 11 cannabis users will become dependent.23 Rates of cannabis dependence in several countries have increased substantially over the past decade as well as the number of individuals seeking treatment. Many individuals seeking treatment for cannabis dependence reported experiencing withdrawal symptoms and that these symptoms made it more difficult to maintain abstinence. As a result, efforts to develop medication for cannabis dependence have primarily focused on relieving withdrawal symptoms. Cannabis withdrawal is characterized by symptoms of irritability, anxiety, sleep disruptions, and aches.24 A growing number of medications have been tested for efficacy in relieving these symptoms, but only one has been demonstrated to be effective—oral ⌬9-THC (dronabinol). The primary reason for evaluating the effects of dronabinol on cannabis withdrawal was based on the idea of substituting a longer-acting pharmaco-
some other source of spiritual strength to help win the struggle with the bottle or needle or pill. For these people, drug treatments, especially of the substitution/maintenance type, are often seen as a crutch that does not address the individual’s basic problem and cannot therefore be of much long-term benefit. To others, substance abuse and dependence can be approached through behavioral techniques such as contingency management or through a variety of psychosocial approaches such as group therapy. For them, medication might be seen as a temporary aid in assisting the person to “reprogram” his or her thinking, routines, and social interactions, but it is ultimately these changes in relationships, attitudes, and activities that are the key to longer-term success. How do you feel about the evidence showing that former heroin users can often be maintained for years on methadone, a legal substitute, while they attend school, work, and otherwise enjoy more productive and less dangerous lives than if they had continued to use heroin?
logically equivalent drug for the abused substance, stabilizing the individual on that drug, and then gradually withdrawing the substituted drug, thus decreasing the likelihood of precipitating abstinence symptoms. It was recently demonstrated that dronabinol markedly reduced symptoms associated with cannabis abstinence including self-reported ratings of cannabis craving, anxiety, misery, and sleep disturbance. The medication also reversed the withdrawal-associated psychomotor performance decrements as well as the anorexia and weight loss associated with cannabis withdrawal. These results indicate that moderate doses of oral dronabinol might be beneficial in the treatment of cannabis dependence.25 To date, no medications are approved for the treatment of cannabis dependence although dronabinol is sometimes used off-label for this purpose. Table 18.1 summarizes medical treatments for substance abuse.
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Treatment: The Big Picture in the United States In each state, the agency that has primary responsibility for public funding of substance abuse treatment programs submits annual reports to the U.S. Substance Abuse and Mental Health Services Administration (SAMHSA). Between 1996 and 2006, the data from more than 1.8 million admissions each year for substance abuse were compiled into the Treatment Episode Data Set.26 In 2006, four substances accounted for about 90 percent of these admissions: alcohol (40 percent), opioids (18 percent), marijuana (16 percent), and cocaine (14 percent). Of those who reported opioids as their primary drug of abuse, 77 percent were heroin users, and 72 percent of those who reported cocaine as the primary drug were crack cocaine smokers. The average age of those admitted with marijuana as the primary drug was 24 years. In 2006, 50 percent of the substance-abuse clients were treated as outpatients, 13 percent as hospital inpatients (detoxification), and 17 percent in a residential setting. These data suggest that the bulk of our substance-abuse treatment should focus on developing more effective interventions for alcohol, opioid, marijuana, and cocaine abuse that can be delivered on an outpatient basis. As reviewed previously, most recent research efforts to develop pharmacotherapies to treat substance abuse have been aimed at decreasing the use of these substances (and nicotine). But, without effective outpatient behavioral/psychosocial interventions, the overall success of pharmacotherapies alone to treat substance abuse is likely to be unimpressive. This is because substance abusers may show poor medication compliance, even on medications that have been demonstrated to be effective at decreasing substance use (e.g., disulfiram for alcohol dependence and naltrexone for opioid dependence). Moreover, substance abusers often present with additional mental disorders and multiple other functional impairments. Thus, behavioral/psychosocial treatments are needed to address these issues so that overall treatment success is enhanced.
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Is Treatment Effective? There is a widespread belief that substanceabuse treatment is often ineffective. We’ve all heard of well-known athletes who have been in treatment programs and later are found to be using illegal drugs, and we might know an alcohol abuser who went into treatment and later began drinking again. Treatment doesn’t work for every client every time, especially if our expectation is that one treatment exposure will eliminate the use of the substance for the rest of the person’s life. Substance dependence is often a chronic illness that shares many characteristics with other chronic illnesses such as diabetes, hypertension, and asthma. There are no reliable “cures,” and all of these conditions may require continuing care throughout the patient’s life. An important question is whether substanceabuse treatment programs have any beneficial effect—and, if they do, are their effects worth the cost? In general, people who go into treatment fare better than those who do not, as measured by reduced crime, increased employment, and better health. A report by the California Department of Alcohol and Drug Programs concluded that, on average, seven dollars are saved for every dollar invested in the treatment of alcohol
Drug treatment doesn’t work for every person every time, but overall, treatment does reduce drug use, reduce associated criminal activity, and increase employment. By continuing to participate in outpatient drug rehabilitation meetings, these teens increase the likelihood that their substance-abuse treatment will be a success over the long term.
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and other drug abuse.27 Alcohol and other drug use was reduced by about two-fifths after treatment; treatment for crack cocaine, powder cocaine, and methamphetamine use was equally effective as for alcohol; and criminal activity declined by about two-thirds after treatment. One report reviewed 53 studies of the effectiveness of substance-abuse treatments for adolescents. Overall, most of the treated adolescents had significant reductions in substance use and problems in other life areas in the year following treatment, and an average of 32 percent remained abstinent at the end of a year. Successful program completion, involvement in outpatient therapy, and the inclusion of the family therapy as one treatment component all appeared to predict success.28 Overall, substance abuse treatment does work. It saves lives, saves money, and is, therefore, a worthwhile investment.
•
Zyban (bupropion) may be used alone or in combination with various forms of nicotine-replacement therapy to aid smoking cessation.
•
Methadone is the drug most commonly used to treat opioid dependence, although buprenorphine is now also available for use in substitution/maintenance treatment. Naltrexone blocks the effects of any opioids the user might take, but it has not been as effective as methadone in helping people to abstain from heroin or other abused opioids. Rapid opioid detoxification is a short-term method to avoid experiencing withdrawal symptoms.
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Although recent findings with modafinil have been encouraging, no medication has yet been developed specifically for treatment of cocaine dependence.
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Cannabis withdrawal symptoms can be relieved by the use of dronabinol, which shows promise as a treatment for cannabis dependence.
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Overall, substance-abuse treatment programs are considered to be effective because they do help many people to abstain, sometimes only for a few months, but often for many years. The benefits far exceed the cost of providing the programs.
Summary •
Treatment for substance abuse and dependence may include both behavioral/ psychosocial approaches and the use of various medications.
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Many of today’s psychosocial treatment programs are heavily influenced by the philosophy developed by Alcoholics Anonymous. These are often referred to as 12-step programs.
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Motivational interviewing is usually used in conjunction with stages of change theory, to help move people from one stage to another in the process of quitting.
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Medications are often used to ease withdrawal during detoxification. Maintaining abstinence may be assisted by either agonist substitution or by antagonist treatment.
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Antabuse (disulfiram) interferes with alcohol metabolism to produce illness if the patient uses alcohol. Naltrexone and acamprosate are also available to assist in preventing relapse.
Review Questions 1. List at least 8 of the 12 steps of Alcoholics Anonymous. 2. What are the four “stages of change” listed in the text? 3. Describe the kinds of contingencies used in contingency management: What happens if the client has several “clean” urine samples in a row? What happens if the client fails one of the urine sample tests? 4. Give one example for each: agonist/substitution therapy, antagonist therapy, and punishment therapy.
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Chapter 18
5. What drugs are typically used to reduce withdrawal symptoms during alcohol detoxification? 6. Compare and contrast the use of disulfiram (Antabuse) versus either naltrexone or acamprosate for alcohol dependence. 7. List four of the five types of available nicotinereplacement therapy. 8. How are methadone and buprenorphine similar to each other and different from naltrexone as treatments for opioid dependence? 9. The effort to develop drugs to treat cocaine dependence has targeted which neurotransmitter systems? 10. How big a problem is cannabis dependence, and what seems to be the most promising drug treatment currently being studied?
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Rollnick, S., and W. R. Miller. “What Is Motivational Interviewing?” Behavioural and Cognitive Psychotherapy 23 (1995), pp. 325–34. Polcin, D. L., G. P. Galloway, J. Palmer, and W. Mains. “The Case for High-Dose Motivational Enhancement Therapy.” Substance Use and Misuse 39 (2004), pp. 331–43. Higgins, S. T., S. H. Heil, and J. P. Lussier. “Clinical Implications of Reinforcement as a Determinant of Substance Use Disorders. Annual Review of Psychology 55 (2004), pp. 431–61. Carroll, K. M., B. J. Rounsaville, C. Nich, L. T. Gordon, P. W. Wirtz, and F. Gawin. “One-year Follow-up of Psychotherapy and Pharmacotherapy for Cocaine Dependence. Delayed Emergence of Psychotherapy Effects.” Archives of General Psychiatry 51 (1994), pp. 989–97. Aharonovich, E., E. Nunes, and D. Hasin. “Cognitive Impairment, Retention and Abstinence Among Cocaine Abusers in Cognitive-behavioral Treatment.” Drug and Alcohol Dependence 71 (2003), pp. 207–11. Chrousos, G. P., and P. W. Gold. “The Concepts of Stress and Stress System Disorders: Overview of Physical and Behavioral Homeostasis.” Journal of the American Medical Association 267 (1992), pp. 1244–52. Woods, J. H., J. L. Katz, and G. Winger. “Benzodiazepines: Use, Abuse, and Consequences.” Pharmacology Review 44 (1992), pp. 151–347. Hald, J., E. Jacobsen, and V. Larsen. “The Sensitizing Effect of Tetraethylthiuram Disulfide (Antabuse) to Ethyl Alcohol.” Acta Pharmocologica et Toxicologica 4 (1948), pp. 285–96. O’Malley, S. S., and others. “Naltrexone and Coping Skills Therapy for Alcohol Dependence: A Controlled Study.” Archives of General Psychiatry 49 (1992), pp. 894–98; and Volpicelli, J., and others. “Naltrexone in the Treatment of
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Alcohol Dependence.” Archives of General Psychiatry 49 (1992), pp. 867–80. Sinclair, J. D. “Evidence About the Use of Naltrexone and for Different Ways of Using It in the Treatment of Alcoholism.” Alcohol 36 (2001), pp. 2–10. Dahchour, A., and P. De Witte. “Ethanol and Amino Acids in the Central Nervous System: Assessment of the Pharmacological Actions of Acamprosate.” Progress in Neurobiology 60 (2000), pp. 343–62. George, T. P., and S. S. O’Malley. “Current Pharmacological Treatments for Nicotine Dependence. Trends in Pharmacological Sciences 25 (2004), pp. 42–48. Ascher, J. A., and others. “Bupropion: A Review of Its Mechanism of Antidepressant Activity.” Journal of Clinical Psychiatry 56 (1995), pp. 395–401; and Slemmer, J. E., B. R. Martin, and M. I. Damaj. “Bupropion Is a Nicotinic Antagonist.” Journal of Pharmacology Experimental Therapies 295 (2000), pp. 321–27. Simon, J. A., C. Duncan, T. P. Carmody, and E. S. Hudes. “Bupropion for Smoking Cessation: A Randomized Trial.” Archives of Internal Medicine 164 (2004), pp. 1797–1803. Stack, N. M. “Smoking Cessation: An Overview of Treatment Options with a Focus on Varenicline.” Pharmacotherapy 27 (2007), pp. 1550–57. Latimer, D., and J. Goldberg. Flowers in the Blood: The Story of Opium. New York: Arno Press, 1981. Comer, S. D., and others. “Depot Naltrexone: Long-lasting Antagonism of the Effects of Heroin in Humans.” Psychopharmacology, 159 (2002), pp. 351–60. Foltin, R. W., and M. W. Fischman. “A Laboratory Model of Cocaine Withdrawal in Humans: Intravenous Cocaine.” Experimental and Clinical Psychopharmacology 5 (1997), pp. 404–11. Gawin, F. H., and H. D. Kleber. “Abstinence Symptomatology and Psychiatric Diagnosis in Cocaine Abusers. Clinical Observations.” Archives of General Psychiatry 43 (1986), pp. 107–13. Hart, C. L. and W. J. Lynch “Developing Pharmacotherapies for Cannabis and Cocaine Use Disorders.” Current Neuropharmacology 3 (2005), pp. 95–114. Dackis, C. A, and others. “A Double-blind, Placebocontrolled Trial of Modafinil for Cocaine Dependence.” Neuropsychopharmacology 30 (2005), pp. 205–11; and Hart, C. L., and others. “Smoked Cocaine Self-Administration is Decreased by Modafinil.” Neuropsychopharmacology 33 (2008), pp. 761–68. Wisor, J. P. and K. S. Eriksson “Dopaminergic-adrenergic Interactions in the Wake Promoting Mechanism of Modafinil.” Neuroscience 132 (2005), pp. 1027–34; Madras, B. K., and others. “Modafinil Occupies Dopamine and Norepinephrine Transporters In Vivo and Modulates the Transporters and Trace Amine Activity In Vitro.” Journal of Pharmacology and Experimental Therapeutics 319 (2006), pp. 561–69; and Ferraro, L., and others. “The Vigilance Promoting Drug Modafinil Increases Extracellular Glutamate Levels in the Medial Preoptic Area and the Posterior Hypothalamus of the Conscious Rat: Prevention by Local GABAA Receptor Blockade.” Neuropsychopharmacology 20 (1999), pp. 346–56. Anthony, J. C., L. A. Warner, and R. C. Kessler. “Comparative Epidemiology of Dependence on Tobacco, Alcohol, Controlled Substances, and Inhalants: Basic Findings
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from the National Comorbidity Survey.” Experimental and Clinical Psychopharmacology 2 (1994), pp. 244–68. Hart, C. L. “Increasing Treatment Options for Cannabis Dependence: A Review of Potential Pharmacotherapies.” Drug and Alcohol Dependence 80 (2005), pp. 147–59. Lichtman, A. H., J. Fisher, and B. R. Martin. “Precipitated Cannabinoid Withdrawal Is Reversed by Delta(9)-tetrahydrocannabinol or Clonidine.” Pharmacology, Biochemistry and Behavior 69 (2001), pp. 181–88. Substance Abuse and Mental Health Services Administration. Treatment Episode Data Set (TEDS). Highlights--
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2006. National Admissions to Substance Abuse Treatment Services. DASIS Series: S-40, DHHS Publication No. (SMA) 08-4313. Rockville, MD: Office of Applied Studies, 2008. Lewis, D. C. “More Evidence That Treatment Works.” The Brown University Digest of Addiction Theory and Application 13 (1994), p. 12. Williams, R. J., and S. Y. Chang. “A Comprehensive and Comparative Review of Adolescent Substance Abuse Treatment Outcome.” Clinical Psychology, Science and Practice 7 (2000), pp. 138–66.
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Appendix A: Drug Names
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B
Abilify (aripiprazole): a typical antipsychotic.
belladonna: poisonous anticholinergic plant.
acamprosate (Campral): treatment for alcohol dependence.
Benzedrine: amphetamine. CNS stimulant and sympathomimetic. Brand name no longer used.
acetaminophen: OTC analgesic. Similar to aspirin in its effects.
benzodiazepines: class of sedative-hypnotics that includes diazepam (Valium).
acetophenazine: Tindal. Antipsychotic.
benztropine: Cogentin. Anticholinergic used to control extrapyramidal symptoms.
acetylsalicylic acid: aspirin. OTC analgesic. alprazolam: Xanax. Benzodiazepine sedative.
black tar: a type of illicit heroin.
Amanita muscaria: hallucinogenic mushroom.
bromide: group of salts with sedative properties.
Ambien: zolpidem. Non-benzodiazepine sedativehypnotic.
buprenorphine (Subutex): opioid used as a maintenance treatment for heroin users.
amitriptyline: Elavil, Endep. Tricyclic antidepressant.
bupropion: Wellbutrin. Atypical antidepressant. Also Zyban, to reduce craving during tobacco cessation.
amobarbital: Amytal. Barbiturate sedative-hypnotic. amoxapine: Asendin. Tricyclic antidepressant. amphetamine: Benzedrine. CNS stimulant and sympathomimetic. Amytal: amobarbital. Barbiturate sedativehypnotic. Anavar: oxandrolone. Anabolic steroid. angel dust: street name for PCP. Antabuse: disulfiram. Alters metabolism of alcohol; used to treat alcohol dependence.
butabarbital: Butisol. Barbiturate sedativehypnotic. Butisol: butabarbital. Barbiturate sedative-hypnotic.
C caffeine: mild stimulant found in coffee and in OTC preparations. cannabis: the marijuana plant.
aprobarbital: Alurate. Barbiturate sedativehypnotic.
carbamazepine: Tegretol. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Artane: trihexyphenidyl. Anticholinergic used to control extrapyramidal symptoms.
Catapres: clonidine. Antihypertensive drug shown to reduce narcotic withdrawal symptoms.
Asendin: amoxapine. Tricyclic antidepressant.
Celexa: citalopram. Atypical antidepressant.
aspirin: acetylsalicylic acid. OTC analgesic.
chloral hydrate: Noctec. Nonbarbiturate sedativehypnotic.
Ativan: lorazepam. Benzodiazepine sedative. atropine: anticholinergic. Aventyl: nortriptyline. Tricyclic antidepressant. ayahuasca: a combination of two plants, one of which contains DMT. Hallucinogen.
chlordiazepoxide: Librium. Benzodiazepine sedative. chlorpheniramine maleate: OTC antihistamine. chlorpromazine: Thorazine. Antipsychotic.
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chlorprothixene: Taractan. Antipsychotic.
dextromethorphan: OTC cough suppressant.
Cibalith: lithium citrate. Salt used in treating mania and bipolar affective disorders.
diazepam: Valium. Benzodiazepine sedative.
Citalopram: Celexa. Atypical antidepressant. clenbuterol: an alpha-2 adrenergic agonist developed to treat asthma, but used by athletes to build muscle. clonidine: Catapres. Antihyperintensive drug shown to reduce narcotic withdrawal symptoms. clorazepate: Tranxene. Benzodiazepine sedative. clozapine: Clozaril. Atypical antipsychotic. Clozaril: clozapine. Atypical antipsychotic. cocaine: CNS stimulant and local anesthetic. codeine: opioid analgesic found in opium. Cogentin: benztropine. Anticholinergic used to control extrapyramidal symptoms.
diethylpropion: Tenuate, Tepanil. Amphetaminelike appetite suppressant. dihydrocodeine: opioid analgesic. Dilaudid: hydromorphone. Opioid analgesic. diphenhydramine: antihistamine. disulfiram: Antabuse. Alters metabolism of alcohol; used to treat alcoholism. DMT: dimethyltryptamine. Hallucinogen. Dolophine: methadone. Opioid analgesic. DOM: hallucinogen. doxepin: Sinequan. Tricyclic antidepressant. dronabinol: Marinol. Prescription form of delta-9tetrahydrocannabinol.
Compazine: prochlorperazine. Antipsychotic. creatine: natural substance found in meat and fish that might have anabolic properties and is used by athletes.
E
Cylert: pemoline. Stimulant used to treat ADD with hyperactivity.
Elavil: amitriptyline. Tricyclic antidepressant.
Effexor: venlafaxine. Antidepressant (SSRI). Endep: amitriptyline. Tricyclic antidepressant. endorphin: endogenous substance with effects similar to those of the opioid analgesics.
D Dalmane: flurazepam. Benzodiazepine hypnotic. Darvon: propoxyphene. Opioid analgesic. Datura: genus of plants, many of which are anticholinergic.
enkephalin: endogenous substance with effects similar to those of the opioid analgesics. ephedrine: sympathomimetic used to treat asthma. Equanil: meprobamate. Nonbarbiturate sedativehypnotic.
Demerol: meperidine. Opioid analgesic.
Eskalith: lithium carbonate. Salt used in treating mania and bipolar affective disorders.
Depakene: valproic acid. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
eszopiclone: Lunesta. Non-benzodiazepine sedative-hypnotic.
desipramine: Norpramin, Pertofrane. Tricyclic antidepressant. Desoxyn: methamphetamine. CNS stimulant and sympathomimetic.
F
Desyrel: trazodone. Atypical antidepressant.
fenfluramine: Pondimin. Appetite suppressant, removed from the market in 1997.
Dexedrine: dextroamphetamine. CNS stimulant and sympathomimetic. dexfenfluramine: Redux. Appetite suppressant, removed from the market in 1997. dextroamphetamine: Dexedrine. CNS stimulant and sympathomimetic.
fentanyl: Sublimaze. Potent synthetic analgesic. flunitrazepam: Rohypnol. Benzodiazepine hypnotic, not sold in the U.S. Known as a “date-rape” drug. fluoxetine: Prozac. Antidepressant (SSRI).
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www.mhhe.com/hart13e fluphenazine: Permitil, Prolixin. Antipsychotic.
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flurazepam: Dalmane. Benzodiazepine hypnotic.
Klonopin: Clonazepam. Benzodiazepine sedativehypnotic, also used as an anticonvulsant.
G
L
GEOdon: Ziprasidone. Atypical antipsychotic.
LAAM: L-alpha-acetyl-methadol. Long-lasting synthetic opioid used in maintenance treatment of narcotic addicts.
GHB: gamma hydroxybutyrate. CNS depressant, produced naturally in small amounts in the human brain. Has been used recreationally and, in combination with alcohol, has some reputation as a “date-rape” drug. Ginkgo biloba: a dietary supplement believed by some to increase blood circulation.
Lamictal: lamotrigine. Anticonvulsant also used as a mood stabilizer in bipolar disorder. lamotrigine: Lamictal. Anticonvulsant also used as a mood stabilizer in bipolar disorder. laudanum: tincture (alcohol solution) of opium. Lexapro: escitalopram. Atypical antidepressant.
H
Librium: chlordiazepoxide. Benzodiazepine sedative. Lithane: lithium carbonate.
Haldol: haloperidol. Antipsychotic.
lithium carbonate, lithium citrate: salts used in treating mania and bipolar affective disorders.
haloperidol: Haldol. Antipsychotic.
Lithobid: lithium carbonate.
henbane: poisonous anticholinergic plant.
lorazepam: Ativan. Benzodiazepine sedative.
heroin: Diacetylmorphine Narcotic analgesic.
Lortab: acetaminophen-hydrocodone combination. Analgesic.
Halcion: triazolam. Benzodiazepine hypnotic.
hydrocodone: Opioid analgesic. hydromorphone: Dilaudid. Opioid analgesic.
loxapine: Loxitane. Antipsychotic. Loxitane: loxapine. Antipsychotic. LSD: lysergic acid diethylamide. Hallucinogen.
I ibogaine: hallucinogen, also proposed to reduce craving in drug addicts. ibuprofen: analgesic and anti-inflammatory.
Ludiomil: maprotiline. Tricyclic antidepressant. Luminal: phenobarbital. Barbiturate sedativehypnotic. Lunesta: eszopiclone. Non-benzodiazepine sedativehypnotic.
imipramine: Janimine, Tofranil. Tricyclic antidepressant. isocarboxazid: Marplan. MAO inhibitor used as antidepressant.
M mandrake: anticholinergic plant.
J Janimine: imipramine. Tricyclic antidepressant.
maprotiline: Ludiomil. Tricyclic antidepressant. Marijuana: Common name for the cannabis plant and for its dried leaves. Marinol: dronabinol. Prescription form of delta-9tetrahydrocannabinol.
K
Marplan: isocarboxazid. MAO inhibitor used as antidepressant.
Ketalar: ketamine. Dissociative anesthetic.
Mazanor: mazindol. Appetite suppressant.
ketamine: Ketalar. Dissociative anesthetic.
mazinodol: Mazanor, Sanorex. Appetite suppressant.
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MDA: hallucinogen.
O
MDMA: hallucinogen. Mebaral: mephobarbital. Barbiturate sedative-hypnotic.
olanzepine: Zyprex. Atypical antipsychotic.
Mellaril: thioridazine. Antipsychotic.
opium: opioid analgesic.
meperidine: Demerol. Opioid analgesic.
oxandrolone: Anavar. Anabolic steroid.
mephobarbital: Mebaral. Barbiturate sedativehypnotic.
oxazepam: Serax. Benzodiazepine sedative.
meprobamate: Equanil, Miltown. Nonbarbiturate sedative-hypnotic.
oxycodone: Percodan. Opioid analgesic. OxyContin: continuous-release form of oxycodone. oxymorphone: Numorphan. Opioid analgesic.
mescaline: hallucinogen found in peyote cactus. mesoridazine: Serentil. Antipsychotic. methadone: Dolophine. Narcotic analgesic.
P
methamphetamine: Desoxyn, Methedrine. CNS stimulant and sympathomimetic.
Pamelor: nortriptyline. Tricyclic antidepressant.
methaqualone: Quaalude, Sopor. Nonbarbiturate sedative-hypnotic.
paraldehyde: nonbarbiturate sedative-hypnotic.
methylphenidate: Ritalin. Stimulant used to treat ADD with hyperactivity.
Parnate: tranylcypromine. MAO inhibitor used as antidepressant.
Metrazol: pentylenetetrazol. Convulsant formerly used in convulsive therapy.
paroxetine: Paxil. Antidepressant (SSRI).
Miltown: meprobamate. Nonbarbiturate sedativehypnotic.
PCP: phencyclidine, angel dust. Hallucinogen.
paregoric: tincture (alcohol solution) of opium.
Paxil: paroxetine. Antidepressant (SSRI).
mirtazapine: Remeron. Atypical antidepressant.
pemoline: Cylert. Stimulant used to treat ADD with hyperactivity.
Moban: molindone. Antipsychotic.
pentazocine: Talwin. Opioid analgesic.
modafinil: Provigil. Atypical CNS stimulant.
pentobarbital: Nembutal. Barbiturate sedativehypnotic.
molindone: Moban. Antipsychotic. morphine: opioid analgesic.
pentylenetetrazol: Metrazol. Convulsant formerly used in convulsive therapy.
N
Percodan: oxycodone. Opioid analgesic.
naloxone: Narcan. Opioid antagonist.
perphenazine: Trilafon. Antipsychotic.
naltrexone: Trexan, reVIA. Opioid antagonist. Used in treating alcoholism.
Pertofrane: desipramine. Tricyclic antidepressant.
Nardil: phenelzine. MAO inhibitor used as antidepressant. Navane: thiothixene. Antipsychotic. Nembutal: pentobarbital. Barbiturate sedativehypnotic.
Permitil: fluphenazine. Antipsychotic.
peyote: cactus containing mescaline (hallucinogenic). phencyclidine: PCP, angel dust. Hallucinogen. phendimetrazine: amphetamine-like appetite suppressant.
Norpramin: desipramine. Tricyclic antidepressant.
phenelzine: Nardil. MAO inhibitor used as antidepressant.
nortriptyline: Aventyl, Pamelor. Tricyclic antidepressant.
phenmetrazine: Preludin. Amphetamine-like appetite suppressant.
Novocain: Procaine. Local anesthetic.
phenobarbital: Luminal. Barbiturate sedative-hypnotic.
Numorphan: oxymorphone. Opioid analgesic.
phentermine: Amphetamine-like appetite suppressant.
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phenylpropanolamine (PPA): OTC appetite suppressant.
secobarbital: Seconal. Barbiturate sedative-hypnotic.
Pondimin: fenfluramine. Appetite suppressant, removed from the market in 1997.
Serax: oxazepam. Benzodiazepine sedative.
Seconal: secobarbital. Barbiturate sedative-hypnotic. Serentil: mesoridazine. Antipsychotic.
Preludin: phenmetrazine. Amphetamine-like appetite suppressant.
Sernyl: former brand name for PCP.
prochlorperazine: Compazine. Antipsychotic.
sertraline: Zoloft. Antidepressant (SSRI).
Prolixin: fluphenazine. Antipsychotic.
Sinequan: doxepin. Tricyclic antidepressant.
propoxyphene: Darvon. Narcotic analgesic.
Sonata: zaleplon. Non-benzodiazepine sedativehypnotic.
protriptyline: Vivactil. Tricyclic antidepressant. Prozac: fluoxetine. Antidepressant (SSRI). pseudoephedrine: OTC sympathomimetic. psilocybin: hallucinogen from the Mexican psilocybe mushroom.
Sopor: methaqualone. Non-barbiturate sedativehypnotic. Steroids: Various important hormones and their chemical derivatives. Usually refers to the anabolic steroids used by athletes and body builders. stanozolol: Winstrol. Anabolic steroid.
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Stelazine: trufluoperazine. Antipsychotic. Sublimaze: fentanyl. Potent synthetic analgesic.
Quaalude: methaqualone. Non-barbiturate sedativehypnotic.
T R Redux: dexfenfluramine. Appetite suppressant, removed from the market in 1997.
Talwin: pentazocine. Opioid analgesic. Taractan: chlorprothixene. Antipsychotic.
Remeron: mirtazapine. Atypical antidepressant.
Tegretol: carbamazepine. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Restoril: temazepam. Benzodiazepine hypnotic.
temazepam: Restoril. Benzodiazepine hypnotic.
reVIA: naltrexone. Opioid antagonist used in treating alcohol dependence.
Tenuate: diethylpropion. Amphetamine-like appetite suppressant.
Risperdal: risperidone. Atypical antipsychotic.
Tepanil: diethylpropion. Amphetamine-like appetite suppressant.
risperidone: Risperdal. Atypical antipsychotic. Ritalin: methylphenidate. Stimulant used to treat ADHD. Rohypnol: flunitrazepam. Benzodiazepine hypnotic, not sold in the U.S., known as a “date-rape” drug.
Teslac: testolactone. Anabolic steroid. testolactone: Teslac. Anabolic steroid. theophylline: mild stimulant found in tea; used to treat asthma. thioridazine: Mellaril. Antipsychotic.
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thiothixene: Navane. Antipsychotic. Thorazine: chlorpromazine. Antipsychotic.
Saint John’s wort: a dietary supplement used by some to treat depression.
Tindal: acetophenazine. Antipsychotic.
SAMe: S-adenosyl-L-methionine. Dietary supplement proposed as a possible treatment for depression.
Tofranil: imipramine. Tricyclic antidepressant.
Sanorex: mazindol. Appetite suppressant.
tranylcypromine: Parnate. MAO inhibitor used as an antidepressant.
scopolamine: anticholinergic.
TMA: indole hallucinogen. Tranxene: clorazepate. Benzodiazepine sedative.
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trazodone: Desyrel. Atypical antidepressant. Trexan: naltrexone. Opioid antagonist.
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triazolam: Halcion. Benzodiazepine hypnotic.
Wellbutrin: bupropion. Atypical antidepressant.
trifluoperazine: Stelazine. Antipsychotic.
Winstrol: stanozolol. Anabolic steroid.
trihexyphenidyl: Artane. Anticholinergic used to control extrapyramidal symptoms. Trilafon: perphenazine. Antipsychotic.
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2-CB: catechol hallucinogen.
Xanax: alprazolam. Benzodiazepine sedative.
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Valium: diazepam. Benzodiazepine sedative.
zaleplon: Sonata. Non-benzodiazepine sedativehypnotic.
valproic acid: Depakene. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Ziprasidone: Gedon. Atypical antipsychotic.
Varenicline: Chantix. To redce nicotine intake and craving during tobacco cessation. Partial nicotine agonist.
Zoloft: Sertraline. Antidepressant (SSRI).
venlafaxine: Effexor. Antidepressant (SSRI).
zolpidem: Ambien. Non-benzodiazepine sedativehypnotic.
Vesprin: triflupromazine. Antipsychotic. Vicodin: Hydrocodone-acetaminophen conbination. Analgesic. Vivactil: protriptyline. Tricyclic antidepressant.
Zyban: bupropion.To reduce craving during tobacco cessation.
Zyprexa: olanzepine. Atypical antipsychotic.
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Appendix
Appendix B: Resources for Information and Assistance
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Federal Government Agencies National Clearinghouse for Alcohol and Drug Information Office of Substance Abuse Prevention (OSAP) P.O. Box 2345 Rockville, MD 20847-2345 Local: (240) 221-4019 T0ll-free: 1-800-729-6686 http://ncadi.samhsa.gov Drugs & Crime Data Center Bureau of Justice Statistics 810 Seventh Street, NW Washington, DC 20531 (202) 307-0765 www.ojp.usdoj.gov/bjs/
Alcohol Alcohol Research Information Service 430 Lanthrop Street Lansing, MI 48912 (517) 485-9900 www.mondaymorningreport.org [email protected] Alcoholics Anonymous World Services P.O. Box 459 New York, NY 10163 (212) 870-3400 www.alcoholics-anonymous.org American Council on Alcoholism 1000 E. Indian School Rd. Phoenix, AZ 85014 Toll-free: 1-800-527-5344 www.aca-usa.org
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Resources for Information and Assistance American Health and Temperance Society 6830 Eastern Ave, NW Washington, DC 20012 (202) 722-6736 BACCHUS of the U.S.(Boost Alcohol Consciousness Concerning the Health of University Students) P.O. Box 100430 Denver, CO 80250-0430 (303) 871-0901 www.bacchusgamma.org Licensed Beverage Information Council 1250 I St., Suite 900 NW Washington, DC 20005 (202) 682-8800 MADD (Mothers Against Drunk Driving) 511 E. John Carpenter Frwy, Suite 700 Irving, TX 75062 Local: (214) 744-6233 Info: 1-800-GET-MADD Help Line: 1-877-MADD-HELP www.madd.org National Alcohol Hotline 24-hr, 7 day/wk 1-800-ALCOHOL National Council on Alcoholism and Drug Dependence 244 E. 58th St. 4th Floor New York, NY 10022 (212)269-7797 Hope-Line: 1-800-NCA-CALL www.ncadd.org
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Appendix B Resources for Information and Assistance
RID (Remove Intoxicated Drivers) P.O. Box 520 Schenectady, NY 12301 (518) 372-0034 Toll-free: 1-888-283-5144 www.rid-usa.org
Smoking ASH (Action on Smoking and Health) 2013 H Street, NW Washington, DC 20006 www.no-smoking.org or www.ash.org Smoking Control Advocacy Resource Center 1730 Rhode Island Ave, Suite 600, NW Washington, DC 20036 (202) 659-8475 Tobacco Institute 2025 M Street, NW Washington, DC 20036 (202) 367-1176 www.tobaccoinstitute.com
Drugs Alcohol and Drug Problems Association of North America 307 N. Main St. Black Walnut, MO 63301 (can’t find phone number- site being built) www.adpana.com American Council for Drug Education 164 W. 74th St. New York, NY 10023 1-800-488-DRUG www.acde.org Do It Now Foundation PO Box 27568 Tempe, AZ 85285-7568 (480)736-0599 www.doitnow.org Drug Policy Foundation changed to: Drug Policy Alliance Network
70 W. 36th St, 16th Floor New York, NY 10018 (212) 613-8020 www.drugpolicy.org Summit Oaks Hospital 19 Prospect St. Box 100 Summit, NJ 07901 (908) 522-0914 I-800-COCAINE www.summitoakshospital.com Narcotic Educational Foundation of America 28245 Avenue Crocker, Suite 230 Santan Clarita, CA 91355-1201 (661)775-1648 Toll-free: (877) 775-NARC www.cnoa.org/NEFA.htm National Drug Information Center of Families in Action, Inc. changed to: National Families in Action 2957 Clairmont Road NE, Suite 150 Atlanta, GA 30329 (404) 248-9676 www.nationalfamilies.org NIDA (National Institute on Drug Abuse) National Institutes of Health 6001 Executive Boulevard, Room 5213 Bethesda, MD 20892-9561 (301) 443-1124 www.nida.nih.gov NORML (National Organization for the Reform of Marijuana Laws) 1600 K St NW, Suite 501 Washington, DC 20006-2832 (202)483-5500 www.norml.org PRIDE (Parent Resource Institute for Drug Education) 50 Hurt Plaza, Suite 210 Atlanta, GA 30303 (404) 577-4500 www.prideusa.org
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Appendix B: Resources for Information and Assistance
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Appendix B Resources for Information and Assistance
Drug Information on the Internet Much information, opinion, misinformation, and discussion about drugs is available on the Internet. It is possible to learn about the latest drug fads, to get involved in arguments about drug policy, and occasionally even to learn some solid facts by browsing on the Internet. But be warned that there is no quality control on many of these
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computer sites—they represent the ultimate in free expression! You’re liable to find such things as a bogus recipe for making LSD from Foster’s beer, warnings about water addiction, and other foolishness mixed in with potentially useful information, so take care. Links to some relevant Internet sites are found on the Online Learning Center.
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Glossary A abstinence Refraining completely from the use of alcohol or another drug. Complete abstinence from alcohol means no drinking at all. Abstinence syndrome: see withdrawal syndrome. abstinence violation effect The tendency of a person who has been abstaining (as from alcohol), and “slips,” to go on and indulge fully, because the rule of abstinence has been broken. acetaldehyde The chemical product of the first step in the liver’s metabolism of alcohol. It is normally present only in small amounts because it is rapidly converted to acetic acid. acetaminophen An aspirinlike analgesic and antipyretic. acetylcholine Neurotransmitter found in the parasympathetic branch and in the cerebral cortex. acetylsalicylic acid The chemical known as aspirin; an over-the-counter drug that relieves pain and reduces fever and inflammation. action potential A brief electrical signal transmitted along a neuron’s axon. active metabolites Pharmacologically active chemicals formed when enzymes in the body act on a drug. acute In general, “sharp.” In medicine, “rapid.” Referring to drugs, the short-term effects or effects of a single administration, as opposed to chronic, or longterm, effects of administration. additive effects When the effects of two different drugs add up to produce a greater effect than either drug alone. As contrasted with antagonistic effects, in which one drug reduces the effect of another, or synergistic effects, in which one drug greatly amplifies the effect of another. adenosine A chemical believed to be a neurotransmitter in the CNS, primarily at inhibitory receptors. Caffeine might act by antagonizing the normal action of adenosine on its receptors.
one example is learning how to achieve certain “feelings” (of excitement or belonging to a group) without using drugs. agonist A substance that facilitates or mimics the effects of a neurotransmitter on the postsynaptic cell. AIDS Acquired immunodeficiency syndrome, a disease in which the body’s immune system breaks down, leading eventually to death. Because the disease is spread through the mixing of body fluids, it is more prevalent in intravenous drug users who share needles. The infectious agent is the human immunodeficiency virus (HIV). alcohol Generally refers to grain alcohol, or ethanol, as opposed to other types of alcohol (for example, wood or isopropyl alcohol), which are too toxic to be drinkable. alcohol abuse In the DSM-IV-TR, defined as a pattern of pathological alcohol use that causes impairment of social or occupational functioning. Compare with alcohol dependence. alcohol dehydrogenase The enzyme that metabolizes almost all of the alcohol consumed by an individual. It is found primarily in the liver. alcohol dependence In the DSM-IV-TR, alcohol dependence is considered a more serious disorder than alcohol abuse, in that dependence includes either tolerance or withdrawal symptoms. alcoholic personality Personality traits, such as immaturity and dependency, that are frequently found in alcoholics in treatment. Many of these consistent traits might be a result of years of heavy drinking rather than a cause of alcoholism. Alcoholics Anonymous (AA) A worldwide organization of self-help groups based on alcoholics helping each other achieve and maintain sobriety.
ADHD Attention deficit hyperactivity disorder, a learning disability. Terminology of the DSM-IV-TR.
alcoholism The word has many definitions and therefore is not a precise term. Definitions might refer to pathological drinking behavior (e.g., remaining drunk for two days), to impaired functioning (e.g., frequently missing work), or to physical dependence. See also alcohol abuse and alcohol dependence.
affective education In general, education that focuses on emotional content or emotional reactions, in contrast to cognitive content. In drug education,
alternatives (to drugs) Assuming that there are motives for drug use, such as the need to be accepted by a group, many prevention and treatment programs
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teach alternative methods for satisfying these motives; may include activities such as relaxation or dancing. Alzheimer’s disease A progressive neurological disease that occurs primarily in the elderly. It causes loss of memory and then progressively impairs more aspects of intellectual and social functioning. Large acetylcholine-containing neurons of the brain are damaged in this disease. Amanita muscaria The fly agaric mushroom, widely used in ancient times for its hallucinogenic properties. amotivational syndrome A hypothesized loss of motivation that has been attributed to chronic marijuana use. amphetamine A synthetic CNS stimulant and sympathomimetic. anabolic Promoting constructive metabolism; building tissue. anabolic steroids Substances that increase anabolic (constructive) metabolism, one of the functions of male sex hormones. The result is increased muscle mass. analgesic Pain-relieving. An analgesic drug produces a selective reduction of pain, whereas an anesthetic reduces all sensation. anandamide A naturally occurring brain chemical with marijuana-like properties. androgenic Masculinizing. anesthetic Sense-deadening. An anesthetic drug reduces all sensation, whereas an analgesic drug reduces pain. angel dust A street name for phencyclidine (PCP) when sprinkled on plant material. anhedonia Lack of emotional response; especially an inability to experience joy or pleasure. animism The belief that objects and plants contain spirits that move and direct them.
antecedents In the context of Chapter 1, behaviors or individual characteristics that can be measured before drug use and might therefore be somewhat predictive of drug use. These are not necessarily causes of the subsequent drug use. anticonvulsant A drug that prevents or reduces epileptic seizures. antidepressant A group of drugs used in treating depressive disorders. The MAO inhibitors, the tricyclics, and the SSRIs are the major examples. antihistamines A group of drugs that act by antagonizing the actions of histamine at its receptors. Used in cold and sinus remedies and in OTC sedatives and sleep aids. anti-inflammatory Reducing the local swelling, inflammation, and soreness caused by injury or infection. Aspirin has anti-inflammatory properties. antipsychotics A group of drugs used to treat psychotic disorders, such as schizophrenia. Also called neuroleptics or major tranquilizers. antipyretic Fever-reducing. Aspirin is a commonly used antipyretic. antitussive Cough-reducing. Narcotics have this effect. OTC antitussives generally contain dextromethorphan. anxiety disorders Mental disorders characterized by excessive worry, fears, avoidance, or a sense of impending danger. At pathological levels, these disorders can be debilitating. anxiolytics Drugs, such as Valium, used in the treatment of anxiety disorders. Literally, “anxiety-dissolving.” aphrodisiac Any substance that is said to promote sexual desire. aspirin Originally Bayer’s brand name for acetylsalicylic acid, now a generic name for that chemical. assassin The story is that this term for a hired killer is derived from a hashish-using cult, the hashshiyya. ataxia Loss of coordinated movement; for example, the staggering gait of someone who has consumed a large amount of alcohol.
Antabuse Brand name for disulfiram, a drug that interferes with the normal metabolism of alcohol, so that a person who drinks alcohol after taking disulfiram will become quite ill. Antabuse interferes with the enzyme aldehyde dehydrogenase, so that there is a buildup of acetaldehyde, the first metabolic product of alcohol.
attention-deficit hyperactivity disorder A learning disability accompanied by hyperactivity. More common in male children. This DSM-IV-TR diagnostic category replaces hyperkinetic syndrome and minimal brain dysfunction.
antagonist A substance that prevents the effects of a neurotransmitter on the postsynaptic cell.
autonomic nervous system The branch of the peripheral nervous system that regulates the visceral,
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www.mhhe.com/hart13e or automatic (“involuntary”) functions of the body, such as heart rate and intestinal motility. In contrast to the somatic, or voluntary, nervous system. axon A region of a neuron that extends from the cell body and is responsible for conducting the electrical signal to the presynaptic terminals. B BAC Blood alcohol concentration, also called blood alcohol level (BAL). The proportion of blood that consists of alcohol. For example, a person with a BAC of 0.10 percent has alcohol constituting one-tenth of 1 percent of the blood and is legally intoxicated in all states.
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and electrical attractions between a specific molecule and its receptor, so that there is a much higher probability that the receptor will be occupied by its proper molecule than by other molecules. biopsychosocial A theory or perspective that relies on the interaction of biological, individual psychological, and social variables. bipolar disorder One of the major mood disorders. Periods of mania and periods of depression have occurred in the same individual. Also called manicdepressive illness.
balanced placebo A research design in which alcohol is compared with a placebo beverage, and subjects either believe they are drinking alcohol or believe they are not.
blackout A period of time during which a person was behaving, but of which the person has no memory. The most common cause of this phenomenon is excessive alcohol consumption, and blackouts are considered to indicate pathological drinking.
barbiturate A major class of sedative-hypnotic drugs, including amobarbital and sodium pentothal.
black tar A type of illicit heroin usually imported from Mexico.
basal ganglia A subcortical brain structure containing large numbers of dopamine synapses. Responsible for maintaining proper muscle tone as a part of the extrapyramidal motor system. Damage to the basal ganglia, as in Parkinson’s disease, produces muscular rigidity and tremors.
blood alcohol concentration A measure of the concentration of alcohol in the blood, expressed in grams per 100 ml (percentage).
behavioral tolerance Repeated use of a drug can lead to a diminished effect of the drug (tolerance). When the diminished effect occurs because the individual has learned to compensate for the effect of the drug, it is called behavioral tolerance. For example, a novice drinker might be unable to walk with a BAC of 0.20 percent, whereas someone who has practiced walking while intoxicated would be able to walk fairly well at the same BAC. behavioral toxicity Refers to the fact that a drug can be toxic because it impairs behavior and amplifies the danger level of many activities. The effect of alcohol on driving is an example. benzodiazepine The group of drugs that includes Valium (diazepam) and Librium (chlordiazepoxide). They are used as anxiolytics or sedatives, and some types are used as sleeping pills. bhang A preparation of cannabis (marijuana) that consists of the whole plant, dried and powdered. The weakest of the forms commonly used in India. binding The interaction between a molecule and a receptor for that molecule. Although the molecules float onto and off the receptor, there are chemical
blood-brain barrier Refers to the fact that many substances, including drugs, that can circulate freely in the blood do not readily enter the brain tissue. The major structural feature of this barrier is the tightly jointed epithelial cells lining blood capillaries in the brain. Drug molecules cannot pass between the cells but must instead go through their membranes. Small molecules and molecules that are lipid- (fat-) soluble cross the barrier easily. Obviously, all psychoactive drugs must be capable of crossing the blood-brain barrier. brain stem The medulla oblongata, pons, and midbrain. Located between the spinal cord and the forebrain, and generally considered to contain the “oldest” (in an evolutionary sense) and most primitive control centers for such basic functions as breathing, swallowing, and so on. brand name The name given to a drug by a particular manufacturer and licensed only to that manufacturer. For example, Valium is a brand name for diazepam. Other companies may sell diazepam, but HoffmanLaRoche, Inc., owns the name Valium. C caffeinism Excessive use of caffeine. Camellia sinesis The plant from which tea is made.
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Cannabis Genus of plants known as marijuana or hemp. Includes C. indica and C. sativa.
comatose A state of unconsciousness from which the individual cannot be aroused.
carbon monoxide A poisonous gas found in cigarette smoke.
congeners In general, members of the same group. With respect to alcohol, the term refers to other chemicals (alcohols and oils) that are produced in the process of making a particular alcoholic beverage.
catheter A piece of plastic or rubber tubing that is inserted or implanted into a vein or other structure. central nervous system Brain and spinal cord. charas A preparation of cannabis, or marijuana, that is similar to hashish. The most potent form of marijuana commonly used in India. chemical name For a drug, the name that is descriptive of its chemical structure. For example, the chemical name sodium chloride is associated with the generic name table salt, of which there may be several brand names, such as Morton’s. chipper An individual who uses heroin occasionally. chlorpheniramine maleate A common over-thecounter antihistamine found in cold products. chronic Occurring over time. Chronic drug use is long-term use; chronic drug effects are persistent effects produced by long-term use. chronic obstructive lung disease A group of disorders that includes emphysema and chronic bronchitis. Cigarette smoking is a major cause of these disorders. cirrhosis A serious, largely irreversible, and frequently deadly disease of the liver. Usually caused by chronic heavy alcohol use. club drugs Drugs associated with use at all-night dance parties, known as “raves,” held in dance clubs, abandoned warehouses, and increasingly in more traditional nightclubs as the rave-party generation moves into its 20s. The drugs most commonly included in this group include the hallucinogen MDMA and the depressants GHB and Rohypnol. coca The plant Erythroxylon coca, from which cocaine is derived. Also refers to the leaves of this plant. cocaethylene A potent stimulant formed when cocaine and alcohol are used together. cocaine A CNS stimulant and local anesthetic; the primary active chemical in coca. cocaine hydrochloride The most common form of pure cocaine; it is stable and water soluble. coca paste A crude, smokable extract derived from the coca leaf in the process of making cocaine. codeine A narcotic chemical present in opium.
controlled drinking The concept that individuals who have been drinking pathologically can be taught to drink in a controlled, nonpathological manner. controlled substance A term coined for the 1970 federal law that revised previous laws regulating narcotics and dangerous drugs. Heroin and cocaine are examples of controlled substances. correlate A variable that is statistically related to some other variable, such as drug use. crack Street name for a smokable form of cocaine. Also called rock. crank Street name for illicitly manufactured methamphetamine. crystal meth Street term for a form of methamphetamine crystals, also called ice. cumulative effects Drug effects that increase with repeated administrations, usually due to the buildup of the drug in the body. CYP450 Cytochrome P450 refers to a group of enzymes found in the liver that are responsible for metabolizing foreign chemicals, including most drugs.
D DARE Drug Abuse Resistance Education, the most popular prevention program in schools. date-rape drug A substance given to someone without her knowledge to cause unconsciousness in order to have nonconsensual sex. Rohypnol and GHB have become known for such use. A 1996 U.S. law provides serious penalties for using drugs in this manner. Datura A plant genus that includes many species used for their hallucinogenic properties. These plants contain anticholinergic chemicals. DAWN Drug Abuse Warning Network, a federal government system for reporting drug-related medical emergencies and deaths. DEA United States Drug Enforcement Administration, a branch of the Department of Justice.
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www.mhhe.com/hart13e delirium tremens Alcohol withdrawal symptoms, including tremors and hallucinations. demand reduction Efforts to control drug use by reducing the demand for drugs, as opposed to efforts aimed at reducing the supply of drugs. Demand reduction efforts include education and prevention programs, as well as increased punishments for drug users. dendrite Treelike region of a neuron that extends from the cell body and contains in its membrane receptors that recognize and respond to specific chemical signals. depolarized When the membrane potential is less polarized. depressant Any of a large group of drugs that generally slow activity in the CNS and at high doses induce sleep. Includes alcohol, the barbiturates, and other sedative-hypnotic drugs. depression A major type of mood disorder. detoxification The process of allowing the body to rid itself of a large amount of alcohol or another drug. Often the first step in a treatment program. deviance Behavior that is different from established social norms and that social groups take steps to change. dextromethorphan An over-the-counter cough control ingredient. diagnosis The process of identifying the nature of an illness. A subject of great controversy for mental disorders. distillation The process by which alcohol is separated from a weak alcohol solution to form more concentrated distilled spirits. The weak solution is heated, and the alcohol vapors are collected and condensed to a liquid form. dopamine A neurotransmitter found in the basal ganglia and other regions of the brain. dose-response curve A graph showing the relationship between the size of a drug dose and the size of the response (or the proportion of subjects showing the response). double-blind procedure A type of experiment in which the patients and those evaluating them do not know which patients are receiving a placebo and which are receiving the test drug. dronabinol The generic name for prescription THC in oil in a gelatin capsule.
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drug Any substance, natural or artificial, other than food, that by its chemical nature alters structure or function in the living organism. drug abuse The use of a drug in such a manner or in such amounts or in situations such that the drug use causes problems or greatly increases the chance of problems occurring. drug dependence A state in which a person uses a drug so frequently and consistently that the individual appears to need the drug to function. This may take the form of physical dependence, or behavioral signs may predominate (e.g., unsuccessful attempts to stop or reduce drug use). drug disposition tolerance The reduced effect of a drug, which can result from more rapid metabolism or excretion of the drug. drug misuse The use of prescribed drugs in greater amounts than, or for purposes other than, those prescribed by a physician or dentist. DSM-IV-TR Diagnostic and Statistical Manual of Mental Disorders, fourth edition text revised, published by the American Psychiatric Association. It has become a standard for naming and distinguishing among mental disorders.
E Ecstasy Street name for the hallucinogen MDMA. Also called “XTC.” ECT Electroconvulsive therapy, or electroconvulsive shock treatment. A procedure in which an electrical current is passed through the head, resulting in an epileptic-like seizure. Although this treatment is now used infrequently, it is still considered to be the most effective and rapid treatment for severe depression. ED50 The effective dose for half the subjects in a drug test. effective dose The dose of a drug that produces a certain effect in some percentage of the subjects. For example, an ED50 produces the effect in 50 percent of the subjects. Note that the dose will depend on the effect that is monitored. emphysema A chronic lung disease in which tissue deterioration results in increased air retention and reduced exchange of gases. The result is difficulty breathing and shortness of breath. An example of a chronic obstructive lung disease, often caused by smoking.
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endorphins Morphine-like chemicals that occur naturally in the brains and pituitary glands of humans and other animals. There are several proper endorphins, and the term is also used generically to refer to both the endorphins and the enkephalins. enkephalins Morphine-like chemicals that occur naturally in the brains and adrenal glands of humans and other animals. The enkephalins are smaller molecules than the endorphins. enzyme A large, organic molecule that works to speed up or help along a specific chemical reaction. Enzymes are found in brain cells, where they are needed for most steps in the synthesis of neurotransmitter molecules. They are also found in the liver, where they are needed for the metabolism of many drug molecules. ephedrine A drug derived from the Chinese medicinal herb ma huang and used to relieve breathing difficulty in asthma. A sympathomimetic from which amphetamine was derived. epilepsy A disorder of the nervous system in which recurring periods of abnormal electrical activity in the brain produce temporary malfunction. There might or might not be loss of consciousness or uncontrolled motor movements (seizures). ergogenic Energy-producing. Refers to drugs or other methods (e.g., blood doping) designed to enhance an athlete’s performance. ergotism A disease caused by eating grain infected with the ergot fungus. There are both psychological and physical manifestations. F FAS Fetal alcohol syndrome. FDA United States Food and Drug Administration. fen-phen A combination of two prescription weightcontrol medications, fenfluramine and phentermine. No longer prescribed due to concerns with toxicity to heart valves. fermentation The process by which sugars are converted into grain alcohol through the action of yeasts. fetal alcohol effect Individual developmental abnormalities associated with the mother’s alcohol use during pregnancy. fetal alcohol syndrome Facial and developmental abnormalities associated with the mother’s alcohol use during pregnancy.
flashback An experience reported by some users of LSD in which portions of the LSD experience recur at a later time without the use of the drug. fly agaric mushroom Amanita muscaria, a hallucinogenic mushroom that is also considered poisonous. freebase In general, when a chemical salt is separated into its basic and acidic components, the basic component is referred to as the free base. Most psychoactive drugs are bases that normally exist in a salt form. Specifically, the salt cocaine hydrochloride can be chemically extracted to form the cocaine free base, which is volatile and can therefore be smoked. functional disorder A mental disorder for which there is no known organic cause. Schizophrenia is a form of psychosis that is considered to be a functional disorder. G GABA An inhibitory neurotransmitter found in most brain regions; gamma-aminobutyric acid. gamma hydroxybutyrate (GHB) CNS depressant, produced naturally in small amounts in the human brain; has been used recreationally and, in combination with alcohol, has some reputation as a date-rape drug; chemically related to GABA. ganja A preparation of cannabis (marijuana) in which the most potent parts of the plant are used. gateway substances Substances, such as alcohol, tobacco, and sometimes marijuana, that most users of illicit substances will have tried before their first use of cocaine, heroin, or other less widely used illicit drugs. generic name For drugs, a name that specifies a particular chemical without being chemically descriptive or referring to a brand name. As an example, the chemical name sodium chloride is associated with the generic name table salt, of which there may be several brand names, such as Morton’s. glia Brain cells that provide firmness and structure to the brain, get nutrients into the system, eliminate waste, form myelin, and create the blood-brain barrier. glutamate An excitatory neurotransmitter found in most brain regions. GRAE “Generally recognized as effective”; a term defined by the FDA with reference to the ingredients found in OTC drugs (see also GRAS).
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www.mhhe.com/hart13e GRAHL “Generally recognized as honestly labeled” (see also GRAE and GRAS). grain neutral spirits Ethyl alcohol distilled to a purity of 190 proof (95 percent). grand mal An epileptic seizure that results in convulsive motor movements and loss of consciousness. GRAS “Generally recognized as safe”; a term defined by the FDA with reference to food additives and the ingredients found in OTC drugs. H hallucinogen A drug, such as LSD or mescaline, that produces profound alterations in perception. hashish A potent preparation of concentrated resin from the Cannabis plant. hash oil A slang term for oil of cannabis, a liquid extract from the marijuana plant. henbane A poisonous plant containing anticholinergic chemicals and sometimes used for its hallucinogenic properties. Hyoscyamus niger. heroin Originally Bayer’s name for diacetylmorphine, a potent narcotic analgesic synthesized from morphine. HIV Human immunodeficiency virus. The infectious agent responsible for AIDS. homeostasis A state of physiological balance maintained by various regulatory mechanisms; body functions such as blood pressure and temperature must be maintained within a certain range.
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I ibogaine A hallucinogen that has been shown to reduce self-administration of cocaine and morphine in rats and is proposed to reduce craving in drug addicts. ibuprofen An aspirin-like analgesic and antiinflammatory. ice The street name for crystals of methamphetamine hydrochloride. illicit drug A drug that is unlawful to possess or use. IND Approval to conduct clinical investigations on a new drug, filed with the FDA after animal tests are complete. indole A type of chemical structure. The neurotransmitter serotonin and the hallucinogen LSD both contain an indole nucleus. inhalants Any of a variety of volatile solvents or other products that can be inhaled to produce intoxication. insomnia Inability to sleep. The most common complaint is difficulty falling asleep. Often treated with a hypnotic drug. intramuscular A type of injection in which the drug is administered into a muscle. intravenous (IV) A type of injection in which the drug is administered into a vein. L
hooka A water pipe, often with more than one mouthpiece. Used to smoke tobacco or marijuana.
laissez-faire A theory that government should not interfere with business or other activities.
human growth hormone A pituitary hormone responsible for some types of giantism.
LD50 The lethal dose for half the animals in a test.
hyperactive Refers to a disorder characterized by short attention span and a high level of motor activity. The DSM-IV-TR term is attention-deficit hyperactivity disorder. hyperpolarized When the membrane potential is more negative. hypnotic Sleep-inducing. For drugs, refers to sleeping preparations. hypodermic syringe A device to which a hollow needle can be attached, so that solutions can be injected through the skin. hypothalamus A group of nuclei found at the base of the brain, just above the pituitary gland.
lethal dose The dose of a drug that produces a lethal effect in some percentage of the animals on which it is tested. For example, LD50 is the dose that would kill 50 percent of the animals to which it was given. leukoplakia A whitening and thickening of the mucous tissues of the mouth. The use of chewing tobacco is associated with an increase in leukoplakia, considered to be a “precancerous” tissue change. limbic system A system of various brain structures that are involved in emotional responses. lipid solubility The tendency of a chemical to dissolve in oils or fats, as opposed to in water. lipophilic The extent to which chemicals can be dissolved in oils and fats.
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lithium A highly reactive metallic element, atomic number 3. Its salts are used in the treatment of mania and bipolar disorder. longitudinal study A study done over a period of time (months or years). look-alikes Drugs sold legally, usually through the mail, that are made to look like controlled, prescriptiononly drugs. The most common types contain caffeine and resemble amphetamine capsules or tablets.
bodies in the midbrain and their terminals in the forebrain, on various structures associated with the limbic system. Believed by some theorists to be important in explaining the therapeutic effects of antipsychotic medications. Also believed by some theorists to be important for many types of behavioral reinforcers. metabolism (of drugs) The breakdown or inactivation of drug molecules by enzymes, often in the liver. metabolite A product of enzyme action on a drug.
M ma huang A Chinese herb containing ephedrine, which is a sympathomimetic drug from which 0 amphetamine was derived. major depression A serious mental disorder characterized by a depressed mood. A specific diagnostic term in the DSM-IV-TR. malting The process of wetting a grain and allowing it to sprout, to maximize its sugar content before fermentation to produce an alcoholic beverage. mandrake Mandragora officinarum, a plant having a branched root that contains anticholinergic chemicals. Now classed among the other anticholinergic hallucinogens, this plant was widely believed to have aphrodisiac properties. marijuana Also spelled marihuana; dried leaves of the Cannabis plant. Marinol The brand name for prescription THC in oil in a gelatin capsule. MDMA Methylenedioxy methamphetamine, a catechol hallucinogen related to MDA. Called “Ecstasy” or “XTC” on the street. medial forebrain bundle A group of neuron fibers that projects from the midbrain to the forebrain, passing near the hypothalamus. Now known to contain several chemically and anatomically distinct pathways, including dopamine and norepinephrine pathways. medical model With reference to mental disorders, a model that assumes that abnormal behaviors are symptoms resulting from a disease. mental illness A term that, to some theorists, implies acceptance of a medical model of mental disorders. mescaline The active hallucinogenic chemical in the peyote cactus. mesolimbic dopamine pathway A group of dopamine-containing neurons that have their cell
metabolize To break down or inactivate a neurotransmitter (or a drug) through enzymatic action. methadone A long-lasting synthetic opioid; commonly used in the long-term treatment for opioid dependence. methadone maintenance A program for treatment of narcotic addicts in which the synthetic drug methadone is provided to the addicts in an oral dosage form, so that they can maintain their addiction legally. methylphenidate A stimulant used in treating ADHD; brand name Ritalin. Mexican brown A form of heroin that first appeared on American streets in the mid-1970s. Because the heroin is made from the hydrochloride salt of morphine, it is brown in its pure form. moist snuff A type of oral smokeless tobacco that is popular among young American men. A “pinch” of this finely chopped, moistened, flavored tobacco is held in the mouth, often between the lower lip and the gum. monoamine A class of chemicals characterized by a single amine group; monoamine transmitters include dopamine, norepinephrine, and serotonin. monoamine oxidase (MAO) inhibitor A drug that acts by inhibiting the enzyme monoamine oxidase (MAO). Used as an antidepressant. mood disorder Mental disorders characterized by depressed or manic symptoms. morphine A narcotic; the primary active chemical in opium. Heroin is made from morphine. morphinism An older term used to describe dependence on the use of morphine. motivational interviewing A technique for encouraging alcoholics or addicts to seek treatment by first assessing their degree of dependence and then discussing the assessment results. Direct confrontation is avoided.
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www.mhhe.com/hart13e N naloxone An opioid antagonist used in treating alcoholism. narcolepsy A form of sleep disorder characterized by bouts of muscular weakness and falling asleep suddenly and involuntarily. The most common treatment employs stimulant drugs such as amphetamine to maintain wakefulness during the day. narcotic Opioid (in pharmacology terms), or a drug that is produced or sold illegally (in legal terms); in the United States, a “controlled substance.” narcotic antagonists Drugs that can block the actions of narcotics. Native American Church A religious organization active among American Indians, in which the hallucinogenic peyote cactus is used in conjunction with Christian religious themes. NDA In FDA procedures, a New Drug Application. This application, demonstrating both safety and effectiveness of a new drug in both animal and human experiments, must be submitted by a drug company to the FDA before a new drug can be marketed. neuroleptic A general term for the antipsychotic drugs (also called major tranquilizers). neuron Brain cell that analyzes and transmits information via chemical and electrical signals. neurotransmitter A chemical messenger that is released by one neuron and that alters the electrical activity in another neuron; its effects are brief and local.
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nonspecific effects Effects of a drug that are not changed by changing the chemical makeup of the drug. Also referred to as placebo effects. norepinephrine A neurotransmitter that might be important for regulating waking and appetite. NORML National Organization for the Reform of Marijuana Laws. NSAIDs Nonsteroidal anti-inflammatory drugs, such as ibuprofen and naproxen. nucleus accumbens A collection of neurons in the forebrain thought to play an important role in emotional reactions to events. nucleus basalis A group of large cell bodies found just below the basal ganglia and containing acetylcholine. These cells send terminations widely to the cerebral cortex. In Alzheimer’s disease, there is a loss of these neurons and a reduction in the amount of acetylcholine in the cortex. O off-label Use of a prescription drug to treat a condition for which the drug has no received U.S. FDA approval. opioid One of a group of drugs similar to morphine, used medically primarily for their analgesic effects. Opioids include drugs derived from opium and synthetic drugs with opium-like effects.
Nicotiana Any of several types of tobacco plant, including N. tobacum and N. rustica.
opioid antagonist Any of several drugs that are capable of blocking the effects of opioids. Used in emergency medicine to treat overdose and in some addiction treatment programs to block the effect of any illicit opioid that might be taken. Nalorphine and naltrexone are examples.
nicotine The chemical contained in tobacco that is responsible for its psychoactive effects and for tobacco dependence.
opium A sticky raw substance obtained from the seed pods of the opium poppy and containing the narcotic chemicals morphine and codeine.
nigrostriatal dopamine pathway A group of dopamine-containing neurons that have their cell bodies in the substantia nigra of the midbrain and their terminals in the corpus striatum (basal ganglia), which is part of the extrapyramidal motor system. It is this pathway that deteriorates in Parkinson’s disease and on which antipsychotic drugs act to produce side effects resembling Parkinson’s disease.
organic disorder For mental disorders, those with a known physical cause (e.g., psychosis caused by long-term alcohol use).
nitrosamines A group of organic chemicals, many of which are highly carcinogenic. At least four are found only in tobacco, and these might account for much of the cancer-causing property of tobacco.
OTC Over-the-counter. OTC drugs are those drugs that can be purchased without a prescription. P Papaver somniferum The opium poppy. paraphernalia In general, the equipment used in some activity. Drug paraphernalia include such items as syringes, pipes, scales, or mirrors.
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parasympathetic The branch of the autonomic nervous system that has acetylcholine as its neurotransmitter and, for example, slows the heart rate and activates the intestine. Parkinson’s disease A degenerative disease of the extrapyramidal motor system, specifically involving damage to the nigrostriatal dopamine system. Early symptoms include muscular rigidity, tremors, a shuffling gait, and a masklike face. Occurs primarily in the elderly. passive smoking The inhalation of tobacco smoke from the air by nonsmokers. patent medicines Proprietary medicines. Originally referred to medicines that were, in fact, treated as inventions and patented in Great Britain. In America, the term came to refer to medicines sold directly to the public. PCP Phenycyclidine; 1-(1-phenylcyclohexl) piperidine. A drug with hallucinogenic properties that was originallly developed as an anesthetic; it is not legally available for human use. This hallucinogen is often referred to as angel dust. PDR Physician’s Desk Reference, a book listing all prescription drugs and giving prescribing information about each. Updated yearly. pekoe A grade of tea. peptide A class of chemicals made up of sequences of amino acids. Enkephalins are small peptides containing only five amino acids, whereas large proteins may contain hundreds.
placebo An inactive drug, often used in experiments to control for nonspecific effects of drug administration. postsynaptic Refers to structures associated with the neural membrane on the receiving side of a synapse. potency Measured by the amount of a drug required to produce a given effect. precursor Something that precedes something else. In biochemistry, a precursor molecule may be acted upon by an enzyme and changed into a different molecule. For example, the dietary amino acid tryptophan is the precursor for the neurotransmitter serotonin. prodrugs Drugs that are administered in an inactive form and become effective after they are chemically modified in the body by enzymes. Prohibition The period 1920–1933, during which the sale of alcoholic beverages was prohibited in the United States. proof A measure of a beverage’s alcohol content; twice the alcohol percentage. proprietary A medicine that is marketed directly to the public. Also called OTC, patent, or nonprescription medicines. prostaglandins Local hormones, some of which are synthesized in response to cell injury and are important for initiating pain signals. Aspirin and similar drugs inhibit the formation of prostaglandins.
peyote A hallucinogenic cactus containing the chemical mescaline.
protective factors Behaviors, attitudes, or situations that correlate with low rates of deviant behavior, including use of illicit drugs. Examples include commitment to school, religiosity, and having parents who communicate opposition to drug use.
phantastica Hallucinogens that create a world of fantasy.
protein binding The combining of drug molecules with blood proteins.
pharmacodynamic tolerance Reduced effectiveness of a drug resulting from altered nervous system sensitivity.
psilocybin The active hallucinogenic chemical in Psilocybe mushrooms.
phenothiazines A group of chemicals that includes several antipsychotic medications.
psychedelic Another name for hallucinogenic drugs. Has a somewhat positive connotation of mind viewing or mind clearing.
phenylpropanolamine (PPA) Until 2000, an active ingredient in OTC weight-control products.
psychoactive A term used to describe drugs that have their principal effect on the CNS.
physical dependence Defined by the presence of a consistent set of symptoms when use of a drug is stopped. These withdrawal symptoms imply that homeostatic mechanisms of the body had made adjustments to counteract the drug’s effects and without the drug the system is thrown out of balance.
psychological dependence Behavioral dependence, indicated by a high rate of drug use, craving for the drug, and a tendency to relapse after stopping use. psychopharmacology Science that studies the behavioral effects of drugs.
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www.mhhe.com/hart13e psychosis A type of mental disorder characterized by a loss of contact with reality and by deterioration in social and intellectual functioning. psychotomimetic Another name for hallucinogenic drugs. Has a negative connotation of mimicking psychosis. Q quid A piece of something to be chewed, such as a wad of chewing tobacco. R receptors Specialized cell structures that recognize and respond to signals from specific chemicals (neurotransmitters or drugs). reinforcement The process of strengthening a behavioral tendency by presenting a stimulus contingent on the behavior. For example, the tendency to obtain and take a drug might be strengthened by the stimulus properties of the drug that occur after it is taken, thus leading to psychological dependence.
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sedative A drug used to relax, tranquilize, or calm a person, reducing stress and excitement. semipermeable Allowing some, but not all, chemicals to pass. serotonin A neurotransmitter found in the raphe nuclei that might be important for impulsivity and depression. shisha Sweetened, flavored tobacco for use in a hooka. side effects Unintended drug effects that accompany the desired therapeutic effect. sidestream smoke Smoke that comes from the ash of a cigarette or cigar. sinsemilla A process for growing marijuana that is especially potent in its psychological effects because of a high THC content; from the Spanish for “without seeds.” smokeless tobacco Various forms of chewing tobacco and snuff. social influence model A prevention model adapted from successful smoking-prevention programs.
reuptake One process by which neurotransmitter chemicals are removed from synapses. The chemical is taken back up into the cell from which it was released.
somatic system The part of the nervous system that controls the voluntary, skeletal muscles, such as the large muscles of the arms and legs.
Reye’s syndrome A rare brain infection that occurs almost exclusively in children and adolescents. There is some evidence that it is more likely to occur in children who have been given aspirin during a bout of flu or chicken pox.
specific effects Those effects of a drug that depend on the amount and type of chemical contained in the drug.
risk factors Behaviors, attitudes, or situations that correlate with, and might indicate the development of, a deviance-prone lifestyle that includes drug or alcohol abuse. Examples are early alcohol intoxification, absence from school, and perceived peer approval of drug use. rock Another street name for crack, a smokable form of cocaine. Rohypnol (flunitrazepam) A benzodiazepine hypnotic; not sold legally in the United States and known as the “date-rape drug.” S safety margin Dose range between an acceptable level of effectiveness and the lowest toxic dose. salicylate A class of chemicals that includes aspirin. schizophrenia A chronic psychotic disorder for which the cause is unknown.
speed A street term used at one time for cocaine, then for injectable amphetamine, and later for all types of amphetamine. Probably shortened from speedball. SSRI Selective serotonin reuptake inhibitor; a class of antidepressants that includes Prozac. stages of change Theoretical description of the cognitive stages through which an addict would go in moving from active use to treatment and abstinence: precontemplation, contemplation, preparation, action, and maintenance. stimulant Any of a group of drugs that has the effect of reversing mental and physical fatigue. subcutaneous Under the skin. A form of injection in which the needle penetrates through the skin (about 3/8 inch) but does not enter a muscle or vein. sympathetic nervous system The branch of the autonomic nervous system that contains norepinephrine as its neurotransmitter and, for example, increases heart rate and blood pressure.
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sympathomimetic Any drug that stimulates the sympathetic branch of the autonomic nervous system—for example, amphetamine. symptom In medical terms, an abnormality that indicates a disease. When applied to abnormal behavior, seems to imply a medical model in which an unseen disease causes the abnormal behavior. synapse The space between neurons. synesthesia A phenomenon in which the different senses become blended or mixed—for example, a sound is “seen.” Might be reported by a person taking hallucinogens.
time course Timing of the onset, duration, and termination of a drug’s effect in the body. tolerance The reduced effectiveness of a drug after repeated administration. toxic Poisonous, dangerous. transporter Mechanism in the nerve terminal membrane responsible for removing neurotransmitter molecules from the synapse by taking them back into the neuron. tricyclics A group of chemicals used in treating depression.
synthesis The formation of a chemical compound. For example, some neurotransmitter chemicals must be synthesized within the neuron by the action of enzymes on precursors.
truth serum Any drugs used to “loosen the tongue,” in association with either psychotherapy or interrogation. Although people might speak more freely after receiving some drugs, there is no guarantee that anything they say is true.
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U
tachyphylaxis A rapid form of tolerance in which a second dose of a drug has a smaller effect than a first dose taken only a short time before.
uptake The process by which a cell expends energy to concentrate certain chemicals within itself. For example, precursor substances to be synthesized into neurotransmitters must be taken up by the neuron.
tar With regard to tobacco, a complex mixture of chemicals found in cigarette smoke. After water, gases, and nicotine are removed from the smoke, the remaining residue is considered to be tar. tardive dyskinesia Movement disorders that appear after several weeks or months of treatment with antipsychotic drugs and that usually become worse if use of the drug is discontinued. temperance With reference to alcohol, temperance originally meant avoiding hard liquor and consuming beer and wine in moderation. Eventually the temperance movement adopted complete abstinence as its goal and prohibition as the means. tetrahydrocannabinol The most active of the many chemicals found in cannabis (marijuana). THC Tetrahydrocannabinol.
V values clarification A type of affective education that avoids reference to drugs but focuses on helping students recognize and express their own feelings and beliefs. W Wernicke-Korsakoff syndrome Chronic mental impairments produced by heavy alcohol use over a long period of time. withdrawal syndrome The set of symptoms that occur reliably when someone stops taking a drug; also called abstinence syndrome.
theobromine A mild stimulant similar to caffeine and found in chocolate; a xanthine.
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theophylline A mild stimulant similar to caffeine and found in tea; a xanthine.
xanthine The chemical class that includes caffeine, theobromine, and theophylline.
therapeutic index (TI) Ratio of the lethal dose to the effective dose for half the animals in an experiment (LD50/ED50).
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Credits Photo Credits Chapter 1 p. 2, Ryan McVay/Getty Images; p. 3L, Emma Lee/Life File/Getty Images; p. 3R, Getty Images; p. 5, Brand X Pictures; p. 11, © The McGraw-Hill Companies, Inc./Gary He, photographer; p. 17, © Brand X Pictures/ PunchStock; p. 19, © BananaStock/PunchStock Chapter 2 p. 25, Brand X Pictures; p. 28, Photodisc Collection/Getty Images; p. 30, © Annie Griffiths Belt/ Corbis; p. 34, McGraw-Hill Companies, Inc./Gary He, photographer; p. 37, © The McGraw-Hill Companies, Inc./Jill Braaten, photographer; p. 40, © Mikael Karlsson Chapter 3 p. 51, National Library of Medicine; p. 54L, Library of Congress Prints and Photographs Division (09335u); p. 54R, Library of Congress Prints and Photographs Division (3C03376U); p. 59, PhotoLink/Getty Images; p. 61, © The McGraw-Hill Companies, Inc./Jill Braaten, photographer; p. 67, © Royalty-Free/Corbis; p. 74, © Thorne Anderson/Corbis Chapter 4 p. 80, Jim Wehtje/Getty Images;
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Index A AA. See Alcoholics Anonymous abortion, spontaneous, 222, 246, 274 abstinence, 430 abstinence violation effect, 226 acamprosate, 435, 436 acetaldehyde, 208, 209 acetaminophen, 295, 298 acetic acid, 208 acetylcholine, 85 pathways, 90 acetylsalicylic acid, 292 acquired immune deficiency syndrome (AIDS), 31 alcohol and, 220 action potential, 84–85 addiction, 6, 34 Check Yourself, 47 heroin, 326 introduction of, 199 addictive personality, 38–39 adenosine, 270 S-adenosyl-L-methionine, 285 ADH. See antidiuretic hormone ADHD. See attention-deficit hyperactivity disorder administration inhalation, 114 injection, 113–114 oral, 111, 113 topical, 114 “Advantages of Substituting the Morphia Habit for the Incurably Alcoholic,” 314 advertising, countering, 417–418 Advisory Committee on Smoking and Health, 238 Afghanistan, 74 agonist, 95 maintenance agents, 435 agoraphobia, 174 agranulocytosis, 179 Agriculture Department, U.S., 56
AIDS. See acquired immune deficiency syndrome Air Surgeons Bulletin, 137 alcohol. See also specific alcoholic beverages absorption, 206 abstinence violation effect and, 226 AIDS and, 220 actions mechanisms of, 209 advertising, 194 as anesthetic, 209 anxiety and, 210 behavioral effects of, 210–216 binge drinking, 205 blackouts from, 215 brain damage and, 218–219 cancer and, 220 cognitive factors regarding, 226 college students and, 206 consumption of, per capita, 198 controlled social drinking of, 430 crime and, 42, 215–216 cultural influence on, 203 death from, 216 dehydrogenase, 208 demonization of, 198 dependence, 39, 40, 222–226, 227 detoxification, 222 disease and, 218, 224 distillation, 193–194, 226 distribution, 206–208 dose-response curves for, 107f driving under influence of, 212–213 Drug Abuse Warning Network and, 28 drug tolerance and, 209 erotic films and, 214, 215 fluid balance and, 216 GABA and, 209 gender and, 205–206, 227 genetics and, 226, 227 as “Good Creature of God,” 198
hallucinations from, 223–224 heart and, 219–220 homicide and, 215 hormonal effects and, 216 immune system and, 220 liver response to, 209 metabolizing, 208–209 minimum age to purchase, 202 morality and, 199 myopia, 211–212, 215, 227 opium v., 310 overdose, 216 penile tumescence and, 214 peripheral circulation and, 216 pharmacology, 206–209 pharmacotherapies for, 435–436 physiological effects of, 216 placebo effects and, 211 poisoning, 216 pregnancy and, 222 problem, 198–203 regulation after 1933, 202 relapse, 224 removal of, 208 sexual assault and, 215 sexual behavior and, 214–215 as social excuse, 226 social stress and, 204–205 suicide and, 216 tax, 201, 202–203 tension and, 204–205 time-out, 211–212 toxicity, 216–221 traffic fatalities involving, 212–213, 227 trends in, 12f trends in, U.S., 203–204, 204f vomiting from, 217 withdrawal syndrome, 222–224 alcohol content, blood (BAC), 206, 207t behavior change and, 210–211, 211t estimating, 208, 227 intake and, 208f
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alcohol effect, fetal, 222 alcohol syndrome, fetal (FAS), 221–222, 223, 227 animal research on, 221 criteria for, 221 diagnosing, 222 gender and, 223 alcoholic dementia, 218 family, 39 hepatitis, 219 personality, 225 Alcoholics Anonymous, 224 Alcoholics Anonymous (AA), 38, 430–432 buddy system, 431 court-ordered referrals to, 431 evaluations of, 431 religion and, 225 twelve step program, 431, 433 aldehyde dehydrogenase, 208 allergy medications, 300 Alpert, Richard, 337–338 dismissal of, 338 alpha-methyltryptamine (AMT), 346 alprazolam, 435 alt.psychoactives newsgroup, 299 Alzheimer’s disease, 90 AMA. See American Medical Association Amanita muscaria, 358–360 Ambien, 162 ambrosia, 358 Amendment, 18th, 200–201 repeal of, 202 Amendment, 21st, 202 American football, 394–395 American Medical Association (AMA), 371 American Psychiatric Association, 36 American Revolution, 263 amino acids, 401 amotivational syndrome, 383 amphetamines, 136–148, 148. See also specific amphetamines absorption, 141 action mechanism of, 141 acute toxicity, 147 in American football, 394–395
appetite-depressant effect of, 137 in athletics, 147, 394 in baseball, 396 beneficial uses of, 141–147 calming effect of, 144 chemical structure of, 140–141 chronic toxicity, 147–148 compulsive/repetitive actions and, 148 concern over, 147–148 dependence potential of, 148 depression and, 141–142 development of, 136–137 early uses for, 136–137 effectiveness of, 397 elimination, 141 euphoria from, 141 history of, 136–140 hyperactive children and, 143–144 in 1960’s, 137–139 legal use of, 143 longterm behavioral consequences of, 147 mood and, 142 Olympics and, 394 paranoid psychosis from, 148 paranoid psychotic reactions to, 137 patent for, 136 pharmacology of, 140–141 tablet, 137 violence and, 147 wartime uses of, 137 weight control and, 142–143 AMT. See alpha-methyltryptamine analgesic-antipyretics, 298 analgesics, 269t, 291–296 ingredients in, 296t anandamide, 374 angel dust, 354 anhedonia, 439 Anheuser-Busch, 195 animal research, 25, 59 benzodiazepine, 164 on beta-2 agonists, 403 on fetal alcohol syndrome, 221 opioid, 322 PCP, 352 on serotonin, 90
animism, 331–332 ANS. See nervous system, autonomic Anslinger, Harry, 63, 75, 369–370 Antabuse, 435 antagonist, 95 opioid, 320 therapy, 435 antianxiety drugs, 173 anticonvulsants, 186 hypnotics as, 163 antidepressants, 105, 173, 180–184 action mechanism of, 184 effectiveness of, 106 lag period, 184 sales of, 182 stimulants and, 117 suicide and, 182 antidiuretic hormone (ADH), 216 Anti-Doping Agency, U.S., 395 Anti-Drug Abuse Acts of 1986/1988, 65–69, 130–131 antihistamine, 290, 298 effectiveness of, 299 antipsychotics, 104, 177–180 action mechanism of, 178–179 agranulocytosis and, 179 allergic reactions to, 179 atypical, 178t conventional, 178t introduction of, 188 long-term effectiveness of, 180 photosensitivity and, 179 side effects of, 179–180 treatment effects of, 178 anxiety, 172 alcohol and, 210 disorders, 173, 174 Aqua-Dots, 169 The Arabian Nights, 369 army LSD research, 337 Artificial Paradises (Baudelaire), 369 As Good as It Gets, 173 aspirin, 291–295 action mechanism of, 294–295 anti-inflammatory properties of, 293 antipyretic properties of, 292–293 bleeding time and, 293
473
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www.mhhe.com/ray13e continued gastrointestinal bleeding and, 294 side effects of, 293 therapeutic dose of, 293 therapeutic use of, 292–293 Assassins, cult of, 371 Association Against Prohibition, 201 ataxia, 107 athletics amphetamines and, 147, 394 banned substances in, 393 caffeine in, 393 cocaine in, 393 historical drug use in, 392–397 international drug testing in, 394 stimulants in, 392–393 atomoxetine, 144 Atropa belladonna, 355 attention-deficit hyperactivity disorder (ADHD), 144 diagnostic criteria for, 145 symptoms of, 146 Avicenna, 309 axon, 83 ayahuasca, 346 B BAC. See alcohol content, blood BALCO Laboratories, 395–396 Balzac, Honoré de, 272 barbital, 154 barbiturates, 153, 154–156. See also specific barbiturates action mechanism, 159 dependence, 156, 163–164 fast-acting, 155 groupings of, 156t short-acting, 155 suicide and, 156 tolerance, 156 basal ganglia, 87 baseball, 396 Baudelaire, Charles, 369 Bayer Laboratories, 291–292 A Beautiful Mind, 173 Bechler, Steve, 282, 398 beer, 194–196 ale, 195 lager, 195 largest selling brands, 195t
© The McGraw−Hill Companies, 2009
INDEX malt liquor, 195 behavior, chemical theories of, 96 belladonna, 355–356, 437 pupil dilation and, 356 Benzedrine, 136 Benzocaine, 290 benzodiazepines, 153, 157–159, 173, 224, 435 animal research and, 164 overdose of, 158 physical dependence of, 158 benzopyrene, 383 beta-2 agonists, 403 Betty Ford Center, 431 Beverly, Robert, 358 bhang, 368 The Bible, 356–357 bipolar disorder, 175 relapses of, 185 Birney’s Catarrh Cure, 53 Biruni, 309 black market steroids, 401 Black Mass, 356 black tar heroin, 318 black tea, 264 blackouts, 215 blockers, 95 starch, 290 blood alcohol content. See alcohol content, blood (BAC) blood proteins, 115 blood-borne diseases, 30–32 blood-brain barrier, 82, 115 in infants, 115 B&M External Remedy, 57 bodybuilding, 404 Bonds, Barry, 395 Boston Tea Party, 263 bourbon, 198 Bourne, Peter, 130 brain alcohol and damage to, 218–219 association areas of, 86 chemical pathways in, 89–91 drugs and, 91–96 major structures of, 86–89, 88f marijuana and damage to, 384 stem, 88 brain-scanning techniques, 38, 96–97 limitations of, 97
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brand names, 102, 119 brandy, 193, 197 Brecher, E.M., 4 British East India Company, 311 bromides, 154 bronchodilation, 375 Buddha, 357 bufotenin, 360 buprenorphine, 438 bupropion, 252, 437 Bureau of International Narcotics and Law Enforcement Affairs, 73 Bureau of Narcotics, 63 Burke, Ken, 127 Bush, George W., 71, 225 C Cade, John, 184 caffeine, 404 action mechanism of, 270 in analgesics, 269t in athletics, 393 behavioral effects of, 272–274 in beverages/food, 266t cancer and, 274 Check Yourself, 277 concern over, 274–275 death from, 275 dependence, 270, 271 in diuretics, 269t headaches and, 272, 273 heart disease and, 274–275 hyperactivity and, 273 panic attacks and, 273 as performance enhancer, 398 pharmacology of, 270–274 physiological effects of, 271–272 reproductive effects and, 274 sobering up with, 274 in soft drinks, 268t in stimulants, 269t time course of, 270 tolerance, 270 caffeinism, 275 calcified lime, 125 calcium acetylhomotaurinate, 435 Camels, 236–237 Caminiti, Ken, 395 camphor, 177 cancan, 259
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cancer, 220 alcohol and, 220 caffeine and, 274 cigarette smoking and, 238 cannabinoids, 373 Cannibas, 365. See also marijuana absorption, 373–374 abuse potential of, 375–376 action mechanism of, 374 active ingredient in, 378 behavioral effects of, 375–378 buyers clubs, 380 distribution, 373–374 elimination, 373–374 history of, 368–373 history of, early, 368–369 in 19th century, 369 medical uses of, 378–381 new science of psychology and, 369 pharmacology of, 373–378 pharmacotherapies, 439 physiological effects of, 374–375 preparations from, 366–368 romantic literature and, 369 Cannibas indica, 366 Cannibas ruderalis, 366 Cannibas sativa, 366 carbamazepine, 60 carbohydrates, 401 Carter, Jimmy, 386 Carter, Rosalynn, 386 cataplexy, 168 catheters, 35 2-CB, 252 CCK. See cholecystokinin “Celebrity Rehab with Dr. Drew,” 431 cell body, 83 Center for Substance Abuse Prevention (CSAP), 421 cereal grains, 193 cerebellum, 374 cerebral atrophy, 384 cerebral cortex, 86 subdivisions of, 87f cerebral trauma, 115 Cerletti, Ugo, 177 champagne, 196 Chantix, 252 charas, 366
Check Yourself addiction, 47 caffeine, 277 consequences, 77 daily mood changes, 189–190 drinking problem, 229 goals/behaviors, 23, 427 hallucinogens, 363 how do drugs work?, 121 memory, 389 natural body cycle, 99 over-the-counter drugs, 303 run the race, 407 sensation-seeking scale, 151 street slang, 329 tobacco awareness, 255 toxicity, 49 Cheek, J. O., 260 Chemical Diversion and Trafficking Act, 67 chemical names, 102 chewing gum, nicotine, 252 chloral hydrate, 154 chlordiazepoxide, 157, 159 chlorpheniramine maleate, 298 chlorpromazine, 177, 350 introduction of, 186 chocolate, 264–266 European introduction of, 265 health warnings, 265 legends surrounding, 264 liquor, 265 milk, 266 preparation of, 265 cholecystokinin (CCK), 290 Chute, Anthony, 233 cigar bars, 243 cigarette smoking, 236–237. See also specific brands in adolescents, 417 advertising of, 238 cancer and, 238 cognitive developmental approach to, 418 current use of, 241 decline in, 253 facial malformations and father’s, 247 filter, 237, 238
hidden costs of, 251 lawsuits regarding, 238–239 low academic performance and, 14 oral gratification from, 250 passive, 244–246 pregnancy and, 246–247 quitting, 251–252 reducing, 416 safer, 240–241 sales of, 239f sidestream smoke from, 245 worldwide, 246 cigars, 236, 242–243 cirrhosis, 219, 220f Civil War, 52 Claviceps purpurea, 333–334 clenbuterol, 403 Clinton, Bill, 12, 13 Clinton, Hilary Rodham, 146 clonidine, 323 clozapine, 179 Le Club de Hachischins, 369 CNS. See nervous system, central coca, 124 paste, 129 wine, 125 Coca-Cola, 125, 266–268 misbranding of, 267 as tonic, 267 trial of, 1911, 267 cocaethylene, 117, 133 cocaine, 54–55, 67, 124–136, 148, 267 absorption, 132 action mechanism of, 132 acute toxicity of, 133 in athletics, 393 beneficial uses of, 132–133 chemical structure of, 132f chronic toxicity of, 133–134 concern for, 133 contemporary legal controls on, 130–132 dangers, 128 dependence potential of, 133–134 early legal controls on, 128–129 early psychiatric uses of, 126–128 elimination of, 132 fame and, 130
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www.mhhe.com/ray13e continued forms of, 129–130 freebasing, 130 friendship and, 135 future of, 135–136 heart muscle and, 133 history of, 124–125 hydrochloride, 129–130 introduction of, 136 as local anesthesia, 125–126, 132–133 media focus on, 130 minimum sentences for, 131 negative publicity for, 129 overuse of, 55 paranoid psychosis from, 133 patterns of use, 135 as performance enhancer, 398 pharmacotherapies, 439 pregnancy and, 134 price of, 74, 135 production of, 135 racial characteristics and, 131t as safe exhilarant, 127 supplies of illicit, 134–135 toxicity, 44 trends in, 12f wealth and, 130 withdrawal symptoms, physical, 134, 439 “Cocaine Lil,” 129 cocoa butter, 265 codeine, 312 antitussive properties of, 322 coffee, 257–261 arabica, 260 commercial roasting of, 260 decaffeinated, 261 economics of, 261 instant, 261 legends surrounding, 257–258 “nerves,” 271 robusta, 260 sexual excitability and, 258 specialty, 259 Cohoba snuff, 345 cold, common, 296–298 treatment of, 298–300 Coleman, Tom, 126 perjury charges, 127 Coleridge, Samuel Taylor, 309 college students
© The McGraw−Hill Companies, 2009
INDEX alcohol and, 206 drug use and, 20 Collier’s, 53 Columbus, Christopher, 232–233 coma, induced, 176 comatose, 107 Communities Mobilizing for Change on Alcohol, 423 Compoz, 290 Comprehensive Drug Abuse Prevention and Control Act of 1970, 64–65 structure of, 64 compulsive behavior, 37 “The Confessions of an English Opium-Eater” (De Quincey), 309–310 congeners, 198, 217 conservatism, 384 Conte, Victor, 395 contingency management, 433–434 “continuum of care,” 412 Controlled Substances Act, 65, 75 Corona, 196 coronaviruses, 297 cotinine, 417 cough suppressants, opioid, 322 Council for Tobacco Research, 238, 243 The Count of Monte Cristo (Dumas), 369 crack, 67, 130 baby, 134 dependence, 66 minimum sentences for, 131 Craig, Elijah, 197 crank, 139 creatine, 403 creativity, 341, 342 crime, 26, 40–43, 44 alcohol and, 42, 215–216 “criminal type,” 41 crystal meth, 139 CSAP. See Center for Substance Abuse Prevention Csikszentmihalyi, Mihaly, 359 2-C-T7, 352 Cuforhedake Brane-Fude, 57 cumulative effects, 111 cyclazocine, 355 Cylert, 145–146
471
D DARE. See Drug Abuse Resistance Education Daruma, 261 date-rape drugs, 67, 159, 160, 168 datura, 357–358 DAWN. See Drug Abuse Warning Network De Quincey, Thomas, 309–310 DEA. See Drug Enforcement Agency deactivation, 116–118, 120 death, 28–29, 29t alcohol related, 216 caffeine related, 275 heroin related, 315 nicotine, 248 tobacco related, 244f death penalty, 63 delirium tremens, 223 Delphi, temple at, 357 delta-9-tetrahydrocannabinol (THC), 71, 366 dendrites, 83 denial, 432 dependence, 6, 26, 32–36, 44 alcohol, 39, 40, 222–226, 227 amphetamine, 148 behavioral, 33–34 biological, 38 biopsychosocial perspective on, 40 caffeine, 270, 271 changing views of, 34–35 cocaine, 133–134 crack, 66 diagnostic criteria for, 36, 432 disease and, 40 family and, 39–40 marijuana, 381–382 medical models for, 34–35 medications used to treat, 440 nicotine, 249–251 potential, 37, 38t as spiritual disorder, 440 Valium, 164 views of, 37–40 dependence, physical, 33, 35–36 barbiturate, 156 opioid, 322–324
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dependence, psychological, 33–34, 35–36 barbiturate, 156, 163–164 benzodiazepine, 158 Librium, 163 opioid, 323–324 Valium, 163 Xanax, 164 depersonalization, 341 depressants, 103–104, 153, 169. See also specific depressants overdose of, 169 stimulants and, 117 depression, 175 Dexatrim, 289 Dexedrine, 141 dextromethorphan (DM), 298, 354 abuse of, 299 diacetylmorphine, 312 diagnosis, 171 diazepam, 158, 159, 223 Dickens, Charles, 296 Dietary Supplement Health and Education Act (DSHEA), 60, 281–282 dietary supplements, 60–61. See also specific dietary supplements dangerous, 283–284t health claims of, 281 diethylene glycol, 58 Dilaudid, 439 dimethyltryptamine (DMT), 345–346 Dionysius, 358 disease, 172 alcohol and, 218, 224 dependence and, 40 distilled spirits, 197–198 disulfiram, 435 diterpines, 275 diuretics, 269t DM. See dextromethorphan DMT. See dimethyltryptamine Dolophine, 438 DOM, 350 The Doors of Perception (Huxley), 349 dopamine, 38, 89–90, 92f precursor, 89
dose-response curve, 106 for alcohol, 107f dose-response relationships, 106–109 double-blind procedure, 106 dronabinol, 71, 379, 440 drug combinations, 29 czar, 69 du jour, 4 illicit, 6 law violations, 43, 44 misuse, 6 Drug Abuse Control Amendments of 1965, 64 Drug Abuse Resistance Education (DARE), 418–420 acceptance of, 419 additional programs, 420 beginnings of, 418–419 components of, 419 ineffectiveness of, 420 studies on, 419–420 Drug Abuse Warning Network (DAWN), 27, 30 alcohol and, 28 heroin in, 30 Drug Enforcement Agency (DEA), 64 drug use alternatives to, 415 antecedents of, 16–18 characteristics of, 32 college students and, 20 concern for, 3 correlates of, 13–20 dangers of, 29–30 deviant, 6, 20 education level and, 14–15 experimenting with, 414 extent of, 8–9 flagged, 414 gender and, 14–15 influences on, 20f initiation of, later, 16 knowledge, 413 models for, 19 motives for, 3, 18–20, 21 positive attitude towards, 413 prevention, 18, 411 progression of, 21
protective factors, 13–14 punitive approach to, 416 race and, 14–15 rate of, 21 reducing, 424 religion and, 14 risk factor, 13–14 social decisions about, 411 stereotypes, 15 trends in, 7, 9–13 trends in, social, 13 Drug-Induced Rape Prevention and Punishment Act, 160 drugs, over-the-counter (OTC), 286 Check Yourself, 303 choosing, 300–301 examples of, 288–291 ingredients in, 300t label standards for, 287 number of, 287 prescription drugs v., 287–288 regulation of, 286–287 sedative, 290–291 sleep aid, 290–291 stimulant, 288–289 weight-control, 289–290 drugs, prescription, 29 effectiveness of, 58–59 “free trial” offers of, 162 marketing new, 59–60 media coverage of, 53 off-label, 60 opioid, 318–319 over-the-counter drugs v., 287–288 preclinical investigations of, 59–60 purity of, 56–58 regulation of, 56–61 rules for, 57 safety of, 58 DSHEA. See Dietary Supplement Health and Education Act Dumas, Alexander, 369 Dutch East India Company, 262 E Ebers papyrus, 307 Eclipse, 241 economies, 7 Ecstasy. See MDMA
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www.mhhe.com/ray13e ECT. See electroconvulsive therapy ED. See effective dose Edgewood Arsenal, 337 Edison, Thomas, 236 education, 411 affective, 414–415 drug use and level of, 14–15 normative, 418 effective dose (ED), 108 electroconvulsive therapy (ECT), 177, 184 Elixir Sulfanilamide, 58 Ellis, Havelock, 349 emergency room, visits to, 27–28, 29t emphysema, 251 endorphins, 91, 320 energy drinks, 268–269 hype surrounding, 269 English East India Company, 262 enkephalins, 320–321 entactogens, 332 entheogens, 332 enzymes, 92 action of, 93f CYP450, 117, 118, 155 metabolic, 94f Enzyte, 285 ephedra, 61, 136, 282, 289, 404 ephedrine, 136, 141 as performance enhancer, 398 epilepsies, 163 E.R., 412 ergogenics, 394 ergotism, 334 erotic films, 214, 215 eszopiclone, 162 evil spirits, 7 Excedrin, 269, 273 F facial malformations, 247 fats, 401 burning, 404 fatty liver, 219 FDA. See Food and Drug Administration fear, 31 fentanyl, 319 fermentation, 192, 226 fetal alcohol syndrome. See alcohol syndrome, fetal (FAS)
© The McGraw−Hill Companies, 2009
INDEX fever, 300 “fight or flight” response, 86 Financial Crimes Enforcement Network, 73 flashbacks, 342 flow, 359 flowering orange pekoe tea, 263 flunitrazepam, 159 fluoxetine, 182, 188 fly agaric, 358–360 flying ointments, 356 Food and Drug Administration (FDA), 57 “Adverse Events Reporting” process of, 282 “Good Manufacturing Practices” regulations of, 282 Modernization Act, 60 Food, Drug and Cosmetic Act, 280, 287 foxy methoxy, 346, 352 freebasing cocaine, 130 Freud, Sigmund, 126–128, 130 G GABA, 90, 98, 119, 159 alcohol and, 209 subtypes, 93 Galen, 161, 307–308 gamma hydroxybutyrate (GHB), 155, 168–169 recreational dose of, 168 structure of, 168 gangrene, 334 ganja, 367 gaseous anesthetics, 166–167 gateway substances, 17–18, 21 interpretation of, 17 gender alcohol and, 205–206, 227 drug use and, 14–15 fetal alcohol syndrome and, 223 generalized anxiety disorder, 174 “generally recognized as effective” (GRAE), 287 “generally recognized as honestly labeled” (GRAHL), 287 “generally recognized as safe” (GRAS), 287
473
generic names, 102 genetics, 16 GHB. See gamma hydroxybutyrate gin, 197 ginkgo biloba, 286 glial cells, 81–82 glue-sniffing, 167 glutamate, 90–91 goals, 410–411 “Good Friday Experiment,” 344 GRAE. See “generally recognized as effective” GRAHL. See “generally recognized as honestly labeled” grain neutral spirits, 197 grapefruit-juice, 103 GRAS. See “generally recognized as safe” green tea, 263 Griffiths, Roland, 344, 345 H habituation, 32 Hague Conference, 1912, 56 Haight-Ashbury district, 138 Halcion, 162 Haldol, 95, 104 Hallucinogen Persisting Perception Disorder, 342 hallucinogen research, government funding of, 345 hallucinogens, 104. See also specific hallucinogens amphetamine derivatives of, 350–352 anticholinergic, 355–360 Check Yourself, 363 deliriants, 352–355 hallucinogens, catechol, 346–352 structure of, 347f hallucinogens, indole, 333–346 structures of, 334f haloperidol, 95, 104 Halsted, W. S., 126 handwashing, 297 hangover, 217–218 products to prevent, 218 harmaline, 346 Harrison Act of 1914, 55–56, 61–63, 75, 129 Boggs amendment to, 63
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continued opioid abuse after, 314–318 opioid abuse before, 313–318 hash oil, 368 hashish, 366, 368 hashishiyya, 368 Hawaiian baby woodroses, 344 Hazelden, 4319 HDL. See high-density lipoproteins head shops, 68–69 headaches, 272, 273 The Health Consequences of Using Smokeless Tobacco, 242 heart muscle alcohol and, 219 cocaine and, 133 Heffter, Arthur, 348–349 Heineken, 196 henbane, 357 hepatitis B, 31 hepatitis C, 31 herbal tea, 264 Herbert, Bob, 126, 127 heroin, 312–313 abuse patterns with, 325–326 addiction, 326 banging, 325 black tar, 318 chippers, 326 cost of, 316, 318 currents use of, 318 death penalty and, 63 deaths, 315 in Drug Abuse Warning Network, 30 epidemics, 308 “French connection” for, 317 injection, 325 maturing out of, 326 Mexican brown, 318 misconceptions about, 326 overdose, 325 preconceptions about, 326 prohibition of, 41 purity of, 316, 318 smoking, 318 street slang, 329 toxicity, 44 variability of, 325 withdrawal symptoms of, 33, 326 Hicks, Thomas, 392 hidden messages, 417
high-density lipoproteins (HDL), 220 hippocampus, 374 Hippocrates, 96 The History and Present State of Virginia (Beverly), 357 “hitting bottom,” 432 HIV. See human immunodeficiency virus Hoa-tho, 378 Hoffman, Albert, 335–336, 360 Holmes, Sherlock, 128 Homeland Security, 67 homeostasis, 81 Homer, 307 homicide, 215 hookahs, 243 Hoover, J. Edgar, 63 hops, 194 hormones, 97 Hornbeck, Mark, 367 horny goat weed, 285 Hostetter’s Bitters, 53 Hotel Pimodan, 369 “How to Create a Nationwide Drug Epidemic” (Brecher), 4 HR 613, 210 Huckleberry Finn, 223–224 human growth hormone, 402 human immunodeficiency virus (HIV), 31, 32 humors, four, 96 Huxley, Aldous, 349 hydrocodone, 318 hydromorphone, 439 hypnotic drug therapy, 161 hypnotics, 153. See also specific hypnotics abuse patterns, 165 as anticonvulsants, 163 as anxiolytics, 160–161 beneficial uses of, 160–163 concern over, 163–165 nonbenzodiazepine, 159 toxicity of, 164–165 withdrawal, 164 hypothalamus, 88 I “I Get a Kick Out of You,” 129 ibotenic acid, 360
ibuprofen, 296 ice, 139 identification, 105, 119 impulsivity, 15, 39 IND. See “Notice of Claimed Investigational Exemption for a New Drug” inhalants, 153, 165–168, 413 examples of, 166 Inhalants: Kids in Danger, Adults in the Dark, 413 inhaler, nicotine, 252 injection heroin, 325 intramuscular, 113–114 intravenous, 113 subcutaneous, 113–114 “An Inquiry into the Effects of Ardent Spirits on the Mind and Body” (Rush), 199 insomnia, 161, 163 insulin, 176 intestinal disorders, 321 “Intoxicating Preparations Made with Cannabis,” 378 iron supplements, 401 J James, William, 349 Jamestown weed, 357–358 jaundice, 219 de Jerez, Rodrigo, 233 jimsonweed, 357–358 Johnson, Alan, 367 Johnson, Gary, 367 Jolt cola, 268 Jones-Miller Act, 62 The Jungle (Sinclair), 55 “Just Say No,” 12 K Kaldi, 258 Kefauver, Estes, 58 Kefauver-Harris amendments, 58–59, 286 Ketalar, 353 ketamine hydrochloride, 353 King, Rodney, 355 knockout drops, 154 Korsakoff’s psychosis, 218 “Kubla Khan” (Coleridge), 309
479
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www.mhhe.com/ray13e L labeling, 280 standards, 287 Laborit, Henri, 177 LaGuardia, Fiorello, 372 LaGuardia Report, 372 laissez-faire, 26, 52 The Lancet, 234 laudanum, 309 laughing gas, 166 LD. See lethal dose League of Spiritual Discovery, 338 Leary, Timothy, 337–338, 339, 373 arrest of, 338 dismissal of, 338 lethal dose (LD), 108 of nicotine, 248 leukoplakia, 242 Librium, 157–158 dependence, 163 Life Skills Training, 421 Liggett, 240–241 limbic system, 88 Linnaeus, 233 lipid solubility, 111 lipophilic molecules, 82 Lipton, Thomas, 264 liqueurs, 198 The Literary Digest, 370 lithium, 184–186, 188 limitations of, 185 noncompliance rate for, 185 liver cirrhosis, 219, 220f disorders, 219 fatty, 219 response to alcohol, 209 Lloyd, Edward, 259 Lloyds of London, 259 loose-leaf tobacco, 242 Louisiana Purchase Exposition, 264 lovastatin, 282–283 lozenges, nicotine, 252 LSD. See d-lysergic acid diethylamide “The LSD Controversy,” 341 Lunesta, 162 d-lysergic acid diethylamide (LSD), 333–344 absorption, 339
© The McGraw−Hill Companies, 2009
INDEX adverse reactions to, 341 army research with, 337 behavioral effects of, 339 beliefs about, 342–343 Central Intelligence Agency research with, 337 creativity and, 341, 342 depersonalization with, 341 discovery of, 335–337 early research, 335–337 emotions and, 340 experience, 340–341 flashbacks, 342 initial effects of, 340–341 large-scale production of, 337 panic reactions to, 342 peak of, 338–339 pharmacology, 339 in psychotherapy, 336 recreational use of, 337–339 therapeutic uses of, 336, 342–343 tolerance, 339 lysergsaurediethylamid, 335 M ma huang, 136, 289 Macbeth (Shakespeare), 160, 214 magnetic resonance imaging (MRI), 97 malaria therapy, 176 male enhancement, natural, 285 malt, 193 mandrake, 356–357 MAO. See monoamine oxidase inhibitors Mariani, Angelo, 125 marijuana, 5, 105, 365. See also Cannibas abuse, 381–382 academic performance and, 14f acute physiological effects of, 382 American society and, 384–386 amotivational syndrome and, 383 availability of, 9–10 blood pressure and, 375 brain damage and, 384 chronic lung exposure to, 382–383
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cognitive processing and, 377 concentration and, 377 concern over, 381–384 cost of, 372 decriminalizing, 385–386 dependence, 381–382 driving ability and, 382 emotions and, 384 epidemiological studies on, 382 heart rate and, 375f high school seniors and, 385 immune system and, 383 inhibitory control and, 377 insanity and, 384 laboratory studies on, 382 memory and, 377 panic reactions to, 382 placebos and, 377 protective factors, 14f “pyramid of prejudice” towards, 371 reproductive effects of, 383 risk, 10, 14f spread of, 385 trends, 9–12, 10f, 12f use by age, 11f violence and, 371 visuospatial processing and, 377 withdrawal, 381–382 zero tolerance seizures and, 386 marijuana, medicinal, 69, 378–381 compassionate use of, 381 media on, 367 Marijuana Tax Act, 63, 371–373, 378 Marinol, 379 Maxwell House, 260 MBD. See minimal brain dysfunction McCarthy, Joseph, 63 MDA, 350 MDMA, 350–352, 359 studies on, 351 de Medici, Catherine, 233 medicine chest, 290 “The Men’s Answer to the Women’s Petition Against Coffee,” 258
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mental disorders, 171–175 classification of, 172–175 diagnosis of, 188 medical model of, 171–172 in movies, 173 treatment of, 175–186 treatment of, before 1950, 175–177 treatment of, consequences of, 186–187 mental hospitals indefinite commitment to, 187 movement out of, 187 patients in, number of, 186f meprobamate, 156–157 Merchandise No. 5, 266–268 “Mescal: A Study of a Divine Plant” (Ellis), 349 mescal beans, 347–348 mescal buttons, 346–347 mescaline, 336, 346–350 discovery of, 348–349 early research on, 348–349 pharmacology of, 349–350 synthesizing, 349 mesolimbic dopamine pathway, 89 metabolic syndrome, 180 metabolite, 116 active, 118 methadone, 322, 430, 435, 438 methamphetamines, 82, 138, 139–140, 288 in community, 8 memory deficits and, 82 stovetop laboratories for, 139 treatment for, 140 methapyrilene, 290 methaqualone, 157 5-methoxy DIPT, 346 methyl donor, 285 methylene chloride, 261 methylphenidate, 144 methylxanthines, 270 Metrazol, 177 Mexican brown, 318 Mickey Finn, 154, 159 microbreweries, 195 Miles Nervine, 290 minerals, 401 minimal brain dysfunction (MBD), 144
misbranding, 55 of Coca-Cola, 267 miscarriage. See abortion, spontaneous Mitchell, Weir, 349 modafinil, 143, 439 moist snuff tobacco, 242 Monitoring the Future Project, 9, 135 monoamine oxidase inhibitors (MAO), 180–181, 250, 346 examples of, 181t limitations of, 181 monoamine theory of mood, 96 Montezuma, 264–265 mood disorder, 174–175 diagnosis of, 176 mood stabilizers, 184–186 moonwalking, 354 Moore, Joe, 126 morality, 199 morning glories, 344 Morpheus, 312 morphine, 311–312 commercial production of, 52 medical value of, 312 Morris, Philip, 236 motivational enhancement therapy, 432–433 action stage, 433 contemplation stage, 433 maintenance stage, 433 motivational interviewing, 432 precontemplation stage, 433 motor cortex, 86 Mountain Dew, 268 movies mental disorders in, 173 tobacco in, 234 Multidisciplinary Association for Psychedelic Studies, 337 “munchies,” 377 muscarine, 359 muscimol, 360 N nalorphine, 320 naloxone, 315, 320, 324 naltrexone, 320, 435, 439 development of, 436 Narcan, 324
narcolepsy, 137, 143, 168 narcosis therapy, 176 Narcotic Control Act of 1956, 63 narcotic farms, 63 Narcotics Division, 61 National Drug Control Policy, Office of, 69 National Drug Control Strategy, 73 The National Formulary, 57 National Organization for the Reform of Marijuana Laws (NORML), 385 National Prohibition Party, 200 National Survey on Drug Use and Health, 11, 135 Native American Church, 348 natural highs, 415 NDA. See new drug application needle exchange programs, 31 freaks, 324 habit, 324 sharing, 31–32 nerve cells, 81–82 nervous system, 81–83 somatic, 85 nervous system, autonomic (ANS), 85–86, 98 parasympathetic, 86 sympathetic, 86 nervous system, central (CNS), 86 overexcitement of, 119 Nestlé, 266 neuroleptic, 177 neurons, 83, 116 depolarized, 85 hyperpolarized, 85 regions of, 83f neurotransmission, 83–85 neurotransmitters, 84, 97–98 availability of, 116 lifecycle of, 91–94, 98 monoamine, 96 release of, 94f new drug application (NDA), 58 New England Journal of Medicine, 53 new science of psychology, 369 The New York Times, 351 “Negro Cocaine ‘Fiends’ are a New Southern Menace,” 129
481
482
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Index
www.mhhe.com/ray13e “This Is Your Brain on Meth: A ‘Forest Fire’ of Damage,” 82 Nicot, Jean, 233 Nicotiana rustica, 234 Nicotiana tobacum, 234 nicotine, 105 absorption, 248 behavioral effects of, 249 chewing gum, 252 deactivation of, 248 death from, 248 dependence, 249–251 inhaler, 252 lethal dose of, 248 lozenges, 252 metabolizing, 248 pharmacology of, 247–251 pharmacotherapies, 436–437 physiological effects of, 248–249 poisoning, 248 reinforcement properties of, 250, 252 replacement therapy, 252, 436 skin patches, 252 structure of, 247f nigrostriatal dopamine pathway, 89, 98 nitrites, 167 nitrous oxide, 166, 354 traveling demonstrations of, 167 NoDoz, 269, 288 Nonprescription Drug Advisory Committee, 288 nonspecific effects, 105–106 nonsteroidal anti-inflammatory drugs (NSAIDs), 296 norepinephrine, 86, 92f, 94 pathways, 90 NORML. See National Organization for the Reform of Marijuana Laws “Notice of Claimed Investigational Exemption for a New Drug” (IND), 59 Novocaine, 133 NSAIDs. See nonsteroidal anti-inflammatory drugs nucleus accumbens, 89, 374 Nutt, Levi G., 62 Nytol, 290
© The McGraw−Hill Companies, 2009
INDEX O obsessive-compulsive disorder, 174 Odyssey (Homer), 307 Olson, Frank, 337 Olympics, 393 amphetamines in, 394 Omnibus Crime Control Act, 402 “On the Preparations of the Indian Hemp, or Gunjah,” 378 One Flew over the Cuckoo’s Nest, 173 oolong tea, 264 Operation Golden Flow, 317 opioid detoxification, rapid, 437 opioids, 104. See also specific opioids action mechanism of, 320–321 animal research on, 322 antagonists, 320 beneficial uses of, 321–322 chemical characteristics of, 319–320 concern over, 322–326 as cough suppressants, 322 cross-tolerance, 322 dependence, 322–324 before Harrison Act, 313–314 history of, 307–319 intestinal disorders and, 321 negative reinforcement of, 324 in 1980s, 317–318 in 1970s, 317–318 in 1960s, 316 pain relief from, 321 pharmacology of, 319–321 pharmacotherapies, 437–438 positive reinforcement of, 323 prescription, 318–319 prohibition, 62 tolerance, 322 toxicity of, 324–325 triad, 324–325 Vietnam War and, 316–317 withdrawal symptoms, 323t opium, 52, 307–311 alcohol v., 310 early history of, 307–309 in Greek medicine, 307–308 harvesting, 307 narcotic agents from, 319f
477
production of, increase in, 74 San Francisco ordinance on, 54 smuggling, 310–311 writers and, 309 Opium Wars, 53–54, 262, 310–311 orange pekoe tea, 263 Orlistat, 289 Orphan Drug Act, 60 Osler, William, 378 OTC. See drugs, over-the-counter outcomes, evaluating, 410–411 overdose alcohol, 216 benzodiazepine, 158 depressant, 169 heroin, 325 Oxford Group, 225 OxyContin, 318–319 P Pahnke, Walter, 344 pain, 291, 321 Pall Mall, 237 panic attacks caffeine and, 273 d-lysergic acid diethylamide and, 342 panic disorder, 174 Paracelsus, 309 paraldehyde, 154 paraphernalia, 68–69 Internet and, 69 prohibition of, 69 parent support groups, 422 parenting skills, 422 Parke-Davis Pharmaceutical Company, 128, 353 Parkinson’s disease, 87, 89, 95, 178, 434 patent medicines, 53, 54 patient, 171 PCP. See phenylcyclohexyl piperidine hydrochloride PDR. See Physician’s Desk Reference “Peace Pill,” 354 peer influence, 421 peer participation, 422 peer programs, 421–422 pekoe tea, 263
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INDEX
Pemberton, J. C., 266 penile tumescence, 214 pentylenetetrazol, 177 People for the Ethical Treatment of Animals (PETA), 108 Perry, Rick, 127 personal skills, 415 personality disorders, 16, 39 personality variables, 15–16 PET. See positron emission tomography PETA. See People for the Ethical Treatment of Animals peyote, 346–350 as sacrament, 348 phantastica, 332 pharm parties, 27 pharmaceuticals. See drugs, prescription pharmacist(s) arrest of, 62 recommendations, 292 Pharmacology and Therapeutics, 313 pharmacotherapies, 434–440 alcohol, 435–436 Cannibas, 439 cocaine, 438–439 detoxification phase, 434–435 maintenance phase, 434–435 nicotine, 436–437 opioid, 437–438 phenacetin, 295 phenobarbital, 159 phenothiazines, 177, 178 phenylcyclohexyl piperidine hydrochloride (PCP), 352–353 as anesthetic, 353 animal research on, 352 folklore, 354–355 as “Peace Pill,” 354 recreational use of, 354–355 violence and, 354 phenylephrine, 288 phenylpropanolamine (PPA), 289 phenytoin, 378 Philip Morris, 250 Phoenix House, 431 photosensitivity, 179
Physician’s Desk Reference (PDR), 105 pipe dreams, 324 pituitary gland, 402 placebo, 105–106 alcohol and, 211 marijuana, 377 response, 106 steroids as, 400 plasma proteins, 115 Playboy Foundation, 385 Pliny, 357 poison arrow frogs, 248 poisoning alcohol, 216 nicotine, 248 Polo, Marco, 368 poppers, 167 Popular Science Monthly, 370, 371 Porter, Cole, 129 positron emission tomography (PET), 96–97, 97f post traumatic stress disorder, 174 postsynaptic cell, 93 potency, 109–110, 119 PPA. See phenylpropanolamine precursors, 67–68 dopamine, 89 uptake of, 91 pregnancy alcohol and, 222 cigarette smoking and, 246 cocaine and, 134 prevention programs and, 423 Premier, 241 Prescription Drug Marketing Act of 1988, 60 prescription drugs. See drugs, prescription pressure resistance, 415–416 presynaptic terminals, 83 prevention community programs for, 423–424 effectiveness of, 414 extracurricular approaches to, 422 family interaction approaches, 422 indicated, 412
informational programs for, 422 jealousy and, 423 knowledge-attitudes-behavior model of, 412–414 mistrust, 423 model programs, 421 parent support groups for, 422 parent/family programs for, 422–423 parenting skills and, 422 peer influence on, 421 peer participation in, 422 peer programs, 421–422 pregnancy and programs for, 423 primary, 411 prime-time programming, 412 programs that work, 420–421 relapse, 434 review of, 415–417 scare stories, 424 in schools, 412–421 secondary, 411–412 selective, 412 social influence model of, 417–418 teen leaders, 418, 419 tertiary, 412 types of, 411–412 universal, 412 value-free, 414–415 in workplace, 424 priest, 7 principles of psychoactive drugs, 4–5 prison Americans in, 68 costs, 73 treatment v., 62–63 problem behaviors, 14 procaine, 133 prodrugs, 118 Prohibition, 194, 195, 198, 200–202, 227 failure of, 201 as “noble experiment,” 201 Project ALERT, 420 proof, 194 propaganda, 411 Proposition 36, 65 prostaglandins, 294
483
484
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www.mhhe.com/ray13e Provigil, 143 Prozac, 90, 182, 188 pseudoephedrine, 288, 298 pseudoparkinsonism, 178–179, 180 psilocin, 344 psilocybe cubensis, 343 psilocybe mexicana, 343 psilocybin, 343–344 mystical experience and, 344 psychedelic, 332 “psychedelic 60s,” 333, 373 psychologist, 5, 183 Psychopharmacology, 345 psychosis, 173 functional, 174 organic, 174 psychotomimetics, 332 public commitment, 417, 419 punishment therapy, 435 Pure Food and Drugs Act, 1906, 55, 75, 314 pyschotherapeutic drugs, 104 Q Quaalude, 157 Quetzalcoatl, 264 Quiet World, 290 R race relations, 52 Raich, Angel, 380 Raich v Ashcroft, 380 Randall, Robert, 379 raves, 359 Reader’s Digest, 238 Reagan, Ronald, 12 receptors, 83, 93, 98, 116 blocking, 95 drug effects on, 95 Red Bull, 268–269 red yeast rice, 282–283 Reefer Madness, 41 reformism, 52 refusal skills, 415–416, 419 training, 417 regulation, 43 of alcohol after 1933, 202 local, 69 of over-the-counter drugs, 286–287
© The McGraw−Hill Companies, 2009
INDEX of prescription drugs, 56–61 state, 69 steroids, 400–402 tobacco, 238, 240 Reid, Samantha, 155 reinforcement, 19, 34, 36 negative, 324 nicotine and, 250, 252 opioid, 323–324 positive, 35 relapse alcohol, 224 prevention, 434 relaxation, 165 religion, 225 drug use and, 14 respiratory depression, 117 resting potential, 84 Reye’s syndrome, 294 Reynolds, 241 rhinoviruses, 297 Ricaurte, George, 351 Richardson, Benjamin, 154 Rig Veda, 358 rimonabant, 374 Ritalin, 144, 146 misuse of, 146 Robinson, F. M., 266 Robitussin, 299 rohypnol, 159, 160 Rolfe, John, 234 romantic literature, 369 Roosevelt, Theodore, 55 Rush, Benjamin, 199 rye whiskey, 198 S safety margin, 109 Saint Anthony’s Fire, 334–335 Saint John’s wort, 118, 279–280, 284–285 effectiveness of, 284–285 prescription drugs and, interactions with, 285 uses of, 284 Sakel, Manfred, 176 Salem witch trials, 335 salicylic acid, 291 salon.com, 412 salt-substitute poisonings, 185 salvia divinorum, 360
479
Samantha Reid Foundation, 155 SAMHSA. See Substance Abuse and Mental Health Services Administration San Pedro cactus, 348 Sandoz Pharmaceutical Company, 336 scare stories, 424 scheduling, 64, 66–67, 69 summary, 66t schizophrenia, 89, 174, 185 diagnosis of, 175 negative symptoms of, 179 positive symptoms of, 179 schools drug-free, 416–417 prevention in, 412–421 store in, 415 Scientific America, 370 scopolamine, 290 Seagram, 194 secobarbital, 158 sedatives, 153 over-the-counter, 290–291 selective reuptake inhibitors, 182–184 examples of, 181t selective serotonin and norepinephrine reuptake inhibitors (SSNRIs), 182 selective serotonin reuptake inhibitors (SSRIs), 182 self-esteem building, 419 “sensation seeking,” 39 sentencing, 67 minimum, 131 Sentencing Commission, U.S., 131 Sernyl, 352 Sernylan, 353 serotonin, 88 animal research and, 90 pathways, 90 reuptake inhibitors, 90 Sertürner, Frederich, 312 sexual assault, 215 sexual behavior, 214–215 sexual excitability, 258 Shafer, Jack, 27 Shakespeare, William, 160, 214 shaman, 7, 332
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INDEX
Shen Nung, 368, 378 Sherley amendment, 1912, 57 sherry, 197 shisha, 243 Shiva, 357 ShowerShock, 272 Sibutramine, 90 side effects, 109 antipsychotics, 179–180 aspirin, 293 SIDS. See sudden infant death syndrome Simpson, Tommy, 394 Sinclair, Upton, 55 sinsemilla, 368 sinus medications, 300 skin patches, nicotine, 252 skin popping, 114, 325 skydiving, 416 Slate, 27 Sleep-Eze, 290 sleeping pills, 138, 142, 161–162 over-the-counter, 290–291 smart pills, 145–147 The Snake Pit, 173 snuff, 233, 235 moist, 242 social failure, 415 social phobia, 174 social skills, 415 society, drug-free, 5 sodium bicarbonate, 401 soft drinks, 266–268 caffeine in, 268t Solanaceae, 355 Soma, 358 Sominex, 290 Sopor, 157 Special K, 353 specific phobia, 174 speed, 138 speedball, 129 SSNRIs. See selective serotonin and norepinephrine reuptake inhibitors SSRIs. See selective serotonin reuptake inhibitors stacking steroids, 399 Stallone, Sylvester, 402 Stamp Act of 1765, 263 Starbucks, 259
stereotypes, 15 steroids, 395 adverse effects on body, 400 anabolic, 394, 399 androgenic effects of, 399 black market, 401 entertainers and, 402 placebo effect of, 400 psychological effects of, 400 regulation, 400–402 research on, 399 stacking, 399 violence and, 400 Stewart, Larry, 127 Stickelmaier, Kate, 367 stimulants, 103. See also specific stimulants antidepressants and, 117 in athletics, 392–393 caffeine in, 269t depressants and, 117 molecular structures of, 140f over-the-counter, 288–289 as performance enhancers, 397–399 Stone, Edward, 291 STP, 350 Strattera, 144 Strengthening Families program, 422–423 strychnine, 392 subculture, deviant, 19 Substance Abuse and Mental Health Services Administration (SAMHSA), 299, 441 Sudafed, 288 sudden infant death syndrome (SIDS), 246 increased risk of, 247 suicide alcohol and, 216 antidepressants and, 182 barbiturates and, 156 methaqualone and, 157 “Suicide Tuesday,” 352 sulfa drugs, 58 Sullivan, John L., 236 Sunday, Billy, 201 Swarbick, Jack, 393 Sydenham, Thomas, 309 sympathomimetic, 136
nasal decongestants, 298 symptoms, 171 synapse, 92 synesthesia, 340 synthesis, 92 T tar, 240 tardive dyskinesia, 179–180 Task Force on Drug Abuse, 316 taurine, 269 Taylor, William, 400 tea, 261–264 bag, 264 black, 264 European record of, 262 fermentation of, 263 flavored, 264 flowering orange pekoe, 263 green, 263 herbal, 264 legends surrounding, 261 as medicinal plant, 262 oolong, 264 orange pekoe, 263 pekoe, 263 smuggling, 263 tax, 262, 263 Technique, 393 temperance movement, 199 teonanacatl, 343 testing, drug in athletics, 394 battles over, 396–397 false-positive results for, 72 federal employees, 70 federal support for, 70–72 hair, 72 methods, 71–72 military and, 70 private employers, 70 public schools, 70–71 transportation workers, 70 testosterone, 395 tetracycline, 113 tetrahydrogestrinone (THG), 395 thalidomide, 58 testing, 108 Thank You For Smoking, 234 THC. See delta-9-tetrahydrocannabinol
485
486
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www.mhhe.com/ray13e Theobroma, 264 Theobroma cacao, 265 theobromine, 266, 270 theophylline, 264, 270 therapeutic index (TI), 108 Theresa, Maria, 265 THG. See tetrahydrogestrinone thiamine, 218 ThinkGeek.com, 272 threshold, 106 TI. See therapeutic index time course, 110 time dependent factors, 110–111 tobacco attacking, 237–243 Check Yourself, 255 Chinese introduction to, 310 concern over, 243–247 deaths, 244f in early America, 235 early medical uses of, 233–234 European introduction of, 233, 252 health effects of, 243–244 history, 232–237 in movies, 234 nitrosamines, 242 as painkiller, 248 regulation of, 238, 240 shisha, 243 spread of, 234–235 surgeon general’s report on, 250 women and, 237 tobacco, chewing, 235–236, 241–242 advantages of, 242 loose-leaf, 242 moist snuff, 242 quid of, 242 tolerance, 33, 118, 120 barbiturate, 156 behavioral, 118–119 caffeine, 270 drug disposition, 118 LSD, 339 opioid, 322 pharmacodynamic, 119 pharmacokinetic, 118 Tour de France, 394 toxicity, 26 acute, 26–27, 28t
© The McGraw−Hill Companies, 2009
INDEX alcohol, 216–221 amphetamine, 147–148 behavioral, 28t categories of, 26–27 Check Yourself, 49 chronic, 26, 28t cocaine, 44, 133–134 heroin, 44 of hypnotics, 164–165 marijuana, 382–384 measuring, 108 monitoring the, 27 of opioids, 324–325 physiological, 26, 28t Trade and Revenue Act of 1767, 263 trafficking penalties, 65–66 Treasury Department, U.S., 56 treatment behavioral, 429–434 celebrity, 431 effectiveness of, 441–442 goals, 430 “magic bullet approach” to, 434 medication, 434–440 prison v., 62–63 psychosocial, 429–434 success of, 430 in United States, 441 Treatment Episode Data Set, 441 “tree of life,” 358 triazolam, 162 tricyclics, 181–182 examples of, 181t truth serum, 176 tuberculosis, 180 Tulia, Texas, 126–127 Twain, Mark, 247 tyramine, 181 U uisgebaugh, 197 Uniform Controlled Substances Act, 69 Unimed, Inc., 379 unipolar disorder, 185 United States Pharmacopoeia, 57, 102 “Unsubstantiated Claims and Documented Health
481
Hazards in the Dietary Supplement Marketplace,” 281 V vaccines, 7 Valium, 158 dependence, 164 values clarification, 414–415, 417 varenicline, 252, 437 vasopressin, 81, 216 Vaughn, William, 234 ventricular fibrillation, 133 Veronal, 154 Vick, Karl, 367 Vietnam War, 316–317 violence, 40–43 alcohol and, 215–216 amphetamines and, 147 marijuana and, 371 PCP and, 354 steroids and, 400 Vioxx, 295 visuospatial processing, 377 vitamins, 401 Vivarin, 288 vodka, 197–198 volatile solvents, 167–168 dangers from, 168 Volkow, Nora, 345 Volstead, Andrew, 200 vomiting center, 88 von Loewi, Otto, 86 von Meduna, Ladislas, 177 W Wafer, Billy, 127 war on drugs, 7 Washington, George, 51, 235 Wasson, Gordon, 343, 360 water, 401 WCTU. See Women’s Christian Temperance Union Wellbutrin, 437 Wernicke-Korsakoff syndrome, 218 What Works: Schools Without Drugs, 416 What Works: Workplaces Without Drugs, 424 whippets, 167 whiskey, 193 rye, 198
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Index
INDEX
Whiskey Rebellion, 51 White, Tonya, 127 Wiley, Harvey, 56, 57 wine, 196–197 coca, 125 dry, 196 generic, 196 medicinal value of, 193 sparkling, 196 sweet, 196 varietal, 196 Winston, 237 de Wit, Harriet, 345 witches, 356 withdrawal symptoms, 33, 34, 118
alcohol, 222–224 amphetamine, 148 avoiding, 109 cocaine, 134, 439 elimination of, 34 heroin, 33, 326 hypnotics, 164 marijuana, 381–382 opioid, 323t reduction of, 34 Women’s Christian Temperance Union (WCTU), 200 “The Women’s Petition Against Coffee,” 258 Wood, Alexander, 312 workplace, “drug-free,” 424
Wright, Hamilton, 55–56 X Xanax, 161 dependence, 164 xanthines, 270 Xenical, 289 Xyrem, 168 Y yeast, 192–193, 226 yin-yang, 96 Z zolpidem, 162 Zyban, 252, 437
487
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McGraw-Hill
McGraw−Hill Primis ISBN−10: 0−39−065732−8 ISBN−13: 978−0−39−065732−9 Text: Drugs, Society and Human Behavior, 13th Edition Hart−Ksir−Ray
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111
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ISBN−10: 0−39−065732−8
ISBN−13: 978−0−39−065732−9
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Contents Hart−Ksir−Ray • Drugs, Society and Human Behavior, 13th Edition Front Matter
1
List of Boxes Preface
1 3
I. Drug Use in Modern Society
7
Introduction 1. Drug Use: An Overview 2. Drug Use as a Social Problem 3. Drug Products and Their Regulations II. How Drugs Work
7 8 31 57 85
Introduction 4. The Nervous System 5. The Actions of Drugs
85 86 107
III. Uppers and Downers
129
Introduction 6. Stimulants 7. Depressants and Inhalants 8. Medication for Mental Disorders
129 130 159 177
IV. Alcohol
197
Introduction 9. Alcohol
197 198
V. Familiar Drugs
237
Introduction 10. Tobacco 11. Caffeine 12. Dietary Supplements and Over−the−Counter Drugs
237 238 262 283
VI. Restricted Drugs
309
Introduction 13. Opioids 14. Hallucinogens 15. Marijuana 16. Performance−Enhancing Drugs
309 310 334 367 393
iii
VII. Prevention and Treatment
411
Introduction 17. Preventing Substance Abuse 18. Treating Substance Abuse and Dependence
411 412 431
Back Matter
447
Appendix A: Drug Names Appendix B: Resources for Information and Assistance Glossary Credits Index
447 453 457 469 472
iv
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List of Boxes
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1
List of Boxes
Drugs in the Media Reporting on the “Drug du Jour” 4 Pharm Parties? 27 Is Media Coverage of New Prescription Drugs Too Rosy? 53 Brain Teasers: What’s in a Pretty Picture? 82 The Grapefruit-Juice Effect 103 The Drug War in Tulia: Aberration or Representative? 126 The Legacy of Samantha Reid 155 Mental Illness at the Movies 173 Advertising Alcohol on Television 194 Tobacco Use in the Movies 234 Fancy Coffee Drinks and Humor 259 Natural Male Enhancement? 258 The Rise and Fall of Heroin “Epidemics” 308 The Psychedelic 60s—Reflections in Film, Music, and Literature 333 Medical Marijuana in the News 367 Banned Substances and How to Avoid Them 393 Prime-Time Drug-Prevention Programming 412 Celebrity Rehab 431
Should We Be Concerned about Steroid Use by Entertainers? 402 Are “Alternatives to Drugs” Really Alternatives? 416
Drugs in Depth Important Definitions—and a Caution! 6 Methamphetamine Use in Your Community 8 Americans in Prison 68 Drug Interactions 117 Alcohol without Liquid 210 Possible New Painkiller? 248 Caffeine and Panic Attacks 273 The Vioxx Controversy 295 Extrapolating Findings from Animals to Humans: What You Need to Know 351 Nutritional Ergogenic Aids 401 How Much Do You Know About DARE? 419 Effective Prevention Programs 421 The 12 Steps of Alcoholics Anonymous 433
Mind/Body Connection Taking Sides Can We Predict or Control Trends in Drug Use? 7 Are Current Laws Fair? 42 Prescription Marijuana? 71 Animal Toxicity Tests 108 Should Psychologists Be Allowed to Prescribe? 183 Protecting the Unborn from Alcohol 223 Caffeine-Dependence Syndrome? 271 Should There Be a Class of “Pharmacist-Recommended” Drugs? 292 Should Naloxone Be Made Available to Heroin Users? 315 Do You Think the Federal Government Should Fund Hallucinogen Research? 345 Should Medical Patients Have Access to Marijuana? 380
Religion and Drug Use 14 Fear and Decision Making 31 Looking for More Humane Policies 65 How Far Should We Go to Enhance Human Abilities? 146 Learning to Relax 165 Is Alcoholics Anonymous a Religion? 225 The Hidden Costs of Smoking 251 Caffeine and the “Geek” Culture: Buying a Dream 272 Abuse of OTC Dextromethorphan 299 Living in the Flow 359 Baseball: Seeking Alternatives to Amphetamines 396 Integrating Treatment and Prevention with Pregnancy Services 423 The Nature of Dependence 440 xv
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List of Boxes
List of Boxes Preventing Inhalant Abuse Avoiding Relapse 434
413
Targeting Prevention Preventing What? 18 Clean Needles? 32 Prescribing Practices 57 Avoiding Withdrawal Symptoms 109 Cocaine and Friendship 135 The Drug-Induced Rape Prevention and Punishment Act 160 Falling Asleep Without Pills 163 Estimating Blood Alcohol Concentration 208 The Medicine Chest 290
DSM-IV-TR Psychiatric Diagnosis of Substance-Use Disorders 36 Diagnostic Criteria for Attention-Deficit Hyperactivity Disorder 145 Anxiety Disorders 174 Diagnosis of Schizophrenia 175 Diagnosis of Mood Disorders 176 Psychiatric Diagnosis of Substance Disorders 432
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
3
Preface Today’s media-oriented college students are aware of many issues relating to drug use. Nearly every day we hear new concerns about methamphetamine, club drugs, legal pharmaceuticals, and the effects of tobacco and alcohol, and most of us have had some personal experience with these issues through family, friends, or co-workers. This course is one of the most exciting students will take because it will help them relate the latest information on drugs to their effects on society and human behavior. Students will not only be in a better position to make decisions to enhance their own health and well-being, but they will also have a deeper understanding of the individual problems and social conflicts that arise when others misuse and abuse psychoactive substances. Much has changed in the 38 years since Drugs, Society, and Human Behavior was first published. The 1970s were a period of widespread experimentation with marijuana and hallucinogens, while the 1980s brought increased concern about illegal drugs and conservatism, along with decreased use of alcohol and all illicit drugs. Not only did drugusing behavior change, but so did attitudes and knowledge. And, of course, in each decade the particular drugs of immediate social concern have changed: LSD gave way to angel dust, then to heroin, then to cocaine and crack. In the 1990s, we saw increased use of LSD and marijuana, but not to the levels of the 1970s.
Recent Trends The most alarming trend in recent years has been the increased misuse of prescription opioid pain relievers such as Oxycontin and Vicodin. These pharmaceuticals have now replaced cocaine as the leading cause of drug overdose deaths in the United States (not counting
alcohol overdoses), and they have joined methamphetamine and Ecstasy as leading causes of concern about drug misuse and abuse. Methamphetamine, Esctasy, GHB, and the misuse of prescription painkillers are the big news items. Meanwhile, our old standbys, alcohol and tobacco, remain with us and continue to create serious health and social problems. Regulations undergo frequent changes, new scientific information becomes available, and new approaches to prevention and treatment are being tested, but the reality of substance use and abuse always seems to be with us. This text approaches drugs and drug use from a variety of perspectives—behavioral, pharmacological, historical, social, legal, and clinical—which will help students connect the content to their own interests.
Special Features Updated Content in the Thirteenth Edition Throughout each chapter, we have included the very latest information and statistics, and the Drugs in the Media feature has allowed us to comment on breaking news right up to press time. In addition, we have introduced many timely topics and issues that are sure to pique students’ interest and stimulate class discussion. The following are just some of the updated topics in the thirteenth edition. For a complete, chapter-by-chapter list of changes, please visit the Online Learning Center for the thirteenth edition (www.mhhe.com/hart13e). •
Statistics on drug use trends, new drug treatments, and drug-related mortality statistics from National Survey on Drug Use and Health, Monitoring the Future, DAWN, TEDS, SAMHSA treatment information (Chapter 1 and throughout) xvii
4
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Front Matter
Preface
© The McGraw−Hill Companies, 2009
Preface
•
Risk and protective factors for drug use, including the influence of gender, race, level of education, personality, and genetics (Chapters 1 and 2)
•
Cocaine sentencing policy (Chapters 3 and 6)
•
Current research on popular recreational drugs, including methamphetamine (Chapter 6), MDMA (Chapter 14), psilocybin (Chapter 14), and marijuana (Chapter 15)
•
Effectiveness and side effects of antidepressants and antipsychotics (Chapter 8)
•
Self-assessment of alcohol use (Chapter 9)
•
Smoking cessation medications (Chapter 10)
•
Behind-the-counter drugs (Chapter 12)
•
Dietary supplement regulation (Chapter 12)
•
Prescribing naloxone to heroin users as a harm-reduction strategy (Chapter 13)
•
Extrapolating findings of animal studies to humans (Chapter 14)
•
Funding for research on hallucinogens (Chapter 14)
•
medical marijuana (Chapter 15)
•
Use of performance-enhancing drugs by athletes and entertainers (Chapter 16)
•
Medications to treat substance abuse and dependence (Chapter 18)
Taking Sides These boxes discuss a particular drug-related issue or problem and ask students to take a side in the debate. This thought-provoking material will help students apply what they learned in the chapter to real-world situations. Taking Sides topics include potential medical uses of marijuana, current laws relating to drug use, and the issue of government funding for research on hallucinogens. Mind/Body Connections The Mind/Body Connection boxes highlight the interface between the psychological and the physiological aspects of substance use, abuse, and dependence. These boxes help students consider influences on their own attitudes toward drug use. Topics include religion and drug use, the social and emotional costs of smoking, and the nature of dependence. Targeting Prevention The Targeting Prevention boxes offer perspective and provoke thought regarding which drugrelated behaviors we, as a society, want to reduce or prevent. Topics include syringe exchange programs, criminal penalties for use of date rape drugs, and nondrug techniques for overcoming insomnia. These boxes help students better evaluate prevention strategies and messages.
Boxes are used in Drugs, Society, and Human Behavior to explore a wide range of current topics in greater detail than is possible in the text itself. The boxes are organized around key themes.
Drugs in Depth These boxes examine specific, often controversial, drug-related issues such as the extrapolation of animal studies to humans, and the growing number of people in prison for drug-related offenses. Drugs in Depth boxes are a perfect starting point for class or group discussion.
Drugs in the Media Our world revolves around media of all types—TV, films, radio, print media, and the Web. To meet students on familiar ground, we have included Drugs in the Media boxes, which take an informative and critical look at these media sources of drug information. Students can build their critical thinking skills while reading about such topics as alcohol advertising, media coverage of prescription drugs, and the presentation of cigarette smoking in films.
Online Learning Center Resources These boxes, found at the opening of each chapter, direct students toward the useful resources available on the Online Learning Center for Drugs, Society, and Human Behavior. These resources include learning objectives, glossary flashcards, Web activities and links, chapter quizzes, audio chapter summaries, and video clips. Students can use Online Learning Center resources to improve their grades and get the most out of this course.
Focus Boxes
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
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Preface
Attractive Design and Illustration Package The inviting look, bold colors, and exciting graphics in Drugs, Society, and Human Behavior draw the reader in with every turn of the page. Sharp and appealing photographs, attractive illustrations, and informative tables support and clarify the chapter material.
Pedagogical Aids Although all the features of Drugs, Society, and Human Behavior are designed to facilitate and improve learning, several specific learning aids have been incorporated into the text: •
Chapter Objectives: Chapters begin with a list of objectives that identify the major concepts and help guide students in their reading and review of the text.
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of drugs and on drug resources and organizations.
Check Yourself! Activities These self-assessments, found at the end of most chapters, help students put health concepts into practice. Each Check Yourself! activity asks students to answer questions and analyze their own attitudes, habits, and behaviors. Self-assessments are included in such areas as sleep habits, daily mood changes, alcohol use, caffeine consumption, and consideration of consequences.
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Summary Drugs Chart: A helpful chart of drug categories, uses, and effects appears on the back inside cover of the text.
Supplements A comprehensive package of supplementary materials designed to enhance teaching and learning is available with Drugs, Society, and Human Behavior.
Online Learning Center www.mhhe.com/hart13e The following instructor resources are available for download from the Online Learning Center; to obtain a password to download these teaching tools, please contact your local sales representative. •
Instructor’s Manual: Organized by chapter, the Instructor’s Manual includes chapter objectives, key terms, chapter outlines, key points, suggested class discussion questions and activities, and video suggestions.
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Test Bank: Revised and expanded for the thirteenth edition, the test bank now includes more questions for each chapter. The questions are available as Word files and with the EZ Test computerized testing software. EZ Test provides a powerful, easyto-use test maker to create printed quizzes and exams. For secure online testing, exams created in EZ Test can be exported to WebCT, Blackboard, and EZ Test Online. EZ Test comes with a Quick Start Guide, user’s manual, and Flash tutorials. Additional help is available online at www.mhhe.com/eztest.
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Definitions of Key Terms: Key terms are set in boldface type and are defined in corresponding boxes. Other important terms in the text are set in italics for emphasis. Both approaches facilitate vocabulary comprehension.
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Chapter Summaries: Each chapter concludes with a bulleted summary of key concepts. Students can use the chapter summaries to guide their reading and review of the chapters.
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Review Questions: A set of questions appears at the end of each chapter to aid students in their review and analysis of chapter content.
PowerPoint Slides: Updated and expanded for the thirteenth edition, the PowerPoint slides include key lecture points and images from the text and other sources.
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Appendices: The appendices include handy references on brand and generic names
Image Bank: Expanded for the thirteenth edition, the image bank contains over 200 images from the text and other sources.
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
Front Matter
© The McGraw−Hill Companies, 2009
Preface
Preface
Student resources on the free Online Learning Center include chapter objectives, glossary flashcards, self-correcting quizzes, Web activities, audio chapter summaries, and links. New for the thirteenth edition are online video clips. These clips feature student interviews on topics related to drugs, alcohol, and tobacco; critical thinking and self-reflection questions accompany each clip.
Classroom Performance System (CPS) CPS, a wireless response system, brings interactivity into the classroom or lecture hall. Each student uses a wireless response pad similar to a television remote to instantly respond to polling or quiz questions. Results can be posted for immediate viewing by the instructor and entire class. Contact your local sales representative for more information about using CPS with Drugs, Society, and Human Behavior.
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Acknowledgments We would like to express our appreciation to the following instructors who reviewed the previous edition and helped lay the groundwork for the improvements and changes needed in the thirteenth edition: Lawrence Anthony University of Cincinnati Rodney Clark Allegheny College Liz Coccia Austin Community College Charles Ellison University of Cincinnati Sandy Festa Rutgers–Camden Marc Gellman University of Miami Janene Grodesky Northern Kentucky University Grace Lartey Western Kentucky University Janet Mason College of Lake County Carl L. Hart
Primis Online www.mhhe.com/primis Primis Online is a database-driven publishing system that allows instructors to create customized textbooks, lab manuals, or readers for their courses directly from the Primis Web site. The custom text can be delivered in print or electronic (eBook) form. A Primis eBook is a digital version of the customized text sold directly to students as a file downloadable to their computer or accessed online by password. Drugs, Society, and Human Behavior can be customized using Primis Online.
Charles Ksir
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
Introduction
© The McGraw−Hill Companies, 2009
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SECTION
ONE Drug Use in Modern Society The interaction between drugs and behavior can be approached from two general perspectives.
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Which drugs are being used and why?
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Certain drugs, the ones we call psychoactive, have profound effects on behavior. Part of what
Drug Use: An Overview Drug Use as a Social Problem Why does our society want to regulate drug use?
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Drug Products and Their Regulations What are the regulations, and what is their effect?
a book on this topic should do is describe the effects of these drugs on behavior, and later chapters do that in some detail. Another perspective, however, views drug taking as behavior. The psychologist sees drug-taking behaviors as interesting examples of human behavior that are influenced by many psychological, social, and cultural variables. In the first section of this text, we focus on drug taking as behavior that can be studied in the same way that other behaviors, such as aggression, learning, and human sexuality, can be studied.
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I. Drug Use in Modern Society
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1. Drug Use: An Overview
© The McGraw−Hill Companies, 2009
Drug Use: An Overview Objectives When you have finished this chapter, you should be able to: • Develop an analytical framework for understanding any specific drug-use issue. • Apply four general principles of psychoactive drug use to any specific drug-use issue. • Explain the differences between misuse, abuse, and dependence. • Describe the general trends of increases and decreases in drug use in the U.S. since 1975.
“The Drug Problem” Talking about Drug Use
• Remember several correlates and antecedents of adolescent drug use. • Describe correlates and antecedents of drug use in the terminology of risk factors and protective factors.
“Drug use on the rise” is a headline that has been seen quite • Discuss motives that people may have for illicit and/or regularly over the years. It gets dangerous drug-using behavior. our attention. At any given time the unwanted use of some kind of drug can be found to be increasing, Journalism students are told that an informaat least in some group of people. How big a tive news story must answer the questions who, problem does the current headline represent? what, when, where, why, and how. Let’s see how Before you can meaningfully evaluate the answering the same questions plus one more extent of such a problem or propose possible question—how much—can help us analyze solutions, it helps to define what you’re talkproblem drug use. ing about. In other words, it helps to be more • Who is taking the drug? We are more conspecific about just what the problem is. Most cerned about a 15-year-old girl drinking a of us don’t really view the problem as drug beer than we are about a 21-year-old woman use, if that includes your Aunt Margie’s takdoing the same thing. We worry more about a ing two aspirins when she has a headache. 10-year-old boy chewing tobacco than we do What we really mean is that some drugs being about a 40-year-old man chewing it (unless we used by some people or in some situations happen to be riding right behind him when constitute problems with which our society he spits out the window). And, although we must deal. 2
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
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Chapter 1
www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips
• don’t like anyone taking heroin, we undoubtedly get more upset when we hear about the girl next door becoming a user. •
What drug are they taking? This question should be obvious, but often it is overlooked. A simple claim that a high percentage of students are “drug users” doesn’t tell us if there has been an epidemic of methamphetamine use or if the drug referred to is alcohol (more likely). If someone begins to talk about a serious “drug problem” at the local high school, the first question should be “what drug or drugs?”
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When and where is the drug being used? The situation in which the drug use occurs often makes all the difference. The clearest
Drug Use: An Overview
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example is the drinking of alcohol; if it is confined to appropriate times and places, most people accept drinking as normal behavior. When an individual begins to drink on the job, at school, or in the morning, that behavior may be evidence of a drinking problem. Even subcultures that accept the use of illegal drugs might distinguish between acceptable and unacceptable situations; some college-age groups might accept marijuana smoking at a party but not just before going to a calculus class!
Online Learning Center Resources
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1. Drug Use: An Overview
Why a person takes a drug or does anything else is a tough question to answer. Nevertheless, it is important in some cases. If a person takes Vicodin because her doctor prescribed it for the knee injury she got while skiing, most of us would not be concerned. If, on the other hand, she takes that drug on her own, just because she likes the way it makes her feel, then we should begin to worry about possible abuse of the drug. The motives for drug use, as with motives for other behaviors, can be complex. Even the person taking the drug might not be aware of all the motives involved. One way a psychologist can try to answer why questions is to look for consistency in the situations in which the behavior occurs (when and where). If a person drinks only with other people who
Our concern about the use of a substance often depends on who is using it, how much is being used, and when, where, and why it is being used.
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
1. Drug Use: An Overview
© The McGraw−Hill Companies, 2009
Section One Drug Use in Modern Society
Drugs in the Media Reporting on the “Drug du Jour” At the beginning of this millennium, newspaper and television stories about drugs are dominated by the so-called club drugs, such as Ecstasy and GHB. Before that there was a wave of media reports about crystal meth and other forms of methamphetamine. In the mid-1980s, it was crack cocaine. Of course these waves of media focus are associated with waves of drug use, but the news media all seem to jump on the latest “drug du jour” (drug of the day) at the same time. One question that doesn’t get asked much is this: What role does such media attention play in popularizing the current drug fad, perhaps making it spread farther and faster than would happen without the publicity? About 40 years ago, in a chapter titled “How to Create a Nationwide Drug Epidemic,” journalist E. M. Brecher described a sequence of news stories that he believed were the key factor
are drinking, we may suspect social motives; if a person often drinks alone, we may suspect that the person is trying to deal with personal problems by drinking. •
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How the drug is taken can often be critical. South American Indians who chew coca leaves absorb cocaine slowly over a long period. The same total amount of cocaine “snorted” into the nose produces a more rapid, more intense effect of shorter duration and probably leads to much stronger dependence. Smoking cocaine in the form of “crack” produces an even more rapid, intense, and brief effect, and dependence occurs very quickly. How much of the drug is being used? This isn’t one of the standard journalism questions, but it is important when describing drug use. Often the difference between what one considers normal use and what one considers abuse of, for example, alcohol or a prescription drug comes down to how much a person takes.
in spreading the practice of sniffing the glues sold to kids for assembling plastic models of cars and airplanes (see volatile solvents in Chapter 7). He argued that, without the well-meant attempts to warn people of the dangers of this practice, it would probably have remained isolated to a small group of youngsters in Pueblo, Colorado. Instead, sales of model glue skyrocketed across America, leading to widespread restrictions on sales to minors. Thinking about the kinds of things such articles often say about the latest drug problem, are there components of those articles that you would include if you were writing an advertisement to promote use of the drug? Do you think such articles actually do more harm than good, as Brecher suggested? If so, does the important principle of a free press mean there is no way to reduce the impact of such journalism?
Four Principles of Psychoactive Drugs Now that we’ve seen how helpful it can be to be specific when talking about drug use, let’s look for some organizing principles. Are there any general statements that can be made about psychoactive drugs—those compounds that alter consciousness and affect mood? Four basic principles seem to apply to all of these drugs. 1.
Drugs, per se, are not good or bad. There are no “bad drugs.” When drug abuse, drug dependence, and deviant drug use are talked about, it is the behavior, the way the drug is being used, that is being referred to. This statement sounds controversial and has angered some prominent political figures and drug educators. It therefore requires some defense. For a pharmacologist, it is difficult to view the drug, the chemical substance itself, as somehow possessing evil intent. It sits there in its bottle and does nothing until we put it into a living system. From the perspective of
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
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1. Drug Use: An Overview
a psychologist who treats drug users, it is difficult to imagine what good there might be in heroin or cocaine. However, heroin is a perfectly good painkiller, at least as effective as morphine, and it is used medically in many countries. Cocaine is a good local anesthetic and is still used for medical procedures, even in the United States. Each of these drugs can also produce bad effects when people abuse them. In the cases of heroin and cocaine, our society has weighed its perception of the risks of bad consequences against the potential benefits and decided that we should severely restrict the availability of these substances. It is wrong, though, to place all of the blame for these bad consequences on the drugs themselves and to conclude that they are simply “bad” drugs. Many people tend to view some of these substances as possessing an almost magical power to produce evil. When we blame the substance itself, our efforts to correct drug-related problems tend to focus exclusively on eliminating the substance, perhaps ignoring all of the factors that led to the abuse of the drug. Every drug has multiple effects. Although a user might focus on a single aspect of a drug’s effect, we do not yet have compounds that alter only one aspect of consciousness. All psychoactive drugs act on more than one place in the brain, so we might expect them to produce complex psychological effects. Also, virtually every drug that acts in the brain also has effects on the rest of the body, influencing blood pressure, intestinal activity, or other functions. Both the size and the quality of a drug’s effect depend on the amount the individual has taken. The relationship between dose and effect works in two ways. By increasing the dose, there is usually an increase in the same effects noticed at lower drug levels. Also, at different dose levels there is often a change in the kind of effect, an alteration in the character of the experience. The effect of any psychoactive drug depends on the individual’s history and expectations.
Chapter 1
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Drug Use: An Overview
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The effects of drugs are influenced by the setting and the expectations of the user.
Because these drugs alter consciousness and thought processes, the effect they have on an individual depends on what was there initially. An individual’s attitude can have a major effect on his or her perception of the drug experience. The fact that relatively inexperienced users can experience a high when smoking oregano and dry oak tree leaves— thinking it’s good marijuana—should come as no surprise to anyone who has arrived late at a party and felt a “buzz” after one drink rather than the usual two or three. It is not possible, then, to talk about many of the effects of these drugs independent of the user’s history and attitude and the setting.
How Did We Get Here? Have Things Really Changed? Drug use is not new. Humans have been using alcohol and plant-derived drugs for thousands of years—as far as we know, since Homo sapiens first appeared on the planet. A truly “drug-free society” has probably never existed, and might never exist. Psychoactive drugs were used in rituals that we could today classify as religious psychoactive: having effects on thoughts, emotions, or behavior. marijuana (mare i wan ah): also spelled “marihuana.” Dried leaves of the Cannabis plant.
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
1. Drug Use: An Overview
© The McGraw−Hill Companies, 2009
Section One Drug Use in Modern Society
Drugs in Depth Important Definitions—and a Caution! Some terms that are commonly used in discussing drugs and drug use are difficult to define with precision, partly because they are so widely used for many different purposes. Therefore, any definition we offer should be viewed with caution because each represents a compromise between leaving out something important versus including so much that the defined term is watered down. The word drug will be defined as “any substance, natural or artificial, other than food, that by its chemical nature alters structure or function in the living organism.” One obvious difficulty is that we haven’t defined food, and how we draw that line can sometimes be arbitrary. Alcoholic beverages, such as wine and beer, may be seen as drug, food, or both. Are we discussing how much sherry wine to include in beef Stroganoff, or are we discussing how many ounces of wine can be consumed before becoming intoxicated? Since this is not a cookbook but, rather, a book on the use of psychoactive chemicals, we will view all alcoholic beverages as drugs. Illicit drug is a term used to refer to a drug that is unlawful to possess or use. Many of these drugs are available by prescription, but when they are manufactured or sold illegally they are illicit. Traditionally, alcohol and tobacco have not been considered illicit substances even when used by minors, probably because of their widespread legal availability to adults. Common household chemicals, such as glues and paints, take on some characteristics of illicit substances when people inhale them to get “high.” Deviant drug use is drug use that is not common within a social group and that is disapproved of by the majority, causing members of the group to take corrective action when it occurs. The corrective action may be informal (making fun of the behavior, criticizing the behavior) or formal (incarceration, treatment). Some examples of drug use might be deviant in the society at large but accepted or even expected in particular subcultures. We still consider this behavior to be deviant, since it makes more sense to apply the perspective of the larger society. Drug misuse generally refers to the use of prescribed drugs in greater amounts than, or for purposes other than, those prescribed by a physician or dentist. For nonprescription drugs or chemicals such as paints, glues, or solvents, misuse might
mean any use other than the use intended by the manufacturer. Abuse consists of the use of a substance in a manner, amounts, or situations such that the drug use causes problems or greatly increases the chances of problems occurring. The problems may be social (including legal), occupational, psychological, or physical. Once again, this definition gives us a good idea of what we’re talking about, but it isn’t precise. For example, some would consider any use of an illicit drug to be abuse because of the possibility of legal problems, but many people who have tried marijuana would argue that they had no problems and therefore didn’t abuse it. Also, the use of almost any drug, even under the orders of a physician, has at least some potential for causing problems. The question might come down to how great the risk is and whether the user is recklessly disregarding the risk. How does cigarette smoking fit this definition? Should all cigarette smoking be considered drug abuse? For someone to receive a diagnosis of having a substance-use disorder (see DSM-IV-TR feature in Chapter 2), the use must be recurrent, and the problems must lead to significant impairment or distress. Addiction is a controversial and complex term that has different meanings for different people. Because the term is so widely used in everyday conversation, it is risky for us to try to give it a precise, scientific definition, and then have our readers use their own long-held perspectives whenever we use the term. Therefore, we have avoided using this term where possible, instead relying on more precisely defined terms such as dependence. Drug dependence refers to a state in which the individual uses the drug so frequently and consistently that it appears that it would be difficult for the person to get along without using the drug. For some drugs and some users, there are clear withdrawal signs when the drug is not taken, implying a physiological dependence. Dependence can take other forms, as shown in the DSM-IV-TR feature in Chapter 2. If a great deal of the individual’s time and effort is devoted to getting and using the drug, if the person often winds up taking more of the substance than he or she intended, and if the person has tried several times without success to cut down or control the use, then the person meets the criteria for dependence.
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
© The McGraw−Hill Companies, 2009
1. Drug Use: An Overview
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Chapter 1
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Drug Use: An Overview
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Taking Sides Can We Predict or Control Trends in Drug Use? Looking at the overall trends in drug use, it is clear that significant changes have occurred in the number of people using marijuana, cocaine, alcohol, and tobacco. However, while it’s easy to describe the changes once they have happened, it’s much tougher to predict what will come next. Maybe even harder than predicting trends in drug use is knowing what social policies are effective in controlling these trends. The two main kinds of activities that we usually look to as methods to prevent or reduce drug use are legal controls and education (including advertising campaigns). How effective do you think laws have been in helping prevent or reduce
in nature, and Chapter 14 provides several examples of hallucinogenic drugs reported to enhance spiritual experiences. A common belief in many early cultures was that illness results from invasion by evil spirits, so in that context it makes sense that psychoactive drugs were often used as part of a purification ritual to rid the body of those spirits. In these early cultures the use of drugs to treat illness likely was intertwined with spiritual use so that the roles of the “priest” and that of the “shaman” (medicine man) often were not separate. In fact, the earliest uses of many of the drugs that we now consider to be primarily recreational drugs or drugs of abuse (nicotine, caffeine, alcohol, and marijuana) were as treatments for various illnesses. Psychoactive drugs have also played significant roles in the economies of societies in the past. Chapter 10 describes the importance of tobacco in the early days of European exploration and trade around the globe as well as its importance in the establishment of English colonies in America; Chapter 6 discusses the significance of the coca plant (from which cocaine is derived) in the foundation of the Mayan empire in South America; and Chapter 13 points out the importance of the opium trade in opening China’s doors to trade with the West in the 1800s. One area in which enormous change has occurred over the past 100-plus years is in the
drug use? Be sure to consider laws regulating sales of alcohol and tobacco to minors in your analysis. What about the public advertising campaigns you are familiar with? How about school-based prevention programs? As you go through the remainder of this book, these questions will come up again, along with more information about specific laws, drugs, and prevention programs. For now, choose which side you would rather take in a debate on the following proposition: broad changes in drug use reflect shifts in society and are not greatly influenced by drug-control laws, antidrug advertising, or drugprevention programs in schools.
development and marketing of legal pharmaceuticals. The introduction of vaccines to eliminate smallpox, polio, and other communicable diseases, followed by the development of antibiotics that are capable of curing some types of otherwise deadly illnesses, laid the foundation for our current acceptance of medicines as the cornerstone of our health care system. Some of the scientific and medical discoveries, problems, and laws associated with these changes are outlined in Chapter 3. The many kinds of legal pharmaceuticals designed to influence mental and behavioral functioning are discussed in Chapter 8. Another significant development in the past 100 years has been government efforts to limit access to certain kinds of drugs that are deemed too dangerous or too likely to produce dependence to allow them to be used in an unregulated fashion. The enormous growth, both in expenditures and in the breadth of substances now controlled, has led many to refer to this development as a “war on drugs.” These laws are also outlined in Chapter 3, but we will trace their effect throughout the chapters on different drug classes, and the chapters on prevention and treatment of drug abuse and dependence. With both of these developments, the proportion of our economy devoted to psychoactive
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
© The McGraw−Hill Companies, 2009
1. Drug Use: An Overview
Section One Drug Use in Modern Society
drugs, both legal and illegal, and to their regulation, has also expanded considerably. So drug use would be an important topic for us to understand if only for that fact. In addition, drug use and its regulation are reflective of changes in our society and in how we as individuals interact with that society. Also, drug problems and our attempts to solve them have in turn had major influences on us as individuals and on our perceptions of appropriate roles for government, education, and health care. Therefore, the topic of psychoactive drugs provides a window through which we can study our own current psychology, sociology, and politics.
Drugs and Drug Use Today Extent of Drug Use In trying to get an overall picture of drug use in today’s society, we quickly discover that it’s not easy to get accurate information. It’s not possible to measure with great accuracy the use of, let’s say, cocaine in the United States. We don’t really know how much is imported and sold, because most of it is illegal. We don’t really know how many cocaine users there are in the country, because we have no good way of counting them. For some things, such as prescription drugs, tobacco, and alcohol, we have a wealth of sales information and can make much better estimates of rates of use. Even there, however, our information might not be complete (home-brewed beer would not be counted, for example, and prescription drugs might be bought and then left unused in the medicine cabinet). Let us look at some of the kinds of information we do have. A large number of survey questionnaire studies have been conducted in junior highs, high schools, and colleges, partly because this is one of the easiest ways to get a lot of information with a minimum of fuss. Researchers have always been most interested in drug use by adolescents and young adults, because this age is when drug use usually begins and reaches its highest levels.
This type of research has a couple of drawbacks. The first is that we can use this technique only on the students who are in classrooms. We can’t get this information from high school dropouts. That causes a bias, because those who skip school or have dropped out are more likely to use drugs. A second limitation is that we must assume that most of the self-reports are done honestly. In most cases, we have no way of checking to see if Johnny really did smoke marijuana last week, as he claimed on the questionnaire. Nevertheless, if every effort is made to encourage honesty (including assurances of anonymity), we expect that this factor is minimized. To the extent that tendencies to overreport or underreport drug use are relatively constant from one year to the next, we can use such results to reflect trends in drug use over time and to compare relative reported use of various drugs.
Drugs in Depth Methamphetamine Use in Your Community Assume that you have just been appointed to a community-based committee that is looking into drug problems. A high school student on the committee has just returned from a residential treatment program and reports that methamphetamine use has become “very common” in local high schools. Some members of the committee want to call in some experts immediately to give schoolwide assemblies describing the dangers of methamphetamine. You have asked for a little time to check out the student’s story to find out what you can about the actual extent of use in the community and report back to the group in a month. Make a list of potential information sources and the type of information each might provide. How close do you think you could come to making an estimate of how many current methamphetamine users there are in your community? Do you think it would be above or below the national average?
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
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Chapter 1
Table 1.1 Percentage of College Students One to Four Years beyond High School Reporting Use of Seven Types of Drugs (2006)
Drug
Used in Used Daily Ever Past for Past Used 30 Days 30 Days
Alcohol
85
65
4.8
Cigarettes
NA
19
9.2
Marijuana/hashish
47
17
4.3
Inhalants
7
0.4
0.0
Amphetamines
11
2.5
0.4
Hallucinogens
11
0.9
0.0
8
1.8
0.1
2.3
0.0
0.0
Cocaine (all) Crack
© The McGraw−Hill Companies, 2009
1. Drug Use: An Overview
Source: Monitoring the Future Project, University of Michigan
Let’s look first at the drugs most commonly reported by young college students in a recent nationwide sample. Table 1.1 presents data from one of the best and most complete research programs of this type, the Monitoring the Future Project at the University of Michigan. Data are collected each year from more than 15,000 high school seniors in schools across the United States, so that nationwide trends can be assessed. Data are also gathered from 8th- and 10th-graders and from college students. Three numbers are presented for each drug: the percentage of college students (one to four years beyond high school) who have ever used the drug, the smaller percentage who report having used it within the past 30 days, and the still smaller percentage who report daily use for the past 30 days.1 Note that most of these college students have tried alcohol at some time in their lives. Half have tried marijuana, and most students report never having tried the rest of the drugs listed. Also note that
Drug Use: An Overview
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daily use of any of these drugs other than cigarettes can be considered rare.
Trends in Drug Use The Monitoring the Future study, which has now been conducted annually for more than 30 years, allows us to see changes over time in the rates of drug use. Figure 1.1 displays data on marijuana use among 12th-graders. Look first at the line labeled “Use.” In 1975, just under 30 percent of high school seniors reported that they had used marijuana in the past 30 days (an indication of “current use”). This proportion rose each year until 1978, when 37 percent of 12th-graders reported current marijuana use. Over the next 13 years, from 1979 to 1992, marijuana use declined steadily so that by 1992 only 12 percent of 12th-graders reported current use (about one-third as many as in 1978). Then the trend reversed, with rates of current use climbing back to 24 percent of 12th-graders by 1997, followed by a slow decline over the past 10 years to just under 20 percent in 2007. Because marijuana is by far the most commonly used illicit drug, we can use this graph to make a broader statement: Illicit drug use among high school seniors has been slowly declining over the past 10 years. Currently, marijuana use is about half as common among 12th-graders as it was in 1978, but it is more common than it was at its lowest point 15 years ago. This is important because there always seem to be people trying to say that drug use is increasing among young people, or that people are starting to use drugs at younger and younger ages, but the best data we have provide no support for such statements (e.g., data from 8th-graders show the same trends as for 12th-graders). How can we explain these very large changes in rates of marijuana use over time? Maybe marijuana was easier to obtain in 1978, less available in 1992, etc.? Each year the same students were asked their opinion about how easy they thought it would be to get marijuana if they wanted to do so. Looking at the “Availability” line, and using the scale on the right-hand side of Figure 1.1,
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Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
I. Drug Use in Modern Society
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1. Drug Use: An Overview
Section One Drug Use in Modern Society 100
50 Availability
90
40
80 70
30 Use
60 50
20
40
Use
30
Risk and Availability
Risk
20
10
10 0
'76 '78 '80 '82 '84 '86 '88 '90 '92 '94 '96 '98 '00 '02 '04 '06 Use: % using once or more in past 30 days (on left-hand scale)
Risk: % saying great risk of harm in regular use (on right-hand scale)
0
Availability: % saying fairly easy or very easy to get (on right-hand scale)
Figure 1.1 Marijuana: Trends in Perceived Availability, Perceived Risk of Regular Use, and Prevalence of Use in the Past 30 Days for 12th-Graders SOURCE: L. D. Johnston, P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg, “Overall, Illicit Drug Use by American Teens Continues Gradual Decline in 2007.” Ann Arbor, MI: University of Michigan News Service [online], available at www.monitoringthefuture.org; accessed December 11, 2007.
we can see that back in 1975 about 90 percent of the seniors said that it would be fairly easy or very easy for them to get marijuana. The interesting thing is that this perception has not changed much, remaining close to 90 percent for over 30 years. Thus, the perceived availability does NOT appear to explain differences in rates of use over time. This is important because it implies that we can have large changes in rates of drug use even when the supply of the drug does not appear to change much. There is another line on Figure 1.1, labeled “Risk” (and also tied to the right-hand scale). In 1975, about 40 percent of 12th-graders rated the risk of harm from regular marijuana use as “great risk of harm.” The proportion of students reporting great risk declined over the same time that use was increasing (up to 1978). Then, as use dropped from 1979 to 1992, perceived risk increased. Perceived risk declined during the 1990s when use was again increasing, and in re-
cent years perceived risk is slowly rising while rates of use are slowly declining. You should be able to see from Figure 1.1 that as time goes by, the line describing changes in perception of risk from using marijuana is essentially a mirror image of the line describing changes in rates of using marijuana. This is important because it seems to say that the best way to achieve low rates of marijuana use is by convincing students that it is risky to use marijuana, whereas efforts to control the availability of marijuana (“supply reduction”) might have less of an influence. However, we must keep in mind that a cause and effect relationship has not been proven. Changes in both rates of use and perceptions of risk could be caused by something else that we are not directly measuring. In addition to the surveys of students, broad-based self-report information is also gathered through house-to-house surveys. With proper sampling techniques, these studies can
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11
40
Percentage Using in Past Month
35 30 25 20
Ages 18–25
15 10 Ages 12–17
5 0 1970
1975
1980
1985
1990 Year
1995
2000
2005
Figure 1.2 Marijuana Use among Persons Ages 12–25, by Age Group: 1971–2006 Source: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
estimate the drug use in most of the population, not just among students. This technique is much more time-consuming and expensive, it has a greater rate of refusal to participate, and we must suspect that individuals engaged in illegal drug use would be reluctant to reveal that
Marijuana is the most commonly used illicit drug, and major surveys including the Monitoring the Future Project and the National Survey on Drug Use and Health track trends in its usage.
fact to a stranger on their doorstep. The National Survey on Drug Use and Health is a face-to-face, computer-assisted interview done with more than 68,000 individuals in carefully sampled households across the United States. Figure 1.2 displays the trends in reported past month use of marijuana for two different age groups. This study shows the same pattern as the Monitoring the Future study of 12th-graders: Marijuana use apparently grew throughout the 1970s, reaching a peak in about 1980, and then declining until the early 1990s, when it increased again. Again, the past few years have seen a slight decline in rates of marijuana use in both age groups, similar to the declines seen in the Monitoring the Future studies. We have seen fairly dramatic trends over time in marijuana use, but what about other substances? Figure 1.3 shows rates of current use of alcohol and cocaine alongside marijuana use for Americans between 18 and 25 years of age. Many more people are current users of alcohol (about two-thirds of adults), and many
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80 Alcohol
Marijuana
Cocaine
70
Percentage Reporting Use
60
50
40
30
20
10
0 1974 1976 1978 1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 2006 Year
Figure 1.3 Trends in Reported Drug Use within the Past 30 Days for Young Adults Ages 18 to 25 SOURCE: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
fewer use cocaine in any given year. But overall, the trends over time are generally similar, with the peak year for all three substances around 1980, lower rates of use in the early 1990s, and less dramatic changes after that. Finding such a similar pattern in two different studies using different sampling techniques gives us additional confidence that these trends have been real and probably reflect broad changes in American society over this time. Political observers will be quick to note that Ronald Reagan was president during most of the 1980s, when use of marijuana and other drugs was declining, while Bill Clinton was in office during most of the 1990s, when these rates rose. Were these changes in drug use the result of more conservative drug-control policies under the Reagan administration and more lib-
eral policies under the Clinton administration? There are two reasons to think that is not the answer. First, the timing is not quite right. President Reagan was elected in 1980, took office in 1981, and didn’t begin focusing on the “Just Say No” antidrug messages until 1983. Most of the important legislation was passed in 1986. All of this was after the downward trend in drug use had already begun. It seems more likely that the Reagan administration recognized the opportunity provided by an underlying change in attitude among the general public. The government’s policies might have helped to amplify the effects of this underlying social change, but they did not create it. The same timing problem is associated with trying to link increased drug use to the Clinton presidency: The election was in 1992, and increased use was already begin-
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ning in 1993, during the first year of the Clinton administration. Also, the Clinton administration can hardly be accused of having liberal drug-control policies—drug-control budgets and arrests for drug violations were both higher than in any previous administration. If we can’t point to government policies as causes of these substantial changes in drug use, how can we explain them? The short answer is that for now, we can’t. We are left with saying that changes in rates of illicit drug use and in alcohol use probably reflect changes over time in a broad range of attitudes and behaviors among Americans—what we can refer to as “social trends.” This isn’t much of an explanation, and that is somewhat frustrating. After all, if we understood why these changes were taking place it might allow us to influence rates of substance use among the general population, or at least to predict what will happen next. Perhaps some of today’s college students will be the ones to develop this understanding over the next few years.
Correlates of Drug Use Once we know that a drug is used by some percentage of a group of people, the next logical step is to ask about the characteristics of those who use the drug, as compared with those who don’t. Often the same questionnaires that ask each person which drugs they have used also include several questions about the persons completing the questionnaires. The researchers might then send their computers “prospecting” through the data to see if certain personal characteristics can be correlated with drug use. But these studies rarely reveal much about either very unusual or very common types or amounts of drug use. For example, if we send a computer combing through the data from 1,000 questionnaires, looking for characteristics correlated with heroin use, only one or two people in that sample might report heroin use, and you can’t correlate much based on one or two people. Likewise, it would be difficult to identify the distinguishing characteris-
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tics of the people who have “ever tried” alcohol, because that group usually represents more than 90 percent of the sample. Much of the research on correlates of drug use has used marijuana smoking as an indicator, partly because marijuana use has been a matter of some concern and partly because enough people have tried it so that meaningful correlations can be done. Other studies focus on early drinking or early cigarette smoking.
Risk and Protective Factors Increasingly, researchers are analyzing the correlates of drug use in terms of risk factors and protective factors. Risk factors are correlated with higher rates of drug use, while protective factors are correlated with lower rates of drug use. A study based on data obtained from the National Survey on Drug Use and Health examined risk and protective factors regarding use of marijuana among adolescents (ages 12–17).2 This largescale study provides some of the best information we have about the correlates of marijuana use among American adolescents. The most significant factors are reported in Table 1.2. In some ways, the results confirm what most people probably assume: the kids who live in rough neighborhoods, whose parents don’t seem to care what they do, who have drugusing friends, who steal and get into fights, who aren’t involved in religious activities, and who don’t do well in school are the most likely to smoke marijuana. The same study analyzed cigarette smoking and alcohol use, with overall similar results. There are some surprising results, however. Those adolescents who reported that their parents frequently monitored their behavior (checking homework, limiting TV watching, and requiring chores, for example) were actually a little more likely to report using marijuana than adolescents who reported less parental correlate (core a let): a variable that is statistically related to some other variable, such as drug use.
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Table 1.2 Risk and Protective Factors Associated with Marijuana Use by Adolescents Risk Factors (in order of importance):
Protective Factors (in order of importance):
1. Having friends who use marijuana or other substances
1. Perceiving that there are strong sanctions against substance use at school
2. Engaging in frequent fighting, stealing, or other antisocial activities 3. Perceiving that substance use is prevalent at your school 4. Knowing adults who use marijuana or other substances 5. Having a positive attitude toward marijuana use
monitoring. This finding points out the main problem with a correlational study: We don’t know if excessive parental monitoring makes adolescents more likely to smoke marijuana, or if adolescents’ smoking marijuana and getting in fights makes their parents more likely to monitor them (the latter seems more likely). Another example of the limitation of correlational studies is the link between marijuana
Mind/Body Connection Religion and Drug Use More than three-fourths of American adolescents report that religion plays an important part in their lives. In study after study, those young people who report more involvement with religion (they attend services regularly and say their religion influences how they make decisions) are less likely to smoke cigarettes, drink alcohol, or use any type of illicit drug. Consider your own feelings about religion and about drug use. Why do you think this relationship between “religiosity” and lower rates of drug use is such a consistent finding? If you have friends from different religious backgrounds, discuss this relationship with them. Some religions have specific teachings against any alcohol use or tobacco use, but the general relationship seems to hold even for those religions that do not forbid these behaviors (at least for adults). What other factors related to religious involvement in general might serve as protective factors against the use of these substances?
2. Having parents as a source of social support 3. Being committed to school 4. Believing that religion is important and frequently attending religious services 5. Participating in two or more extracurricular activities
smoking and poor academic performance. Does smoking marijuana cause the user to get lower grades? Or is it the kids who are getting low grades anyway who are more likely to smoke marijuana? One indication comes from the analysis of risk and protective factors for cigarette smoking in this same study. The association between low academic performance and cigarette smoking was even stronger than the association between low academic performance and marijuana smoking. This leads most people to conclude that it’s the kids who are getting low grades anyway who are more likely to be cigarette smokers, and the same conclusion can probably be reached about marijuana smoking. The overall picture that emerges from studies of risk and protective factors is that the same adolescents who are likely to smoke cigarettes, drink heavily, and smoke marijuana are also likely to engage in other deviant behaviors, such as vandalism, stealing, fighting, and early sexual behavior—what some researchers refer to as problem behaviors. We all can think of individual exceptions to this rule, but correlational studies over many years all come to the same conclusion: If you want to find the greatest number of young people who use illicit drugs, look among the same people who are getting in trouble in other ways.
Race, Gender, and Level of Education Table 1.3 shows how some demographic variables are related to current use of some drugs of interest. The first thing to notice is
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Table 1.3 Drug Use among 18- to 25-year-olds: Percentage Reporting Use in the Past 30 Days
Drug
Male
African Female White American Hispanic
Native American Asian
High School College Graduate Graduate
Alcohol (Age 21+)
66
58
69
47
52
53
50
57
80
Tobacco (all types)
51
37
51
33
31
56
26
48
34
Marijuana
20
13
19
15
10
25
7
17
12
Cocaine
3
2
3
0.5
3
3
0.7
2
1
Source: Substance Abuse and Mental Health Services Administration, Results from the 2006 National Survey on Drug Use and Health (Rockville, MD: Office of Applied Studies, NSDUH Series H-32, DHHS Publication No. SMA 07-4293, 2007).
something that has been a consistent finding over many kinds of studies for many years, and that is that males are more likely to drink alcohol, use tobacco, smoke marijuana, and use cocaine than are females. This probably doesn’t surprise most people too much, but it is good to see that in many cases the data do provide support for what most people would expect. Expectations regarding ethnic and racial influences on drug use are more likely to clash with the data from the National Survey on Drug Use and Health. For example, overall, whites are much more likely to drink alcohol, use tobacco, or use cocaine than are African Americans, and whites are slightly more likely to use marijuana as well. These results do not conform to many peoples’ stereotypes, so let’s remind ourselves that we are talking about household surveys that cut across socioeconomic and geographic lines and attempt to examine American society at large. Also, remember that we are getting data simply about recent use of these substances, which for most people means relatively low-level and infrequent use, at least for alcohol, marijuana, and cocaine. If we restricted ourselves to looking at the smaller group of people who can be classified as substance abusers, and if we compared urban neighborhoods with high minority populations to suburban white neighborhoods, we would find higher rates of drug abuse in the
urban “ghetto.” But within the general population, it appears that rates of use are lower among blacks than among whites. We do see from Table 1.3 that the group labeled “Native American” (American Indian and Alaskan Native groups) have somewhat higher rates of tobacco and marijuana use, and across Asian groups there is a generally lower rate of use of all these substances. Education level is powerfully related to two common behaviors: young adults with college degrees (compared to those who only completed high school) are much more likely to drink alcohol and much less likely to use tobacco. Those with more education are also somewhat less likely to use marijuana or cocaine.
Personality Variables The relationships between substance use and various indicators of individual differences in personality variables have been studied extensively over the years. In general, large-scale survey studies of substance use in the general population have yielded weak or inconsistent correlations with most traditional personality traits as measured by questionnaires. So, for example, it has been difficult to find a clear relationship between measures of self-esteem and rates of using marijuana. More recently, several studies have found that various ways of measuring a factor called “impulsivity” can be correlated with rates
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of substance use in the general population.3 Impulsivity is turning out to be of much interest to drug researchers, but also hard to pin down in that different laboratories have different ways of measuring it. In general, it seems to relate to a person’s tendency to act quickly and without consideration of the longer-term consequences. We can expect to see more research on this concept over the next few years. Instead of looking at any level of substance use within the general population, we can look for personality differences between those who are dependent on substances and a “normal” group of people. When we do that, we find many personality differences associated with being more heavily involved in substance abuse or dependence. The association with impulsivity, for example, is much stronger in this type of study. Likewise, if we look at groups of people who are diagnosed with personality disorders, such as conduct disorder or antisocial personality disorder, we find high rates of substance use in these groups. Overall, it seems that personality factors may play a small role in whether someone decides to try alcohol or marijuana, but a larger role in whether that use develops into a serious problem. Because the main focus of this first chapter is on rates of drug use in the general population, we will put off further discussion of personality variables to the next chapter.
Genetics There is increasing interest in genetic influences on drug use. Again, studies looking across the general population and asking simply about recent use are less likely to produce significant results than studies that focus on people diagnosed with substance-use disorders. Genetic factors probably play a small role in whether someone tries alcohol or marijuana, but a larger role in whether that use develops into a serious problem. Studies of genetic variability in impulsivity and related traits are beginning to show clear association with substance-use disorders.4 Genetic factors in dependence are discussed further in Chapter 2.
Antecedents of Drug Use Finding characteristics that tend to be associated with drug use doesn’t help us understand causal relationships very well. For example, do adolescents first become involved with a deviant peer group and then use drugs, or do they first use drugs and then begin to hang around with others who do the same? Does drug use cause them to become poor students and to fight and steal? To answer such questions, we might interview the same individuals at different times and look for antecedents, characteristics that predict later initiation of drug use. One such study conducted in Finland found that future initiation of substance use or heavy alcohol use can be predicted by several of the same risk factors we have already discussed: aggressiveness, conduct problems, poor academic performance, “attachment to bad company,” and parent and community norms more supportive of drug use.5 Because these factors were measured before the increase in substance use, we are more likely to conclude that they may be causing substance use. But some other, unmeasured, variables might be causing both the antecedent risk factors and the subsequent substance use to emerge in these adolescents’ lives. A few scientists have been able to follow the same group of people at annual intervals for several years in what is known as a longitudinal study. One such study has tracked more than 1,200 participants from a predominantly African American community in Chicago from ages 6 through 32.6 Males who had shown a high “readiness to learn” in first grade were less likely to be cocaine users as adults, but females with poor academic performance in first grade had lower rates of cocaine use than females with higher first-grade scores. Males who were either “shy” or “aggressive” in first grade were more likely to be adult drug users compared to the students who had been considered neither shy nor aggressive 26 years earlier. It is much more difficult to obtain this type of data, and it is somewhat surprising that any variables measured at age six could reliably predict adult drug use.
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Males who are aggressive in early elementary school are more likely to be drug users as adults.
Gateway Substances One very important study from the 1970s pointed out a typical sequence of involvement with drugs.7 Most of the high school students in that group started their drug involvement with beer or wine. The second stage involved hard liquor, cigarettes, or both; the third stage was marijuana use; and only after going through those stages did they try other illicit substances. Not everyone followed the same pattern, but only 1 percent of the students began their substance use with marijuana or another illicit drug. It is as though they first had to go through the gateway of using alcohol and, in many cases, cigarettes. The students who had not used beer or wine at the beginning of the study were much less likely to be marijuana smokers at the end of the study than the students who had used these substances. The cigarette smokers were about twice as likely as the nonsmokers to move on to smoking marijuana. If the gateway theory can explain something about later drug use, then perhaps looking at
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those people who followed the traditional order of substance use (alcohol/cigarettes, followed by marijuana, followed by other illicit drugs) and comparing them to people who followed different orders of use might tell us something useful about the importance of particular orders of initiation. One recent study examined 375 homeless “street” youth, ages 13–21, in Seattle.8 They were asked at what age they first started using various substances, and then grouped into categories depending on whether they followed the traditional gateway order or some other order of initiation. The order of use did not predict current levels or types of drug use in this population, leading the study’s authors to conclude that knowing which substances people use first might not be very important in helping to prevent future escalation of drug use. One possible interpretation of the gateway phenomenon is that young people are exposed to alcohol and tobacco and that these substances somehow make the person more likely to go on to use other drugs. Because most people who use these gateway substances do not go on to become cocaine users, we should be cautious about jumping to that conclusion. More likely is that early alcohol use and cigarette smoking are common indicators of the general deviance-prone pattern of behavior that also includes an increased likelihood of smoking marijuana or trying cocaine. Because beer and cigarettes are more widely available to a deviance-prone young person than marijuana or cocaine, it is logical that beer and cigarettes would most often be tried first. The socially conforming students are less likely to try even these relatively available substances until they are older, and they are less likely ever to try the illicit substances. Let’s
antecedent (ant eh see dent): a variable that occurs before some event such as the initiation of drug use. longitudinal study (lon jeh too di nul): a study done over a period of time (months or years). gateway: one of the first drugs (e.g., alcohol or tobacco) used by a typical drug user.
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Targeting Prevention Preventing What? Chapter 1 provides an overview of psychoactive drug use, primarily based on data from the United States. As we look forward to the topic of prevention, it’s appropriate to think about what aspects of psychoactive drug use we would most like to reduce. Following are some perspectives: • We should work to prevent any use of tobacco or alcohol by those under age 21, as well as any use of drugs such as marijuana, cocaine, and LSD. These drugs are all illegal, and we know that early use of tobacco and alcohol is associated with a greatly increased risk of illicit drug use in the future. • Focusing only on drug use ignores the fact that illicit drug use is usually part of a larger pattern of deviant or antisocial behavior. Therefore, our efforts would be more effective if we were to target younger people and work to prevent poor
ask the question another way: If we developed a prevention program that stopped all young people from smoking cigarettes, would that cut down on marijuana smoking? Most of us think it might, because people who don’t want to suck tobacco smoke into their lungs probably won’t want to inhale marijuana smoke either. Would such a program keep people from getting D averages or getting into other kinds of trouble? Probably not. In other words, we think of the use of gateway substances not as the cause of later illicit drug use but, instead, as an early indicator of the basic pattern of deviant behavior resulting from a variety of psychosocial risk factors.
Motives for Drug Use To most of us, it doesn’t seem necessary to find explanations for normative behavior; we don’t often ask why someone takes a pain reliever when she has a headache. Our task is to try to explain the drug-taking behavior that frightens and infuriates—the deviant drug use. We
academic performance, fighting, shoplifting, and other early indicators of this lifestyle, in addition to early experimentation with tobacco and alcohol. • Wait a minute! We’re confusing what might be desirable with what might be possible. We can’t prevent everyone from doing things we don’t like. For example, as adults most people will drink alcohol at least once in a while, yet perhaps only 10 percent of drinkers have most of the problems. Trying to prevent all drug use and other undesirable behavior is just too big a job, and it violates our sense of individual freedom. We need to focus our efforts on preventing abuse and the crime that goes with it. That’s a much smaller problem, and we have a better chance of success. With which of these perspectives do you most agree at this point? Are there other perspectives not represented by these three?
should keep one fact about human conduct in mind throughout this book: Despite good, logical evidence telling us we “should” avoid certain things, we all do some of them anyway. We know that we shouldn’t eat that second piece of pie or have that third drink on an empty stomach. Cool-headed logic tells us so. We would be hard pressed to find good, sensible reasons why we should smoke cigarettes, drive faster than the speed limit, go skydiving, sleep late when we have work to do, flirt with someone and risk an established relationship, or use cocaine. Whether one labels these behaviors sinful or just stupid, they don’t seem to be designed to maximize our health or longevity. But humans do not live by logic alone; we are social animals who like to impress each other, and we are pleasure-seeking animals. These factors help explain why people do some of the things they shouldn’t, including using drugs. The research on correlates and antecedents points to a variety of personal and social variables that influence our drug taking, and many psychological and sociological theorists have proposed
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People who use drugs and who identify with a deviant subculture are more likely to engage in a variety of behaviors not condoned by society.
models for explaining illegal or excessive drug use. We have seen evidence for one common reason that some people begin to take certain illegal drugs: usually young, and somewhat more often male than female, they have chosen to identify with a deviant subculture. These groups frequently engage in a variety of behaviors not condoned by the larger society. Within that group, the use of a particular drug might not be deviant at all but might, in fact, be expected. Occasionally the use of a particular drug becomes such a fad among a large number of youth groups that it seems to be a nationwide problem. However, within any given community there will still be people of the same age who don’t use the drug. Rebellious behavior, especially among young people, serves important functions not only for the developing individual but also for the evolving society. Adolescents often try very hard to impress other people and may find it especially difficult to impress their parents. An adolescent who is unable to gain respect from people or who is frustrated in efforts to “go his or her own way” might engage in a particularly dangerous or disgusting behavior as a way of demanding that people be impressed or at least pay attention. One source of excessive drug use may be found within the drugs themselves. Many of these drugs are capable of reinforcing the behavior that gets the drug into the system. Reinforce-
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ment means that, everything else being equal, each time you take the drug you increase slightly the probability that you will take it again. Thus, with many psychoactive drugs there is a constant tendency to increase the frequency or amount of use. Some drugs (such as intravenous heroin or cocaine) appear to be so reinforcing that this process occurs relatively rapidly in a large percentage of those who use them. For other drugs, such as alcohol, the process seems to be slower. In many people, social factors, other reinforcers, or other activities prevent an increase. For some, however, the drug-taking behavior does increase and consumes an increasing share of their lives. Most drug users are seeking an altered state of consciousness, a different perception of the world than is provided by normal, day-to-day activities. Many of the high school students in the nationwide surveys report that they take drugs “to see what it’s like,” or “to get high,” or “because of boredom.” In other words, they are looking for a change, for something new and different in their lives. This aspect of drug use was particularly clear during the 1960s and 1970s, when LSD and other perception-altering drugs were popular. We don’t always recognize the altered states produced by other substances, but they do exist. A man drinking alcohol might have just a bit more of a perception that he’s a tough guy, that he’s influential, that he’s well liked. A cocaine user might get the seductive feeling that everything is great and that she’s doing a great job (even if she isn’t). Many drug-abuse prevention programs have focused on efforts to show young people how to feel good about themselves and how to look for excitement in their lives without using drugs. Another thing seems clear: Although societal, community, and family factors (the outer areas of Figure 1.4) play an important role in determining whether an individual will first try a reinforcement: a procedure in which a behavioral event is followed by a consequent event such that the behavior is then more likely to be repeated. The behavior of taking a drug may be reinforced by the effect of the drug.
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Societal Laws and Penalties
Availability and Cost
Community and Family Family Political Statements
Peers Antidrug Commercials
Individual
Schools
Alcohol and Tobacco Ads
Personality Knowledge/Attitudes/Beliefs Personal Drug Experience Motives/Needs Biology
Clubs/ Organizations
Church
Statements by Authorities/ Celebrities
Gangs Local Police Portrayal in News Articles/Shows
Portrayal in Movies/Novels
Figure 1.4 Influences on Drug Use drug, with increasing use the individual’s own experiences with the drug become increasingly important. For those who become seriously dependent, the drug and its actions on that individual become central, and social influences, availability, cost, and penalties play a less important role in the continuation of drug use.
•
Deviant drug use includes those forms of drug use not considered either normal or acceptable by the society at large. Drug misuse is using a drug in a way that was not intended by its manufacturer. Drug abuse is drug use that causes problems. (If frequent and serious, then a diagnosis of substance-use disorder is applied.) Drug dependence involves using the substance more often or in greater amounts than the user intended, and having difficulty stopping or cutting down on its use.
•
Among American college students, about 65 percent can be considered current (within the past 30 days) users of alcohol, about 20 percent current smokers of tobacco cigarettes, less than 20 percent current marijuana users, and less than 2 percent current users of cocaine.
Summary •
•
In discussing a drug-use issue, you must consider who is using the drug, what drug is being used, when and where the drug use is occurring, why the person is using the drug, how the person is taking the drug, and how much drug is being used. No drug is either entirely good or bad, and every drug has multiple effects. The size and type of effect depends on the dose of the drug and the user’s history and expectations.
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•
•
•
•
Both alcohol and illicit drug use reached an apparent peak around 1980, then decreased until the early 1990s, with a slower increase after that. Current rates of use are lower than at the peak. Adolescents who use illicit drugs (mostly marijuana) are more likely to know adults who use drugs, less likely to believe that their parents would object to their drug use, less likely to see their parents as a source of social support, more likely to have friends who use drugs, less likely to be religious, and more likely to have academic problems. A typical progression of drug use starts with cigarettes and alcohol, then marijuana, then other drugs such as amphetamines, cocaine, or heroin. However, there is no evidence that using one of the “gateway” substances causes one to escalate to more deviant forms of drug use. People may use illicit or dangerous drugs for a variety of reasons: They may be part of a deviant subculture, they may be signaling their rebellion, they may find the effects of the drugs to be reinforcing, or they may be seeking an altered state of consciousness. The specific types of drugs and the ways they are used will be influenced by the user’s social and physical environment. If dependence develops, then these environmental factors may begin to have less influence.
Chapter 1
4. 5.
6. 7. 8.
Review Questions
2. 3.
Besides asking a person the question directly, what is one way a psychologist can try to determine why a person is taking a drug? What two characteristics of a drug’s effect might change when the dose is increased? In about what year did drug use in the United States peak?
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About what percentage of college students use marijuana? What do the results of the National Survey on Drug Use and Health tell us about the overall rates of marijuana and cocaine use among whites compared to African Americans in the United States? How does having a college degree influence rates of drinking alcohol? Using tobacco? Name one risk factor and one protective factor related to the family/parents. How does impulsivity relate to rates of drug use in the general population? How does impulsivity relate to substance dependence?
References 1.
2.
3.
4.
5.
1.
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Johnston, L. D., P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg. Monitoring the Future National Survey Results on Drug Use, 1975–2004. Volume II: College Students and Adults Ages 19–45 (NIH Publication No. 05-5728). Bethesda, MD: National Institute on Drug Abuse, 2005. Wright, D., and M. Pemberton. Risk and Protective Factors for Adolescent Drug Use: Findings from the 1999 National Household Survey on Drug Abuse (DHHS Publication No. SMA 04-3874, Analytic Series A-19). Rockville, MD: Substance Abuse and Mental Health Services Administration, Office of Applied Studies, 2004. Vangsness, L., B. H. Bry, and E. W. LaBouvie. “Impulsivity, Negative Expectancies, and Marijuana Use: A Test of the Acquired Preparedness Model.” Addictive Behaviors 30 (2005), pp. 1071–76. Kreek, M. J., D. A. Nielsen, E. R. Butelman, and K. S. LaForge. “Genetic Influences on Impulsivity, Risk Taking, Stress Responsivity and Vulnerability to Drug Abuse and Addiction.” Nature Neuroscience 8 (2005), pp. 1450–57. Poikolainen, Kari. “Antecedents of Substance Use in Adolescence.” Current Opinion in Psychiatry 15 (2002), pp. 241–45. Ensminger, M. E., H. S. Juon, and K. E. Fothergill. “Childhood and Adolescent Antecedents of Substance Use in Adulthood.” Addiction 97 (2002), pp. 833–44. Kandel, D., and R. Faust. “Sequence and Stages in Patterns of Adolescent Drug Use.” Archives of General Psychiatry 32 (1975), pp. 923–32. Ginzler, J. A., and others. “Sequential Progression of Substance Use among Homeless Youth: An Empirical Investigation of the Gateway Theory.” Substance Use & Misuse 38 (2003), pp. 725–58.
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Check Yourself
Name
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Date
Do Your Goals and Behaviors Match? One interesting thing about young people who get into trouble with drugs or other types of deviant behavior is that they often express fairly conventional long-term goals for themselves. In other words, they want or perhaps even expect to be successful in life, but then do things that interfere with that success. One way to look at this is that their long-term goals don’t match up with their short-term behavior. Everyone does this sort of thing to some extent—you want to get a good grade on the first exam, but then someone talks you into going out instead of studying for the next one. Or perhaps you hope to lose five pounds but just can’t pass up that extra slice of pizza. Make yourself a chart that lists your long-term goals down one side and has a space for short-term behaviors down the other side, like the one below.
Write in your goal under each category as best you can. Then think about some things you do occasionally that tend to interfere with your achieving that goal and put a minus sign next to each of those behaviors. After you have gone through all the goals, write down some short-term behaviors that you could practice to assist you in achieving each goal, and put a plus sign beside each of those behaviors. How does it stack up? Are there some important goals for which you have too many minuses and not enough plusses? If study skills and habits, relationship problems, or substance abuse appear to be serious roadblocks for your success, consider visiting a counselor or therapist to get help in overcoming them.
Goals (Long-Term)
Behaviors (Short-Term)
Educational
Physical health and fitness
Occupational
Spiritual
Personal relationships
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Drug Use as a Social Problem Objectives When you have finished this chapter, you should be able to: • Distinguish between the federal government’s regulatory approach before the early 1900s and now. • Distinguish between acute and chronic toxicity and between physiological and behavioral toxicity. • Describe the two types of data collected in the DAWN system and know the top four drug classes for emergency room visits and for mortality. • Understand why the risks of HIV/AIDS and hepatitis are higher among injection drug users.
As we look into the problems ex• Define tolerance, physical dependence, and behavioral perienced by society as a result of dependence. the use of psychoactive drugs, we need to consider two broad catego• Understand that the scientific perspective on substance ries. The first category is the probdependence has changed in recent years. lems directly related to actually • Differentiate between substance abuse and substance taking the drug, such as the risk dependence using diagnostic criteria. of developing dependence or of overdosing. Second, because the • Debate the various theories on the cause of dependence. use of certain drugs is considered • Describe four ways it has been proposed that drug use a deviant act, the continued use of might cause an increase in crime. those drugs by some individuals represents a different set of social problems, apart from the direct dangers of the drugs themselves. These problems include arrests, fines, jailing, and the expenses associated with efforts to prevent misuse and to Laissez-Faire treat abuse and dependence. We begin by examIn the 1800s, the U.S. government, like the ining the direct drug-related problems that first majority of countries around the world, had raised concerns about cocaine, opium, and other virtually no laws governing the sale or use of drugs. Problems related to law enforcement, premost drugs. The idea seemed to be that, if the vention, and treatment will be examined more seller wanted to sell it and the buyer wanted to thoroughly in Chapters 3, 17, and 18. 25
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Toxicity
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The word toxic means “poisonous, deadly, or dangerous.” All the drugs we discuss in this text can be toxic if misused or abused. We will use the term to refer to those effects of drugs that interfere with normal functioning in such a way as to produce dangerous or potentially dangerous consequences. Seen in this way, for example, alcohol can be toxic in high doses because it suppresses respiration—this can be dangerous if breathing stops long enough to induce brain damage or death. But we can also consider alcohol to be toxic if it causes a person to be so disoriented that, for them, otherwise normal behaviors, such as driving a car or swimming, become dangerous. This is an example of something we refer to as behavioral toxicity. We make a somewhat arbitrary distinction, then, between behavioral toxicity and “physiological” toxicity—perhaps taking advantage of the widely assumed mind-body distinction, which is more convenient than real. The only reason for making this distinction is that it helps remind us of some important kinds of toxicity that are special to psychoactive drugs and that are sometimes overlooked. Why do we consider physiological toxicity to be a “social” problem? One view might be that if an individual chooses to take a risk and harms his or her own body, that’s the individual’s business. But impacts on hospital emergency rooms, increased health insurance rates, lost productivity, and other consequences of physiological toxicity mean that social systems also are affected when an individual’s health is put at risk, whether by drug use or failure to wear seat belts. Another distinction we make for the purpose of discussion is acute versus chronic. Most of the time when people use the word acute, they mean “sharp” or “intense.” In medicine an acute condition is one that comes on suddenly, as opposed to a chronic or long-lasting condition. When talking about drug effects, we can think of the acute effects as those that result
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buy it, let them do it—laissez-faire, in French. This term has been used to characterize the general nature of the U.S. government of that era. In the 21st century, hundreds of drugs are listed as federally controlled substances, the U.S. government spends more than $12 billion each year trying to control their sale and use, and 1.5 million arrests are made each year for violating controlled substance laws. What happened to cause the leaders of the “land of the free” to believe it was necessary to create especially restrictive regulations for some drugs? Three main concerns aroused public interest: (1) toxicity: some drug sellers were considered to be endangering the public health and victimizing individuals because they were selling dangerous, toxic chemicals, often without labeling them or putting appropriate warnings on them; (2) dependence: some sellers were seen as victimizing individuals and endangering their health by selling them habit-forming drugs, again often without appropriate labels or warnings; and (3) crime: the drug user came to be seen as a threat to public safety—the attitude became widespread that drug-crazed individuals would often commit horrible, violent crimes. In Chapter 3, we will look at the roots of these concerns and how our current legal structures grew from them. For now, let’s look at each issue and develop ground rules for the discussion of toxicity, dependence, and drug-induced criminality.
Categories of Toxicity
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Drugs in the Media Pharm Parties? As evidence from various sources points to an increasing problem with misuse of prescription medications, especially opioids such as Oxycontin and Vicodin, it should not be surprising that sometimes drug “experts” and news organizations will sensationalize the issue. In 2006, USA Today reported that drug counselors across the country were beginning to hear about “pharm” or “pharming” parties, at which young people bring whatever prescription pills they can acquire, put them all into a large bowl, and then just take pills at random from the bowl. The problem with the story was that no actual data on these practices were presented, leading Jack Shafer, a columnist for the online magazine Slate, to respond with an
from a single administration of a drug or are a direct result of the actual presence of the drug in the system at the time. For example, taking an overdose of heroin can lead to acute toxicity. By contrast, the chronic effects of a drug are those that result from long-term exposure and can be present whether or not the substance is actually in the system at a given point. For example, smoking cigarettes can eventually lead to various types of lung disorders. If you have emphysema from years of smoking, that condition is there when you wake up in the morning and when you go to bed at night, and whether your most recent cigarette was five minutes ago or five days ago doesn’t make much difference. Using these definitions, Table 2.1 (p. 28) can help give us an overall picture of the possible toxic consequences of a given type of drug. However, knowing what is possible is different from knowing what is likely. How can we get an idea of which drugs are most likely to produce adverse drug reactions?
Drug Abuse Warning Network In an effort to monitor the toxicity of drugs other than alcohol, the U.S. government set up the Drug Abuse Warning Network (DAWN). This
article, “Phar-fetched Pharm Parties: Real or a Media Invention?” After looking into the origins of these stories, Shafer became even more convinced that this was just a sensationalistic story with little or no basis in fact. It’s not to say that such a party has never happened anywhere—indeed, those of us who have been watching the drug scene for decades recall similar media stories in the early 1970s. But is this really something that has become as frequent as USA Today implied? One concern about such media reports is that they might encourage some young people to try this, because it is reported to be a craze that’s currently sweeping the nation. You can read Shafer’s article online at http://www.slate.com/id/2143982.
system collects data on drug-related emergency room visits from hospital emergency departments in major metropolitan areas around the country. When an individual goes to an emergency room with any sort of problem related to drug misuse or abuse, each drug involved (up to six) is recorded. For each drug or drug type, staff members can add up the number of visits associated with that particular drug. The visit could be for a wide variety of reasons, such as injury due to an accident, accidental overdose, a suicide attempt, or a distressing panic reaction that is not life-threatening to the patient. The emergency
laissez-faire (lay say fair): a hands-off approach to government. toxic: poisonous, dangerous. behavioral toxicity: toxicity resulting from behavioral effects of a drug. acute: referring to drugs, the short-term effects of a single dose. chronic: referring to drugs, the long-term effects from repeated use. DAWN: Drug Abuse Warning Network. System for collecting data on drug-related deaths or emergency room visits.
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Table 2.1 Examples of Four Types of DrugInduced Toxicity Acute (immediate) Behavioral
“Intoxication” from alcohol, marijuana, or other drugs that impair behavior and increase danger to the individual
Physiological
Overdose of heroin or alcohol causing the user to stop breathing
Chronic (long-term) Behavioral
Personality changes reported to occur in alcoholics and suspected by some to occur in marijuana users (a motivational syndrome)
Physiological
Heart disease, lung cancer, and other effects related to smoking; liver damage resulting from chronic alcohol exposure
room personnel who record these incidents do not need to determine that the drug actually caused the visit, only that some type of drug misuse or abuse was involved. This avoids many of the subjective judgments that would vary from place to place and from day to day, especially when (as is often the case) more than one drug is involved. If someone is in an automobile accident after drinking alcohol, smoking marijuana, and using some cocaine, rather than trying to say which one of these substances was responsible for the accident, each of them is counted as being involved in that emergency room visit. Because not every emergency room in the U.S. participates in the DAWN system, for many years the sampled data were used to estimate the overall number of emergency room visits for the entire country. Because of concerns about the accuracy of those estimates, more recent results are not used in that way. The numbers for emergency room visits for
2005 shown on the left side of Table 2.2 (p. 29) are the totals from the sampled hospitals.1 The DAWN system collects another set of data on drug-related deaths, with the reports being completed by medical examiners (coroners) in the same metropolitan areas around the U.S. The agency responsible for the DAWN data (the Office of Applied Studies from the Substance Abuse and Mental Health Services Administration) became so concerned about the accuracy of national estimates that they have stopped providing overall national totals and rankings by drug type. The numbers on the right side of Table 2.2 were derived by adding up the reported number of deaths in 2003 related to each drug type from each of the 32 major metropolitan areas.2 Alcohol is treated somewhat differently than other drugs in the sample. Whenever an emergency room visit or a death is related only to alcohol use by an adult, the DAWN system does not keep track of that. Alcohol-related problems are counted when alcohol and some other drug are involved (alcohol-in-combination); in the latest report alcohol alone is recorded if the individual is under 21 years of age. Notice that alcohol-in-combination is near the top ranking in both types of data, a place it has held for many years. In fact, if alcohol were counted alone its numbers would be large enough to make the other drugs seem much less important beside it. This seems to indicate that alcohol is a fairly
The Drug Abuse Warning Network (DAWN) uses data from hospital emergency rooms to monitor drug toxicity.
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Table 2.2 Toxicity Data from the Drug Abuse Warning Network (DAWN) DRUG-RELATED EMERGENCY ROOM VISITS (2005) Rank
DRUG-RELATED DEATHS (2003)
Drug
Number
Rank
1.
Cocaine
448,481
1.
Opioids (not heroin)
3,667
2.
Alcohol-in-combination
394,224
2.
Cocaine
3,142
3. 4.
Marijuana Prescription opioids
242,200 196,225
3. 4.
Alcohol-in-combination Benzodiazepeines
2,482 1,611
5. 6. 7.
Benzodiazepines Heroin Methamphetamine
172,388 164,572 108,905
5. 6. 7.
1,566 1,171 882
8. 9.
Antidepressants Acetaminophen
61,023 39,494
Antidepressants Methadone Sedative-Hypnotics (non-benzodiazepeine)
8.
Heroin
792
Antipsychotics
37,327
9.
Stimulants (includes methamphetamine) Marijuana
584
10.
10.
Drug
Number
304
Source: Drug Abuse Warning Network, 2005: National Estimates of Drug-Related Emergency Department Visits. DAWN Series D-29, DHHS Publication No. (SMA) 07-4256. Rockville, MD, March 2007; and Drug Abuse Warning Network, 2003: Area Profiles of Drug-Related Mortality. DAWN Series D-27, DHHS Publication No. (SMA) 05-4023. Rockville, MD, 2005.
toxic substance. It can be, but let us also remember that about half of all adult Americans drink alcohol at least once a month, whereas only a small percentage of the adult population uses cocaine, a drug that is also at the top of both lists. The DAWN system does not correct for differences in rates of use, but rather gives us an idea of the relative impact of a substance on medical emergencies and drug-related deaths. Cocaine has vied with alcohol-in-combination for the top spot on these lists since the mid-1980s. Legal drugs are found on both lists, with prescription opioids now at the top of the mortality data. Including the widely prescribed hydrocodone (Vicodin) and oxycodone (Oxycontin), these drugs are increasingly marketed through Internet pharmacies that might be contributing to the increased number of toxic reactions. Other groups of prescription drugs, such as benzodiazepine sedatives (e.g., Xanax) and sleeping pills (e.g., Halcion) and the antidepressants, are relatively
important, especially in the category of drugrelated deaths. The importance of drug combinations, particularly combinations with alcohol, in contributing to these numbers cannot be overstressed. Typically about half of the emergency room visits involve more than one substance, and about three-fourths of the drug-related deaths include multiple drugs. By far the most common “other” drug is alcohol. The most dramatic case is for the benzodiazepines. In 2003, only 16 of the 1,611 benzodiazepine-related deaths were reported as single-drug deaths, implying that the real danger lies in combining sedatives or sleeping pills with alcohol.
How Dangerous Is the Drug? Now that we have some idea of the drugs contributing to the largest numbers of toxic reactions in these two sets of data, let’s see if we can
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use that information to ask some questions about the relative danger to a person taking one drug versus another. We mentioned that the DAWN data do not correct for frequency of use. However, in Chapter 1 we reviewed other sets of data that provide information on the relative rates of use of different drugs, such as the National Survey on Drug Use and Health discussed on pages 10–15. The populations and sampling methods are different, so we’re not going to be able to make fine distinctions with any degree of accuracy. But we know, for example, that roughly eight times as many people report current use of marijuana as report current use of cocaine. The 2003 DAWN mortality report shows roughly six times as many cocaine-related deaths as marijuana-related deaths. If one-eighth as many users experience six times as many deaths, can we say that the risk of death to an individual cocaine user is 48 times the risk of death to an individual marijuana user? That’s too precise an answer, but is seems pretty clear that cocaine is relatively much more toxic than marijuana. We should point out an important difference in the latest DAWN report for 2003 regarding heroin. In past DAWN reports, if a blood sample was positive for morphine, this was recorded under the heroin/morphine category, because it is not possible to distinguish heroin from morphine with the standard toxicology screens. However, morphine is also fairly widely used as a legal prescription pain reliever, so previous reports probably overestimated the number of toxic reactions to heroin itself. In the 2003 data, for the first time heroin is counted separately only if there is specific information that the person actually used heroin. Since that information is not always available, especially after someone has died, the new reports probably underestimate the total number of toxic reactions to heroin. As a result, heroin appears to have dropped from third place in drug-related deaths to eighth place. This change is likely due to changes in the way the records are kept rather than to changes in heroin itself or in its use. We cannot tell precisely from the DAWN data how many total deaths are related to the use of cocaine or heroin, because not all coroners are
included in the system. Data are gathered from metropolitan areas that include about a third of the U.S. population, but they are areas that have higher than average use of illicit drugs. A very rough estimate of the total annual number of deaths related to cocaine, for example, might be three times the reported DAWN figure, or about 9,000 per year. The total for all illicit drugs, including cocaine, heroin, marijuana, and methamphetamine, might be approximately 15,000. Using the same proportions, estimated annual deaths associated with the use of the prescription narcotic analgesics, antidepressants, benzodiazepines, and over-the-counter pain relievers would be roughly 20,000. For comparison, alcohol is estimated to be responsible for 100,000 deaths annually (see Chapter 9), and more than 400,000 annual deaths are attributed to cigarette smoking (see Chapter 10). Of course, many more people use those substances, and in terms of relative danger of toxicity, heroin and cocaine are undoubtedly more dangerous than prescription drugs, alcohol, or cigarettes. However, in looking at the total impact of these drug-related deaths on American society, you might conclude that politicians and the news media have been paying a disproportionate amount of attention to cocaine, heroin, and methamphetamine.
Blood-Borne Diseases One specific toxicity concern for users who inject drugs is the potential for spreading
Needles are collected through an exchange program in an effort to prevent the spread of HIV among needle-using drug users.
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Mind/Body Connection Fear and Decision Making Fear is a useful emotion. Being afraid of something that threatens you helps you to avoid the real dangers that do exist in our world. But, of course, fear also can be irrational, far out of proportion to any real threat. When that happens, as individuals we might be hampered by being unable to use elevators or ride in airliners, or fear of contamination might seriously interfere with our social lives. Fear is also a favorite tool of many politicians. If they can convince us that there is a real threat of some kind and they offer to protect us from it, we are likely to elect them and to give them the power or funding they seek to provide that protection. Again, this is a rational and perfectly appropriate governmental response to the extent that the threat is both real and likely to harm us, but sometimes it is difficult to get it right. Maybe the U.S. government has underestimated the threat of global climate change. Maybe because of the horrible televised images of the World Trade Center attack we overestimate the threat of Al Quaeda. Raising fears about specific types of drugs has been a staple of politics and government in the U.S. for more than 100
blood-borne diseases, such as HIV, AIDS, and the life-threatening liver infections hepatitis B and hepatitis C. These viral diseases can all be transmitted through the sharing of needles. In a recent study of injecting drug users in six U.S. cities, rates of HIV infection ranged from a low of 3 percent to a high of almost 30 percent, representing a serious public health hazard. Rates of hepatitis B infection among injecting drug users were higher, ranging from 50 percent to 80 percent, and rates were even higher for hepatitis C (66 percent to 93 percent). Since rates increased with age, the authors stressed the need for prevention programs targeting younger people who have recently begun injecting drugs.3 This type of drug-associated toxicity is not due to the action of the drug itself, but is incidental to the sharing of needles, no matter which drug is injected or whether the injection is intravenous or intramuscular. An individual drug user may inject 1,000 times a year, and
years, from the age of Demon Rum through heroin, marijuana, LSD, PCP, cocaine, MDMA (Ecstasy), and methamphetamine. How do we get it right? On an individual level, most of us are sufficiently afraid of the possible consequences of using illicit drugs that we avoid using them at all. If those fears are overblown, so what? As long as we avoid using dangerous drugs we can see those fears as being useful. But a politician can easily amplify fears about a drug and use that fear to help get elected, and to pass laws that go too far, compared to the actual magnitude of the threat. Think about frightening things you have heard about specific drugs. For example, there has been a lot of talk about “meth” labs exploding and about the toxic effects of exposure to the harsh chemicals used in making methamphetamine. How can you evaluate such stories other than to go look up statistics on the actual occurrences of such events? Remember to use your common sense. If a story seems to be outrageous, there’s a pretty good chance that someone is overstating the actual risk.
that represents a lot of needles. In several states and cities, drug paraphernalia laws make it illegal to obtain syringes or needles without a prescription, and the resulting shortage of new, clean syringes increases the likelihood that drug users will share needles. One response to this has been the development of syringe exchange programs, in which new, clean syringes are traded for used syringes. Although the U.S. Congress has prohibited the use of federal funds to support these programs, based on the theory that they provide moral encouragement for illegal drug use, exchange programs have been funded by state and local governments, and many other countries support such programs. Evidence shows that given the opportunity, drug
HIV: human immunodeficiency virus. AIDS: acquired immunodeficiency syndrome.
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Targeting Prevention Clean Needles? The spread of the human immunodeficiency virus (HIV) among drug users is associated primarily with the sharing of the needles used for injecting heroin and other drugs. Evidence from several studies indicates that HIV transmission can be reduced if clean syringes and needles are made readily available to injecting drug users. Do you know whether a user of illicit drugs in your community can get access to clean syringes and needles? You might start learning about this by asking a local pharmacist to see what the rules are for purchasing these items, as well as how expensive they are. It will also be interesting to see how the pharmacist reacts to your questions about this topic. How do you react to the idea of possibly being
injectors increase their use of clean syringes, rates of infection are lowered, and the programs more than pay for themselves in the long run.4 Despite political opposition, syringe exchange currently represents one of the most practical ways to prevent the spread of these blood-borne diseases among drug users and from them to the non-drug-using population.
Substance Dependence: What Is It? All our lives we have heard people talk about “alcoholics” and “addicts,” and we’re sure we know what we’re talking about when one of these terms is used. Years ago when people first became concerned about some people being frequent, heavy users of cocaine or morphine, the term habituation was often used. If we try to develop scientific definitions, terms such as alcoholic or addict are actually hard to pin down. For example, not everyone who is considered an alcoholic drinks every day—some drink in binges, with brief periods of sobriety in between. Not everyone who drinks every day is considered an alcoholic—a glass of wine with
looked at as a user of illegal drugs? You might take this book along to show that you do have an academic reason for asking! Once you find out what the situation is with direct purchasing, see if you can discover if there is a needle exchange program in your community. This will be a little harder, but you can start by looking up “public health” in the phone book and calling that office. Are there steps your community could take to make clean needles more readily available to users of illicit drugs? Do you believe that such programs encourage or condone drug use? Would the program help prevent the spread of HIV in your community? Visit the Online Learning Center for links to more information on needle exchange programs.
dinner every night doesn’t match most people’s idea of alcoholism. The most extreme examples are easy to spot: the homeless man dressed in rags, drinking from a bottle of cheap wine, or the heroin user who needs a fix three or four times a day to avoid withdrawal symptoms. No hard-and-fast rule for quantity or frequency of use can help us draw a clear line between what we want to think of as a “normal drinker” or a “recreational user” and someone who has developed a dependence on the substance, who is compelled to use it, or who has lost control over use of the substance. It would be nice if we could separate substance use into two distinct categories: In one case, the individual controls the use of the substance; in the other case, the substance seems to take control of the individual. However, the real world of substance use, misuse, abuse, and dependence does not come wrapped in such convenient packages.
Three Basic Processes The extreme examples mentioned above, of the homeless wine drinker or the frequent heroin user, typically exhibit three characteristics of their substance use that distinguish
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them from first-time or occasional users. These appear to represent three processes that may occur with repeated drug use, and each of these processes can be defined and studied by researchers interested in understanding drug dependence. Tolerance Tolerance refers to a phenomenon seen with many drugs, in which repeated exposure to the same dose of the drug results in a lesser effect. There are many ways this diminished effect can occur, and some examples are given in Chapter 5. For now, it is enough for us to think of the body as developing ways to compensate for the chemical imbalance caused by introducing a drug into the system. As the individual experiences less and less of the desired effect, often the tolerance can be overcome by increasing the dose of the drug. Some regular drug users might eventually build up to taking much more of the drug than it would take to kill a nontolerant individual. Physical Dependence Physical dependence is defined by the occurrence of a withdrawal syndrome. Suppose a person has begun to take a drug and a tolerance has developed. The person increases the amount of drug and continues to take these higher doses so regularly that the body is continuously exposed to the drug for days or weeks. With some drugs, when the person stops taking the drug abruptly, a set of symptoms begins to appear as the drug level in the system drops. For example, as the level of heroin drops in a regular user, that person’s nose might run and he or she might begin to experience chills and fever, diarrhea, and other symptoms. When we have a drug that produces a consistent set of these symptoms in different individuals, we refer to the collection of symptoms as a withdrawal syndrome. These withdrawal syndromes vary from one class of drugs to another. Our model for why withdrawal symptoms appear is that the drug initially disrupts the body’s normal physiological balances. These imbalances are detected by the nervous system, and over a period of re-
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peated drug use the body’s normal regulatory mechanisms compensate for the presence of the drug. When the drug is suddenly removed, these compensating mechanisms produce an imbalance. Tolerance typically precedes physical dependence. To continue with the heroin example, when it is first used it slows intestinal movement and produces constipation. After several days of constant heroin use, other mechanisms in the body counteract this effect and get the intestines moving again (tolerance). If the heroin use is suddenly stopped, the compensating mechanisms produce too much intestinal motility. Diarrhea is one of the most reliable and dramatic heroin withdrawal symptoms. Because of the presumed involvement of these compensating mechanisms, the presence of a withdrawal syndrome is said to reflect physical (or physiological) dependence on the drug. In other words, the individual has come to depend on the presence of some amount of that drug to function normally; removing the drug leads to an imbalance, which is slowly corrected over a few days. Psychological Dependence Psychological dependence (also called behavioral dependence) can be defined in terms of observable behavior. It is indicated by the frequency of using a drug or by the amount of time or effort an individual spends in drug-seeking behavior. Often it is accompanied by reports of craving the drug or its effects. A major contribution of behavioral psychology has been to point out the scientific
tolerance: reduced effect of a drug after repeated use. withdrawal syndrome: a consistent set of symptoms that appears after discontinuing use of a drug. physical dependence: drug dependence defined by the presence of a withdrawal syndrome, implying that the body has become adapted to the drug’s presence. psychological dependence: behavioral dependence; indicated by high rate of drug use, craving for the drug, and a tendency to relapse after stopping use.
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weak-willed, lazy, or immoral (the “moral model”). Then medical and scientific studies began of users of alcohol and opioids. It seemed as if something more powerful than mere selfindulgence was at work, and the predominant view began to be that dependence is a druginduced illness.
Frequent drug use, craving for the drug, and a high rate of relapse after quitting indicate psychological dependence.
value of the concept of reinforcement for understanding psychological dependence. The term reinforcement is used in psychology to describe a process: A behavioral act is followed by a consequence, resulting in an increased tendency to repeat that behavioral act. The consequence may be described as pleasurable or as a “reward” in some cases (e.g., providing a tasty piece of food to someone who has not eaten for a while). In other cases, the consequence may be described in terms of escape from pain or discomfort. The behavior itself is said to be strengthened, or reinforced, by its consequences. The administration of certain drugs can reinforce the behaviors that led to the drug’s administration. Laboratory rats and monkeys have been trained to press levers when the only consequence of lever pressing is a small intravenous injection of heroin, cocaine, or another drug. Because some drugs but not others are capable of serving this function, it is possible to refer to some drugs as having “reinforcing properties” and to note that there is a general correlation between those drugs and the ones to which people often develop psychological dependence.
Changing Views of Dependence Until the 20th century, the most common view was probably that dependent individuals were
Early Medical Models If heroin dependence is induced by heroin, or alcohol dependence by alcohol, then why do some users develop dependence and others not? An early guess was simply that some people, for whatever reasons, were exposed to large amounts of the substance for a long time. This could happen through medical treatment or self-indulgence. The most obvious changes resulting from long exposure to large doses are the withdrawal symptoms that occur when the drug is stopped. Both alcohol and the opioids can produce rather dramatic withdrawal syndromes. Thus, the problem came to be associated with the presence of physical dependence (a withdrawal syndrome), and enlightened medically oriented researchers went looking for treatments based on reducing or eliminating withdrawal symptoms. According to the most narrow interpretation of this model, the dependence itself was cured when the person had successfully completed withdrawal and the symptoms disappeared. Pharmacologists and medical authorities continued into the 1970s to define “addiction” as occurring only when physical dependence was seen. Based on this view, public policy decisions, medical treatment, and individual drug-use decisions could be influenced by the question “Is this an addicting drug?” If some drugs produce dependence but others do not, then legal restrictions on specific drugs, care in the medical use of those drugs, and education in avoiding the recreational use of those drugs are appropriate. The determination of whether a drug is or is not “addicting” was therefore crucial. In the 1960s, some drugs, particularly marijuana and amphetamines, were not considered to have well-defined, dramatic, physical withdrawal syndromes. The growing group of interested scientists began to refer to drugs
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such as marijuana, amphetamines, and cocaine as “merely” producing psychological dependence, whereas heroin produced a “true addiction,” which includes physical dependence. The idea seemed to be that psychological dependence was “all in the head,” whereas with physical dependence actual bodily processes were involved, subject to physiological and biochemical analysis and possibly to improved medical treatments. This was the view held by most drug-abuse experts in the 1960s.
the basis of what had been called psychological dependence. Drugs such as amphetamines and cocaine could easily be used as reinforcers in these experiments, and they were known to produce strong psychological dependence in humans. Animal experiments using drug selfadministration are now of central importance in determining which drugs are likely to be used repeatedly by people, as well as in exploring the basic behavioral and biological features associated with drug dependence.5
Positive Reinforcement Model In the 1960s, a remarkable series of experiments began to appear in the scientific literature—experiments in which laboratory monkeys and rats were given intravenous catheters connected to motorized syringes and controlling equipment so that pressing a lever would produce a single brief injection of morphine, an opioid very similar to heroin. In the initial experiments, monkeys were exposed for several days to large doses of morphine, allowed to experience the initial stages of withdrawal, and then connected to the apparatus to see if they would learn to press the lever, thereby avoiding the withdrawal symptoms. These experiments were based on the predominant view of drug use as being driven by physical dependence. The monkeys did learn to press the levers. As these scientists began to publish their results and as more experiments like this were done, interesting facts became apparent. First, monkeys would begin pressing and maintain pressing without first being made physically dependent. Second, monkeys who had given themselves only fairly small doses and who had never experienced withdrawal symptoms could be trained to work very hard for their morphine. A history of physical dependence and withdrawal didn’t seem to have much influence on response rates in the long run. Clearly, the small drug injections themselves were working as positive reinforcers of the lever-pressing behavior, just as food can be a positive reinforcer to a hungry rat or monkey. Thus, the idea spread that drugs can act as reinforcers of behavior and that this might be
Which Is More Important, Physical Dependence or Psychological Dependence? The animal research that led to the positive reinforcement model implies that psychological dependence is more important than physical dependence in explaining repeated drug use, and this has led people to examine the lives of heroin users from a different perspective. Stories were told of users who occasionally stopped taking heroin, voluntarily going through withdrawal so as to reduce their tolerance level and get back to the lower doses of drug they could more easily afford. When we examine the total daily heroin intake of many users, we see that they do not need a large amount and that the agonies of withdrawal they experience are no worse than a case of intestinal flu. We have known for a long time that heroin users who have already gone through withdrawal in treatment programs or in jail have a high probability of returning to active heroin use. In other words, if all we had to worry about was users’ avoiding withdrawal symptoms, the problem would be much smaller than it actually is.
reinforcement: a procedure in which a behavioral event is followed by a consequent event such that the behavior is then more likely to be repeated. The behavior of taking a drug may be reinforced by the effect-of the drug. catheters (cath a ters): plastic or other tubing implanted into the body.
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DSM-IV-TR Psychiatric Diagnosis of Substance-Use Disorders Diagnostic Criteria for Substance Dependence A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of the substance to achieve intoxication or desired effect b. Markedly diminished effect with continued use of the same amount of the substance 2. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the substance b. The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms 3. The substance is often taken in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful efforts to cut down or control substance use. 5. A great deal of time is spent in activities necessary to obtain the substance. 6. Important social, occupational, or recreational activities are given up or reduced because of substance use. 7. The substance use is continued despite knowledge of having a persistent or recurrent physical or
Psychological dependence, based on reinforcement, is increasingly accepted as the real driving force behind repeated drug use, and tolerance and physical dependence are now seen as related phenomena that sometimes occur but probably are not critical to the development of frequent patterns of drug-using behavior. Researchers and treatment providers rely heavily on the definitions of substance dependence and substance abuse developed by the American Psychiatric Association and presented in their Diagnostic and Statistical Manual (DSM-IV-TR).6 These are presented in
psychological problem that is likely to have been caused or exacerbated by the substance. • With physiological dependence: evidence of tolerance or withdrawal (i.e., either Item 1 or 2 is present) • Without physiological dependence: no evidence of tolerance or withdrawal (i.e., neither Item 1 nor 2 is present) Diagnostic Criteria for Substance Abuse A. A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: 1. Recurrent substance use resulting in failure to fulfill major role obligations at work, school, or home 2. Recurrent substance use in situations in which it is physically hazardous 3. Recurrent substance-related legal problems 4. Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance B. The symptoms have never met the criteria for substance dependence for this class of substance.
outline form above. Notice that both substance dependence and substance abuse are complex behavioral definitions, and the exact set of behaviors seen may vary from person to person. Also, please note that three of the seven criteria must be met for substance dependence, and that five of the seven describe behaviors, such as taking more of the substance than was intended or giving up other important activities because of substance use. This again points out that these substance-use disorders are primarily seen as behavioral in nature, with tolerance and physical dependence being less important.
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Broad Views of Substance Dependence If we define drug dependence not in terms of withdrawal but in more behavioral or psychological terms, as an overwhelming involvement with getting and using the drug, then might this model also be used to describe other kinds of behavior? What about a man who visits prostitutes several times a day; someone who eats large amounts of food throughout the day; or someone who places bets on every football and basketball game, every horse race or automobile race, and who spends hours each day planning these bets and finding money to bet again? Shouldn’t these also be considered examples of dependence? Do the experiences of overeating, gambling, sex, and drugs have something in common—a common change in physiology or brain chemistry or a common personality trait that leads to any or many of these compulsive behaviors? Are all of these filling an unmet social or spiritual need? More and more, researchers are looking for these common threads and discussing “dependencies” as a varied set of behavioral manifestations of a common dependence process or disorder.
Is Dependence Caused by the Substance? Especially with chemical dependence, many people speak as though the substance itself is the cause of the dependence. Certainly some drugs are more likely than others to result in dependence. For example, it is widely believed that heroin and crack cocaine are both extremely likely to lead to compulsive use. In contrast, most users of marijuana report occasional use and little difficulty in deciding when to use it and when not to. We also know that some methods of taking a drug (e.g., intravenous injection) are more likely to result in repeated use than other methods of taking the same drug (by mouth, for instance). We can determine which drugs, or which methods of using those drugs, pose the greatest risk for dependence. One major study reviewed 350 published articles to come up with relative ratings, then had the prelimi-
Alcohol causes serious dependence in perhaps 1 of 10 drinkers.
nary tables reviewed by a panel of psychopharmacologists for suggested changes.7 Based on that report, we can classify psychoactive drugs into seven categories of “dependence potential.” Smoked or injected methamphetamine would probably be in one of the top two categories in such a ranking (see Table 2.3). The range of risk of dependence depends to some extent upon the drug itself, but also depends upon its method of use (as well as a variety of other biological, psychological, and social factors). Thus, the substance itself cannot be seen as the entire cause of the problem, even though some people would like to put all the blame on “demon rum” or on heroin or crack cocaine. When we extend the concept of dependence to other activities, such as gambling, sex, or overeating, it seems harder to place the entire blame on the activity, again because many people do not exhibit compulsive patterns of such behaviors. Some activities might be more of a problem than others—few people become dependent on filling out income tax forms, whereas a higher proportion of all those who gamble become overwhelmingly involved. Still, it is wrong to conclude that any activity is by its nature always “habit forming.” When a chemical is seen as causing the dependence, there is a tendency to give that substance a personality and to ascribe motives to it. When we listen either to a practicing user’s loving description of his interaction with the drug
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Table 2.3 Dependence Potential of Psychoactive Drugs Very high:
Heroin (IV) Crack cocaine
High:
Morphine (injected) Opium (smoked)
Moderate/high:
Cocaine powder (snorted) Tobacco cigarettes PCP (smoked)
Moderate:
Diazepam (Valium) Alcohol Amphetamines (oral)
Moderate/low:
Caffeine MDMA* (Ecstasy) Marijuana
Low:
Ketamine (see Chapter 14)
Very low:
LSD† Mescaline Psilocybin
*MDMA, methylenedioxy methamphetamine †
LSD, lysergic acid diethylamide
or to a recovering alcoholic describe her struggle against the bottle’s attempts to destroy her, the substance seems to take on almost human characteristics. We all realize that is going too far, yet the analogy is so powerful that it pervades our thinking. Alcoholics Anonymous (AA) members often describe alcohol as being “cunning, baffling, and powerful” and admit that they are powerless against such a foe. And those seeking the prohibition of alcohol, cocaine, marijuana, heroin, and other drugs have over the years tended to demonize those substances, making them into powerful forces of evil. The concept of a “war on drugs” reflects in part such a perspective—that some drugs are evil and war must be waged against the substances themselves.
Is Dependence Biological? In recent years, interest has increased in the possibility that all compulsive behaviors might
have some common physiological or biochemical action in the brain. For example, many theorists have recently focused on dopamine, one of the brain’s important neurotransmitters, which some believe to play a large role in positive reinforcement. The idea is that any drug use or other activity that has pleasurable or rewarding properties spurs dopamine activity in a particular part of the brain. This idea is discussed more fully in Chapter 4. Although this theory has been widely tested in animal models and much evidence is consistent with it, considerable evidence also shows that this model is too simple and that other neurotransmitters and other brain regions are also important. A great deal of attention has been given to reports from various brain-scanning experiments done on drug users. For example, cues that stimulate craving for cocaine activate many areas that are widely separated in the brain, including some that are known to be dopamine-rich areas and some that are not.8 Although these studies show some of the physiological consequences produced by cocaine or by even thinking about cocaine, they have not yet been useful in examining the possible biological causes of dependence. One important question that remains is whether the brains of people who have used cocaine intermittently show different responses, compared with the brains of dependent cocaine users. Ultimately, the strongest demonstration of the power of such techniques would be if it were possible to know, based on looking at a brain scan, whether a person had developed dependence. Many previous biological theories of dependence have failed this test: so far, no genetic, physiological or biochemical marker has been found that strongly predicts drug dependence.
Is There an “Addictive Personality”? Perhaps the explanation for why some people become dependent but others do not lies in the personality—that complex set of attributes and attitudes that develops over time, partly as a result of particular experiences. Is there a common
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personality factor that is seen in compulsive drug users but not in others? We’ve known for some time that people who are diagnosed with certain types of personality disorders, such as antisocial personality or conduct disorder, are more likely to also have one of the substanceuse disorder diagnoses (substance abuse or substance dependence). We’ve also known that people who have a long history of alcohol dependence or heroin dependence will demonstrate a variety of differences from the normal population on personality tests. But neither of these findings tells us anything about what caused these relationships. Conduct disorder and antisocial personality disorder reflect a general tendency for a person to violate social norms. Perhaps drug use is just one of many ways this person might choose to break the rules? And someone who has been drinking heavily for many years, has had health problems, perhaps lost a job and family, might well have developed personality differences due to the consequences of years of substance abuse. So we have not had much good information until fairly recently about personality differences that might predispose individuals to develop a substance-use disorder. One personality trait that has frequently been associated with greater risk for abuse of stimulants such as amphetamine or cocaine is called “sensation-seeking.” The sensation-seeking scale, which is discussed further in Chapter 6 and is printed on page 151, measures the person’s preference for variety, risk, and various physical sensations. People who score higher on this scale tend to report a greater “high” and a greater “liking” for the drug when given amphetamine in a laboratory setting.9. Another, possibly related, personality factor is often referred to as impulsivity—the tendency to act quickly without as much regard to long-term consequences. The relationships between impulsivity and drug use are complex, and researchers are becoming more sophisticated in trying to understand the relationships among impulsivity, specific types of drug use, and the setting in which the drug is used. In
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other words, being impulsive might have more to do with whether a person drinks heavily when away from home on a weekend night than it does with whether a person has a glass of wine with dinner.10
Is Dependence a Family Disorder? Although few scientific studies have been done, examination of the lives of alcohol-dependent individuals reveals some typical patterns of family adaptation to the problem. A common example in a home with an alcohol-dependent father is that the mother enables this behavior, by calling her husband’s boss to say he is ill or by making excuses to family and friends for failures to appear at dinners or parties and generally by caring for her incapacitated husband. The children might also compensate in various ways, and all conspire to keep the family secret. Thus, it is said that alcohol dependence often exists within a dysfunctional family—the functions of individual members adjust to the needs created by the presence of excessive drinking. This new arrangement can make it difficult for the drinker alone to change his or her behavior, because doing so would disrupt the family system. Some people suspect that certain family structures actually enhance the likelihood of alcohol abuse or dependence developing. For example, the “codependent” needs of other family members to take care of someone who is dependent on them might facilitate drunkenness. Much has been written about the effects on children who grow up in an “alcoholic family,” and there is some indication that even as adults these individuals tend to exhibit certain personality characteristics. The “adult children of alcoholics” are then perhaps more likely to become involved in dysfunctional relation-
Alcoholics Anonymous (AA): a worldwide organization of self-help groups based on alcoholics helping each other achieve and maintain sobriety.
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ships that increase the likelihood of alcohol abuse, either in themselves or in another family member. Again, the evidence indicates that such influences are statistical tendencies and are not all-powerful. It is perhaps unfortunate that some people with alcoholic parents have adopted the role of “adult children” and try to explain their entire personalities and all their difficulties in terms of that status.
Is Substance Dependence a Disease? The most important reason for adopting a disease model for dependence is based on the experiences of the founders of AA and is discussed in Chapter 9. Psychiatrists had commonly assumed that alcohol dependence was secondary to another disorder, such as anxiety or depression, and often attempted to treat the presumed underlying disorder while encouraging the drinker to try to “cut down.” The founders of AA believed that alcohol dependence itself was the primary problem and needed to be recognized as such and treated directly. This is the reason for the continued insistence that alcohol dependence is a disease—that it is often the primary disturbance and deserves to stand in its own right as a recognized disorder requiring treatment. On the other hand, Peele11 and others have argued that substance dependence does not have many of the characteristics of some classic medical diseases, such as tuberculosis or syphilis: We can’t use an X-ray or blood test to reveal the underlying cause, and we don’t have a way to treat the underlying cause and cure the symptoms—we don’t really know that there is an underlying cause, because all we have are the symptoms of excessive involvement. Furthermore, if substance dependence itself is a disease, then gambling, excessive sexual involvement, and overeating should also be seen as diseases. This in turn weakens our normal understanding of the concept of disease. The disease model is perhaps best seen as an analogy—substance dependence is like a disease in many ways, but that is different from insisting
that it is a disease. One reason for the conflict over the disease model of dependence may be differences in how we think of the term disease. For example, many would agree that high blood pressure is considered a disease—it’s certainly viewed as a medical disorder. We know that high blood pressure can be produced by genetic factors, cigarette smoking, diet, lack of exercise, or by other medical conditions. In that context, the idea that alcohol or drug dependence is like a disease doesn’t seem so far-fetched. This is taking a broad, biopsychosocial perspective that dependence might be related to dysfunctions of biology, personality, social interactions, or a combination of these factors.
Crime and Violence: Does Drug Use Cause Crime? It might seem obvious to a reader of today’s newspapers or to a viewer of today’s television that drugs and crime are linked. There are frequent reports of killings attributed to warring gangs of
There are more than 1.5 million drug arrests every year.
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drug dealers. Our prisons house a large population of people convicted of drug-related crimes, and several reports have revealed that a large fraction of arrestees for nondrug felonies have positive results from urine tests for illicit substances. The belief that there is a causal relationship between many forms of drug use and criminality probably forms the basis for many of our laws concerning drug use and drug users. The relationship between crime and illegal drug use is complex, and only recently have, 5' dimethoxy –4' – methylamphetamine (DOM)
3, 4 methylenedioxy amphetamine (MDA) 3, 4, 5 trimethoxyphenylethylamine (mescaline)
Carbon Oxygen Hydrogen Nitrogen
3,4 methylenedioxy methamphetamine (MDMA)
Figure 14.2 Catechol Hallucinogens known as “mescal buttons,” remain psychoactive indefinitely and are the source of the drug between the yearly harvests. The indigenous peoples’ journey in November and December to harvest the peyote is an elaborate ceremony, sometimes taking almost a month and a half. When the mescal buttons are to be used, they are soaked in the mouth until soft, then formed by hand into a bolus and swallowed. Mescal buttons should not be confused with mescal beans—or with mescal liquor,
which is distilled from the fermentation of the agave cactus and is the starting point for making tequila. Mescal buttons are slices of the peyote cactus and contain mescaline as the primary active agent. Mescal beans, however,
peyote (pay oh tee): a type of hallucinogenic cactus. mescaline (mess ka lin): the active chemical in the peyote cactus.
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are dark red seeds from the shrub Sophora secundiflora. These seeds, formerly the basis of a vision-seeking cult, contain a highly toxic alkaloid, cytisine, the effects of which resemble those of nicotine, causing nausea, convulsions, hallucinations, and occasionally death from respiratory failure. The mescal bean has a long history, and there is some evidence that use of the bean diminished when the safer peyote became available in the southwestern United States. In the transition from a mescal bean to a mescal button cult, some tribes experienced a period in which a mixture of peyote and mescal seeds was concocted and drunk. These factors contributed to considerable confusion in the early (and some recent) literature.28 Although there was evidence that the use of peyote had moved north into the United States as early as 1760, it was not until the late 19th century that a peyote cult was widely established among the Native Americans of the plains. From that time to the present, Native American missionaries have spread the peyote religion to almost a quarter of a million Native Americans, some as far north as Canada. The Native American Church of the United States was first chartered in Oklahoma in 1918 and is an amalgamation of Christianity and traditional beliefs and practices of the Native Americans, with peyote use incorporated into its ceremonies. Peyotism continues to be an important religious practice among the Indians of the United States between the Rocky Mountains and the Mississippi. Peyote is also used in other ways because the Native Americans attribute spiritual power to the peyote plant. As such, peyote is believed to be helpful, along with prayers and modern medicines, in curing illnesses. It is also worn as an amulet, much as some Christians wear a Saint Christopher’s medal, to protect the wearer from harm. For many years the use of peyote as a sacrament by the Native American Church was protected by the constitutional guarantee of freedom of religion. That protection had inspired Timothy Leary to attempt a similar exclusion for LSD in his newly founded 1960s
Peyotism remains an important religious practice among Native Americans in certain areas of the United States. This painting from the early 20th century includes scenes of peyote cult practices.
League of Spiritual Discovery. However, in 1990 the Supreme Court ruled that the State of Oregon could prosecute its citizens for using peyote, and the freedom of religion argument was not allowed. A large group of religious and civil liberties organizations asked the court to reconsider its decision, but it declined to do so. The two defendants in the case were Native Americans and members of the Native American Church. Federal law and many state laws specifically exclude sacramental peyote use, and the court pointed out that Oregon could exclude such use, too. Other states have not moved to outlaw religious use of peyote. San Pedro Cactus Another mescaline-containing cactus, Trichocereus pachanoi, whose common name is the San Pedro cactus, is native to the Andes Mountains of Peru and Ecuador and has been used for thousands of years as a religious sacrament.32 The San Pedro is a large, multibranched cactus, often growing to heights of 10 to 15 feet. Its mescaline content is less than that of peyote, and its recreational use more often results in adverse side effects than in the desired hallucinogenic experience. Discovery and Early Research on Mescaline Near the end of the 19th century, Arthur Heffter isolated several alkaloids from peyote and showed that
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mescaline was the primary agent for the visual effect induced by peyote. Mescaline was synthesized in 1918, and most experiments on the psychoactive and/or behavioral effects since then have used synthesized mescaline. More than 30 psychoactive alkaloids have now been identified in peyote, but mescaline does seem to be the agent responsible for the vivid colors and other visual effects. The fact that mescaline is not equivalent to peyote is not always made clear in the literature. One of the early investigators of the effects of peyote was Dr. Weir Mitchell, who used an extract of peyote and reported, in part: The display which for an enchanted two hours followed was such as I find it hopeless to describe in language which shall convey to others the beauty and splendor of what I saw. Stars, delicate floating films of color, then an abrupt rush of countless points of white light swept across the field of view, as if the unseen millions of the Milky Way were to flow in a sparkling river before my eyes . . . zigzag lines of very bright colors . . . the wonderful loveliness of swelling clouds of more vivid colors gone before I could name them.33
Another early experimenter was Havelock Ellis. Interestingly, he took his peyote on Good Friday in 1897, 65 years before the Good Friday experiment with psilocybin. His experience is described in detail in a 1902 article titled “Mescal: A Study of a Divine Plant” in Popular Science Monthly, but a brief quotation gives the essence of the experience: On the whole, if I had to describe the visions in one word, I should say that they were living arabesques. There was generally a certain incomplete tendency to symmetry, the effect being somewhat as if the underlying mechanism consisted of a large number of polished facets acting as mirrors. It constantly happened that the same image was repeated over a large part of the field, though this holds good mainly of the forms, for in the colors there would still remain all sorts of delicious varieties. Thus at a moment when uniformly jewelled flowers seemed to be springing up and extending all over the field of vision,
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the flowers still showed every variety of delicate tone and tint.34
Not every individual wants every educational opportunity. William James, surprisingly, was one who did not. He wrote to his brother Henry: “I ate one but three days ago, was violently sick for twenty-four hours, and had no other symptoms whatever except that and the Katzenjammer the following day. I will take the visions on trust.” Even Dr. Weir Mitchell, who had the effect previously recorded, said, “These shows are expensive. . . . The experience, however, was worth one such headache and indigestion but was not worth a second.” Even if you get by without too much nausea and physical discomfort, which the Native Americans also report, all might not go well. Huxley, whose 1954 The Doors of Perception35 made him a guru in this area, admitted, “Along with the happily transfigured majority of mescaline takers there is a minority that finds in the drug only hell and purgatory.” It is reported that natives sometimes wished for bad trips when taking this or other plants. By meeting their personal demons, they hoped to conquer them and remove problems from their lives. Pharmacology of Mescaline Mescaline is readily absorbed if taken orally, but it poorly passes the blood-brain barrier (which explains the high doses required). There is a maximal concentration of the drug in the brain after 30 to 120 minutes. About half of it is removed from the body in six hours, and there is evidence that some mescaline persists in the brain for up to 10 hours. Similar to the indole hallucinogens, the effects obtained with low doses, about 3 mg/kg body weight, are primarily euphoric, whereas doses in the range of 5 mg/kg give rise to a full set of hallucinations. Most of the mescaline is excreted unchanged in the urine, and the metabolites identified thus far are not psychoactive. A dose that is psychoactive in humans causes pupil dilation, pulse rate and blood pressure increases, and an elevation in body
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temperature. All of these effects are similar to those induced by LSD, psilocybin, and most other alkaloid hallucinogens. There are other signs of central stimulation, such as EEG arousal, after mescaline intake. In rats the LD50 is about 370 mg/kg body weight, 10 to 30 times the dose that causes behavioral effects. Death results from convulsions and respiratory arrest. Tolerance develops more slowly to mescaline than to LSD, and there is cross-tolerance between them. As with LSD, mescaline intoxication can be blocked with chlorpromazine. Although mescaline and the other catechol hallucinogens have a structure that resembles the catecholamine neurotransmitters, they act indirectly on the serotonin 2A receptor. Amphetamine Derivatives A large group of synthetic hallucinogens is chemically related to the amphetamines. However, most of these drugs have little amphetamine-like stimulant activity. Thanks to certain chemical substitutions on the ring part of the catechol nucleus, these drugs are more mescaline-like (Figure 14.2). DOM (STP) DOM is 2,5-dimethoxy-4-methylamphetamine. In the 1960s and 1970s, DOM was called STP, and street talk was that the initials stood for serenity, tranquility, and peace. Its actions and effects are similar to those of mescaline and LSD, with a total dose of 1 to 3 mg yielding euphoria and 3 to 5 mg a six- to eighthour hallucinogenic period. This makes DOM about a hundred times as potent as mescaline but only one-thirtieth as potent as LSD. MDA and Others In addition to DOM, many other amphetamine derivatives have been synthesized and shown to have hallucinogenic properties. Most of these have effects very similar to those of DOM and mescaline, as well as LSD and the indole types. There is some indication that one type of derivative, MDA (Figure 14.2), has effects that are subjectively somewhat different. MDA, which is somewhat more potent than mescaline, has seen some recreational use through illicit manufacture. Because of the variety of possible
Some evidence suggests that Ecstasy may be neurotoxic, affecting serotonin neurons in the brain.
hallucinogenic amphetamine derivatives and because most of these chemicals are not specifically listed as controlled substances, illicit drug makers were drawn to this group of chemicals in the production of various designer drugs to be sold on the street as hallucinogens. MDMA One of the amphetamine derivatives— MDMA—received special attention in July 1984 when the DEA first proposed scheduling it. Although there had been some recreational use of MDMA (it is called “Ecstasy” or “XTC”), a number of psychiatrists testified against the scheduling of MDMA. They insisted that it was not a true hallucinogen and that it had a special ability to promote empathy, thus aiding the psychoanalytic process.36 There is some evidence supporting this claim of increased empathy: In one study, 100 people completed detailed questionnaires describing the effects of their previous use of MDMA.37 Although such retrospective reports are less reliable than reports obtained during or immediately after the experience, a remarkably common report (90 percent of the individuals) was that they experienced a heightened sense of “closeness” with other people. And like other amphetamines, MDMA increases euphoria, sociability, blood pressure, and heart rate. Although several people reported that objects seemed more “luminescent,” very few reported actual visual hallucinations.
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Drugs in Depth Extrapolating Findings from Animals to Humans: What You Need to Know “The amount of the drug Ecstasy that some recreational users take in a single night may cause permanent brain damage and lead to symptoms like those of Parkinson’s disease,” read an article published in The New York Times on September 27, 2002. This and similar statements were based on assertions made in a scientific paper that had just appeared in the highly respected and influential journal Science.38 George Ricaurte and his team of researchers gave nonhuman primates three doses of MDMA (also known as Ecstasy) over the course of six hours and, then, a couple of weeks later evaluated neuroanatomical and neurochemical alterations. They found extensive damage to dopamine and serotonin neurons as well as reduced levels of these neurotransmitters in the brain. The finding that MDMA damaged brain cells was not new. Several studies documented the neurotoxic effects of MDMA in laboratory animals.39 The majority of these studies, however, had used dosing regimens that were much larger and longer than those used by recreational MDMA users. Studies using laboratory animals, for instance, typically administer MDMA via routes other than oral, and in doses greater than 5 mg/kg twice a day for four or more consecutive days. By contrast, human recreational drug users almost always administer the drug orally and typically do not exceed 2–4 mg/kg in only one evening. What made Ricaurte and colleagues’ results intriguing was that the doses of MDMA used and the pattern of drug administration were claimed to be comparable to those used by recreational human users. The researchers injected MDMA at a dosage of 2 mg/kg, three times, at three-hour intervals, for a total dose of 6 mg/kg. As noted above, even this dosing regimen does not exactly correspond with those typically used by humans. Importantly, the route of drug administration is a critical determinant of neurochemical consequences (e.g., toxicity) because these effects depend on the rate of rise of drug concentrations and the maximum brain concentrations achieved. Recall from Chapter 5 that drugs administered by injection result in a more rapid onset of effects and greater brain concentrations. Furthermore, potential toxicity is decreased when a drug is self-administered compared to experimenteradministered.40 Thus, these two factors increased
the likelihood of observing toxicity in the Ricaurte study. Nevertheless, the study findings generated a wave of controversy. Critics argued that the total dose given to the animals far exceeded doses taken by humans and that the kind of brain damage observed has never been found in humans. They also noted that 20 percent of the animals died following MDMA administrations, whereas human mortality is rare. Supporters, in contrast, took the findings as evidence that MDMA is a highly toxic drug that should not be taken even once. But in an embarrassing turn of events, Ricaurte and colleagues were forced to retract their paper one year after its publication because they discovered that methamphetamine had been mistakenly given, rather than MDMA.41 This was deduced after several unsuccessful attempts by the researchers to replicate their original findings. It is noteworthy that those negative data were never published. This suggests that there is a bias toward publishing positive results (i.e., demonstration of MDMA-induced neurotoxicity). A similar situation has been noted regarding antidepressant medications (see Chapter 8). Even so, these events raise important questions about drug-induced neurotoxicity observed in laboratory animals and the relevancy of such findings for the human drug users. Unfortunately, uneven (and sometimes sensationalized) reports about drug-induced toxicity can be discouraging to students. As a result, some may reject all related information from scientific sources. Who should you believe? How do you determine which dataset is more compelling? In your attempt to understand research investigating drug-induced toxicity, you should ask a few simple questions: (1) What was the drug dosing regimen used and is it similar to regimens used by humans? (2) what was the route of drug administration used and do humans use the drug in this manner? (3) Was the drug self-administered or administered by the experimenter? (4) Because the development of tolerance can be protective against some types of toxicity, like human drug-taking behavior, were the animals administered escalating doses prior to receiving a larger dose? All of these factors potentially impact neurochemical findings and should be considered when making extrapolations about data collected in laboratory animals to humans.
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Anecdotal reports suggest that MDMA users report substantially more negative or depressed mood states in the days immediately following MDMA administration. Colloquially, this phenomenon is frequently referred to as “Suicide Tuesday.” Some have speculated that initially MDMA administration causes a substantial release of serotonin, followed by a marked reduction of the neurotransmitter, lasting several hours to days after the last dose. Because serotonin plays a major role in mood regulation, this produces the depressed mood state reported by MDMA users in the days following drug use. But there is no hard evidence. In fact, preliminary data collected in our laboratory at Columbia University do not indicate the emergence of depressed mood states in the days after MDMA use, even when the drug is given repeatedly. Another frequently mentioned potential negative consequence of MDMA is damage to brain cells. Several investigators have shown that large doses of MDMA given to laboratory animals can destroy serotonin neurons, but the relevance of this and related findings for human recreational use is unclear (see the Drugs in Depth box). Recreational users of the drug perform similar to their education- and agematched counterparts on cognitive tests and do not typically use doses as large as those used in animal experiments. However, this does not suggest that the drug should be used recreationally. MDMA remains listed as a Schedule I controlled substance, which means its recreational use is prohibited. 2-CB and 2-C-T 7 It’s happened before and it will happen again: As federal and state agencies work to limit access to one drug, another arrives to fill the gap. In this case, two drugs have arrived to share the rave scene with MDMA: 4-bromo-2,5-dimethoxyphenethylamine (known as 2-CB) and 4-propylthio-2, 5-dimethoxyphenethylamine (2-C-T7). As phenylethylamines, both are chemical cousins to the amphetamine series of hallucinogens. Along with the recently popularized tryptamine deriv-
atives MTA and “foxy methoxy” (see page 346), a confusing array of chemicals is being made available to “ravers,” who may find themselves trying unknown amounts of unfamiliar drugs more often than they’d like.
Deliriants If the indole and catechol hallucinogens are grouped together as “phantastica” with all having similar effects, and acting primarily through the serotonin 2A receptor, then how do we classify all the remaining hallucinogens? We have chosen the term deliriants, implying that the drugs to follow have somewhat more of a tendency to produce mental confusion and a loss of touch with reality. The drugs we describe next represent a variety of effects and act through different brain mechanisms, so it is perhaps better to think of each type by itself rather than as belonging to a group with common effects.
PCP In the 1950s, Parke, Davis & Company investigated a series of drugs in the search for an efficient intravenous anesthetic. On the basis of animal studies, the company selected 1-(1phenylcyclohexyl) piperidine hydrochloride (PCP, generic name phencyclidine) for testing in humans. The studies on monkeys had indicated that PCP was a good analgesic but did not produce good muscle relaxation or sleep. Instead, the animals showed a sort of “dissociation” from what was happening: “During the operation the animal had its eyes open and looked about unconcernedly.” In 1958, the first report was published on the use of PCP (Sernyl) for surgical anesthesia in humans. Sernyl produced good analgesia without depressing blood circulation or respiration and did not produce irregularities in heartbeat. Loss of sensation occurred within two or three minutes of beginning the intravenous infusion, after about 10 mg of the drug had been delivered. The patients later had no memory of the procedure, did not
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remember being spoken to, and remembered no pain. Compared with existing anesthetics, which tend to depress both respiration and circulation through general depression of the CNS, this type of “dissociative” anesthetic seemed to be quite safe. However, the psychological reactions to the drug were unpredictable. During administration of the drug a few patients became very excited, and a different anesthetic had to be used. Several patients were “unmanageable” as they emerged from the anesthetic, exhibiting severely manic behavior. This and later reports indicated that many people given anesthetic doses of Sernyl reported changes in body perception and hallucinations, and about 15 percent of the patients experienced a “prolonged confusional psychosis,” lasting up to four days after the drug was given. This period of confusion was characterized by feelings of unreality, depersonalization, persecution, depression, and intense anxiety. News of this new hallucinogen soon reached Dr. Luby, a psychiatrist, who began testing it in both normal and schizophrenic subjects.42 All the subjects reported changes in perception of their own bodies, with one normal subject saying, “my arm feels like a twenty-mile pole with a pin at the end.” Another said, “I am a small . . . not human . . . just a block of something in a great big laboratory.” There were a number of reports of floating, flying, dizziness, and alternate contraction and expansion of body size. All subjects also showed a thought disorder. Some made up new words, uttered strings of unrelated words, or repeated words or simple phrases. Also, all became increasingly drowsy and apathetic. At times a subject would appear to be asleep but when asked a direct question would respond. When asked, “Can you hear me?” subjects often responded, “No.” The majority became either angry or uncooperative. Many of the normal subjects said they felt as if they were drunk from alcohol. All subjects displayed diminished pain, touch, and position sense, and all showed nystagmus (rapid oscillations of the eyes) and a slapping, ataxic walk. Luby and his colleagues felt that PCP was dif-
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ferent from LSD or mescaline in that there were few reports of intense visual experiences and many more reports of body image changes. The disorganized thinking, suspiciousness, and lack of cooperation made the PCP state resemble schizophrenia much more than the LSD state. Thus, by 1960, PCP had been characterized as an excellent anesthetic for monkeys, a medically safe but psychologically troublesome anesthetic for humans, and a hallucinogen different from LSD and mescaline, with profound effects on body perception. Parke, Davis withdrew Sernyl as an investigational drug for humans in 1965 and in 1967 licensed another company to sell Sernylan as an animal anesthetic. It was primarily used with primates, in both research laboratories and zoos. Also, because of its rapid action and wide safety margin, Sernylan was used in syringe bullets to immobilize stray, wild, or dangerous zoo animals. Because of the popular term tranquilizer gun for this use, PCP became popularly, and inaccurately, known as an animal “tranquilizer.” Other PCP-like Drugs: Ketamine, Dextromethorphan, and Nitrous Oxide Even though Sernyl was never marketed for human use, a related chemical from the same series was marketed as a dissociative anesthetic. Ketamine hydrochloride (Ketalar) has been in continued human use for more than 30 years. Although ketamine has more depressant effects than PCP and fewer prolonged reactions, clinical reports indicate that emergence reactions occur in about 12 percent of patients. These reactions include hallucinations and delirium, sometimes accompanied by confusion and irrational behavior. In 1999, widespread reports of ketamine abuse and its notoriety as a party drug (called Special K, or K) caused the Department of Health and Human Services to recommend adding ketamine to the list of Schedule III controlled substances.
PCP: phencyclidine; originally developed as an anesthetic; has hallucinogenic properties.
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Like PCP and ketamine, two more common substances are also capable of causing dissociative effects, perhaps by blocking NMDA-type glutamate receptors in the brain. Nitrous oxide (laughing gas, Chapter 7) and dextromethorphan, an over-the-counter cough suppressant (Chapter 12) can, at very high doses, produce dissociative-type hallucinations similar to those produced by PCP. Unfortunately, at these doses there is also evidence of pathological changes to neurons in the cerebral cortex of animals. It was reported that the combination of nitrous oxide and ketamine, sometimes used for general anesthesia, produces synergistic neurotoxic effects in animals.43 Recreational Use of PCP In late 1967, workers at the Haight-Ashbury Medical Clinic obtained samples of a substance being distributed as the “Peace Pill.” The drug was analyzed and determined to be PCP, and its identity and dangers were publicized in the community in December 1967. By the next year, it was reported that this drug had enjoyed only brief popularity and then disappeared. It appeared briefly in New York in 1968 as “hog” and at other times as “trank.” Into the early 1970s, PCP was apparently regarded as pretty much a “garbage” drug by street people. In the early 1970s, PCP crystals were sometimes sprinkled onto oregano, parsley, or alfalfa and sold to unsuspecting youngsters as marijuana. In this form, it became known as angel dust. Because PCP can be made inexpensively and relatively easily by amateur chemists, when it is available it usually doesn’t cost much. Eventually, the rapid and potent effects of angel dust made it a desired substance in its own right. Joints made with PCP sometimes contained marijuana, sometimes another plant substance, and were known as “killer joints” or “sherms” (because they hit the user like a Sherman tank). In the late 1970s, PCP use was the most common cause of drug-induced visits to hospital emergency rooms in many communities, and in some neighborhoods young users could be seen “moonwalking” down the street (taking
very high, careful, and slow steps) on any Saturday night. The dependence-producing properties of PCP have also been studied in monkeys, which will press a lever to obtain access to the drug.44 This is in contrast to LSD and other hallucinogens, which do not support animal self-administration and do not produce psychological dependence in most users. Because some PCP users have been reported to behave violently, there is a question as to whether PCP tends to promote violence directly or whether violence is a side effect of the suspicion and anesthesia produced by the drug. Most users do not report feeling violent and feel so uncoordinated that they can’t imagine starting a fight. However, police who have tried to arrest PCP users have had trouble subduing them because many of the commonly used arrest techniques rely on restraining holds that result in pain if the arrestee resists. Because the PCP user is anesthetized, these restraint techniques are less effective. Manual restraint by more than one officer might be required to arrest some PCP users, although one might question how different this is from the problem of arresting a greatly alcohol intoxicated person who is “feeling no pain.” That PCP users might not feel pain has resulted in some gruesome legends about users biting or cutting off their own fingers and so forth. Like earlier stories about LSD users blinding themselves by staring at the sun, these legends cannot be substantiated and most likely have not really occurred. One oft-repeated story probably falls into the category of police folklore. Every cop knows for a fact the story about the PCP user who was so violent, had such superhuman strength, and was so insensitive to pain that he was shot 28 times (or a similar large number of times) before he fell. Although everyone “knows” that this happened, no one can tell you exactly when or where. One might dismiss such folklore as harmless, unless it contributes to events such as the shooting, six times at close range, of an unarmed, naked, 35year-old biochemist who was trying to climb the
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street sign outside his laboratory. This story really did happen, on August 4, 1977, during the height of PCP use in the U.S. The lethal shots were fired by a Los Angeles police officer. The coroner’s office reported that the victim’s blood did contain traces of a drug similar to PCP.45 Several years later, Los Angeles police officers involved in the widely publicized videotaped beating of Rodney King said during their trial that they used such force because they believed King might have been “dusted”—under the influence of PCP. The mechanism of PCP’s action on the brain was a mystery for several years, because PCP alters many neurotransmitter systems but does not appear to act directly on any of them. In 1979, it was reported that a specific receptor for PCP was present in the brain, and in 1981 the identity between the receptor and another that had previously been considered a subtype of opiate receptor was reported. The drug cyclazocine, which has some opiate activity and has also been reported to produce hallucinations, binds well to this “sigma” receptor, but morphine, naloxone, and other opiates do not. Thus, the sigma receptor is probably better characterized as being selective for PCP, ketamine, and other similar drugs rather than as a type of opiate receptor. The presence of the sigma receptor implies that some endogenous substance should bind to it, but more than 20 years of research has not yet determined what that might be or what the normal functions are for this receptor. Several drugs have been developed that bind to the sigma receptor, but none has reached the market.46
The family of plants in which all these genera are found is Solanaceae, “herbs of consolation,” and three pharmacologically active alkaloids are responsible for the effects of these plants. Atropine, which is dl-hyoscyamine, scopolamine, or l-hyoscine, and l-hyoscyamine are all potent central and peripheral cholinergic blocking agents. These drugs occupy the acetylcholine receptor site but do not activate it; thus, their effect is primarily to block muscarinic cholinergic neurons, including the parasympathetic system. These agents have potent peripheral and central effects, and some of the psychological responses to these drugs are probably a reaction to peripheral changes. These alkaloids block the production of mucus in the nose and throat. They also prevent salivation, so the mouth becomes uncommonly dry, and perspiration stops. Temperature can increase to fever levels (109°F has been reported in infants with atropine poisoning), and heart rate can show a 50-beat-per-minute increase with atropine. Even at moderate doses these chemicals cause considerable dilation of the pupils of the eyes, with a resulting inability to focus on nearby objects. With large enough doses, a behavioral pattern develops that resembles toxic psychosis; there is delirium, mental confusion, loss of attention, drowsiness, and loss of memory for recent events. These two characteristics—a clouding of consciousness and no memory for the period of intoxication—plus the absence of vivid sensory effects separate these drugs from the indole and catechol hallucinogens. The anticholinergics are the original deliriants.
Anticholinergic Hallucinogens
Belladonna Atropine, which was isolated in 1831, is the active ingredient in the deadly nightshade, Atropa belladonna. The name of the plant reflects two of its major uses in the Middle Ages and before. The genus name
The potato family contains all the naturally occurring agents to be discussed in this section. Three of the genera—Atropa, Hyoscyamus, and Mandragora—have a single species of importance and were primarily restricted to Europe. The fourth genus, Datura, is worldwide and has many species containing the active agents.
angel dust: the street name for PCP sprinkled on plant material.
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Belladonna, or deadly nightshade, is a poisonous plant that contains an anticholinergic hallucinogen.
reflects its use as a poison. Deadly nightshade was one of the plants used extensively by both professional and amateur poisoners; 14 of its berries contain enough of the alkaloid to cause death. Belladonna, the species name, meaning “beautiful woman,” comes from the use of the extract of this plant to dilate the pupils of the eyes. Interestingly, ancient Roman and Egyptian women knew something that science did not learn until more recently. In the 1950s, it was demonstrated, by using pairs of photographs identical except for the amount of pupil dilation, that most people judge the girl with the more dilated eyes to be prettier. Of more interest here than pretty girls or poisoned men is the sensation of flying reported by some users of belladonna. The origin of this story goes back at least to the Middle Ages in Europe, and in particular to descriptions of witches and witchcraft. Every early society for which we have any history has a tradition of people with special knowledge of useful plants. In Europe, the people who were consulted for their special arcane knowledge of plant potions were most often women, and their traditions are kept alive in our modern concept of “witches.” Among the rich folklore about witches are several
accounts from the 1400s describing “flying ointments” (e.g., The Book of the Sacred Magic of Abremelin the Mage, 1458), and one ingredient often included in these ointments was deadly nightshade. The notion is that this ointment was spread upon the body and/or on a stick, or “staffe,” which was straddled. This is certainly the origin of our notion that witches flew about on broomsticks, though in many accounts it seems that the sticks were used more as phallic symbols and were perhaps ridden in a different manner. What is actually known about witches and witchcraft of this era is confused considerably by what was written about witches by Catholic priests during the Inquisition. During the Middle Ages, all such pagan rituals were considered to be heresy, and practitioners were tortured and killed. Admissions by witches that they “flew” long distances to celebrate Black Mass were extracted during torture and were likely to have reflected the beliefs of the inquisitors more than the history of the person being tortured. Some incredibly lurid accounts of the practices of witches associated drugs, sex, and human sacrifice. Similar lurid accounts linking other drugs (marijuana, LSD, cocaine) to sexual abandon and criminal violence have appeared during more recent years, also promoted by those protecting the established order. The facts are usually not so exciting. Anticholinergics can make people feel lightheaded, and in conjunction with the power of suggestion one might get the sensation of floating, or flying, but it’s not a realistic way to get from New York to Chicago. Mandrake The mandrake plant (Mandragora officinarum) contains all three alkaloids. Although many drugs can be traced to the Bible, it is particularly important to do so with mandrake because its close association with love and lovemaking has persisted from Genesis to recent times: In the time of wheat-harvest Reuben went out and found some mandrakes in the open country
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www.mhhe.com/hart13e and brought them to his mother Leah. Then Rachel asked Leah for some of her son’s mandrakes, but Leah said, “Is it so small a thing to have taken away my husband, that you should take my son’s mandrakes as well?” But Rachel said, “Very well, let him sleep with you tonight in exchange for your son’s mandrakes.” So when Jacob came in from the country in the evening, Leah went out to meet him and said, “You are to sleep with me tonight; I have hired you with my son’s mandrakes.” That night he slept with her.47
The mandrake root is forked and, if you have a vivid imagination, resembles a human body. The root contains the psychoactive agents and was endowed with all sorts of magical and medical properties. The association with the human form is alluded to in Shakespeare’s Juliet’s farewell speech: “And shrieks like mandrakes torn out of the earth, That living mortals hearing them run mad.” Henbane Compared with deadly nightshade and mandrake, Hyoscyamus niger has had a most uninteresting life. This is strange, because it is pharmacologically quite active and contains both scopolamine and l-hyoscyamine. Other plants of this genus contain effective levels of the alkaloids, but it is Hyoscyamus niger that appears throughout history as henbane, a highly poisonous substance and truly the bane of hens, as well as other animals. Pliny in AD 60 said, “For this is certainly known, that, if one takes it in drink more than four leaves, it will put him beside himself.” Shakespeare’s Hamlet’s father must have had more than four leaves because it was henbane that was used to poison him. Datura The distribution of the many Datura species is worldwide, but they all contain the three alkaloids under discussion—atropine, scopolamine, and hyoscyamine—in varying amounts. Almost as extensive as the distribution are its uses and its history. Although it is not clear when the Chinese first used Datura metel as a medicine to treat colds and nervous
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disorders, the plant was important enough to become associated with Buddha: The Chinese valued this drug far back into ancient times. A comparatively recent Chinese medical text, published in 1590, reported that “when Buddha preaches a sermon, the heavens bedew the petals of this plant with rain drops.”48
Halfway around the world 2,500 years before the Chinese text, virgins sat in the temple to Apollo in Delphi and, probably under the influence of Datura, mumbled sounds that holy men interpreted as predictions that always came true. Engraved on the temple at Delphi were the words “Know thyself.” Datura is associated with the worship of Shiva in India, where it has long been recognized as an ingredient in love potions and has been known as “deceiver” and “foolmaker.” In Asia the practice of mixing the crushed seeds of Datura metel in tobacco, cannabis, and food persists even today. One interesting use of Datura stramonium, which is native and grows wild in the eastern United States, was devised by the Algonquin Indians. They used the plant to solve the problem of the adolescent search for identity: The youths are confined for long periods, given “ . . . no other substance but the infusion or decoction of some poisonous, intoxicating roots . . . ” and “they became stark, staring mad, in which raving condition they were kept eighteen or twenty days.” These poor creatures drink so much of that water of Lethe that they perfectly lose the remembrance of all former things, even of their parents, their treasure, and their language. When the doctors find that they have drunk sufficiently of the wysoccan . . . they gradually restore them to their senses again. . . . Thus they unlive their former lives and commence men by forgetting that they ever have been boys.48
The same plant is now called Jamestown weed, or jimsonweed, as a result of an incident in the 17th century. This was recorded for history in the book The History and Present State
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of Virginia, published first in 1705 by Robert Beverly.49 The James-Town Weed (which resembles the Thorny Apple of Peru, and I take to be the Plant so call’d) is supposed to be one of the greatest Coolers in the World. This being an early Plant, was gather’d very young for a boil’d Salad, by some of the Soldiers sent thither, to pacifie the Troubles of Bacon; and some of them eat plentifully of it, the Effect of which was a very pleasant Comedy; for they turn’d natural Fools upon it for several Days.
Although there has been some recent abuse of jimsonweed, the unpleasant and dangerous side effects of this plant limit its recreational use. Synthetic Anticholinergics Anticholinergic drugs were once used to treat Parkinson’s disease (before the introduction of L-dopa) and are still widely used to treat the pseudoparkinsonism produced by antipsychotic drugs (see Chapter 8). Particularly in older people there is concern about inadvertently producing an “anticholinergic syndrome,” characterized by excessive dry mouth, elevated temperature, delusions, and hallucinations. Anticholinergic drugs such as trihexyphenidyl (Artane) and benztropine (Cogentin) have only rarely been abused for their delirium-producing properties.
Amanita Muscaria The Amanita muscaria mushroom is also called “fly agaric,” probably because of what it does to flies. It doesn’t kill them, but when they suck its juice, it puts them into a stupor for two to three hours. It is one of the common poisonous mushrooms found in forests in many parts of the world. The older literature suggests that eating 5 to 10 Amanita mushrooms results in severe effects of intoxication, such as muscular twitching, leading to twitches of limbs and raving drunkenness, with agitation and vivid hallucinations. Later follow many hours of partial paralysis with sleep and dreams.
The red- and white-speckled mushroom Amanita muscaria played a major role in the early history of Indo-European and Central American religions.
When the ancient Aryan invaders swept down from the north into India 3,500 years ago, they took soma, itself considered a deity. The cult of Soma ruled India’s religion and culture for many years—the poems of the Rig Veda celebrate the sacramental use of this substance. It has only been within the past 30 years that scholars have discovered and agreed on the identity of soma as Amanita.1 The suggestion has been made that the ambrosia (“food of the gods”) mentioned in the secret rites of the god Dionysius in Greece was a solution of the Amanita mushroom. And based on paintings representing the “tree of life” found in ancient European cave paintings, it has been suggested that Amanita muscaria use formed a basis for the cult that originated about 2,000 years ago and today calls itself Christianity.50 Until the Russians introduced them to alcohol, many of the isolated nomadic tribes of Siberia had no intoxicant but Amanita: Use of the Amanita mushroom by Siberian tribes continues today largely free from social control of any sort. Use of the drug has a Shamanist aspect, and forms the basis for orgiastic communal
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Mind/Body Connection Living in the Flow During the 1960s, the spirit of kinship with a peer group helped fuel the spread of LSD. More recently, the feeling of making intense emotional connections seems to have helped spread a “rave” subculture in the United States and elsewhere. This scene, known for its all-night dance parties featuring techno tunes and the drug Ecstasy, has had a dedicated following since the early 1990s. It’s not, however, just about the music or the drugs, according to those in the rave community. It’s about being in the moment, having a brief conversation with a stranger who affects you, having an emotional internal experience. What really makes people glad to be alive? What are the inner experiences that make life worthwhile? It’s easier to talk about dancing than it is to describe a moment of mystical union with the universe. Joy can find us and lift us in moments of ordinary connection, though, and the opening we feel to life is not unlike that experienced through a spiritual quest or mystical practice. The elation comes when we know we belong—to another, to ourselves, to the mystery that is larger than ourselves. In our society, celebrations and relaxation often involve moving away from the emotion, numbing ourselves with alcohol or drugs. Dance and music are exceptions to this, but too often we are simply spectators in our lives. Sometimes we discount the small joys in daily living. Sometimes we spoil the good by focusing on the less than perfect or seemingly
indulgences. Since the drug can induce murderous rages in addition to more moderate hallucinogenic experiences, serious injuries frequently result.51
In the frozen northland, these mushrooms are expensive; sometimes several reindeer are exchanged for an effective number of the mushrooms. During the long winter months they might be worth the price. While the mushrooms themselves are not reusable (once eaten, they’re gone), the hallucinogen is excreted unchanged in the urine. When the effect begins to wear off, “midway in the party the cry of ‘pass
incompatible. Perhaps we don’t want to be let down, so we anticipate disappointment rather than expect success and happiness. Can you think of a time when joy came unexpectedly and caught you off guard? Maybe it was a sudden realization that made you smile. Perhaps it was something you didn’t even know you were looking for. Chances are it was a moment when you felt so alive that, ironically, you forgot yourself. Mihaly Csikszentmihalyi, a University of Chicago psychology professor who has devoted his life’s work to studying what makes people happy, satisfied, and fulfilled, describes “flow” as a state of consciousness so focused that you are totally absorbed in an activity and lose track of time. It is a state of complete engagement with life in which you feel strong, alert, in effortless control, unself-conscious, and at the peak of your abilities. Examples of when you might experience flow include after completing a hard task, when feeling the wind in your hair during a walk on the beach, during yoga or sex, and when seeing your child respond to your smile for the first time. What activities usually make you feel happy and completely engaged? During the next week, be aware of and record what activities give you this feeling of deep enjoyment. Then try to build some of these activities into your daily routine to improve the spiritual and emotional quality of your life.
the pot’ goes out.”52 The active ingredient can be reused four or five times in this way. There is evidence that Amanita was also used as a holy plant by several tribal groups in the Americas, ranging from Alaska and the Great Lakes to Mexico and Central America. In several of the legends, its origin is associated with thunder and lightning.1 For many years the active agent in this mushroom was thought to be muscarine (for which the muscarinic cholinergic receptors were named). This substance activates the same type of acetylcholine receptor that
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is blocked by the anticholinergics. However, pharmacological studies with other cholinergic agonists did not produce similar psychoactive effects. Next, attention focused on bufotenin, an indole that is found in high concentrations in the skins of toads. However, the hallucinogenic properties of bufotenin have been in doubt, and Amanita species contain only small amounts of it. In the mid-1960s, meaningful amounts of two chemicals were found: ibotenic acid and muscimol. The effects of Amanita ingestion are not similar to those of other hallucinogens, and that helped confuse the picture with regard to the mechanism. Muscimol can act as an agonist at GABA receptors, which are inhibitory and found throughout the CNS. Muscimol is more potent than ibotenic acid, and drying of the mushroom, which is usually done by those who use it, promotes the transformation of ibotenic acid to muscimol. Muscimol has been given to humans, resulting in confusion, disorientation in time and place, sensory disturbances, muscle twitching, weariness, fatigue, and sleep.28 Amanita muscaria and other related poisonous mushrooms are found in North America, and they are a particularly dangerous type of plant with which to experiment.
Salvia Divinorum This member of the mint family is known by its botanical name, which is translated as “diviner’s sage.” It has been used for centuries by the Mazatec people of Oaxaca, Mexico, in religious ceremonies, and more recently some young people in Mexico have smoked it as a substitute for marijuana. The traditional methods of using the plant include chewing the leaves, drinking a tea made from the crushed leaves, or smoking the dried leaves. The resulting hallucinatory effect is reported to last for up to an hour.53 People in the United States and in Europe have cultivated the plant for the past several years and use it as a legal hallucinogen. Salvia is not currently listed as a controlled substance in the United States.
The plant was identified in 1962 by Wasson and Hoffman, and the active agent, salvinorin A, was identified in 1982. Salvinorin A is nearly as potent as LSD, in that an effective human dose may be as little as 200 μg (micrograms) when smoked. It was reported in 1994 that salvinorin A binds selectively to the kappa opioid receptor, where it acts as an agonist. Thus, this drug represents a newly discovered type of chemical structure and a unique pharmacological effect, which is stimulating research to develop new, related compounds.53 Meanwhile, it will be interesting to see what happens to the legal status of Salvia and of salvinorin A. That will no doubt be influenced by whether there are highly publicized examples of abuse.
Summary •
Hallucinogenic plants have been used for many centuries, not only as medicines but for spiritual and recreational purposes as well.
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LSD, a synthetic hallucinogen, alters perceptual processes and enhances emotionality, so that the real world is seen differently and is responded to with great emotion.
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Other chemicals that contain the indole nucleus, such as psilocybin (from the Mexican mushroom), have effects similar to those of LSD.
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Mescaline, from the peyote cactus, and synthetic derivatives of the amphetamines represent the catechol hallucinogens. They have psychological effects quite similar to those of the indole types.
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PCP, or angel dust, produces more changes in body perception and fewer visual effects than LSD.
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Anticholinergics are found in many plants throughout the world and have been used not only recreationally, medically, and spiritually but also as poisons.
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Review Questions 1. What are the distinctions among phantastica, deliriants, psychedelics, psychotomimetics, entheogens, and hallucinogens? 2. What is the precise relationship between ergotism and LSD? 3. Why was LSD used in psychoanalysis in the 1950s and 1960s? How does this relate to its proposed use by the Army and the CIA? 4. Describe the dependence potential of LSD in terms of tolerance, physical dependence, and psychological dependence. 5. What is the diagnostic term for flashbacks? 6. What is the active agent in the “magic mushrooms” of Mexico, and is it an indole or a catechol? 7. Besides the psychological effects, what other effects are reliably produced by peyote? 8. Contrast MDMA and PCP in terms of how they appear to make people feel about being close to others. 9. Which of the hallucinogenic plants was most associated with witchcraft? 10. What can be concluded from the evidence regarding the neurotoxic effects of MDMA? 11. Which hallucinogen acts as an agonist at kappa opiate receptors?
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Schultes, R. E., and A. Hofmann. Plants of the Gods. New York: McGraw-Hill, 1979. Caporael, L. R. “Ergotism: The Satan Loosed in Salem.” Science 192 (1976), pp. 21–26. Gottlieb, J., and N. P. Spanos. “Ergotism and the Salem Village Witch Trials.” Science 194 (1976), pp. 1390–94. Hofmann, A. “Psychotomimetic Agents.” In A. Burger, ed. Drugs affecting the central nervous system (Vol. 2). New York: Marcel Dekker, 1968. Segal, J., ed. Research in the Service of Mental Health, Research on Drug Abuse. National Institute on Mental Health, Pub. No. (ADM) 75-236, U.S. Department of Health, Education, and Welfare. Washington, DC: U.S. Government Printing Office, 1975. Johnston, L. “Ford Signs Grant of $750,000 in LSD Death in CIA Test.” The New York Times, October 14, 1976, p. C43. Treaster, J. B. “Mind-Drug Test a Federal Project for Almost 25 Years.” The New York Times, August 11, 1975, p. M42.
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“CIA Considered Big LSD Purchase.” Washington Star, August 4, 1975. See also Knight, M. “LSD Creator Says Army Sought Drug.” The New York Times, August 1, 1975. Taylor, J. R., and W. N. Johnson. Use of Volunteers in Chemical Agent Research. Inspector General Report No. DAIGIN 21-75, Washington, DC: U.S. Department of Army, March 10, 1976. Weil, A. T. “The Strange Case of the Harvard Drug Scandal.” Look, November 5, 1963, pp. 38–48. Blumenthal, R. “Leary Drug Cult Stirs Millbrook.” The New York Times, June 14, 1967, p. 49. “Celebration #1.” New Yorker 42 (1966), p. 43. Council on Mental Health and Committee on Alcoholism and Drug Dependence. “Dependence on LSD and Other Hallucinogenic Drugs.” Journal of the American Medical Association 202 (1967), pp. 141–44. Leary and Liddy, Debating Specialists. The New York Times, September 3, 1981, p. B26. Appel, J. B., and J.A. Rosecrans. “Behavioral Pharmacology of Hallucinogens in Animals: Conditioning Studies.” In B. L. Jacobs, ed. Hallucinogens: Neurochemical, Behavioral and Clinical Perspectives. New York: Raven Press, 1984. Julien, R. M. A Primer of Drug Action, 10th ed. New York: Worth, 2005. Siegel, R. K. “The Natural History of Hallucinogens.” In B. L. Jacobs, ed. Hallucinogens: Neurochemical, Behavioral and Clinical Perspectives. New York: Raven Press, 1984. Krippner, S. “Psychedelic Experience and the Language Process.” Journal of Psychedelic Drugs 3, no. 1 (1970), pp. 41–51. Levine, J., and A. M. Ludwig. “The LSD Controversy.” Comprehensive Psychiatry 5, no. 5 (1964), pp. 318–19. Forsch, W. A., E. S. Robbins, and M. Stern. “Untoward Reactions to Lysergic Acid Diethylamide (LSD) Resulting in Hospitalization.” New England Journal of Medicine 273 (1965), pp. 1235–39. Halpern, J. H., and others. “Hallucinogen Persisting Perceptual Disorder: What Do We Know after 50 Years?” Drug & Alcohol Dependence 69 (2003), pp. 109–19. Zegans, L. S., J. C. Pollard, and D. Brown. “The Effects of LSD-25 on Creativity and Tolerance to Regression.” Archives of General Psychiatry 16 (1967), pp. 740–49. Spitzer, M., and others. “Increased Activation of Indirect Semantic Associations Under Psilocybin.” Biological Psychiatry 39 (1996), pp. 1055–57. Hollister, L. E., J. Shelton, and G. Krieger. “A Controlled Comparison of Lysergic Acid Diethylamide (LSD) and Dextroamphetamine in Alcoholics.” American Journal of Psychiatry 125 (1969), pp. 1352–57. NIMH Research on LSD. “Extramural Programs Fiscal Year 1948 to Present.” Prepared September 1, 1975. Pahnke, W. “Drugs and Mysticism: An Analysis of the Relationship Between Psychedelic Drugs and the Mystical Consciousness.” Ph.D. thesis, Harvard University, 1963. Griffiths R. R., W. A. Richards, U. McCann, and R. Jesse. “Psilocybin Can Occasion Mystical-type Experiences Having Substantial and Sustained Personal Meaning and Spiritual Significance.” Psychopharmacology 187 (2006), pp. 268–83. Schultes, R. E., and A. Hofmann. The Botany and Chemistry of Hallucinogens. Springfield, IL: Charles C. Thomas, 1980.
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Al-Assmar, S. E. “The Seeds of the Hawaiian Baby Woodrose Are a Powerful Hallucinogen [letter].” Archives of Internal Medicine 159 (1999), p. 2090. Strassman, R. J., and others. “Differential Tolerance to Biological and Subjective Effects of Four Closely-Spaced Doses of N,N-dimethyltryptamine in Humans.” Biological Psychiatry 39 (1996), pp. 784–95. Grob, C. S., and others. “Human Psychopharmacology of Hoasca, a Plant Hallucinogen Used in Ritual Context in Brazil.” Journal of Nervous and Mental Disease 184 (1996), pp. 86–94. Dobkin de Rios, M., and M. Cardenas. “Plant Hallucinogens, Shamanism, and Nazca Ceramics.” Journal of Ethnopharmacology 2 (1980), pp. 233–46. De Ropp, R. S. Drugs and the Mind. New York: Grove Press, 1957. Ellis, H. “Mescal: A Study of a Divine Plant.” Popular Science Monthly 61 (1902), pp. 59, 65. Huxley, A. The Doors of Perception. New York: Harper & Row, 1954. MDMA. “Compound Raises Medical, Legal Issues.” Brain/ Mind Bulletin, April 15, 1985. Peroutka, S. J., and others. “Subjective Effects of 3,4-methylenedioxymethamphetamine in Recreational Users.” Neuropsychopharmacology 1 (1988), pp. 273–77. Ricaurte, G. A., J. Yuan, G. Hatzidimitriou, B. J. Cord, and U. D. McCann. “Severe Dopaminergic Neurotoxicity in Primates after a Common Recreational Dose Regimen of MDMA (Ecstasy).” Science 297 (2002), pp. 2260–3. Ricaurte, G. A., J. Yuan, and U. D. McCann. “(⫹/⫺)3,4-Methylenedioxymethamphetamine (‘Ecstasy’)-induced Serotonin Neurotoxicity: Studies in Animals.” Neuropsychobiology 42 (2000), pp. 5–10. Dworkin, S. I., S. Mirkis, and J. E. Smith. “Responsedependent versus Response-independent Presentation of Cocaine: Differences in the Lethal Effects of the Drug.” Psychopharmacology 117 (1995), pp. 262–6. Ricaurte, G. A. , J. Yuan, G. Hatzidimitriou, B. J. Cord, and U. D. McCann. “Retraction.” Science 301(2003), p. 1479.
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Luby, E., and others. “Study of a New Schizophrenomimetic Drug—Sernyl.” American Medical Association Archive of Neurological Psychiatry 81 (1959), pp. 113–19. Jevtovic-Todorovic, V., and others. “Ketamine Potentiates Cerebrocortical Damage Induced by the Common Anaesthetic Agent Nitrous Oxide in Adult Rats.” British Journal of Pharmacology 130 (2000), pp. 1692–98. Cosgrove, K. P., and M. E. Carroll. “Differential Effects of Bremazocine on Oral Phencyclidine (PCP) Self-Administration in Male and Female Rhesus Monkeys.” Experimental & Clinical Psychopharmacology 12 (2004), pp. 111–17. Overend, W. “PCP: Death in the ‘Dust.’ ” Los Angeles Times, September 26, 1977. Guitart, X., and others. “Sigma Receptors: Biology and Therapeutic Potential.” Psychopharmacology 174 (2004), pp. 301–19. Genesis 30:14–16. The New English Bible. Oxford University Press and Cambridge University Press, 1970. Schultes, R. E. “The Plant Kingdom and Hallucinogens (Part III).” Bulletin on Narcotics 22, no. 1 (1970), pp. 43–46. Beverly, R. The History and Present State of Virginia, 1705. Chapel Hill: University of North Carolina Press, 1947. Allegro, J. M. The Sacred Mushroom and the Cross. New York: Doubleday, 1970. Wasson, R. G. “Fly Agaric and Man.” In D.H. Efron, ed. Ethnopharmacologic Search for Psychoactive Drugs. Washington, DC: National Institute of Mental Health, 1967. See also Wasson, R. G. Soma, Divine Mushroom of Immortality. New York: Harcourt Brace Jovanovich, 1971. “Hallucinogens.” Columbia Law Review 68, no. 3 (1968), pp. 521–60. Sheffler, D. J., B. L. Roth, and A. Salvinorin. “The ‘Magic Mint’ Hallucinogen Finds a Molecular Target in the Kappa Opioid Receptor.” Trends in Pharmacological Sciences 24 (2003), pp. 107–09.
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Check Yourself
Name
Date
Hallucinogens from Plants Match the plants on the left with the appropriate hallucinogenic chemical on the right:
ayahuasca
mescaline
peyote
muscimol
sacred mushrooms (from Mexico)
d-lysergic acid amide
morning glories
atropine
belladonna
DMT and harmaline
Amanita
psilocybin
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Marijuana Objectives When you have finished this chapter, you should be able to: • Describe the relationship among marijuana, cannabis, and THC and discuss different preparations of cannabis. • Describe how Europeans became exposed to the psychological effects of cannabis. • Explain how marijuana was described in the years leading up to the 1937 Marijuana Tax Act. • Discuss the legal status of marijuana in the U.S. since 1937, including current debates. • Draw parallels among the various scientific and medical
Marijuana has meant so many studies on marijuana. things to so many people over • Describe the type of receptor THC acts on in the brain the years that it is hard to deand compare the time course of smoked vs. oral THC. scribe it from a single perspective. The matter of classifying • List the two most consistent physiological effects of marijuana among the other psymarijuana. choactive drugs is so complex • Discuss evidence for the abuse potential of marijuana that we, like most authors, avoid and influences on the psychological effects of marijuana. the issue by setting it off by itself. Marijuana can produce some • Describe the effects of marijuana use on driving ability, sedative-like effects, some pain the lungs, sperm motility, and the immune system. relief, and, in large doses, hal• Describe the range of evidence relating to whether lucinogenic effects. Thus, many marijuana smoking leads to brain damage in humans. of its users treat it as a depressant; it has been called a narcotic (for both pharmacological, as well as political, reasons); and it is often included among descriptions of hallucinogenic plants. Cannabis, the Plant However, the effects it produces when used as most people use it are sufficiently different Marijuana (or marihuana; either spelling is corfrom those of other psychoactive drugs to jusrect) is a preparation of leafy material from the tify its consideration as a unique substance. Cannabis plant that is smoked. The question is 365
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Online Learning Center Resources www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. • • • • • •
Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips
which Cannabis plant, because there is still botanical debate over whether there is one, three, or more species of Cannabis. In previous years, this issue spurred legal arguments because the laws mentioned only Cannabis sativa. Does that include all marijuana or not? The evidence is strong that there are three separate species. Cannabis sativa originated in Asia but now grows worldwide and primarily has been used for its fibers, from which hemp rope is made. This is the species that grows as a weed in the United States and Canada. Cannabis indica is grown for its psychoactive resins and is cultivated in many areas of the world, including selected planters and backyards of the United States. The third species, Cannabis ruderalis, grows primarily in Russia and not at all in America. The plant Linnaeus named C. sativa in 1753 is what is still known as C. sativa.1 C. sativa that is cultivated for use as hemp grows as a lanky plant up to 18 feet high. C. indica plants cultivated for their psychoactive effects are more compact and usually only two or three feet tall. The psychoactive potency results from an interaction between genetics and environmental conditions. Plants of different species grown under identical conditions produce different amounts of psychoactive material, and the same plants vary in potency from year to year, depending on the amount of sunshine, warm weather, and moisture.
A leaf of the Cannabis (marijuana) plant.
Preparations from Cannabis The primary psychoactive agent, delta-9tetrahydrocannabinol (THC), is concentrated in the resin of Cannabis; most of the resin is in the flowering tops, less is in the leaves, and there is little in the fibrous stalks. The psychoactive potency of a Cannabis preparation depends on the amount of resin present and therefore varies, depending on the part of the plant used.1 India has produced three traditional Cannabis preparations, each of which corresponds roughly to preparations available in the United States. The most potent of these is called charas in India, and it consists of pure resin that has been carefully removed from the surface of leaves and stems. Hashish, or hasheesh, is a substance widely known around the world and in its purest form is pure resin, like charas. It may be less pure, depending on how carefully the resin has been separated from the plant material. Hashish is rare in the United States, constituting less than 1 percent of all confiscated marijuana samples in the past 10 years. The average THC content of hashish has ranged from 3 to 7 percent with rare samples as high as about 20 percent.
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Drugs in the Media Medical Marijuana in the News Probably no single psychoactive drug topic has received more publicity in the past few years than the issue of medical marijuana, which has been placed as a referendum on the ballot in several states. Each time, there are stories about the plight of people with AIDS who say they need marijuana to stimulate their appetites. And each time there are stories reflecting the views of local police and federal drug-control officials who say that medical marijuana is just an excuse for people who want to grow and use an illegal substance. Here is a sampling of a few days’ headlines that reveal the complexity of the issues raised when these laws are considered and then passed: “Medical cannabis may be legalized in Illinois,” by Kate Stickelmaier, Daily Vidette, March 18, 2008. NORMAL, IL—In a decision on March 5, the Senate Public Health Committee voted 6–4 in favor of allowing the medical use of marijuana to become legal for those with debilitating diseases. “Pot for medical use on ballot: Supporters gather signatures to ensure the initiative will go before public in November,” by Mark Hornbeck, Detroit News, March 4, 2008. LANSING, MI—An initiative to legalize marijuana for medical use likely is headed for the November ballot in Michigan, following certification Monday of supporters’ petitions by a state elections panel. “Medical marijuana may go on Ohio ballot,” by Alan Johnson, The Columbus Dispatch, August 18, 2007. COLUMBUS, OH—A statewide issue to legalize medical marijuana is headed for the ballot in Michigan next year—and could swing south to Ohio shortly thereafter. “Doctors group backs marijuana for medical uses,” by Will Dunham, Reuters, February 15, 2008.
The second most potent preparation is traditionally called ganja in India, and it consists of the dried flowering tops of plants with pistillate flowers (female plants). The male plants are removed from the fields before the female plants can become pollinated and put their energy into seed production. This increases the potency of the female plants and produces high-grade
WASHINGTON, DC—A leading U.S. doctors’ group has endorsed using marijuana for medical purposes, urging the government to roll back a prohibition on using it to treat patients and supporting studies into its medical applications. “Calif. Firms Can Fire Medical Marijuana Users: State’s High Court Finds Compassionate Use Act Does Not Affect Employers’ Rights, by Karl Vick, Washington Post, January 25, 2008. LOS ANGELES, CA—The California Supreme Court ruled Thursday that employers can fire workers who test positive for marijuana even if they have a note from a doctor recommending its use for medical reasons. Judging from the small but increasing number of states that permit seriously ill patients to grow and use marijuana under medical supervision (California took the lead in 1996), the issue isn’t going away anytime soon. And this is separate from the issue of general legalization. Currently, marijuana maintains a slot alongside heroin and methamphetamine as a “drug of concern” in its listing on the federal Drug Enforcement Administration’s Web site. The average American so far seems uninterested in a serious national debate on the use of marijuana. The mere mention of legalizing any illegal drug means political suicide for any politician willing to broach the subject. A notable exception is former New Mexico Governor Gary Johnson, a Republican. An outspoken advocate for legalizing pot while in office, Johnson is also a triathlete who maintained steady popularity ratings in his state. Although most U.S. citizens may not be ready to embrace his stance, we will certainly be seeing more arguments in the media for legalizing medical marijuana use.
Cannabis (can a biss): the genus of plant known as marijuana. THC: delta-9-tetrahydrocannabinol, the most active chemical in marijuana. hashish (hash eesh or hash eesh): concentrated resin from the Cannabis plant.
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Hashish, concentrated resin from the Cannabis plant, is relatively rare in the United States.
marijuana known as sinsemilla (from the Spanish sin semilla, “without seeds”). The average THC content of sinsemilla samples from the United States also varies widely, ranging from 7 to 12 percent. The weakest form in India is bhang, which is made by using the entire remainder of the plant after the top has been picked, then drying it and grinding it into a powder. The powder can then be mixed into drinks or candies.1 This type of preparation is rare in the United States, but it is similar to low-grade marijuana, which consists of the leaves of a plant, perhaps even a sativa plant found growing as a weed. Some of this low-grade marijuana contains less than 1 percent THC. Manually scraping exuded resin off the plant to make hashish is a tedious process, and a more efficient method of separating the resin from plants has been known for many years. The plants are boiled in alcohol, then the solids filtered out and the liquid evaporated down to a thick, dark substance once known medically as “red oil of cannabis” and now referred to as hash oil. Again, this product varies widely in its potency but can contain more than 50 percent THC. Until fairly recently, both the medical and the psychological effects of Cannabis preparations were variable. All the traditional methods could do was produce relatively pure
plant resin, but that resin could vary considerably in its THC content. If we consider only the marijuana available for smoking in the United States, we can see that it can vary widely in potency from a low-grade product containing less than 1 percent THC to a high-grade sinsemilla containing 9 percent or more THC. The usual range of potency for marijuana seems to be 2 to 8 percent, however. Since the early 1980s, repeated reports have stated that the marijuana available on the streets today is “10 times” more potent than the marijuana of the 1960s. The political message behind this is that the marijuana of the 1960s may have been relatively harmless, but the current marijuana is more dangerous. In fact, the entire range of these traditional preparations has been known, and scientific, literary, and medical descriptions of the wide range of effects have been based on this entire range of potencies, for 150 years. But it is true that U.S. marijuana growers are becoming more sophisticated and producing more sinsemilla.
History Early History The earliest reference to Cannabis is in a pharmacy book written in 2737 BC by Chinese emperor Shen Nung. Referring to the euphoriant effects of Cannabis, he called it the “Liberator of Sin.” He recommended it for some medical uses, including “female weakness, gout, rheumatism, malaria, beriberi, constipation and absent-mindedness.” Social use of the plant had spread to the Muslim world and North Africa by AD 1000. In this period in the eastern Mediterranean area, a legend developed around a religious cult that committed murder for political reasons. The cult was called “hashishiyya,” from which our word assassin developed. In 1299, Marco Polo told the story he had heard of this group and its leader. It was a marvelous tale and had all the ingredients necessary for a tale to survive through the
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ages: intrigue, murder, sex, the use of drugs, and mysterious lands. The story of this group and its activities was told in many ways over the years, and Boccaccio’s Decameron contained one story based on it. Stories of this cult, combined with the frequent reference to the power and wonderment of hashish in The Arabian Nights, were widely circulated in Europe over the years.
The 19th Century: Romantic Literature and the New Science of Psychology At the start of the 19th century, world commerce was expanding. New and exciting reports from the world travelers of the 17th and 18th centuries introduced new cultures and new ideas to Europe. Asia and the Middle East had yielded exotic spices, as well as the stimulants coffee and tea. Europe was ready for another new sensation, and got it. The returning veteran, as usual, gets part of the blame for introducing what Europe was ready to receive: Napoleon’s campaign to Egypt at the beginning of the nineteenth century increased the Romantic’s acquaintance with hashish and caused them to associate it with the Near East. . . . Napoleon was forced to give an order forbidding all French soldiers to indulge in hashish. Some of the soldiers brought the habit to France, however, as did many other Frenchmen who worked for the government or traveled in the Near East.2
By the 1830s and 1840s, everyone who was anyone was using, thinking about using, or decrying the use of mind-tickling agents such as opium and hashish. One of the earliest (1844) popular accounts of the use of hashish is in The Count of Monte Cristo by Alexander Dumas. The story includes a reference to the Assassins tale and contains statements about the characteristics of the drug that still sound contemporary. During the 1840s, a group of artists and writers gathered monthly at the Hotel Pimodan in Paris’s Latin Quarter to use drugs. This group became famous because one of the participants, Gautier, wrote a book, Le Club de Hachischins, that described their activities. From this group
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have come some of the best literary descriptions of hashish intoxication. These French Romantics, like the Impressionist painters of a later period, were searching for new experiences, new sources of creativity from within, and new ways of seeing the world outside. A few of the regulars were well-known writers, including Baudelaire, Gautier, and Dumas. Baudelaire used hashish and was an astute observer of its effects in himself and in others. In his book Artificial Paradises, he echoed what Dumas had written about the kind of effect to expect from hashish: The intoxication will be nothing but one immense dream, thanks to intensity of color and the rapidity of conceptions; but it will always preserve the particular tonality of the individual. . . . The dream will certainly reflect its dreamer. He is only the same man grown larger . . . sophisticate and ingenu . . . will find nothing miraculous, absolutely nothing but the natural to an extreme.3
As the end of the 19th century approached, the use of psychoactive drugs increased, but the hashish experience held little interest for the dweller in middle America.
“Marijuana, Assassin of Youth” At the beginning of the 20th century, public interest in Cannabis and its use was not widespread. In the early 1920s, a few references in the mass media reported the use by Mexican Americans of something the newspapers called marijuana, but public concern was not aroused. In 1926, however, a series of articles associating marijuana and crime appeared in a New Orleans newspaper. As a result, the public began to take an interest in this “new” drug. The U.S. commissioner of narcotics, Harry Anslinger, said that in 1931 the Bureau of Narcotics’ file on marijuana was less than two
sinsemilla (sin se mee ya): “without seeds”; a method of growing more potent marijuana.
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inches thick. The same year, the Treasury Department stated: A great deal of public interest has been aroused by the newspaper articles appearing from time to time on the evils of the abuse of marijuana, or Indian hemp. This publicity tends to magnify the extent of the evil and lends color to an inference that there is an alarming spread of the improper use of the drug, whereas the actual increase in such use may not have been inordinately large.4
Even so, by 1935, 36 states had laws regulating the use, sale, and/or possession of marijuana. By the end of 1936, all 48 states had similar laws. The Federal Bureau of Narcotics also changed its tune. In 1937, at congressional hearings, Anslinger stated, “Traffic in marihuana is increasing to such an extent that it has come to be the cause for the greatest national concern.”5 From 1931 to 1937, the use of marijuana had spread throughout the country, but there is no evidence that there was extensive use in most communities. The primary motivation for the congressional hearings on marijuana came not because of the use of marijuana as an inebriant or a euphoriant but because of reports by police and in the popular literature stating, “Most crimes of violence are laid to users of marihuana.”6 Scientific American reported in March 1936: Marijuana produces a wide variety of symptoms in the user, including hilarity, swooning, and sexual excitement. Combined with intoxicants, it often makes the smoker vicious, with a desire to fight and kill.7
And Popular Science Monthly in May 1936 contained a lengthy article with such statements as this: The Chief of Philadelphia County detectives declared that whenever any particularly horrible crime was committed—and especially one pointing to perversion—his officers searched first in marijuana dens and questioned marijuana smokers for suspects.8
It hardly seemed necessary for readers to be told that marijuana had arrived as “the foremost menace to life, health, and morals in the list of drugs used in America.”8 In this period the association was repeatedly made between crime, particularly violent and/or perverted crime, and marijuana use. A typical report follows: In Los Angeles, Calif., a youth was walking along a downtown street after inhaling a marijuana cigarette. For many addicts, merely a portion of a “reefer” is enough to induce intoxication. Suddenly, for no reason, he decided that someone had threatened to kill him and that his life at that very moment was in danger. Wildly he looked about him. The only person in sight was an aged boot-black. Drug-crazed nerve centers conjured the innocent old shoe-shiner into a destroying monster. Mad with fright, the addict hurried to his room and got a gun. He killed the old man, and then, later, babbled his grief over what had been wanton, uncontrolled murder. “I thought someone was after me,” he said. “That’s the only reason I did it. I had never seen the old fellow before. Something just told me to kill him!” That’s marijuana!9
However, not all articles condemned marijuana as the precipitator of violent crimes. An article in The Literary Digest reported that the chief psychiatrist at Bellevue Hospital in New York City had reviewed the cases of more than 2,200 criminals convicted of felonies. Referring to marijuana, he said, “None of the assault cases could be said to have been committed under the drug’s influence. Of the sexual crimes, there was none due to marihuana intoxication. It is quite probable that alcohol is more responsible as an agent for crime than is marihuana.”10 There was very poor documentation of the relationship between marijuana and crime, which in the 1930s was stated as if it had been proved. A thorough review of Commissioner Anslinger’s writings on marijuana concluded: In the works of Mr. Anslinger, there are either no references or references to volumes which my
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www.mhhe.com/hart13e assistants and I have checked and which, in our checking, we find to be based upon much hearsay and little or no experimentation. We found a mythology in which later writers cite the authority of earlier writers, who also had little evidence. We have found, by and large, what can most charitably be described as a pyramid of prejudice, with each level of the structure built upon the shaky foundations of earlier distortions.11
Examples of this “pyramid of prejudice” abound, but here’s one way it worked: One of Mr. Anslinger’s Treasury agents would testify before Congress and relate one of the outrageous stories of marijuana-induced violence. Next, the testimony would be referred to in an editorial in a medical journal, such as the Journal of the American Medical Association (JAMA). Then Anslinger or one of his people would write a magazine article, citing the prestigious JAMA as the source of the information. With such poor evidence supporting the relationship between marijuana use and crime, it seems strange that the true story was never told. There are probably several reasons. One was the Great Depression, which made everyone acutely sensitive to, and wary of, any new and particularly foreign influences. The fact that it was lower-class Mexican Americans and African Americans who were associated with use of the drug made the drug doubly dangerous to the white middle class. Another contributing factor probably was the regular reference in associating marijuana and crime to the murdering cult of Assassins as suggestive of the characteristics of the drug. The 1936 Popular Science Monthly reference to the Assassins is the most concise: The origin of the word “assassin” has two explanations, but either demonstrates the menace of Indian hemp. According to one version, members of a band of Persian terrorists committed their worst atrocities while under the influence of hashish. In the other version, Saracens who opposed the Crusaders were said to employ the services of hashish addicts to secure secret murderers of the leaders of the Crusades. In both
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versions, the murderers were known as “haschischin,” “hashshash” or “hashishi” and from those terms comes the modern and ominous “assassin.”8
In none of the original stories and legends were the murders committed by individuals under the influence of hashish; rather, hashish may have been part of the reward for carrying out various crimes. No matter. As the 1930s rolled on, fear of marijuana users and of marijuana itself increased, as did state marijuanacontrol laws. In the mid-1930s, the Narcotics Bureau acted to support federal legislation, and in the spring of 1937 congressional hearings were held.
The Marijuana Tax Act of 1937 Passage of the Marijuana Tax Act was a foregone conclusion. Few witnesses testified other than law enforcement officers. People dealing in birdseed had the act modified so they could import sterilized Cannabis seed for use in their product. An official of the American Medical Association (AMA) testified on his own behalf, not representing the AMA, against the bill. His reasons for opposing the bill were multiple. Primarily, he thought the state antimarijuana laws were adequate and that the social-menace case against Cannabis had not been proved. It might be that most other medical doctors didn’t associate the old remedies based on Cannabis with this new, foreign-sounding drug marijuana. The bill was passed in August and became effective on October 1, 1937. The general characteristics of the law followed the regulation-by-taxation theme of the Harrison Act of 1914. The federal law did not outlaw Cannabis or its preparations; it just taxed the grower, distributor, seller, and buyer and made it, administratively, almost impossible for anyone to have anything to do with Cannabis. In addition, the Bureau of Narcotics prepared a uniform law that many states adopted. The uniform law on marijuana specifically named C. sativa as the species of plant whose leafy material is illegal.
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In later years, the defense in some court cases argued that the material confiscated by the police had come from C. indica and thus was not illegal. In the usual specimens obtained by police or presented in court, all distinguishing characteristics between species are either not present or are obliterated by drying and crushing. Because the cannabinoids are present in all species, there is no way of telling what species most confiscated marijuana belongs to. The current federal and uniform laws refer only to Cannabis. The state laws made possession and use of Cannabis illegal per se. In May 1969, 32 years later, the U.S. Supreme Court declared the Marijuana Tax Act unconstitutional and overturned the conviction of Timothy Leary because there was in the Federal anti-marijuana law—a section that requires the suspect to pay a tax on the drug, thus incriminating himself, in violation of the Fifth Amendment: and a section that assumes (rather than requiring proof) that a person with foreign-grown marijuana in his possession knows it is smuggled.12
After the Marijuana Tax Act Passage of the Marijuana Tax Act had an amazing effect. Almost immediately there was a sharp reduction in the reports of heinous crimes committed under the influence of marijuana. The price of the merchandise increased rapidly (the war came along, too), so that five years after passage of the act the cost of a marijuana cigarette—a reefer—had increased 6 to 12 times and cost about a dollar. The year after the law was enacted, 1938, Mayor Fiorello LaGuardia of New York City remembered what no one else wanted to recall. What he recalled were two army studies on marijuana use by soldiers in the Panama Canal Zone around 1930. Both reports had found marijuana to be innocuous and had said that its reputation as a troublemaker “was due to its association with alcohol which was always found the prime agent.”13 Mayor LaGuardia asked the New York Academy of Medicine to study marijuana, its
use, its effects, and the necessity for control. The report, issued in 1944, was intensive and extensive and a very good study for its time. Following is only a part of the report’s summary:14 It was found that marihuana in an effective dose impairs intellectual functioning in general. . . . Marihuana does not change the basic personality structure of the individual. It induces a feeling of self-confidence, but this expressed in thought rather than in performance. There is, in fact, evidence of a diminution in physical activity. . . . Those who have been smoking marihuana for a period of years showed no mental or physical deterioration which may be attributed to the drug.14
This 1944 report, which was completed by a reputable committee of the New York Academy of Medicine, brought a violent reaction. The AMA stated in a 1945 editorial: For many years medical scientists have considered cannabis a dangerous drug. Nevertheless, a book called “Marihuana Problems” by New York City Mayor’s Committee on Marihuana submits an analysis of seventeen doctors of tests on 77 prisoners and, on this narrow and thoroughly unscientific foundation, draws sweeping and inadequate conclusions which minimize the harmfulness of marijuana. Already the book has done harm. One investigator has described some tearful parents who brought their 16 year old son to a physician after he had been detected in the act of smoking marihuana. A noticeable mental deterioration had been evident for some time even to their lay minds. The boy said he had read an account of the LaGuardia Committee report and that this was his justification for using marihuana.15
As in all such reports and reactions to reports, there is little dispute over the facts, only over the interpretation. The LaGuardia Report is consistent with the Indian Hemp Commission Report of the 1890s, the Panama Canal Zone reports of the 1930s, and the comprehensive reports in the 1970s by the governments of New Zealand, Canada, Great Britain, and the United States, in addition to the 1981 report to the World Health Organization and the 1982 report
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Figure 15.1 Delta-9 THC, The Most Active Substance Found in Cannabis, and Anandamide, Isolated from Brain Tissue by the National Academy of Science to the Congress of the United States, so it is likely that the conclusions of the LaGuardia Report were and are for the most part valid. The 1950s and 1960s were a unique period in the history of marijuana. There was a hiatus in scientific research on Cannabis, but experimentation in the streets increased. With the arrival of the “psychedelic ’60s,” the popular press emphasized the more sensational hallucinogens. Marijuana, however, became the most common symbol of youthful rejection of authority and identification with a new era of personal freedom. According to the annual high school senior survey and the NIDA household survey (see Chapter 1), marijuana apparently peaked in popularity in the United States in the late 1970s. During the mid-1980s and early 1990s, marijuana use became much less popular than it had been in the 1970s, but the mid-1990s saw the beginning of a significant rise in the number of young people using marijuana.
Pharmacology Cannabinoid Chemicals The chemistry of Cannabis is quite complex, and the isolation and extraction of the active ingredient are difficult even today. The active
agent in Cannabis is unique among psychoactive plant materials in that it contains no nitrogen and thus is not an alkaloid. There are more than 400 chemicals in marijuana, but only 66 of them are unique to the Cannabis plant—these are called cannabinoids. One of them, delta-9-tetrahydrocannabinol (THC), was isolated and synthesized in 1964 and is clearly the most pharmacologically active. Structures of some of these chemicals are shown in Figure 15.1. The major active metabolite in the body of THC is 11-hydroxy-delta-9-THC. The relationship of THC to Cannabis is probably more similar to the relationship of nicotine to tobacco than of alcohol to beer, wine, or distilled spirits. Alcohol is the only behaviorally active agent in alcoholic beverages, but there might be several active agents in Cannabis.
Absorption, Distribution, and Elimination When smoked, THC is rapidly absorbed into the blood and distributed first to the brain, then redistributed to the rest of the body, so that within 30 minutes much is gone from the brain. The peak psychological and cardiovascular effects occur together, usually within 5 to 10 minutes. The THC remaining in the blood has a half-life of about 19 hours, but metabolites (of
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which there are at least 45), primarily 11hydroxy-delta-9-THC, are formed in the liver and have a half-life of 50 hours. After one week, 25 to 30 percent of the THC and its metabolites might still remain in the body. Complete elimination of a large dose of THC and its metabolites might take two or three weeks. THC taken orally is slowly absorbed, and the liver transforms it to 11-hydroxy-delta-9-THC; therefore, much less THC reaches the brain after oral ingestion, and it takes much longer for it to have psychological and cardiovascular effects. The peak effects following oral ingestion usually occur at about 90 minutes. The high lipid solubility of THC means that it (like its metabolites) is selectively taken up and stored in fatty tissue to be released slowly. Excretion is primarily through the feces. All of this has two important implications: (1) there is no easy way to monitor (in urine or blood) THC/metabolite levels and relate them to behavioral and/or physiological effects, as can be done with alcohol, and (2) the long-lasting, steady, low concentration of THC and its metabolites on the brain and other organs might have effects not yet determined.
Mechanism of Action Scientists searched for years for a key to help them unlock the mystery of marijuana’s action on the central nervous system. The identification and purification of THC was a necessary step. A significant breakthrough was made by researchers in 1988 who developed a technique to identify and measure highly specific and selective binding sites for THC and related compounds in rat brains. One result was the development and testing of more potent marijuana analogues. Another result was the 1992 discovery of a natural substance produced in the body that has marijuana-like effects when administered to animals. This endogenous substance (see Figure 15.1) is called anandamide (ananda is sanskrit for “bliss”).16 THC and other cannabinoids are known to bind to two receptors, designated CB1 and
CB2.17 There are substantial differences in the structures of these two receptors and their anatomical distribution in the body. CB2 receptors are found mainly outside the brain in immune cells, suggesting that cannabinoids may play a role in the modulation of the immune response. CB1 receptors are found throughout the body, but primarily in the brain. These receptors are much more abundant than receptors for morphine and heroin,17 suggesting that the potential actions of cannabinoids are widespread. The locations of CB1 receptors in the brain also may provide some clues about their functions. For example, the highest density of CB1 receptors has been found in cells of the basal ganglia; its primary components include the caudate nucleus, putamen, and globus pallidus. Cells of the basal ganglia are involved in coordinating body movements. Other regions that also contain a larger number of CB1 receptors include the cerebellum, which coordinates fine body movements; hippocampus, which is involved in aspects of memory storage; cerebral cortex, which regulates the integration of higher cognitive functions; and nucleus accumbens, which is involved in reward. A number of drugs have been developed in an effort to more selectively act on these receptors. Rimonabant, a selective CB1 receptor antagonist, is currently available in several countries as an anti-obesity agent. The U.S. Food and Drug Administration, however, declined to approve it for use because of concerns about side effects such as depression and anxiety.
Physiological Effects One of the most consistent acute physiological effects of both smoked marijuana and oral THC is an increase in heart rate. Figure 15.2 shows that both smoked marijuana and oral THC increased the heart rate of marijuana smokers in a dose-dependent fashion (i.e., larger THC doses produced larger heart rate elevations).18,19 While the peak effects produced by smoking marijuana containing 4 percent THC are similar to 20 mg oral THC, the drug’s time course of action is
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Figure 15.2 The Time Course for Heart Rate after Smoking Marijuana (left) and Ingesting Oral THC (right) different. Peak heart-rate elevations produced by smoked marijuana occurred within 10 minutes and returned to baseline levels after about 90 minutes, whereas peak heart-rate elevations produced by oral THC did not occur until 90 minutes following ingestion and remained elevated for at least four hours after drug administration. The effect of cannabis-based drugs on blood pressure is more variable, with some studies reporting slight increases and others reporting no effect. Concern has been raised that smoking marijuana might have permanent deleterious effects on the cardiovascular system, but there is no evidence to indicate that marijuana-related cardiovascular effects are associated with serious health problems for most young, healthy users.20 Patients with hypertension, cerebrovascular disease, and coronary atherosclerosis, however, should probably avoid smoking marijuana or ingesting THC because of the drug’s effects on heart rate. Other consistent acute effects of smoked marijuana are reddening of the eyes and dryness of the mouth and throat. Except for bronchodilation, acute exposure to marijuana has little effect on breathing as measured by conventional pulmonary tests. Heavy marijuana smoking over a much longer period could lead to clinically signifi-
cant and less readily reversible impairment of pulmonary function.
Behavioral Effects While physiological effects produced by cannabis-based drugs provide important information, the behavior of most interest for the assessment of abuse potential is drug taking. Until recently, cannabinoids were not shown to maintain self-administration in laboratory animals, suggesting that the abuse potential of cannabis-based drugs was minimal. This seemed inconsistent with epidemiological data showing that marijuana is the most widely used illicit drug in the world21 and that a substantial proportion of Americans seek treatment for marijuana abuse and dependence each year.22 Findings from recent studies, however, demonstrate clearly that rats and squirrel monkeys will consistently self-administer cannabinoids.23 The success of recent attempts to obtain reliable selfadministration in laboratory animals has been
anandamide (an and a mide): a chemical isolated from brain tissue that has marijuana-like properties.
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attributed to intravenously injecting THC doses more rapidly than had been previously tried. Several laboratory studies have shown that marijuana produces robust self-administration by human marijuana smokers, and that marijuana self-administration is related to the THC content of the cigarettes. That is, marijuana cigarettes containing a higher concentration of THC are preferred to those containing a lower THC concentration.24 These findings not only confirm the abuse potential of smoked marijuana, but they also suggest that THC administered alone (e.g., oral administration of THC capsules) might have abuse potential. In a recent study, experienced marijuana smokers were given repeated opportunities to self-administer oral THC capsules or to receive $2. Several important findings from that study are worth mentioning. Participants selected: (1) money on more occasions than the capsules; (2) more drugcontaining capsules than placebo; and (3) more THC capsules during social/recreational periods compared to non–social/recreational periods. These observations indicate that oral THC’s abuse potential is modest at best, experienced marijuana smokers can readily distinguish THCrelated effects, and cannabis self-administration is influenced by social factors.19 Some have argued that before novice marijuana smokers are able to experience marijuanaassociated positive subjective effects (e.g., euphoria, stoned), they must go through a process by which they learn to recognize and interpret the psychoactive effects produced by smoked marijuana.25 While this position remains open for debate, the subjective effects on experienced marijuana smokers have been well characterized. In general, experienced smokers report increased ratings of euphoria, “high,” mellowness, hunger, and stimulation after smoking marijuana. These effects peak within 5 to 10 minutes and last for about two hours; they are usually THC concentration-dependent (i.e., the magnitude of effects is increased with increasing THC concentrations). Subjective effects reported by infrequent smokers are similar but more intense because these individuals are
Experienced marijuana smokers report euphoria, “high,” hunger, and mellowness after smoking; the magnitude of the effects depends on the THC concentration.
less tolerant to marijuana-associated effects. Also, at higher THC concentrations some infrequent smokers may report negative effects such as mild paranoia and hallucination. As seen with heart rate, peak subjective effects of oral THC are similar to those produced by smoked marijuana except that the time course of the effects is different. Peak subjective effects occur about 90 minutes following oral ingestion and can last for several hours. An important factor in determining whether a drug is likely to be abused is the rapidity of the onset of its effects. The more rapidly a drug’s effects are experienced, the more likely it will be abused. This might be why the abuse potential of oral THC is limited.
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While an earlier study demonstrated that relatively less-experienced marijuana smokers reported being intoxicated after smoking a placebo cigarette, more recent studies demonstrate that regular marijuana smokers are not so readily duped. Placebo cigarettes were made by extracting the THC and other cannabinoids from marijuana—the cigarettes looked and smelled like regular marijuana cigarettes. In these studies, participants “sampled” marijuana cigarettes (containing placebo or different THC concentrations) and alternative reinforcers (e.g., money or snack food), and subsequently were given an option to choose. Participants selected cigarettes containing THC on more than 75 percent of choice opportunities compared to only about 40 percent when placebo cigarettes were available.26 Furthermore, subjective effects produced by the placebo cigarette were identical to baseline levels, whereas subjective effects produced by cigarettes containing THC were significantly elevated. The effect of marijuana on cognitive performance has received a great deal of attention in the popular press and the scientific literature for many years with little resolution. Unfortunately, many discussions on this topic add to the confusion because they fail to differentiate between the direct (acute) effects and long-term (chronic) effects of marijuana. They also fail to consider the marijuana use history of the user. Following acute administration of smoked marijuana to infrequent marijuana smokers, cognitive performance is disrupted temporarily in several domains: The amount of time that is required to complete cognitive tasks is increased (slowed cognitive processing); performance on immediate recall tasks is decreased (impaired short-term memory); premature responding is increased (impaired inhibitory control); performance on tracking tasks is decreased (loss of sustained concentration or vigilance); and performance on tasks requiring participants to reproduce computer-generated patterns is disrupted (impaired visuospatial processing). The acute effects of marijuana on the performance of frequent smokers are less dramatic, leading
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some to hypothesize that regular marijuana smokers are tolerant to many marijuana-related cognitive effects.18 Some negative cognitive effects, however, have been reported. For example, slowing of cognitive performance is a consistent finding, even in regular users. This effect may have significant behavioral consequences under circumstances requiring complex operations that must be accomplished in a limited time frame, such as certain workplace tasks and the operation of machinery and automobiles. It is also difficult to make definitive statements about long-term cognitive effects of marijuana use because of divergent findings and interpretations. More general conclusions, however, are possible. Based on the available evidence, it appears that following a sufficient period of abstinence (greater than one month), regular marijuana use produces minimal effects on cognition as measured by standard neuropsychological tests.27 The reader is cautioned, though, because as the number of better controlled studies increase, the current conclusions about the long-term effects of marijuana on cognition may change. We’ve all heard about someone smoking marijuana and then getting a case of the “munchies,” a marked increase in food intake. Data from a large number of studies clearly demonstrate that marijuana and oral THC significantly increase food intake. These findings provided the basis for at least one clinical use of cannabisbased drugs—appetite stimulation (see “Medical Uses of Cannabis”). A related question that has received less scientific attention is: Why aren’t most chronic marijuana users overweight? Some have speculated that tolerance develops to the food intake-enhancing effect of cannabis-based drugs, but no empirical data support this view. The bottom line is that the average weight of chronic marijuana users is not known because there have been no studies addressing this issue. So, the average chronic marijuana user may indeed be overweight. Or it could be that most marijuana use occurs during youth (this is certainly supported by data from national surveys), when people and their metabolism are most active.
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Another consistent behavioral effect of marijuana is on verbal behavior (talking). Stimulant drugs such as amphetamines have been shown to increase verbal interactions, as have moderate doses of alcohol. Marijuana appears to be different. Several researchers have reported that while nonverbal social interactions are increased following marijuana smoking, verbal exchanges are dramatically decreased.28
Medical Uses of Cannabis Cannabis has never attained the medical status of opium, but the first report of medical use was by Shen Nung in 2737 BC. About 2,900 years after the Shen Nung report, another Chinese physician, Hoa-tho (AD 200) recommended Cannabis resin mixed with wine as a surgical anesthetic. Although Cannabis preparations were used extensively in medicine in India and after about AD 900 in the Near East, almost nothing about it appeared in European medical journals until the 1800s. Early reports in Europe, such as de Sacy’s 1809 article titled “Intoxicating Preparations Made with Cannabis,” awakened more interest among the writers and artists of the period than among physicians. In 1839, however, a lengthy article, “On the Preparations of the Indian Hemp, or Gunjah,” was published by a British physician working in India.29 He reviewed the use of Cannabis in Indian medicine and reported on his own work with animals, which suggested that Cannabis preparations were quite safe. Having shown Cannabis to be nontoxic, he used it clinically and found it to be an effective anticonvulsant and muscle relaxant, as well as a valuable drug for the relief of the pain of rheumatism. In 1860, the Ohio State Medical Society’s Committee on C. indica reported its successful use in the treatment of stomach pain, chronic cough, and gonorrhea. One physician felt he had to “assign to the Indian hemp a place among the so-called hypnotic medicines next to opium.”30 One difficulty that has always plagued the scientific, medical, and social use of Cannabis is
the variability of the product. An 1898 brochure reviewed the assay and standardization techniques used with many of the common plant drugs and stated: “In Cannabis Indica we have a drug of great importance and one which of all materia medica is undoubtedly the most variable.”31 Four years later, Parke, Davis,32 using new standardization procedures, claimed that “each lot sent out upon the market by us is of full potency and to be relied upon.” The company listed a variety of Cannabis products available for medical use, including “a Chocolate Coated Tablet Extract Indian Cannabis 1/4 grain.” Passage of the Marijuana Tax Act of 1937 resulted in all 28 of the legal Cannabis preparations being withdrawn from the market, and in 1941 Cannabis was dropped from The National Formulary and The U.S. Pharmacopoeia. The decline in the medical use of Cannabis occurred long before 1937, and the law did not eliminate an actively used therapeutic agent. Four factors, however, contributed to the declining prescription rate of this plant. One was the development of new and better drugs for most illnesses. Second was the variability of the available medicinal preparations of Cannabis, which was repeatedly mentioned in the 1937 hearings.5 Third, the active ingredient is very insoluble in water and thus not amenable to injectable preparations. Last, taken orally it has an unusually long (oneto two-hour) latency to onset of action. With the recent renewed interest in marijuana as a social drug has come some reevaluation of the implications of some of the older therapeutic reports. Scientists have looked again at some of the most interesting reported therapeutic effects of Cannabis. One is its anticonvulsant activity. A 1949 report found it effective in some cases in which phenytoin (Dilantin), the anticonvulsant of choice both then and now, was ineffective.33 The fact that both Queen Victoria’s physician and Sir William Osler, as well as others, found Cannabis to be very effective against tension and migraine headaches also caused some interest. A 1971 report showed that marijuana smoking was effective in reducing the fluid pressure
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evidence is most impressive in glaucoma . . . ; in asthma . . . ; and in the nausea and vomiting of cancer chemotherapy . . . and might also be useful in seizures, spasticity, and other nervous system disorders.36
The potential medical benefits of marijuana is an issue with a long and controversial history.
of the eye in a glaucoma patient.34 That report became a cause célèbre in 1975, when Robert Randall, a glaucoma patient, was arrested for growing marijuana plants on his back porch for medical purposes. Fifteen months later, he (1) saw the charges against him dropped, (2) had his physician certify that the only way for him to avoid blindness was to smoke five joints a day, and (3) had these marijuana joints legally supplied to him by the United States government.35 This began a limited program in which the National Institute on Drug Abuse (NIDA) provided marijuana cigarettes to patients with the FDA’s approval of a “compassionate use” protocol. A second possible important medical use was reported in 1975. Medication containing THC was found to be effective in reducing the severe nausea caused by certain drugs used to treat cancer. A 1982 report from the National Academy of Sciences stated: Cannabis and its derivatives have shown promise in the treatment of a variety of disorders. The
In 1985, the FDA licensed a small drug company, Unimed, Inc., to begin producing a capsule containing THC for sale to cancer chemotherapy patients who are experiencing nausea. The drug is referred to by the generic name dronabinol and the brand name Marinol. Dronabinol has helped cancer chemotherapy patients gain weight, and in 1993 the FDA also approved its use for stimulating appetite in AIDS patients. Proponents of medical marijuana argue that the smoked version of the drug should be made legally available as well. They contend that smoked marijuana has several advantages relative to oral THC, including a more rapid onset of effects and greater ability of the patient to control medication effects. It is also possible that marijuana plant constituents other than THC may contribute to the drug’s therapeutic effects, that is the combination and/or balance of the chemicals contained in the plant may be an important factor for beneficial effects. Such arguments, however, have not been successful in terms of reclassifying marijuana under the U.S. Controlled Substance Act. Marijuana remains a Schedule I drug, which means, from a federal government perspective, it cannot be legally prescribed because it has no acceptable medical use. Of course, many citizens and medical professionals disagree with the U.S. government’s position regarding the medical utility of marijuana. This has become more apparent in recent years as citizens have attempted to take action at the state level. In November 1996, both Arizona and California voters passed ballot initiatives allowing physicians to recommend marijuana
dronabinol (dro nab i noll): the generic name for prescription THC in oil in a gelatin capsule. Marinol (mare i noll): the brand name for dronabinol.
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Taking Sides Should Medical Patients Have Access to Marijuana? At least 12 states have passed ballot initiatives allowing patients to use marijuana on the advice of their physicians. Passage of these initiatives has fueled public interest in this topic. The bestdemonstrated effects of marijuana (and of THC) are the reduction of the nausea caused by chemotherapy for cancer and the stimulation of appetite, which might benefit AIDS patients. With such serious illnesses involved, many feel that the compassionate thing is to allow marijuana to be used if it might help, since the risk of dependence seems to be a rather small issue in such cases. In fact, “Cannabis buyers clubs” sprang up in many large cities—most notably, San Francisco—and patients who had notes from the physicians could purchase from them. These clubs were illegal, but local law enforcement agencies for the most part left them alone, not wanting to arrest seriously ill patients. Of course, because the clubs were illegal and informally operated, there was no guarantee that everyone purchasing marijuana was, in fact, seriously ill. Following the passage of the first ballot initiatives, the U.S. government in December 1996 announced that it would move to revoke the DEA registration of any physician who advised a patient to use illegal drugs. This caused some to wonder about violations of the tradition of privileged communications between doctors and patients, and so far the legality of all of this is open to question. In early 1998, the U.S. Justice Department announced plans to shut down all Cannabis buyers clubs in California. In September 2000, the U.S. District Court in San Francisco issued an injunction permanently barring the government from revoking a physician’s
for serious illnesses and allowing patients to possess and use marijuana if their physicians recommend it. There was still no legal way for patients to purchase marijuana, of course, and no legal growers or distributors. More than half the states had previously passed laws allowing medicinal use of marijuana, so in a sense this was not new. However, those previous laws had passed in the 1970s, when
license to prescribe medicine “merely because the doctor recommends medical marijuana to a patient based on a sincere medical judgement.” The court also prevented the government from initiating an investigation of a doctor’s other prescribing practices solely because he or she had recommended marijuana. In November 2000, at the White House’s request, the U.S. Supreme Court issued an emergency ban (by a vote of 7–1) on the distribution of marijuana for medical purposes. The court struck down the U.S. Court of Appeals ruling in San Francisco, which would have made “medical necessity” a defense against violation of federal drug statutes. The court voted 8–0 against such defenses in May 2001. In November 2004, the Supreme Court heard arguments in Raich v Ashcroft, a case brought on behalf of Angel Raich, a California patient, and others. They asserted that because the marijuana was provided to Ms. Raich free, the transactions did not constitute “commerce.” And, since the growing, transfer, and use of the marijuana were all done within California, the federal government could not assert jurisdiction based on its ability to regulate interstate commerce. In June 2005, the U.S. Supreme Court disagreed ruling that federal law enforcement personnel could prosecute patients for possessing marijuana even if their physicians recommended marijuana use for a serious illness. Despite this ruling, the medical marijuana issue is far from being resolved. In fact, in July 2007, New Mexico became the twelfth state to legalize the medical use of marijuana. Do you think medical necessity is a compelling argument for the use of marijuana? Why or why not?
decriminalization and even legalization of marijuana were being debated openly. Also, many of those older laws allowed marijuana to be used only as part of an approved research effort, not for individual patients. As of early 2008, 12 states had some form of legislation allowing a patient, with a physician’s authorization (or prescription), to use marijuana for medical purposes (see Taking Sides).
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In 1997, in response to public pressure to allow the medical use of marijuana, the White House Office of National Drug Control Policy funded another study by the Institute of Medicine (IOM) of the National Academy of Sciences to perform a comprehensive review of the scientific evidence for potential benefits and risks of using marijuana as a medicine. The resulting 1999 report has been pointed to by proponents of medical marijuana as supporting the idea that marijuana is a relatively safe and effective medicine for patients suffering from chronic conditions, such as AIDS wasting syndrome or chronic pain. However, the report also recommends more research on cannabinoid biology, additional clinical studies on marijuana and synthetic cannabinoids, and the development of an effective inhaler to solve the problem of poor oral absorption of THC. In the meantime, the panel recommended that the compassionate use of smoked marijuana cigarettes be allowed for no more than six months for patients with debilitating, intractable pain or vomiting, when the following conditions are met: •
The failure of approved medications to provide relief has been documented.
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The symptoms can reasonably be expected to be relieved by rapid-onset cannabinoid drugs.
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Such treatment is administered under medical supervision in a manner that allows for the assessment of treatment effectiveness.
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An oversight strategy is in place to approve or reject requests within 24 hours after a physician seeks permission to provide marijuana to a patient for a specified use.
The entire report can be found on the Internet at books.nap.edu/catalog/9586.html.
Causes for Concern Abuse and Dependence The evidence now suggests that if high levels of marijuana are used regularly over a sustained
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period, tolerance can develop to many marijuanarelated effects, including the cognitive- impairing, physiological, and subjective effects. However, tolerance may not develop uniformly across each of these variables. For example, it has been demonstrated that heavy marijuana smokers exhibit minimal cognitive impairment following acute marijuana smoking, while showing dramatic heart rate increases and reporting significant levels of euphoria. These findings suggest that tolerance may develop more readily to marijuana-related cognitive effects than to heart rate responses and subjective effects.18 Relative to other drugs of abuse, many people perceive marijuana to be an innocuous drug with limited abuse potential. People have made comparisons between marijuana abuse and abuse of other drugs such as crack cocaine. However, the social consequences associated with marijuana use and those associated with crack cocaine use are dissimilar, making oneto-one comparisons imperfect. Research showing that THC and marijuana produce robust self-administration in laboratory animals and in human research participants clearly demonstrates that the drug has some abuse potential. In addition, of the 7 million Americans classified with dependence on or abuse of illicit drugs in 2006, 4.2 million were dependent on or abused marijuana.37 Although this number represents a relatively small fraction of current marijuana users (less than 30 percent), it shows that a significant number of marijuana smokers do suffer ill effects from using the drug. Can regular marijuana use produce a withdrawal syndrome? According to the DSM-IV-TR (the standard diagnostic instrument), the answer is no. The DSM-IV-TR does not recognize a diagnosis of cannabis withdrawal. Data from a variety of human laboratory and clinical studies, however, demonstrate that an abstinence syndrome can be observed following abrupt cessation of several days of smoked marijuana administration or oral ⌬9-THC administration. Cannabinoid withdrawal is not life threatening, but symptoms can be unpleasant. Marijuana
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withdrawal syndrome in humans may include negative mood states (e.g., anxiety, restlessness, depression, and irritability), disrupted sleep, decreased food intake, and in some cases, aggressive behavior. These symptoms have been reported to begin 1 day after cannabinoid cessation and persist from 4 to 12 days, depending on an individual’s level of marijuana dependence. Clearly, the majority of marijuana users do not experience withdrawal symptoms nor do they meet DSM-IV-TR criteria for cannabis-use disorders. But these findings indicate that regular marijuana use may not be as innocuous as previously perceived.38
Toxicity Potential Acute Physiological Effects The acute physiological effects of marijuana, primarily an increase in heart rate, have not been thought to be a threat to health. However, as the marijuanausing population ages, there is concern that individuals with high blood pressure, heart disease, or hardening of the arteries might be harmed by smoking marijuana.39 The lethal dose of THC has not been extensively studied in animals, and no human deaths have been reported from “overdoses” of Cannabis. Driving Ability A large number of studies have investigated the effects of marijuana on driving performance, but the findings have been inconsistent. Some studies have reported marijuanarelated driving impairments, while others have not. Traditionally, two types of studies have been conducted: (1) epidemiological: These studies determine whether marijuana use is over-represented among drivers involved in automobile accidents; and (2) laboratory: These studies determine the direct effects of marijuana on skills related to driving performance. Findings from the majority of the epidemiological studies show little evidence that drivers who use marijuana alone are more likely to be involved in an accident than nondrug-using drivers. But data from laboratory studies of computer-controlled driving simula-
Inhaling marijuana smoke.
tors indicate that marijuana produces significant impairments.40 Most of the laboratory studies have employed relatively infrequent marijuana users as participants, a group that would be expected to show marked impairments. Because tolerance can develop to many of the cognitive-impairing effects of marijuana, further laboratory studies should include heavy marijuana smokers. Panic Reactions The other major behavioral problem associated with acute marijuana intoxication is the panic reaction. Much like many of the bad trips with hallucinogens, the reaction is usually fear of loss of control and fear that things will not return to normal. This reaction is more common among less-experienced marijuana users. Even Baudelaire understood this and advised his readers to surround themselves with friends and a pleasant environment before using hashish. Although many people do seek emergency medical treatment for marijuana-induced panic and are sometimes given sedatives or tranquilizers, the best treatment is probably “talking down,” or reminding the person of who and where they are, that the reaction is temporary, and that everything will be all right. Chronic Lung Exposure There has been a great deal of concern about the possible long-term effects of chronic marijuana use. A couple of
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physiological concerns merit attention. One is the effect on lung function and the concern about lung cancer. Experiments have shown that chronic, daily smoking of marijuana impairs air flow in and out of the lungs.41 It is hard to tell yet whether years of such an effect results in permanent, major obstructive lung disease in the same way that smoking tobacco cigarettes does. Also, no direct evidence links marijuana smoking to lung cancer in humans. Remember that it took many years of cigarette smoking by millions of Americans before the links between tobacco and lung cancer and other lung diseases were shown. Marijuana smoke has been compared with tobacco smoke.42 Some of the constituents differ (there is no nicotine in marijuana smoke and no THC in tobacco), but many of the dangerous components are found in both. Total tar levels, carbon monoxide, hydrogen cyanide, and nitrosamines are found in similar amounts (except for tobacco-specific nitrosamines, which are carcinogens). Another potent carcinogen, benzopyrene, is found in greater amounts in marijuana than in tobacco. Everyone suspects that marijuana smoking will eventually be shown to cause cancer, but how much of a problem this will be compared with tobacco is hard to say. On the one hand, few marijuana smokers smoke 20 marijuana cigarettes every day, whereas tobacco smokers regularly smoke this much. On the other hand, the marijuana cigarette is not filtered and the user generally gets as much concentrated smoke as possible as far down in the lungs as possible and holds it there. So, while some wait and see when the data will come out, others are participating in the experiment. Reproductive Effects Another area of concern is reproductive effects in both men and women. Heavy marijuana smoking can decrease testosterone levels in men, although the levels are still within the normal range and the significance of those decreases is not known. Diminished sperm counts and abnormal sperm structure in heavy marijuana users has been
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reported, perhaps because anandamide plays a role in normal sperm function.43 A number of studies have reported either lower birth weight or shorter length at birth for infants whose mothers smoked marijuana during pregnancy, but because so many of the women also smoked tobacco or drank alcohol, it is not possible to determine the exact contribution of marijuana to these effects. It is, of course, wise to avoid the use of all drugs during pregnancy. The Immune System Effects There have also been reports that marijuana smoking impairs some measures of the functioning of the immune system.44 Animal studies have found that THC injections can reduce immunity to infection, but at doses well above those obtainable by smoking marijuana. Some human studies of marijuana smokers have suggested reduced immunity, but most have not. If the effect were real, it could result in marijuana smokers’ being more susceptible to infections, cancer, and other diseases, such as genital herpes. One might suspect that such problems would eventually be reflected in the overall death rate of marijuana users. However, a report examining 10 years of mortality data for more than 65,000 people found no relationship between marijuana use and overall death rates.45 Amotivational Syndrome Since 1971, when some psychiatric case reports were published identifying an amotivational syndrome in marijuana smokers, concern has been expressed about the effect of regular marijuana use on behavior and motivation. A number of experiments and correlational studies have been aimed at answering this question. There does seem to be evidence for this diminished motivation, impaired ability to learn, and school and family problems in some adolescents who are chronic, heavy marijuana smokers. If they stop smoking and remain in counseling, the condition improves.46 This probably implies a constant state of intoxication rather than a long-lasting change in brain function or personality.
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Insanity The connection between marijuana use and insanity was one of the main arguments for outlawing the drug in the 1930s, and the notion still remains that marijuana can cause a type of psychosis. There have been reports of psychotic “breakdowns” occurring with rare frequency after marijuana has been smoked, but the causal relationship is in question. The psychotic episodes are generally self-limiting and seem to occur in individuals with a history of psychiatric problems.46 Brain Damage For about 30 years, it has been speculated that amotivational or prolonged psychotic reactions could reflect an underlying damage to brain tissue produced by marijuana. For example, a 1972 report from England indicated that two individuals who demonstrated cerebral atrophy had a history of smoking marijuana. They also had a history of using many other illicit drugs, plus other medical problems, but it was suggested that the brain damage might have been caused by the marijuana. Several experiments have since been done, and all have failed to find a relationship between marijuana smoking and cerebral atrophy. Ironically, some of the nonpsychoactive ingredients in marijuana, including cannabidiol, have been shown to have powerful antioxidant properties that protect brain cells from the toxic effects of other chemicals.47 This effect was strong enough that the NIMH filed a patent in 1988 entitled “Cannabinoids as Antioxidants and Neuroprotectants.” Emotion has played an obvious and influential role. Scientists on both sides have become crusaders for their cause. Some individuals seem to think it is their professional duty to seek out and publicize every potential evil associated with marijuana, even if no strong scientific evidence supports their views. Others seem to automatically question the negative reports and look for ways to discredit them. We can predict that the emotion, the premature announcements of new scary findings, the repeating of long discredited stories, and the conflicting reports will continue.
Marijuana and American Society Our patterns of drug use are but one facet of our evolving society. Drug use affects and is affected by other social trends, including a couple of significant themes from the 1980s. One trend was the increased emphasis on physical health. Jogging, working out, dieting, drinking less alcohol and caffeine, and smoking less all were reflections of our national concern over shaping up. The health trend obviously worked against marijuana use: How many people who wouldn’t smoke tobacco felt good about inhaling marijuana smoke? Second, the 1980s saw a move toward social and political conservatism, which worked against such counterculture behavior as marijuana smoking. And, of course, drug use tends to be faddish. If marijuana was the fashionable drug of the 1970s, then it couldn’t be the fashionable drug of the 1980s. However, in the 1990s the drug came back into fashion, at least somewhat.
Federal and state laws and penalties related to marijuana possession tend to reflect other social trends, becoming more severe in periods of social and political conservatism.
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Data from the yearly survey of high school seniors shows the trends most clearly. After peaking in 1978–1979, the number of high school seniors who had ever smoked marijuana dropped from just over 60 percent to 32 percent in 1992, then rebounded to 45 percent by the class of 2005. Equally dramatic were the trends in daily use, which went from 11 percent in 1978 to 2 percent in 1992 and back to 6 percent by 2005.48 The earlier decreases in marijuana use went along with a steady increase in the belief among these students that “people risk harming themselves if they smoke marijuana regularly.” Whereas just over one-third of the high school seniors agreed with that statement in 1978, more than three-fourths agreed in 1992. Fads being what they are, this downward trend in marijuana use had to end sometime, and the turnaround was seen in the high school senior class of 1992. Significant increases in marijuana use in the 1992–2005 period were accompanied by decreased estimates of risk (see Chapter 1). Although marijuana is not used by most Americans, it is still remarkable how many people have used and continue to use a substance that shouldn’t exist at all in our society, according to the Controlled Substances Act and the DEA. That a large fraction of the society continues to violate the laws regarding marijuana is a matter for concern. It is easy to look back and wish that the 1937 Marijuana Tax Act had never happened. Marijuana use was spreading slowly across the United States and, with any luck, it might have become acculturated. Society would have adapted to marijuana and adapted marijuana to society. Soon it would have become part of society: Perhaps most people would never have used it regularly; of those who did use it, most would have known how to use it; some, of course, would have abused it. It has happened before with coffee, tea, tobacco, and alcohol. The 1937 law prevented all that. It didn’t affect most Americans a great deal until the 1960s, when a large number of young people began experimenting with drugs. Marijuana,
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more than anything else, convinced many young people that the government had been lying to them about drugs. They had been told that marijuana would make them insane, enslave them in drug dependence, and lead to violence and perverted sexual acts. Their experience told them that marijuana was pretty innocuous, compared with those stories, and it became an important symbol: Smoking marijuana struck a blow for truth and freedom. The problem was that laws existed that allowed young people to be sent to jail for 20 years for striking this blow, and that didn’t sit well with some people. Voice was given to the millions of marijuana users in 1970 when a young Washington lawyer established the National Organization for the Reform of Marijuana Laws (NORML) with a grant from the Playboy Foundation. As the founder of NORML put it, “The only people working for reform then were freaks who wanted to turn on the world, an approach that was obviously doomed to failure. I wanted an effective, middle-class approach, not pro-grass but antijail.” Also, in 1970 the Comprehensive Drug Abuse Prevention and Control Act of 1970 established the Commission on Marijuana and Drug Abuse. Its 1972 report recommended that federal and state laws be changed so that private possession of small amounts of marijuana for personal use, and casual distribution of small amounts without monetary profit, would no longer be offenses. The year 1972 was a turning point in the fight to decriminalize marijuana. In June the American Medical Association came out in favor of dropping penalties for possession of “insignificant amounts” of marijuana and noted that “there is no evidence supporting the idea that marijuana leads to violence, aggressive behavior, or crime.” In August the American Bar Association called for the reduction of criminal penalties for possession, and a year later the organization recommended decriminalization. Both traditional liberals and conservatives could support the idea, not to declare marijuana legal but to make possession of marijuana a civil offense, punishable only by a fine.
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In October 1973, Oregon abolished criminal penalties for marijuana use, substituting civil fines of up to $100. Marijuana offenders were given citations that are processed similar to traffic tickets. Did marijuana use increase in Oregon as a result of the decriminalization? Yes. By leaps and bounds? No. From the fall of 1974, a year after decriminalization, to the fall of 1977, the percentage of adults over 18 who had ever used marijuana went from 19 percent to 25 percent. Current users went from 9 percent to 10 percent over the same period. However, marijuana use was increasing toward its 1978 to 1979 peak all over the country at the same time. Possession of a small amount of marijuana was made only a civil offense by eight other states: Maine, Colorado, California, Ohio, Minnesota, Mississippi, New York, and North Carolina. In Alaska, private possession of up to four ounces of marijuana was not illegal. Changing marijuana possession from a felony to a misdemeanor saved money on court costs, juries, and jails. The state of California enjoyed an estimated average annual savings of more than $95 million between 1976 and 1985 as a result of its citation plan for marijuana possession.49 At the federal level, action picked up in 1977. In January, Rosalynn Carter joined her husband, the president, in calling for the decriminalization of marijuana and revealed that their oldest son had been discharged from the Navy for smoking marijuana. Bills to decriminalize marijuana possession were introduced into both houses of Congress, and in August President Carter sent a message to Congress in which he asked them to abolish all federal criminal penalties for the possession of small amounts of marijuana. In the late 1970s, de facto decriminalization had already occurred in many areas of the country. Law enforcement agencies in many of the larger U.S. cities had stopped arresting marijuana users and did not search out those with small amounts for personal use. When the Reagan administration came into office in 1981, any hope of federal decriminal-
ization was gone, replaced by a “get tough” attitude toward all illegal drugs. Marijuana was no exception. In addition to increased efforts to intercept marijuana shipments from abroad, a nationwide effort was launched to combat the cultivation of marijuana plants. More than 100 million plants were tugged out of the ground in 1987 by state, local, and federal law enforcement teams.50 Add to that the zero tolerance seizures of boats, cars, and planes containing even traces of marijuana and the 1988 legislation putting extra pressure on the user (e.g., $10,000 fines at the federal level; see Chapter 3), and we can see that the pendulum had definitely swung back. The states began to follow suit: In 1989, Oregon raised its civil penalty for possession from a $100 maximum to a $500 minimum. In 1990, Alaska voters approved the recriminalization of marijuana possession, making it a misdemeanor punishable by a jail term and up to a $1,000 fine. In 1993, an Alaska Court of Appeals ruled that individuals did have the right to possess up to four ounces of marijuana for personal use. An initiative in 2004 that would have removed criminal penalties for marijuana possession and allowed its regulated (and taxed) sale in Alaska failed to pass.
Summary •
Cannabis has a rich history relating both to its medicinal use and to its recreational uses.
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Marijuana became famous as the “Assassin of Youth” in the 1930s and was outlawed in 1937.
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Cannabis contains many active chemicals, but the most active is delta-9-THC.
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THC is absorbed rapidly by smoking but slowly and incompletely when taken by mouth.
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THC has a long half-life of elimination, and its metabolites can be found in the body for up to several weeks after THC enters the body.
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Selective THC receptors exist in brain tissue, leading to the discovery of a naturally occurring brain cannabinoid, anandamide.
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Marijuana causes an increase in the heart rate and reddening of the eyes as its main physiological effects.
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Psychologically, THC has some sedative properties, produces some analgesia, and at high doses can produce hallucinations.
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Marijuana is useful in the treatment of glaucoma, the reduction of nausea in patients undergoing cancer chemotherapy, and the increase of appetite in AIDS patients. A legal form of THC is available by prescription.
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Although strong dependence is not common, it does occur in some individuals.
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Marijuana can impair driving skills, but it is not clear that smoking marijuana leads to an increased frequency of accidents.
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Most experts agree that chronic smoking of marijuana impairs lung function somewhat and probably increases the risk of lung cancer.
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1. What are the major differences between C. sativa and C. indica? 2. How are hashish and sinsemilla produced? 3. When and where was the earliest recorded medical use of cannabis? 4. Why were Harry Anslinger’s writings on marijuana referred to as a “pyramid of prejudice”? 5. What were the general conclusions of the 1944 LaGuardia Commission? 6. What is meant by “cannabinoid,” and about how many are there in Cannabis? What is the cannabinoid found in brain tissue? 7. How is the action of THC in the brain terminated after about 30 minutes, when the halflife of metabolism is much longer than that? 8. What are the two most consistent physiological effects of smoking marijuana?
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9. What two medical uses have been approved by the FDA for dronabinol? 10. What evidence suggests that marijuana use might interfere with reproduction?
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Schultes, R. E., and A. Hofmann. The Botany and Chemistry of Hallucinogens. Springfield, IL: Charles C Thomas, 1980. Mickel, E. J. The Artificial Paradises in French Literature. Chapel Hill: University of North Carolina Press, 1969. Baudelaire, C. P. Artificial Paradises; on Hashish and Wine as Means of Expanding Individuality. Translated by Ellen Fox. New York: Herder & Herder, 1971. Musto, D. F. The American Disease: Origins of Narcotic Control, 3rd ed. New York: Oxford, 1999, p. 221. Taxation of Marihuana, Hearings before the Committee on Ways and Means, House of Representatives, Seventy-fifth Congress, First Session, on HR 6385, April 27–30 and May 4, 1937. Washington, DC: U.S. Government Printing Office. Parry, A. “The Menace of Marihuana.” American Mercury 36 (1935), pp. 487–88. “Marihuana Menaces Youth.” Scientific American 154 (1936), p. 151. Wolf, W. “Uncle Sam Fights a New Drug Menace . . . Marijuana.” Popular Science Monthly 128 (1936), p. 14. Anslinger, H. J., and C. R. Cooper. “Marijuana: Assassin of Youth.” The American Magazine 124 (1937), pp. 19, 153. “Facts and Fancies about Marihuana.” Literary Digest 122 (1936), pp. 7–8. Whitlock, L. “Review: Marijuana.” Crime and Delinquency Literature 2, no. 3 (1970), p. 367. Fort, J. “Pot: A Rational Approach.” Playboy, October 1969, pp. 131, 154. “The Marihuana Bugaboo.” Military Surgeon 93 (1943), p. 95. “Mayor LaGuardia’s Committee on Marijuana.” In D. Solomon, ed. The Marihuana Papers. New York: New American Library, 1966. “Marijuana Problems.” Journal of the American Medical Association 127 (1945), p. 1129. DiMarzo, V., and others. “Formation and Inactivation of Endogenous Cannabinoid Anandamide in Central Neurons.” Nature 372 (1994), p. 686. Sim, L. I., and others. “Differences in G-protein Activation by Mu- and Delta-opioid, and Cannabinoid, Receptors in Rat Striatum.” European Journal of Pharmacology 307 (1996), pp. 97–105. Hart, C. L., and others. “Effects of Acute Smoked Marijuana on Complex Cognitive Performance.” Neuropsychopharmacology 25 (2001), pp. 757–65. Hart, C. L., and others. “Reinforcing Effects of Oral ⌬9-THC in Male Marijuanna Smokers in a Laboratory Choice Procedure.” Psychopharmacology, 181 (2005) pp. 237–243. Jones, R. T. “Cardiovascular System Effects of Marijuana.” Journal of Clinical Pharmacology 42, no. 11 (2002), pp. 585–635. Anthony, J. C., and J. Helzer. “Epidemiology of Drug Dependence.” In M.T. Tsuang and others, eds. Textbook in
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Psychiatric Epidemiology. New York: John Wiley & Sons, 1995, pp. 361–406. Substance Abuse and Mental Health Services Administration. Treatment Episode Data Set (TEDS): 1995–2005. National Admissions to Substance Abuse Treatment Services. DASIS Series: S-37, DHHS Publication No. SMA 074234. Rockville, MD: Office of Applied Studies, 2007. Justinova, Z., and others. “Self-Administration of Delta9tetrahydrocannabinol (THC) by Drug Naive Squirrel Monkeys.” Psychopharmacology 169 (2003), pp. 135–40. Kelly, T. H., and others. “Effects of D9-THC on Marijuana Smoking, Dose Choice, and Verbal Report of Drug Liking.” Journal of the Experimental Analysis of Behavior 61 (1994), pp. 203–11. Becker, H. S. “Becoming a Marijuana User.” American Journal of Sociology 59 (1953), pp. 235–43. Ward, A. S., and others. “The Effects of a Monetary Alternative on Marijuana Self-administration.” Behavioural Pharmacology 8 (1997), pp. 275–86. Pope, H. G., and others. “Neuropsychological Performance in Long-Term Cannabis Users.” Archives of General Psychiatry 58 (2001), pp. 909–15. Foltin, R. W., and M. W. Fischman. “Effects of Smoked Marijuana on Human Social Behavior in Small Groups.” Pharmacology, Biochemistry, and Behavior 30 (1988), pp. 539–41. O’Shaughnessy, W. B. “On the Preparations of the Indian Hemp, or Gunja.” Transactions of the Physical and Medical Society of Bengal, 1838–1840, pp. 71–102, 1842, pp. 421–61. Mikuriya, T. H. “Marijuana in Medicine: Past, Present and Future.” California Medicine 110 (1969), pp. 34–40. Standardization of Drug Extracts, promotional brochure. Detroit: Parke, Davis & Co., 1898. Letter to EP Delabarre, 9 Arlington Ave., Providence, RI, from Parke, Davis & Co., Manufacturing Department, Main Laboratories, Detroit, Superintendent’s Office, Control Department, March 10, 1902. Davis, J. P., and H. H. Ramsey. “Antiepileptic Action of Marihuana-active Substances.” Federation Proceedings 8 (1949), pp. 284–85. Hepler, R. S., and I. R. Frank “Marijuana Smoking and Intraocular Pressure.” Journal of the American Medical Association 217 (1971), pp. 1392. “Medical Therapy, Legalization Issues Debated at Marijuana Reform Conference.” National Drug Reporter 7, no. 1 (1977), pp. 3–5. Institute of Medicine, National Academy of Sciences. Marijuana and Health. Washington, DC: National Academy Press, 1982. Substance Abuse and Mental Health Services Administration. Results from the 2006 National Survey on Drug
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Use and Health: National Findings. NSDUH Series H-32, DHHS Publication No. SMA 07-4293. Rockville, MD: Office of Applied Studies, 2007. Hart, C. L. “Increasing Treatment Options for Cannabis Dependence: A Review of Potential Pharmacotherapies.” Drug and Alcohol Dependence 80 (2005), pp. 147–59. Aryana, A., and M. A. Williams. “Marijuana as a Trigger of Cardiovascular Events: Speculation or Scientific Certainty?” International Journal of Cardiology 118 (2007), pp. 141–44. Ramaekers, J. G., and others. “Dose-related Risk of Motor Vehicle Crashes after Cannabis Use.” Drug and Alcohol Dependence 73 (2004), pp. 109–19. Tashkin, D. P. “Airway Effects of Marijuana, Cocaine and Other Inhaled Illicit Agents.” Current Opinion in Pulmonary Medicine 7 (2001), pp. 43–61. Moir, D., and others. “A Comparison of Mainstream and Sidestream Marijuana and Tobacco Cigarette Smoke Produced under Two Machine Smoking Conditions.” Chemical Research and Toxicology 21 (2008), pp. 494–502. Schuel, H., and others. “Evidence That Anandamidesignalling Regulates Human Sperm Functions Required for Fertilization.” Molecular Reproduction and Development 63 (2002), pp. 376–87. Shay, A. H., and others. “Impairment of Antimicrobial Activity and Nitric Oxide Production in Alveolar Macrophages from Smokers of Marijuana and Cocaine.” Journal of Infectious Diseases 187 (2003), pp. 700–04. Sidney, S., J. E. Beck, and G. D. Friedman. “Marijuana Use and Mortality.” American Journal of Public Health 87 (1997), pp. 585–90. Smith, D. E., R. B. Seymour. “Clinical Perspectives on the Toxicology of Marijuana: 1967–1981.” In Marijuana and Youth: Clinical Observations on Motivation and Learning. Washington, DC: U.S. Department of Health and Human Services, U.S. Government Printing Office, 1982. Hampson, A. J., and others. “Neuroprotective Antioxidants from Marijuana.” Annals of the New York Academy of Sciences 899 (2000), pp. 274–82. Johnston, L. D., P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg. “Monitoring the Future National Results on Adolescent Drug Use: Overview of Key Findings, 2005.” NIH Publication No. 06-5882. Bethesda, MD: National Institute on Drug Abuse, 2006. Aldrich, M. R., and T. Mikuriya. “Savings in California Marijuana Law Enforcement Costs Attributable to the Moscone Act of 1976—a Summary.” Journal of Psychoactive Drugs 20 (1988), pp. 75–81. Drug Enforcement Administration, 1987 Domestic Cannabis Eradication/Suppression Program Final Report. Washington, DC: U.S. Department of Justice, 1987.
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Short-term Memory One of the most consistent findings about the effects of marijuana is that it impairs short-term memory. To learn more about short-term memory and get an idea of the types of tests that are used to measure it, go
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PerformanceEnhancing Drugs Objectives When you have finished this chapter, you should be able to: • Relate historical uses of performance-enhancing drugs by athletes. • Describe the history of use of stimulants to enhance performance. • Describe the development and current state of drug testing in sports. • Explain why the BALCO scandal received so much publicity. • Describe the performance-enhancing effects and primary dangers of stimulant drugs.
Why is there so much concern • Distinguish between androgenic and anabolic effects of over drug use by athletes? Why testosterone and other related steroid hormones. not focus on drug use by clarinet • Describe the desired effects and undesirable side-effects players or muffler repair people? of steroids in men, women, and adolescents. There are several answers to this question, and together they dem• Explain the effects of human growth hormone as well as onstrate the special reasons to its dangers. be concerned about drug use in • Explain the effects of creatine. sports. First, well-known athletes are seen as role models for young • Discuss the usefulness of dietary supplements in relation people, portraying youth, strength, to their label claims. and health. When a famous athlete is reported to be using steroids or some other illicit substance, there our tradition of fair play in sports, and wideis concern that impressionable young people will spread cheating of any kind tends to diminish a see drug use in a more positive light. Corporate sport and public interest in it. Professional wressponsors pay these athletes to endorse their prodtling, which is widely viewed as being rigged ucts, from shoes to breakfast cereal, based on this or staged, is enjoyed more as a form of comic presumed influence over young consumers. entertainment than as an athletic contest. Most Second, some of the drugs used by athletes professional and amateur athletes guard their are intended to give the user an advantage over honor carefully, and the use of performancethe competition, an advantage that is clearly enhancing drugs is seen as a threat to that honor. viewed as being unfair. This is inconsistent with 391
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Online Learning Center Resources www.mhhe.com/hart13e Visit our Online Learning Center (OLC) for access to these study aids and additional resources. • • • • • •
Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips One of the major concerns over the use of performance-enhancing drugs is that they violate the tradition of fair play in sports.
Third, there is a concern that both the famous and the not-so-famous athletes who use drugs are endangering their health and perhaps their lives for the sake of a temporary burst of power or speed. Athletes should be aware of the risks associated with the use of these drugs. Because these drugs are often obtained illicitly, we can assume that the providers of the drugs do not present a balanced cost/benefit analysis to the potential user but, instead, probably maximize any possible benefit and minimize the dangers.
Historical Use of Drugs in Athletics Ancient Times Although we tend to think of drug use by athletes as a recent phenomenon, the use of chemicals to enhance performance might be as old as sport itself. As with many early drugs, some of these concoctions seemed to make sense at the time but probably had only placebo value. We no longer think that the powdered hooves of an ass will make our feet fly as fast as that animal’s, but perhaps it was a belief in that powder that helped the ancient Egyptian competitor’s self-confidence. Also, if all the others are using it, why take chances? The early Greek Olympians used various herbs and mushrooms that might have had
some pharmacological actions as stimulants, and Aztec athletes used a cactus-based stimulant resembling strychnine. Athletic competitions probably developed in tribal societies as a means of training and preparing for war or for hunting, and various psychoactive plants were used by tribal peoples during battles and hunts, so it is not surprising that the drugs were also used in athletic contests from the beginning.
Early Use of Stimulants During the 1800s and early 1900s, three types of stimulants were reported to be in use by athletes. Strychnine, which became famous as a rat poison, can at low doses act as a central nervous system stimulant. However, if the dose is too high, seizure activity will be produced in the brain. The resulting convulsions can paralyze respiration, leading to death. At least some boxers were reported to have used strychnine tablets. This might have made them more aggressive and kept them from tiring very quickly, but it was a dangerous way to do it. We’ll never know how many of those rugged heroes were killed in this way, but there must have been a few. Thomas Hicks won the marathon in the 1904 St. Louis Olympics, then collapsed and had to be revived. His race was partly fueled by
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Drugs in the Media Banned Substances and How to Avoid Them Television and other news from the past several Olympic games reported multiple instances of athletes being disqualified for using banned substances. In some cases, the disqualification was not contested, but in others the athletes thought they had been disqualified unfairly because they had taken something prescribed for them or something that they were not aware had been banned. The following list, from an article in Technique magazine by Jack Swarbick, lawyer for USA Gymnastics, includes tips for athletes on how to avoid the problem. Even if you aren’t an Olympic competitor, these tips should give you an idea of how complex and difficult this problem can be. 1. Be familiar with the banned substances list of the governing body (International Olympic Committee or NCAA). This means knowing not only what drugs are on the list but also the types of medications or even foods in which those drugs are often found. 2. Make certain that others who ought to know, such as your parents, physician, and school nurse, are also familiar with the banned substances list. 3. Know what medications you are using. Athletes should consult with the governing body regarding the potential for any medications to contain elements of banned substances and should be careful to list
a mixture of brandy and strychnine.1 Although the availability of amphetamines later made highly dangerous drugs such as strychnine less attractive, some evidence indicates the occasional use of strychnine continued at the level of world competition into the 1960s. Cocaine was also available in the 1800s, at first in the form of Mariani’s Coca Wine (used by the French cycling team), which was referred to in some advertisements as “wine for athletes.”2 When pure cocaine became available, athletes quickly adopted this more potent form. Many athletes used coffee as a mild stimulant, and some added pure caffeine to their coffee or took caffeine tablets. There were numerous reports
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all medications when completing the screening form as part of the drug-testing program. At competitions, drink only out of containers that were sealed when you got them, and once you have begun drinking out of a container do not leave it unattended. Several sports have implemented fairly rigorous security measures for the handling of coolers and water bottles. When you are required to produce a urine sample as part of the drug-testing procedures, never surrender possession of the sample or leave it unattended until after you have sealed it inside the shipping canister provided by the officials. If there are any irregularities in the process by which you give a urine sample and place that sample in the sealed container (e.g., a cracked beaker, a spilled sample, or unauthorized individuals on-site), immediately bring those irregularities to the attention of the drug-control administrator on-site. If you are informed that you have tested positive for a banned substance (and you dispute that result), you will be invited to witness the testing of the second half (i.e., the “B sample”) of your urine sample. Attend the test of the B sample, take with you an individual qualified to evaluate the process, and consider videotaping the test.
of the suspected doping of swimmers, cyclists, boxers, runners, and other athletes during this period. Then, as now, some of the suspicions were raised by the losers, who might or might not have had any evidence of doping. Our use of the word dope for illicit drugs is derived from a Dutch word used in South Africa to refer to a cheap brandy, which was sometimes given to racing dogs or horses to slow them down. From this came the term for doping horses and then people, more often in an effort to improve rather than impair performance. Dogs and horses received all the substances used by humans, including coca wine and cocaine, before the days of testing for drugs.
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Amphetamines It isn’t clear when athletes first started using amphetamines for their stimulant effects, but it was probably not long after the drugs were introduced in the 1930s. Amphetamines were widely used throughout the world during World War II, and in the 1940s and 1950s there were reports of the use of these pep pills by professional soccer players in England and Italy. Boxers and cyclists also relied on this new synthetic energy source. More potent than caffeine, longer-lasting than cocaine, and safer than strychnine, it seemed for a while to be the ideal ergogenic (energy-producing) drug for both training and competition. In 1952, the presence of syringes and broken ampules in the speed-skating locker room at the Oslo Winter Olympics was an indication of amphetamines’ presence in international competition. There were other reports from the 1952 summer games in Helsinki and the 1956 Melbourne Olympics. Several deaths during this period were attributed to overdoses of amphetamines or other drugs. By the time of the 1960 Rome games, amphetamine use had spread around the world and to most sports. On opening day a Danish cyclist died during time trials. An autopsy revealed that his death resulting from “sunstroke” was aided by the presence of amphetamines, which reduce blood flow to the skin, making it more difficult for the body to cool itself. Three other cyclists collapsed that day, and two were hospitalized.1 This and other examples of amphetamine abuse led to investigations and to antidoping laws in France and Belgium. Other nations, including the United States, seemed less concerned.
International Drug Testing Some sports, especially cycling, began to test competitors for drugs on a sporadic basis. Throughout the 1960s, some athletes refused to submit to tests or failed tests and were disqualified. These early testing efforts were not enough to prevent the death of cyclist Tommy Simpson, an ex-world champion, who died during the
1967 Tour de France. His death was seen on television, and weeks later it was reported that his body contained two types of amphetamines and that drugs had been found in his luggage. This caused the International Olympic Committee in 1968 to establish rules requiring the disqualification of any competitor who refuses to take a drug test or who is found guilty of using banned drugs. Beginning with fewer than 700 urine tests at the 1968 Mexico City Olympics, each subsequent international competition has had more testing, more disqualifications, and more controversy.
American Football Most Americans did not seem to be very concerned about drug use by athletes until reports surfaced in the late 1960s and early 1970s that professional football players were using amphetamines during games. Before that, people might not have been very concerned about it even if they had known. Remember from Chapter 6 that the amphetamines underwent a major status change in the United States during the 1960s. For years an increasing number of Americans had used amphetamines to keep them awake, to provide extra energy, or to lose weight. They were seen by most people as legal, harmless pep pills. It was in that context that the physicians for professional football teams ordered large quantities of the drugs as a routine part of their supplies, and trainers dispensed them liberally. At the end of the 1960s, amphetamines were widely considered to be drugs of abuse, dangerous drugs that could lead to violent behavior. In this context, revelations that many professionals were playing high made for sensational headlines. Several National Football League (NFL) players sued their teams for injuries received while playing under the influence of drugs, and the NFL officially banned the distribution of amphetamines by team physicians and trainers in 1971. Although the drugs were no longer condoned by the league, the NFL did little at that time to enforce the ban, except to request
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copies of each team’s orders for medical supplies. Athletes who wanted amphetamines still obtained and used them, often through a legal prescription from their own physicians. The attitude seemed to be that, if the players wanted to use pep pills and obtained them on their own, that was their business, but team physicians and trainers shouldn’t be using medications to push the athletes beyond their normal endurance. The current NFL policy, of course, restricts all use of amphetamines, as well as many other drugs, no matter where they are obtained.
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were a Bulgarian discus thrower, a Romanian shotputter, a Polish discus thrower, and weight lifters from several countries. By that time, individual Western athletes might have chosen to use steroids, but some of the eastern European countries seemed to have adopted their use almost as a matter of official policy. When the East German swimming coach was asked during the 1976 Olympics why so many of their women swimmers had deep voices, the answer was, “We have come here to swim, not sing.”4
The BALCO Scandal Steroids During and after World War II, it was found that malnourished people could gain weight and build themselves up more rapidly if they were given the male hormone testosterone. The Soviets were the first to put this hormone to use on a wide scale to build up their athletes. An American team physician at the 1956 Olympics reported that the Soviet athletes were using straight testosterone, sometimes in excessive doses and with unfortunate side effects. Testosterone helps both men and women become more muscular, but its masculinizing effects on women and enlargement of the prostate gland in men are definite drawbacks. The American physician at the 1956 Olympics returned to the United States and helped develop and test anabolic steroids, which were quickly adopted by American weight lifters and bodybuilders.3 American and British athletes in events such as discus and shotput were the first to acknowledge publicly that they had used steroids, and there was evidence that steroid use was widespread during the 1960s in most track and field events. These drugs were not officially banned, nor were they tested for in international competition until the early 1970s, mainly because a sensitive urine test was not available until then. Of the 2,000 urine samples taken during the 1976 Olympics, fewer than 300 were tested for the presence of steroids, and 8 of those were positive.1 The first international athletes to be found guilty of taking steroids
For years, rumors had circulated around professional baseball that certain players were using steroids, but Major League Baseball did not test for them. When Barry Bonds came into the 2001 season looking bigger and stronger, and went on to hit a record 79 home runs, some speculated that he might have used steroids, but the rumors were always denied. In 2002, former player Ken Caminiti admitted to using steroids and claimed that “half” the Major League players were doing so. Major League Baseball did institute a limited testing program that was generally considered to be too weak to have much effect. In June 2003, an unidentified track coach delivered to the U.S. Anti-Doping Agency a syringe containing an “undetectable” steroid, naming the source as Victor Conte, founder of BALCO Laboratories. Analysis determined that the syringe contained tetrahydrogestrinone (THG), a steroid previously unknown to the agency that did not show up in agency tests. The BALCO investigation led to a raid on the laboratory and the discovery of other steroids and human-growth hormone.5 Conte testified before a grand jury in San Francisco after being given immunity from prosecution and named a long list of Olympic and professional athletes who ergogenic (er go gen ic): producing work or energy; a general term for performance enhancement. anabolic (an a ball ick): promoting constructive metabolism; building tissue.
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Mind / Body Connection Baseball: Seeking Alternatives to Amphetamines Psychologically, amphetamine increases feelings of alertness and well-being and improves attention, focus, reaction time, and vigilance. The drug also reverses psychological decrements caused by fatigue and sleep deprivation. Physically, it increases motor and cardiovascular activity. Undoubtedly, these features have contributed to the use of this drug in Major League Baseball for at least a half of a century. It is important to note that amphetamine use in baseball has continued, despite the fact that it has been available only by prescription in the U.S. since 1970. According to investigations of drug use in baseball, this legal technicality did not seem to interfere with the widespread use of amphetamine. However, under baseball’s new drug policy, which took effect at the start of the 2006 season, amphetamine is now banned. While penalties associated with amphetamine infractions are not as severe as steroid violations, players consistently testing positive for the substance run the risk of being banned from the game. The Major League Baseball season is a grueling endurance test, comprised of seven weeks of spring training followed by 162 games in six months. There are also double-headers (two games in one day), rain delays, cross-country flights, and the expectation that players perform at their peak each game. Given this situation, it is not difficult to see why amphetamine use was common. One frequently asked question is what impact will the ban have on the players and game? Some observers have speculated that ultimately it will be
had been his clients, including Barry Bonds and many other professional baseball players. As a result of this and other developments, at the start of the 2006 season, Major League Baseball instituted more frequent testing and toughened penalties for drug policy violations. In addition, testing for amphetamines was included as part of the new policy for the first time (see the Mind/Body Connection box). Under the current policy, each player is tested at least twice: once during the preseason and
a positive development, prompting players to seek healthier and natural alternatives. For example, some players might adapt strategies to improve their physical conditioning. Others may seek out sport psychologists to learn mental skills necessary to perform consistently in training and competition. Some may alter their lifestyles such that they decrease their alcohol intake and attend more carefully to their diet and sleep habits. Another view is that players will continue to use pharmacological tools to aid them through marathon seasons. It has been suggested that high caffeinecontaining energy drink consumption will increase as well as the use of over-the-counter stimulants. Although it is difficult to track this type of stimulant use, information is available regarding the number of players granted therapeutic-use exemptions for Attention-Deficit Hyperactivity Disorder (ADHD). As discussed in Chapter 6, stimulants, including amphetamine, are used to treat this disorder, and its diagnosis could provide a legal avenue through which a player could obtain amphetamine. In 2006, for example, of the 1,354 Major League Baseball players, 28 were granted therapeutic-use exemptions for ADHD. In 2007, this number dramatically increased to 103.6 It is worth noting that the U.S. adult prevalent rate for ADHD is substantially lower than baseball’s 2007 exemptions. It is too early to know for certain the impact of baseball’s ban on amphetamine. But, judging from these early indications, a significant number of individuals will employ strategies, both pharmacological and nonpharmacological, to circumvent the ban.
once during the regular season. All players are also subjected to additional random tests throughout the season. Table 16.1 summarizes the penalties associated with violations.
The Battle over Testing During the 1980s, public revelations of drug use by athletes became common and cocaine was often mentioned. Professional basketball, baseball, and football players in the United States
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Table 16.1 Penalties for Violating Major League Baseball Drug Policy Penalty Steroid First positive test Second positive test
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were being sent into treatment centers for cocaine dependence, and several either dropped out or were kicked out of professional sports. Most amateur and professional sports organizations adopted longer and more complicated lists of banned substances and rules providing for more and more participants to be tested. For example, in 1986, the National Collegiate Athletic Association (NCAA) adopted a list of more than 3,000 brand-name drugs containing banned substances. All participants are to be tested during the championship contest and after all postseason football games. In many events around the world, all contestants must now be subjected to urine tests as a matter of routine. Because of both the expense and the inconvenience, some have questioned the wisdom of trying to test every athlete for everything. Despite the enormous expense to which sports organizations have gone, the use of steroids, stimulants, and other performance-enhancing substances seems to be as great as ever. Both the extent of testing and the ingenuity of athletes trying to beat the tests continue to escalate. The BALCO scandal demonstrates that chemists will keep coming up with new ways to help the athletes avoid detection.
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Stimulants as Performance Enhancers The first question to be answered about the use of a drug to increase energy or otherwise enhance athletic performance is, Does it work? We might not worry so much about unfair competition if we didn’t feel that the use of a drug would really help the person using it. Also, if we could prove that these drugs were ineffective, then we could presumably convince young people not to take the risk of using drugs because there would be no gain to be had. But experiments can never prove that a drug has no effect—you might have done a hundred experiments and not used the right dose or the right test (peak output? endurance? accuracy?). The possibility always exists that someone will come along later with the right combination to demonstrate a beneficial effect. Therefore, be wary when someone tries to use scientific evidence to argue that a drug doesn’t work, has no effect, is not toxic, or is otherwise inactive. We’ve had a pretty good idea of the effectiveness of the amphetamines since 1959, when Smith and Beecher published the results of a double-blind study comparing amphetamines and placebos in runners, swimmers, and weight throwers.7 They concluded that most of the athletes performed better under amphetamines, but the improvement was small (a few percentage points’ improvement). Several studies have reported no differences or very small differences
Stimulants have been shown to improve endurance.
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in performance, and some medical experts in the 1960s wanted to argue that amphetamines were essentially ineffective and there was no reason for people to use them. An excellent 1981 review of the existing literature put it all into perspective. Pointing out that it had been taking athletes an average of about seven years for each 1 percent improvement in the world record speed for the mile run, if amphetamines produced even a 1 percent improvement they could make an important difference at that level of competition. The study concluded that there is an amphetamine margin. It is usually small, amounting to a few percent under most circumstances. But even when that tiny, it can spell the difference between a gold medal and sixth place.8 Whether amphetamines or other stimulants increase physical ability (provide pep or energy) or produce their actions only through effects on the brain is an interesting question, which might not be answerable. Surely a person who feels more confident will train harder, compete with a winning attitude, try harder, and keep trying longer. With amphetamines, improvements have been seen both in events requiring brief, explosive power (shotput) and in events requiring endurance, such as distance running. In laboratory studies, increases have been found in isometric strength and in work output during endurance testing on a stationary bicycle (the subjects rode longer under amphetamine conditions). This endurance improvement could be due to the masking of fatigue effects, allowing a person to compete to utter exhaustion. Caffeine has also been shown to improve endurance performance under laboratory conditions. In one experiment, 330 mg of caffeine (approximately equivalent to three cups of brewed coffee) increased the length of a stationary bicycle ride by almost 20 percent. In another experiment, when subjects rode for two hours, their total energy output was 7 percent higher after 500 mg caffeine than in the control condition.9 The effectiveness of caffeine might depend on other factors: For example, one study reported no benefit from caffeine when athletes ran long
distances (12 miles) in hot, humid conditions.10 Small amounts of caffeine are acceptable in most sports, but a urine level above 12 μg/mL will lead to disqualification in many competitions. The doses needed to produce large performance increases produce much higher levels than that, but there could still be a slight improvement even at legal levels. Apparently no controlled laboratory or field experiments have tested the performanceenhancing capabilities of cocaine, but especially during the 1980s many athletes believed in its power. Cocaine’s stimulant properties are generally similar to those of the amphetamines, so we can assume that cocaine would be effective under some circumstances. Given cocaine’s shorter duration of action, it would not be expected to improve endurance over a several-hour period as well as either amphetamines or caffeine. For years, athletes had another readily available stimulant in the form of ephedrine, either as a drug or in the form of ephedra extract. Ephedra (ma huang) was introduced in Chapter 6 as the herbal source of ephedrine, and it was the ephedrine molecule that was modified in the 1920s to produce amphetamine. When Olympic and NCAA officials developed lists of banned substances, ephedrine soon made its way onto the lists (except for people whose physicians said they suffered from asthma—ephedrine relaxes bronchial passages and is an ingredient in asthma medications). Professional sports organizations were at first less concerned about ephedrine, but eventually the National Football League also banned it. Major League Baseball did not, and baseball players used it to provide extra energy, or in some cases to reduce weight, since ephedra was also found in many weight-control dietary supplements (Chapter 12). In 2003, Baltimore Orioles pitcher Steve Bechler died after collapsing during practice—his temperature rose to 108 degrees in the hospital before his death, which was attributed to heat stroke due to the ingestion of “significant amounts” of ephedrine from a dietary supplement.11 This widely publicized death finally gave the FDA enough political backing to go along with the years of
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evidence it had been accumulating, leading to the 2004 ban on ephedra and ephedrine in dietary supplements. With all these and several other CNS stimulants banned by most sports associations, some athletes have continued to use them during training, to allow them to run, ride, or swim harder. They then do not use the drug for several days before the competition or during the competition, hoping that traces of the substance will not appear in the urine test. This might make sense, but no one knows whether training under one drug condition has an effect on competition under another condition. Also, overexertion under the influence of a fatigue-masking drug might be most dangerous during training, leading to muscle injury, a fall or another accident, or heat exhaustion. Athletes and others who use amphetamines or cocaine regularly run the risk of developing a dependence on the drug, developing paranoid or violent behavior patterns, and suffering from the loss of energy and psychological depression that occur as the drugs wear off (see Chapter 6).
Steroids The male sex hormone testosterone has two major types of effects on the developing man. Androgenic effects are masculinizing actions: Initial growth of the penis and other male sex glands, deepening of the voice, and increased facial hair are examples. This steroid hormone also has anabolic effects. These include increased muscle mass, increases in the size of various internal organs, control of the distribution of body fat, increased protein synthesis, and increased calcium in the bones. In the 1950s, drug companies began to synthesize various steroids that have fewer of the androgenic effects and more of the anabolic effects than testosterone. These are referred to as anabolic steroids, although none of them is entirely free of some masculinizing effect. Whether these drugs are effective in improving athletic performance has been controversial:
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For many years the medical position was that they were not, whereas the lore around the locker room was that they would make anyone bigger, stronger, and more masculine-looking. A lot of people must have had more faith in the locker-room lore than in the official word. The 1989 Physician’s Desk Reference contained the following statement in boldface type: “Anabolic Steroids Have Not Been Shown to Enhance Athletic Ability.” Try telling that to any current major league baseball player, sports writer, or fan. That disclaimer is no longer required by the FDA. There is no doubt that testosterone has a tremendous effect on muscle mass and strength during puberty, and experiments on castrated animals clearly show the muscle-developing ability of the synthetic anabolics.12 What is not so clear is the effect of adding additional anabolic stimulation to adolescent or adult males who already have normal circulating levels of testosterone. Laboratory research on healthy men who are engaged in weight training and are maintained on a proper diet has often found that anabolic steroids produce small increases in lean muscle mass and sometimes small increases in muscular strength. There is no evidence for an overall increase in aerobic capacity or endurance in those studies. However, it might never be possible to conduct experiments demonstrating the effectiveness of the high doses used by some athletes. Many athletes report that they take 10 or more times the dose of a steroid that has been tested and recommended for treatment of a deficiency disorder.13 It is also common for athletes to take more than one steroid at a time (both an oral and an injectable form, for example). This practice is known as “stacking.” To expose research subjects to such massive doses would clearly be unethical. Another impediment to doing careful research on this topic is that these steroids produce detectable psychological effects. When double-blind experiments have been attempted,
androgenic (an drow gen ick): masculinizing.
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almost always the subjects have known when they were on steroids, thus destroying the blind control.14 This is important because steroid users report that they feel they can lift more or work harder when they are on the steroids. This may be due to CNS effects of the steroids leading to a stimulant-like feeling of energy and loss of fatigue or to increased aggressiveness expressed as more aggressive training. There is a further possibility of what is known as an active placebo effect, with a belief in the power of steroids, enhanced by the clear sensation that the drug is doing something because one can “feel” it. Until recently, many of the scientists studying steroid hormones believed that their main effects were psychological, combined with a “bloating” effect on the muscle, in which the muscle retains more fluids, is larger, weighs more, but has no more physical strength.1
Psychological Effects of Steroids The reported psychological effects of steroids, including a stimulant-like high and increased aggressiveness, might be beneficial for increasing the amount of work done during training and for increasing the intensity of effort during competition. However, there are also concerns that these psychological effects might produce great problems, especially at high doses. One concern is that a psychological dependence seems to develop in some users, who feel great when they are on the steroids but become depressed when they are off them. Many users take the drugs in cycles, and their mood swings can interfere with their social relationships and other life functions. There has been a great deal of discussion about “roid rage,” a kind of manic rage that has been reported by some steroid users.15 We should be careful about attributing instances of violence to a drug on the basis of uncontrolled retrospective reports, especially when the perpetrator of a violent crime might be looking for an excuse.16 However, there are a suffi-
cient number of reports of violent feelings and actions among steroid users for us to be concerned and to await further research. Says Dr. William Taylor, a leading authority on anabolic steroids, “I’ve seen total personality changes. A passive, low-key guy goes on steroids for muscle enhancement, and the next thing you know, he’s being arrested for assault or disorderly conduct.”17
Adverse Effects on the Body There are many concerns about the effects of steroid use on the body. In young users who have not attained their full height, steroids can cause premature closing of the growth plates of the long bones, thus limiting their adult height. For all users the risk of peliosis hepatitis (bloody cysts in the liver) and the changes in blood lipids possibly leading to atherosclerosis, high blood pressure, and heart disease are potentially serious concerns. Acne and baldness are reported, as are atrophy of the testes and breast enlargement in men using anabolic steroids. There are also considerations for women who use anabolic steroids. Because women usually have only trace amounts of testosterone produced by the adrenals, the addition of even relatively small doses of anabolic steroids can have dramatic effects, in terms of both muscle growth and masculinization. Some of the side effects, such as mild acne, decreased breast size, and fluid retention, are reversible. The enlargement of the clitoris might be reversible if steroid use is stopped soon after it is noticed. Other effects, such as increased facial hair and deepening of the voice, might be irreversible.14
Regulation As we found in Chapter 2, when a drug produces dependence, violent behavior, and toxic side effects, society may feel justified in trying to restrict the drug’s availability. In 1988, congressional hearings were held on the notion
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Drugs in Depth Nutritional Ergogenic Aids If athletes can’t get or refuse to use pharmacological aids in athletic competition, most believe that certain foods or nutritional supplements are a “natural” way to enhance their performance. Following is a very abbreviated description of a more complete review of this topic.18 Amino acids are the natural building blocks of the protein required to build muscle, and one certainly requires a basic minimum intake. There is some evidence that very active people can benefit from a somewhat increased intake of dietary protein, slightly above the recommended daily allowances, but there is no demonstrated need to purchase expensive amino acid supplements to achieve this. Marketers of these “muscle-building” dietary supplements walk a fine line by avoiding making specific claims on the product labels, so they do not fall under the FDA’s rules for demonstrating effectiveness. Usually nearby posters or pamphlets link amino acids to the idea of muscle growth. These supplements are probably of little or no value to an athlete who is receiving proper nutrition. Carbohydrates are burned as fuels, especially during prolonged aerobic exercise. Carbohydrates taken two to four hours before an endurance performance lasting for more than an hour may enhance the performance by maintaining blood glucose levels and preventing the depletion of muscle stores of glycogen. Carbohydrate loading before marathon runs consists of resting for the last day or two while ingesting extra carbohydrates, increasing both muscle and liver stores of carbohydrates. In either case, there is not much evidence to support the value of carbohydrate supplements for athletic performances lasting less than an hour. Fats, in experiments with fat supplements, have not been found to be a useful ergogenic aid. Vitamins, especially the water-soluble B vitamins, are necessary for normal utilization of food energy.
of placing anabolic steroids on the list of controlled substances. Evidence was presented that a large black market had developed for these drugs, amounting to perhaps $100 million per
Deficiencies in these vitamins, such as might result when a wrestler is dieting to meet a weight limit, can clearly impair physical performance. However, once the necessary minimum amount is available for metabolic purposes, further supplements are of no value. Many experiments have been done with supplements of C, E, and B-complex vitamins or with multivitamin supplements, the so-called vitamin B15, and with bee pollen, and there is no evidence for enhanced performance or faster recovery after workouts. Again, these supplements are probably of no value to an athlete who is receiving proper nutrition. Minerals, in the form of various mineral supplements, are widely used by athletes. Once again, most are probably not needed or useful, but there may be some exceptions. Electrolyte drinks are designed to replace both fluids and electrolytes, such as sodium and chloride that are lost in sweat. Actually, sweat contains a lower concentration of these electrolytes than does blood, so it is more important to replace the fluids than the electrolytes under most circumstances. Sodium supplementation may be useful for those engaged in ultraendurance events, such as 100-mile runs. Iron supplements are helpful in athletes who are iron-deficient, as may occur especially in female distance runners. However, if iron status is normal, there is probably no value in iron supplements. The jury is still out on whether “buffering” the blood pH with sodium bicarbonate (baking soda) enhances performance in anaerobic events, such as 400- to 800-meter runs. Some studies indicate improvements, whereas others do not. Water is needed by endurance athletes to keep their body temperatures down, especially in a warm environment. Drinking water both before and during prolonged exercise can deter dehydration and improve performance. Visit the Online Learning Center for links to more information on supplements.
year. In addition, there was concern that adolescent boys, many of whom were not athletic at all, had begun to use steroids in the belief that they would quickly become more muscular
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Taking Sides Should We Be Concerned about Steroid Use by Entertainers? In recent years, the U.S. Congress has focused much attention on Major League Baseball players’ alleged use of performance-enhancing drugs. However, some are warning that steroids and human growth hormone are being illegally prescribed throughout the country at an alarming rate under the belief they will aid healing, enhance physical attractiveness, and/or slow aging. The list of people accused of using these drugs is extensive and ranges from ordinary citizens to prominent entertainers. For example, in March 2007, Sylvester Stallone was required to pay a fine of nearly $3,000 to Australian officials after they discovered in his luggage several vials of human growth hormone. The use of antiaging, anti-obesity, and anti-fatigue agents in the entertainment industry has been known and accepted for decades. But recent claims that some members of the industry are using steroids and related compounds raise similar questions to those mentioned
and “macho” looking. As part of the Omnibus Crime Control Act of 1990, anabolic steroids became listed as a Schedule III controlled substance, requiring more record-keeping and limited prescription refills.19
Other Hormonal Manipulations Whereas the anabolic steroids have been in wide use, other treatments have been experimented with on a more limited basis. Female sex hormones have been used to feminize men, so that they could compete in women’s events. The women’s gold medal sprinter in the 1964 Olympics was shown by chromosome testing to have been a man, and he had to return the medal. Hormone receptor–blocking drugs have probably been used to delay puberty in female gymnasts. In women, puberty shifts the center of gravity lower in the body and changes body proportions in ways that adversely affect performance in some gymnastic events. Smaller
regarding the use of these drugs by athletes. Entertainers are role models for young people. Will their steroid use suggest to impressionable youngsters that this type of drug use is acceptable? Performance-enhancing drugs are usually taken to create an advantage over the competition. For example, professional models may take amphetamines in an effort to decrease body weight and enhance their chances of landing the “supermodel” contract. This is clearly viewed as being unfair to models not taking antiobesity drugs. And of course, there are healthrelated risks associated with these drugs, especially when taken illicitly. As a result of these issues, should we increase our monitoring of performance-enhancing drug use by members of the entertainment industry? Should Congress also conduct investigations of drug use in the entertainment industry? Or should Congress refrain from such drug-use investigations altogether?
women appear to be more graceful, spin faster on the uneven bars, and generally have the advantage, which is why top female gymnasts are usually in their teens. However, the Soviets were suspected of tampering with nature: Their top three international gymnasts in 1978 were all 17 or 18 years old, but the following were their heights and weights: 53 inches, 63 pounds; 60 inches, 90 pounds; and 57 inches, 79 pounds. We have certainly not seen the end of growth-promoting hormonal treatments. Human growth hormone, which is released from the pituitary gland, can potentially increase the height and weight of an individual to gigantic proportions, especially if administered during childhood and adolescence. In rare instances, the excessive production of this hormone creates giants well over 7 feet tall. These giants usually die at an early age because their internal organs continue to grow. However, administration of a few doses of this hormone at the right time might produce a more controlled increase
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in body size. Likewise, the growth-hormonereleasing hormone, and some of the cellular intermediary hormones by which growth hormone exerts its effects, might work to enhance growth. It is difficult to test for the presence of these substances. Despite the possible dangers, the lure of an otherwise capable basketball player growing a couple of inches taller or of a football player being 30 pounds heavier has no doubt caused many young athletes to experiment with these substances. Studies have shown that growth hormone increases lean body mass but may not improve strength.20 The 1990 legislation that placed anabolic steroids on the list of controlled substances also made it a crime to distribute human growth hormone for nonmedical purposes.
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is no evidence that beta-2 agonists improve athletic performance.21
Creatine One widely used substance among bodybuilders has been creatine, a natural substance found in meat and fish. This legal product is sold as a food supplement. There is clear evidence that creatine helps regenerate ATP, which provides the energy for muscle contractions. Users of creatine tend to gain some weight, some of which is water weight. There is considerable evidence that the use of creatine can improve strength and short-term speed in sprinting. However, studies of longer-distance running, cycling, and swimming often find no effect, and in one case a significant slowing was reported, probably due to weight gain.4
Beta-2 Agonists At the beginning of the 1992 Olympics, the leader of the British team was disqualified because of the detection of a new drug. Clenbuterol was developed as a treatment for asthma and is a relative of several other bronchodilators that are found in prescription inhalers. These drugs have sympathomimetic effects on the bronchi of the lungs but are designed to be more specific than older sympathomimetics, such as ephedrine or the amphetamines (see Chapter 6). Their specificity comes from a selective stimulation of the beta-2 subtype of adrenergic receptors. Research with cows had revealed an increase in muscle mass, and speculation was beginning that this might represent a new type of nonsteroidal anabolic agent. Apparently someone in Great Britain was keeping an eye on the animal research literature and decided to try the anabolic actions on at least one Olympic athlete. Presumably it was hoped that such a new drug would not be tested for, but the Olympic officials were also well informed and ready, at least for clenbuterol. Human studies have shown some increases in strength of selected muscle types with clenbuterol or a similar drug, but there
Getting “Cut” If getting “cut,” “ripped,” and “shredded” sounds like something you’d want to avoid, then you’re probably not into bodybuilding. These terms refer to the appearance of someone who is both muscular and lean. Because amateur wrestlers compete in weight classes and they need to be strong, they have always had the problem of eating well to build strength and train hard, but then needing to “cut” weight before the weigh-ins for matches. Jockeys have had a similar problem. Over the years, some of these athletes have engaged in fairly extreme methods to achieve short-term weight reduction, such as purging, taking diuretic drugs to lose water weight, and exercising in a heated environment or wearing nonporous clothing to maximize sweating. The entire list of weight-control drugs mentioned in Chapters 6 and 12 have been used as
human growth hormone: a pituitary hormone responsible for some types of giantism.
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Bodybuilders and other athletes have used steroids or other supplements to develop a lean, strong, muscular body—to become “cut” or “ripped.”
well, ranging from amphetamine to ephedrine to caffeine. Increasingly, bodybuilders are seeking the look of someone who is both strong and lean, with lots of muscle definition. That appearance is referred to as looking “cut,” probably derived from the idea of cutting weight or cutting fat, but perhaps also carrying the connotation of “sculpted.” A more extreme version of looking cut is looking “ripped,” or sometimes “shredded.” These are the men and women whose every muscle fiber and vein can be seen through the skin, perhaps with a body fat percentage down to an unhealthy 6 to 9 percent (14 to 20 percent is considered ideal for a healthy male). They also are using drugs and nutritional supplements to help achieve this appearance. Steroids increase muscle mass, but they don’t produce this kind of lean definition. A brisk market has developed in dietary supplements containing the word ripped in their name, such as “Ripped Fuel” and “Ripped Fast.” For many years these products relied mainly on ephedra as the main active ingredient. Once ephedra was banned, these
profitable products did not go away, they simply changed their formulas and kept making the same claims about being “fat burners” and promising incredible results. They contain a bewildering variety of plant extracts, many of which contain caffeine in unknown amounts (e.g., guarana extract, green tea extract, and coffee bean extract). Remember that these dietary supplements do not have to be demonstrated to be effective, and the beneficial claims have not been evaluated by the FDA (or anyone else). If an included ingredient should turn out to be dangerous, it might take a long time for this to come to the attention of the FDA, and it would then take a long time for the agency to build a case to remove the ingredient from the market (it took 10 years for ephedra). No such product has ever been shown to actually be a “fat burner,” so it’s unlikely that these are either. If you buy them, the closest you’ll get to being “ripped” as a result is probably feeling “ripped off” when the magic pill doesn’t deliver what you hoped.
Summary •
Performance-enhancing drugs have been used by athletes throughout history.
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Athletic use of stimulants appears to have increased and spread to most sports with the use of amphetamines during the 1950s and 1960s.
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Amphetamines and caffeine have both been shown to increase work output and to mask the effects of fatigue.
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Some athletes continue to use stimulants for training, despite the dangers of injury and overexertion.
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Anabolic steroids are capable of increasing muscle mass and probably strength, although it has been difficult to separate the psychological stimulant-like effect of these drugs from the physical effects on the muscles themselves.
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Anabolic steroids can also produce a variety of dangerous and sometimes irreversible side effects.
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It is difficult to do ethical and well-controlled research on the effects of steroids.
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Misuse of human growth hormone and related substances might be the next problem to arise.
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Creatine is a legally available nutritional supplement that can increase strength but might slow distance runners because of resultant weight gain.
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4. 5.
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Review Questions 1. What was the first type of stimulant drug reported to be used by boxers and other athletes in the 1800s? 2. What was the first type of drug known to be widely used in international competition and that led to the first Olympic urine-testing programs? 3. When and in what country were the selective anabolic steroids first developed? 4. Do amphetamines and caffeine actually enhance athletic performance? If so, how much? 5. How was ephedrine used by athletes, and what happened to it? 6. What muscle effect do we know for certain that anabolic steroids can produce in healthy men? 7. What is meant by “roid rage,” and what double-blind studies have been done on this phenomenon? 8. What specific effect of anabolic steroids might be of concern to young users? to females? 9. Why do “pituitary giants” often die at an early age? 10. How does creatine increase strength?
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8. 9. 10.
11. 12. 13. 14. 15.
16.
17. 18.
19.
20.
21.
Donohue, T., and N. Johnson. Foul Play: Drug Abuse in Sports. Oxford, England: Basil Blackwell, 1986. Asken, M. J. Dying to Win: The Athlete’s Guide to Safe and Unsafe Drugs in Sports. Washington, DC: Acropolis, 1988. Eichner, E. R. “Ergogenic Aids: What Athletes Are Using— and Why.” Physician and Sportsmedicine 25 (1997), pp. 70–83. Goldman, B. Death in the Locker Room. South Bend, IN: Icarus Press, 1984. Fainaru-Wada, M., and L. Williams. “Sports and Drugs: How the Doping Scandal Unfolded. Fallout from BALCO Probe Could Taint Olympics, Pro Sports.” San Francisco Chronicle, December 21, 2003. Schmidt, M. S., and A. Schwarz. “Baseball Is Challenged on Rise in Stimulant Use.” The New York Times, January 16, 2008. Smith, G. M., and H. K. Beecher. “Amphetamine Sulfate and Athletic Performance.” Journal of the American Medical Association 170 (1959), pp. 542–57. Laties, V. G., and B. Weiss. “The Amphetamine Margin in Sports.” Federation Proceedings 40 (1981), pp. 2689–92. Noble, B. J. Physiology of Exercise and Sport. St Louis: Mosby, 1986. Cohen, B. S., and others. “Effects of Caffeine Ingestion on Endurance Racing in Heat and Humidity.” European Journal of Applied Physiology 73 (1996), pp. 358–63. Bodley, H. “Medical Examiner: Ephedra a Factor in Bechler Death.” USA Today, March 13, 2003. Williams, M. H. Ergogenic Aids in Sports. Champaign, IL: Human Kinetics, 1983. Marshall, E. “The Drug of Champions.” Science 242 (1983), pp. 183–84. Taylor, W. N. Hormonal Manipulation: a New Era of Monstrous Athletes. Jefferson, NC: McFarland & Co., 1985. Pope, H. G., and D. L. Katz. “Affective and Psychotic Symptoms Associated with Anabolic Steroid Use.” American Journal of Psychiatry 145 (1988), pp. 487–90. Lubell, A. “Does Steroid Abuse Cause— or Excuse— Violence? Physician and Sportsmedicine 17 (1989), pp. 176–85. Fultz, O. “’Roid Rage.” American Health 10 (1991), p. 60. Burke, L., and others. “Supplements and Sports Foods.” Clinical Sports Nutrition, 3rd ed. Edited by L. Burke and V. Deakin. Sydney: McGraw-Hill, 2006, pp. 485–579. Available at http://www.ais.org.au/nutrition/documents/ 16Complete.pdf Nightingale, S. L. “Anabolic Steroids as Controlled Substances.” Journal of the American Medical Association 265 (1991), p. 1229. Liu, H., and others. “Systematic Review: The Effects of Growth Hormone on Athletic Performance.” Annals of Internal Medicine (2008) [March 17 Epub ahead of print] Spann, S. “Effect of Clenbuterol on Athletic Performance.” Annals of Pharmacotherapy 29 (1995), p. 75.
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How Would You Run the Race? Imagine that you have gone out for the track team. You compete in the 3,000-meter races and have been training hard for the past two years. It seems as though you have worked as hard as you could every day, yet it’s clear that your times have gotten as fast as they’re going to get. The conference championships are tomorrow. Your parents have traveled 300 miles to see you run, and lots of your friends will be there, cheering you on. You know your own times, and you know the competition, and, although you expect a close race for the top three spots, you figure to come in fourth. You yourself have never used any type of stimulant drug, but you have heard rumors that several of the fastest runners take amphetamines before the race, and you suspect that it is true. Your conference has not yet adopted a drug-screening program for track, however, so there’s no way to know for sure.
Under these circumstances, what would you do if 1. Someone you don’t know very well but who you heard is a drug dealer offers you some “speed” just for the race? 2. A friend of yours has some prescription diet pills that contain amphetamines, and the friend offers you one? 3. You are offered some cocaine to snort right before the race? 4. You are offered coffee or tea? Or would you rather not take artificial stimulants at all, come in fourth, and know you did your best and ran a clean race?
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SEVEN Prevention and Treatment This final section on prevention and treatment comes at the end of the book for a reason. Now
17 Preventing Substance Abuse What kinds of prevention programs have been tested in the schools, and which ones seem to be effective? What can parents and communities do?
that you’re more familiar with the wide spectrum of substances that people can abuse, and also
18 Treating Substance Abuse and Dependence What are the differences among the various approaches to treating alcohol, opioid, cocaine dependence, and others? How well do these programs work?
with the wide variety of forms of substance abuse and dependence, we are better able to talk about what we’re trying to prevent, and what we’re trying to treat. Because many of the medication-based treatments depend on specific interactions with the targeted substances of abuse, you now should understand how those medications have been developed and used.
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Preventing Substance Abuse Objectives After you have studied this chapter, you should be able to: • Distinguish between education and propaganda programs based on their goals and approaches. • Describe two systems for classifying prevention programs: one based on stages of involvement, the other based on target populations defined by risk for drug use. • Describe the historical shifts in substance abuse prevention programs from the knowledge-attitudes-behavior model to affective education to anti-drug norms. • Explain how the social influence model for smoking prevention led to the development of DARE and similar programs.
Why can’t we do something to keep young people from ruining their lives with drugs? As • Describe the outcome of research on DARE’s effectiveness our society seeks to prevent drug and how DARE America has responded. abuse by limiting the availabil• List some examples of effective prevention programs that ity of such drugs as heroin and have been adopted as model programs by SAMHSA. cocaine, we are forced to recognize several other facts. First, as • Give some examples of peer, family, and community long as there is a sizable market approaches to prevention. for these substances, there will • Describe the most consistent feature of workplace prevenbe people to supply them. Thus, tion programs. only if we can teach people not to want the drugs can we attack the source of the problem. Second, these substances will never disappear, so we should try to teach people to Defining Goals and live in a world that includes them. Third, our Evaluating Outcomes society has accepted the continued existence Think about the process you are engaged in of tobacco and alcohol, yet some people are while reading and studying this book. The text harmed by them. Can we teach people to coexis aimed at teaching its readers about drugs: ist with both legal and illegal substances and their effects, how they are used, and how they to live in such a way that their lives and health relate to society. The goal of the authors is are not impaired by them? 410
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education. A person who understands all this information about all these drugs will perhaps be better prepared to make decisions about personal drug use, more able to understand drug use by others, and better prepared to participate in social decisions about drug use and abuse. We hope that a person who knew all this would be in a position to act more rationally, neither glorifying a drug and expecting miraculous changes from using it nor condemning it as the essence of evil. But our ultimate goal is not to change the readers’ behavior in a particular direction. For example, the chapter on alcohol, although pointing out the dangers of its use and the problems it can cause, does not attempt to influence readers to avoid all alcohol use. The success of this book is measured by how much a person knows about alcohol, tobacco, or marijuana, not by whether he or she is convinced never to drink or smoke. On the other hand, a tradition exists, going back to the “demon rum” programs of the late 1800s, of presenting negative information about alcohol and other drugs in the public schools with the clear goal of prevention of use. Some of these early programs presented information that was so clearly one-sided that they could have been classified as propaganda rather than education. We would not measure the success of such a program by how much objective information the students gained about the pharmacology of cocaine, for example. A more appropriate index might be how many of the
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students did subsequently experiment with the drugs against which the program was aimed. Until the early 1970s, it was simply assumed that these programs would have the desired effect, and few attempts were made to evaluate them.
Types of Prevention The goals and methods of a prevention program also depend on the drug-using status of those served by the program. The programs designed to prevent young people from starting smoking might be different from those used to try to prevent relapse in smokers who have quit, for example. Until recently, drug-abuse prevention programs have been classified according to a public health model: •
Primary prevention programs are those aimed mainly at young people who have not yet tried the substances in question or who may have tried tobacco or alcohol a few times. As discussed in the section “Defining Goals and Evaluating Outcomes,” such programs might encourage abstinence from specific drugs or might have the broader goal of teaching people how to view drugs and the potential influences of drugs on their lives, emotions, and social relationships. Because those programs are presented to people with little personal experience with drugs, they might be expected to be especially effective. But, there is the danger of introducing large numbers of children to information about drugs that they might otherwise never have heard of, thus arousing their curiosity.
•
Secondary prevention programs can be thought of as designed for people who have tried the drug in question or a variety of other substances. The goals of such programs are usually the prevention of the use of other, more dangerous substances and the prevention of the development of more dangerous forms of use of the substances they are already experimenting with. We
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Drugs in the Media Prime-Time Drug-Prevention Programming In late 1997, the U.S. Congress approved the expenditure of $1 billion over a five-year period for anti-drug advertising on television networks. This was a lot of revenue for the networks, but the catch was that they had to broadcast the messages at half the normal market price. After industry protests, the White House Office of National Drug Control Policy struck deals to discharge networks from the halfcost advertising time requirements if they would incorporate drug-abuse prevention messages into the content of television shows. For example, the program “E.R.,” about a hospital emergency room,
might describe the clientele here as more “sophisticated” substance users who have not suffered seriously from their drug experiences and who are not obvious candidates for treatment. Many college students fall into this category, and programs aimed at encouraging responsible use of alcohol among college students are good examples of this stage of prevention. •
Tertiary prevention, in our scheme, is relapse prevention, or follow-up programs. For alcohol-or heroin-dependent individuals, treatment programs are the first order of priority. However, once a person has been treated or has stopped the substance use without assistance, we enter another stage of prevention.
The Institute of Medicine has proposed a new classification of the “continuum of care,” which includes prevention, treatment, and maintenance.1 Prevention efforts are categorized according to the intended target population, but the targets are not defined only by prior drug use: •
Universal prevention programs are designed for delivery to an entire population—for example, all schoolchildren or an entire community.
has included several episodes dramatizing the consequences of illicit drug use. The agreement was brought to light in early 2000 by the online newsmagazine salon.com, which raised concerns about hidden government “propaganda.” See if you can get a few people to keep an eye out for such integrated anti-drug content for one week. Did you find some obvious examples? Have you been aware of this type of integrated content before? What is the danger involved in having the federal government influence the content of television programming in this subtle way?
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Selective prevention strategies are designed for groups within the general population that are deemed to be at high risk—for example, students who are not doing well academically or the poorest neighborhoods in a community.
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Indicated prevention strategies are targeted at individuals who show signs of developing problems, such as a child who began smoking cigarettes at a young age or an adult arrested for a first offense of driving under the influence of alcohol.
Prevention Programs in the Schools The Knowledge-Attitudes-Behavior Model After the increase in the use of illicit drugs by young middle-class people in the 1960s, there was a general sense that society was not doing an adequate job of drug education, and most school systems increased their efforts. However, there was confusion over the methods to be used. Traditional anti-drug programs had relied heavily on representatives of the local police, who went into schools and told a few horror stories, describing the legal trouble due anyone who got caught with illicit drugs. Sometimes
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Targeting Prevention Preventing Inhalant Abuse The abuse by children of spray paints and other products containing solvents appears to have increased somewhat in recent years (see Chapter 7). Several characteristics of this type of abuse make it an interesting problem for prevention workers. First, the variety of available products and their ready availability in stores, the home, and even in schools make preventing access to the inhalants an impossibility. Second, most of the kids who use these substances probably know it’s unhealthy and dangerous to do so, so further information of that sort may not add much in the way of preventing their use. Third, this use is very “faddish”—a group of eighthgraders in one school might start inhaling cleaning fluid; a group of sixth-graders in another neighborhood might be into gold paint (in distinct preference to black, yellow, or white). Given these characteristics, where does a school-based prevention education program begin
the officers showed what the drugs looked like or demonstrated the smell of burning marijuana, so that the kids would know what to avoid. Sometimes, especially in larger cities, a former user described how easy it was to get “hooked,” the horrible life of the junkie, and the horror of withdrawal symptoms. The 1960s saw more of that, plus the production of a large number of scary anti-drug films. Teachers and counselors knew little about these substances, and many teachers attended courses taught by experts. Some of the experts were enforcement-oriented and presented the traditional scare-tactics information, whereas others were pharmacologists who presented the “dry facts” about the classification and effects of various drugs. The teachers then brought many of these facts into their classrooms. It was later pointed out that the programs of this era were based on an assumed model: that providing information about drugs would increase the students’ knowledge of drugs and their effects, that this increased knowledge would lead to
to attack the problem? Does it focus on a particular product and try to talk kids out of using gold paint? Does it talk about a whole variety of products and thereby perhaps introduce the kids to new things they hadn’t thought of? One videotape (Inhalants: Kids in Danger, Adults in the Dark) took the approach of attempting to inform parents and teachers of the varieties of paints, perfumes, solvents, and other spray products used by abusers and to inform them of some of the subterfuges used by some of the kids (carrying a small cologne vial to school, spraying paint into empty soft drink cans, etc.). However, this video is not meant to be shown to children, because it describes exactly what to do and how to do it. Probably the best idea in prevention classes is to reinforce to children in general terms the dangers of inhalants without describing a particular substance or method of use.
changes in attitudes about drug use, and that these changed attitudes would be reflected in decreased drug-using behavior.2 In the early 1970s, this model began to be questioned. A 1971 study indicated that students who had more knowledge about drugs tended to have a more positive attitude toward drug use.3 Of course, it may have been that prodrug students were more interested in learning about drugs, so this was not an actual assessment of the value of drug education programs. A 1973 report by the same group indicated that four different types of drug education programs were equally effective in producing increased knowledge about drugs and equally ineffective in altering attitudes or behavior.4 Nationwide, drug use had increased even with the greater emphasis on drug education. Concern arose about the possibility that drug education may even have contributed to increased drug use. Before the 1960s, the use of marijuana and LSD was rare among school-age youngsters. Most of them didn’t know much about these things, had
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given them little thought, and had probably never considered using them. Telling them over and over not to use drugs was a bit like telling a young boy not to put beans in his nose. He probably hadn’t thought of it before, and your warning gives him the idea. These concerns led the federal government in 1973 to stop supporting the production of drug-abuse films and educational materials until it could determine what kinds of approaches would be effective. The question of effectiveness depended greatly on the goals of the program. Did we want all students never to experiment with cigarettes, alcohol, marijuana, or other drugs? Or did we want students to be prepared to make rational decisions about drugs? For example, a 1976 report indicated that students in drug education programs did increase their use of drugs over the two years after the program, but they were less likely to show drastic escalation of the amount or type of drug use over that period, when compared with a control group.5 Perhaps by giving the students information about drugs, we make them more likely to try them, but we also make them more aware of the dangers of excessive use. For a time in the 1970s, it seemed as though teaching students to make rational decisions about their own drug use with the goal of reducing the overall harm produced by misuse and abuse could be a possible goal of prevention programs.
Affective Education Educators have been talking for several years about education as including both a “cognitive domain” and an “affective domain,” the domain of emotions and attitudes. One reason that young people might use psychoactive drugs is to produce certain feelings: of excitement, of relaxation, of power, of being in control. Or perhaps a child might not really want to take drugs but does so after being influenced by others. Helping children know their own feelings and express them, helping them achieve altered emotional states without drugs, and teaching them to feel valued,
Helping young people learn to deal with emotions in healthy ways and giving them successful experiences may reduce their rates of smoking, drinking, and drug use.
accepted, and wanted are all presumed to be ways of reducing drug use. Values Clarification The values clarification approach makes the assumption that what is lacking in drug-using adolescents is not factual information about drugs but, rather, the ability to make appropriate decisions based on that information.6 Perhaps drug use should not be “flagged” for the students by having special curricula designed just for drugs but, instead, emphasis should be placed on teaching generic decision-making skills. Teaching students to analyze and clarify their own values in life is accomplished by having them discuss their reactions to various situations that pose moral and ethical dilemmas. Groups of parents or other citizens who are concerned about drug abuse sometimes have great difficulty understanding and accepting these approaches because they do not take a direct anti-drug approach. In the 1970s, when these programs were developed, it seemed important that the schools not try to impose a particular set of values but, rather, allow for differences in religion, family background, and so on. For this reason, the programs were often said to be value-free. To many parents, the purpose of values clarification training is not
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immediately clear, and teaching young children to decide moral issues for themselves may run contrary to the particular set of values the parents want their children to learn. Alternatives to Drugs Along with values clarification, another aspect of affective education involves the teaching of alternatives to drug use. Under the assumption that students might take drugs for the experience, for the altered states of consciousness that a drug might produce, students are taught so-called natural highs, or altered states, that can be produced through relaxation exercises, meditation, vigorous exercise, or an exciting sport. Students are encouraged to try these things and to focus on the psychological changes that occur. These alternatives should be discussed with some degree of sensitivity to the audience; for example, it would make little sense to suggest to many inner-city 13-year-olds that expensive activities such as scuba diving and snow skiing would be good alternatives to drugs. Personal and Social Skills Several studies indicate that adolescents who smoke, drink, or use marijuana also get lower grades and are less involved in organized sports or school clubs. One view of this is that students might take up substance use in response to personal or social failure. Therefore, teaching students how to communicate with others and giving them success experiences is another component of affective education approaches. For example, one exercise that has been used is having the students operate a school store. This is done as a group effort with frequent group meetings. The involved students are expected to develop a sense of social and personal competence without using drugs. Another approach is to have older students tutor younger students, which is designed to give the older students a sense of competence. An experiment carried out in Napa, California, combined these approaches with a drug education course, small-group discussions led by teachers, and classroom management techniques designed to teach
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discipline and communication skills and to enhance the students’ self-concepts.7 Although a small effect on alcohol, marijuana, and cigarette use was found among the girls, the effects were gone by the one-year follow-up.
Anti-drug Norms A 1984 review of prevention studies concluded that (1) most substance abuse prevention programs have not contained adequate evaluation components; (2) increased knowledge has virtually no impact on substance abuse or on intentions to smoke, drink, or use drugs; (3) affective education approaches appear to be experiential in their orientation and to place too little emphasis on the acquisition of skills necessary to increase personal and social competence, particularly those skills needed to enable students to resist the various interpersonal pressures to begin using drugs; and (4) few studies have demonstrated any degree of success in terms of actual substance abuse prevention.8
This last point is not entirely a criticism of the programs themselves but reflects the difficulty of demonstrating statistically significant changes in behavior over a period of time after the programs. Refusal Skills In response to the third point, that affective education approaches were too general and experiential, the next efforts at preventing drug use focused on teaching students to recognize peer pressure to use drugs and on teaching specific ways to respond to such pressures without using drugs. This is sometimes referred to as psychological inoculation. In addition to the focus on substance use, “refusal skills” and “pressure resistance” strategies are
values clarification: teaching students to recognize and express their own feelings and beliefs. alternatives: alternative nondrug activities, such as relaxation or dancing.
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Taking Sides Are “Alternatives to Drugs” Really Alternatives? As one part of many drug education programs, students are taught that they can produce natural highs—that is, altered states of consciousness similar to those produced by drugs, but without using drugs. One such alternative that has been mentioned in these programs is skydiving. Obviously an activity of that sort has all the glamour, danger, and excitement most of us would want. Maybe if the kids could do this whenever they wanted, they wouldn’t want to try cocaine or marijuana. But let’s examine this as an alternative for a bunch of junior high school kids. First, there’s the matter of cost and availability. How realistic is it to think that most of these kids would have access to skydiving? Second, there’s the issue of convenience. Even if you were a rich kid, with your own airplane, parachute, and pilot, it’s unlikely that you’d be able to go skydiving every afternoon after school. Drugs and alcohol may not provide the best
taught in a broader context of self-assertion and social skills training. The first successful application of this technique was a film in which young actors acted out situations in which one person was being pressured to smoke cigarettes. The film then demonstrated effective ways of responding to the pressure gracefully without smoking. After the film, students discuss alternative strategies and practice the coping techniques presented in the film. This approach has been demonstrated to be successful in reducing cigarette smoking in adolescent populations. It has been adapted for use with groups of various ages and for a wider variety of drugs and other behaviors, and students are taught from kindergarten on to “just say no” when someone is trying to get them to do something they know is wrong. Drug-Free Schools In 1986 the federal government launched a massive program to support “drug-free schools and communities.” Among other things, the government provided mil-
highs in the world, but often they are easy to get and use, compared with activities such as skydiving. Maybe skydiving isn’t a practical alternative to drugs for a lot of people. Still, it seems more wholesome and desirable. Let’s become social philosophers and ask ourselves why the image of a person skydiving is more positive than the image of a person snorting cocaine. After all, skydiving doesn’t make any obvious contributions to society. Let’s play devil’s advocate and propose that skydiving is not preferable to taking cocaine. Either way, the person is engaged in dangerous, expensive, self-indulgent activity. Contrast skydiving with cocaine, and see if you can answer for yourself why skydiving has a more positive image than cocaine use. You may have to talk about this with several people before you get a consistent feeling for why our society respects one of these activities so much more than the other. What about skiing? bungee-cord jumping?
lions of dollars’ worth of direct aid to local school districts to implement or enhance drugprevention activities. Along with this, the Department of Education produced a small book called What Works: Schools Without Drugs,9 which made specific recommendations for schools to follow. This book did not recommend a specific curriculum; its most significant feature was the emphasis on factors other than curriculum, such as school policies on drug and alcohol use. It suggested policies regarding locker searches, suspension, and expulsion of students. The purpose was not so much to take a punitive approach to alcohol or drug use as to point out through example and official policy that the school and community were opposed to drug and alcohol use by minors. Following this general drug-free lead, schools adopted “tobacco-free” policies, stating that not only the students but also teachers and other staff people were not to use tobacco products at school or on school-sponsored trips or activities.
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According to this approach, the curriculum should include teaching about the laws against drugs, as well as about the school policies. In other words, as opposed to the 1970s values clarification approach of teaching students how to make responsible decisions for themselves, this approach wants to make it clear to the students that the society at large, the community in which they live, and the school in which they study have already made the decision not to condone drug use or underage alcohol use. This seems to be part of a more general educational trend away from “value-free” schools toward teaching values that are generally accepted in our society. For schools to be eligible for federal Drug-Free Schools funding, they must certify that their program teaches that “illicit drug use is wrong and harmful.”
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the social influence model.10 Out of all this research, certain consistencies appear. The most important of these is that it is possible to design smoking prevention programs that are effective in reducing the number of adolescents who begin smoking. Some practical lessons about the components of those programs have also emerged.11 For example, presenting information about the delayed consequences of smoking (possible lung cancer many years later) is relatively ineffective. Information about the immediate physiological effects (increased heart rate, shortness of breath) is included instead. Some of the most important key elements that were shown to be effective were the following:. •
Training refusal skills (for example, eight ways to say no). This was originally based on films demonstrating the kinds of social pressures that peers might use to encourage smoking and modeling a variety of appropriate responses. Then the students engage in role-playing exercises in which they practice these refusal skills. By using such techniques as changing the subject or having a good excuse handy, students learn to refuse to “cooperate” without being negative. When all else fails, however, they are taught to be assertive and insist on their right to refuse.
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Public commitment. Researchers found that having each child stand before his or her peers and promise not to start smoking and sign a pledge not to smoke are effective prevention techniques. Countering advertising. Students are shown examples of cigarette advertising, and then the “hidden messages” are discussed (young, attractive, healthy, active models are typically used; cigarette smoking might be associated with dating or with sports). Then the logical inconsistencies
Development of the Social Influence Model Some of the most sophisticated prevention research in recent years has been focused directly on cigarette smoking in adolescents. This problem has two major advantages over other types of drug use, as far as prevention research is concerned. First, a large enough fraction of adolescents do smoke cigarettes so that measurable behavior change is possible in a group of reasonable size. In contrast, one would have to perform an intervention with tens of thousands of people before significant alterations in the proportion of heroin users would be statistically evident. Second, the health consequences of smoking are so clear with respect to cancer and heart disease that there is a fairly good consensus over goals: We’d like to prevent adolescents from becoming smokers. One research advantage is the relatively simple verification available for self-reported use of tobacco: Saliva samples can be measured for cotinine, a nicotine metabolite. Virtually all the various approaches to drug-abuse prevention have been tried with smoking behavior; in fact, Evans’s 1976 smoking prevention paper introduced the use of the psychological inoculation approach based on
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social influence model: a prevention model adopted from successful smoking programs
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Training in refusal skills, including role-playing exercises, is a key component of the social influence model.
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between these hidden messages and the actual effects of cigarette smoking (e.g., bad breath, yellow teeth, shortness of breath) are pointed out. The purpose of this is to “inoculate” the children against cigarette advertising by teaching them to question its messages. Normative education. Adolescents tend to overestimate the proportion of their peers who smoke. Presenting factual information about the smoking practices of adolescents provides students with a more realistic picture of the true social norms regarding smoking and reduces the “everybody is doing it” attitude. When possible, statistics on smoking from the specific school or community should be used in presenting this information.
Use of teen leaders. Presenting dry facts about the actual proportion of smokers should ideally be reinforced by example. If you’re presenting the program to junior high students, it’s one thing to say that fewer than one-fifth of the high school students in that community smoke, but it’s another to bring a few high school students into the room and have them discuss the fact that neither they nor their friends smoke, their attitudes about smokers, and ways they have dealt with others’ attempts to get them to smoke.
Possible improvements to those approaches are offered by the cognitive developmental approach to smoking behavior. McCarthy criticized the social influence/social skills training model for assuming that all students should be taught social skills or refusal skills without regard to whether they need such training.12 The model “is that of a defenseless teenager who, for lack of general social skills or refusal skills, passively accedes to social pressures to smoke.” Alternative models have been proposed in which the individual makes active, conscious decisions in preparation for trying cigarettes, trying smoking and becoming an occasional or regular user. The decision-making processes, and thus the appropriate prevention strategy, might be different at each of these “stages of cognitive development” as a smoker. Furthermore, smokers who begin smoking very young behave differently than smokers who begin as older adolescents (e.g., those who start young show more unanimity in selecting the most popular brand). Unfortunately, adolescents continue to initiate smoking every year, and the risk and protective factors reviewed in Chapter 1 have more influence on smoking behavior (and on alcohol and other drug use) than any information or education programs yet devised.13
DARE Perhaps the most amazing educational phenomenon in a long time had fairly modest beginnings in 1983 as a joint project of the Los
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Angeles police department and school district. Those who are familiar with the Drug Abuse Resistance Education (DARE) program will have recognized its components described under the social influence model of smoking cessation. The difference here is that the educational program with DARE is delivered by police officers, originally in fifth- and sixth-grade classrooms. By basing the curriculum on sound educational research, by maintaining strict training standards for the officers who were to present the curriculum, and by encouraging the classroom teacher to participate, some of the old barriers to having nonteachers responsible for curriculum were overcome. The officers are in uniform, and they use interactive techniques as described for the social influence model. Most of the components are there: refusal skills, teen leaders, and a public commitment not to use illicit drugs. In addition, some of the affective education components are included: self-esteem building, alternatives to drug use, and decision making. The component on consequences of drug abuse is, no doubt, enhanced by the presence of a uniformed officer who can serve as an information source and symbol for concerns over gang activity and violence and can discuss arrest and incarceration. The 17-week program is capped by a commencement assembly at which certificates are awarded. This program happened to be in place at just the right time, both financially and politically. With the assistance of drug-free schools money and with nationwide enthusiasm for new drug-prevention activities in the 1980s, the program spread rapidly across the United States. By the early 1990s, DARE programs were found in every state. This program was accepted quickly by many schools, and endorsed enthusiastically by educators, students, parents, and police participants, even though its effectiveness in preventing drug use was not evaluated extensively until 1994. In 1994, two important, large-scale studies of the effects of DARE were reported. One was based on a longitudinal study in rural, suburban,
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Drugs in Depth How Much Do You Know about DARE? 1. Almost everyone in the United State has heard of DARE. What do the letters stand for? 2. One component of DARE is practicing how to refuse using drugs. Do you know the origin of DARE’s eight ways to say no? 3. DARE has been implemented in more schools than any other substance-abuse prevention program. Does research on its effectiveness show that it’s one of the best at preventing drug abuse? 4. Besides school-based programs, what other kinds of substance-abuse prevention programs have been developed? 5. The Institute of Medicine has a relatively new way of categorizing prevention programs into various types. Do you know what factor is used to differentiate among the types? Answers 1. Drug Abuse Resistance Education 2. This and most components of DARE were adopted from smoking prevention programs developed in the 1970s. 3. Research on the effectiveness of DARE has not demonstrated a strong impact on preventing drug use. Other programs described in this chapter appear to be more effective. 4. Parent, family, and community programs and public media campaigns have also been developed to prevent drug abuse. 5. The target population (the entire population, at-risk populations, and individuals with early signs of problems).
and urban schools in Illinois, comparing students exposed to DARE with students who were not.14 Although the program had some effects on reported self-esteem, there was no evidence DARE: Drug Abuse Resistance Education, the most popular prevention program in schools.
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for long-term reductions in self-reported use of drugs. The other report was based on a review of eight smaller outcome evaluations of DARE, selected from 18 evaluations based on whether the reports had a control group, a pretest-posttest design, and reliable outcome measures.15 The overall impact of these eight programs was to increase drug knowledge and knowledge about social skills, but the effects on drug use were marginal at best. There was a very small but statistically significant reduction of tobacco use and no reliable effect on alcohol or marijuana use. A more recent review of all the experimental studies on DARE published in peer-reviewed journals found an average effect size that was small and not statistically significant. The authors reported that their results supported previous conclusions about the ineffectiveness of DARE.16 The repeated failures to demonstrate a significant impact of the DARE program on drug use remain a dilemma in light of its widespread popularity. Communities have not abandoned the program. Instead, DARE America has developed additional programs, including DARE + PLUS (Play and Learn Under Supervision) as an extension to the elementary program, and curriculum for middle school and high school DARE programs designed to follow up with these older adolescents. We cannot yet evaluate the effectiveness of these additional programs.
Programs That Work Several school-based drug-use prevention programs have been modeled after the successful social influence model and have components similar to those of DARE. A few of these programs have been demonstrated to have beneficial effects on actual drug use: Project ALERT was first tested in 30 junior high schools in California and Oregon.17 The program targeted cigarette smoking, alcohol use, and marijuana use. Before the program, each student was surveyed and classified as a nonuser, an experimenter, or a user for each of the three substances. The curriculum was taught either by health educators or by educa-
School-based drug-use prevention programs have been shown to reduce initiation and levels of drug use.
tors with the assistance of trained teen leaders. Control schools simply continued whatever health or drug curriculum they had been using. The program was delivered in the seventh grade, and follow-up surveys were done 3, 12, and 15 months later. Three “booster” lessons were given in the eighth grade. The program surprisingly had no measurable effect on initiation of smoking by nonusers. However, those who were cigarette experimenters before the program began were more likely to quit or to maintain low rates of smoking than the control group. The group with teen leader support showed the largest reduction: 50 percent fewer students were weekly smokers at the 15-month follow-up. The experimental groups drank less alcohol soon after the program was presented, for previous alcohol nonusers, experimenters, and users. However, this effect diminished over time and disappeared by the end of the study. The most consistent results were in reducing initiation of marijuana smoking and reducing levels of marijuana smoking. For example, among those who were not marijuana users at the beginning, about 12 percent of the controlgroup students had begun using marijuana
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Drugs in Depth Effective Prevention Programs The Center for Substance Abuse Prevention (CSAP), a branch of the Substance Abuse and Mental Health Administration in the U.S. Department of Health and Human Services, has been studying research on effective prevention programs. It has developed a list of model programs. Some of the programs on this partial list are described within this chapter, and more information on the others can be obtained from the SAMHSA Web site. Also, as new programs are approved, they are being added to the list, so for the most current list, check on the Web at prevention.samhsa.gov. Model Programs • Across Ages • Athletes Training and Learning to Avoid Steroids (ATLAS)
by the 15-month follow-up. In the treatment groups, only 8 percent began using during that time period, representing a one-third decrease in initiation to marijuana use. Another program, the Life Skills Training program, has been subjected to several tests and has shown long-term positive results. This three-year program is based on the social influence model and teaches resistance skills, normative education, and media influences. Self-management skills and general social skills are also included. One study of this program found significantly lower use of marijuana, alcohol, and tobacco after six years. A subsequent application of this program among ethnic minority youth (Latino and African American) in New York City found reduced use on a two-year follow-up.18
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that is why most efforts at drug-abuse prevention have been carried out there. However, peers, parents, and the community at large also exert powerful social influences on young people. Because these groups are less accessible than the schools, fewer prevention programs have been based on using parent and community influences. Nevertheless, important efforts have been made in all these areas.
Peer Programs Most peer programs have occurred in the school setting, but some have used youth-oriented community service programs (such as YMCA, YWCA, and recreation centers) or have focused on “street” youth by using them in group community service projects. •
Peers, Parents, and the Community Our nation’s public schools clearly are the most convenient conduit for attempts to achieve widespread social changes among young people, and
Child Development Project Communities Mobilizing for Change on Alcohol Creating Lasting Family Connections Dare to Be You Families and Schools Together Keep a Clear Mind Life Skills Training Project ALERT Project Northland Project Towards No Tobacco Use Reconnecting Youth Residential Student Assistance Program Safe Dates SMART Team Strengthening Families Program Too Good for Drugs
Peer influence approaches start with the assumption that the opinions of an adolescent’s peers are significant influences on the adolescent’s behavior. Often using an adult group facilitator/coordinator, the program’s emphasis is on open discussion among a group of children or adolescents.
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These discussions might focus on drugs, with the peer group discussing dangers and alternatives, or they might simply have the more general goal of building positive group cohesiveness, a sense of belonging, and communication skills. •
Peer participation programs often focus on groups of youth in high-risk areas. The idea here is that young people participate in making important decisions and in doing significant work, either as “peers” with cooperating adults or in programs managed almost entirely by the youth themselves. Sometimes participants are paid for community service work, in other cases they engage in money-making businesses, and sometimes they provide youth-oriented information services. These groups almost never focus on drug use in any significant way; rather, the idea is to help people become participating members of society.
The benefits of these “extracurricular” peer approaches are measurable in terms of acquired skills, improved academic success, higher selfesteem, and a more positive attitude toward peers and school. As to whether they alter drug use significantly, the data either are not available or are inconclusive for the most part.
Parent and Family Programs The various programs that have worked with parents have been described as taking at least one of four approaches.19 Most of the programs include more than one of these approaches. •
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Informational programs provide parents with basic information about alcohol and drugs, as well as information about their use and effects. Although the parents often want to know simply what to look for, how to tell if their child is using drugs, and what the consequences of drug abuse are, the best programs provide additional information. One important piece of information is the actual extent of the use of various types of drugs among young people. Another goal
might be to make parents aware of their own alcohol and drug use to gain a broader perspective of the issue. A basic rationale is that well-informed parents will be able to teach appropriate attitudes about drugs, beginning when their child is young, and will be better able to recognize potential problems relating to drug or alcohol use. •
Parenting skills might be taught through practical training programs. Communication with children, decision-making skills, how to set goals and limits, and when and how to say no to your child can be learned in the abstract and then practiced in role-playing exercises. One risk factor for adolescent drug and alcohol use is poor family relationships, and improving family interaction and strengthening communication can help prevent alcohol and drug abuse.
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Parent support groups can be important adjuncts to skills training or in planning community efforts. Groups of parents meet regularly to discuss problem solving, parenting skills, their perceptions of the problem, actions to be taken, and so on.
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Family interaction approaches call for families to work as a unit to examine, discuss, and confront issues relating to alcohol and drug use. Other exercises might include more general problem solving or response to emergencies. Not only do these programs attempt to improve family communication, but also the parents are placed in the roles of teacher of drug facts and coordinator of family action, thus strengthening their knowledge and skills.
One selective prevention program, called the Strengthening Families program, targets children of parents who are substance abusers. This program has been successfully implemented several times within diverse populations. It has three major goals: improving parenting skills, increasing children’s skills (such as communication skills, refusal skills, awareness of feelings, and emotion expression
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skills), and improving family relationships (decreasing conflict, improving communication, increasing parent-child time together, and increasing the planning and organizational skills of the family). Children and parents attend evening sessions weekly for 14 weeks to learn and practice these skills. Evaluations of this program indicate that it reduces tobacco and alcohol use in the children as well as reduces substance abuse and other problems in the parents.20
Community Programs Two basic reasons exist for organizing prevention programs at the community level. The first is that a coordinated approach using schools, parent and peer groups, civic organizations, police, newspapers, radio, and television can have a much greater impact than an isolated program that occurs only in the school, for example. Another reason is that drug-abuse prevention and drug education are controversial and emotional topics. Parents might question the need for or the methods used in drug education programs in the schools. Jealousy and mistrust about approaches can separate schools, police, church, and parent groups. A program that starts by involving all these groups in the planning stages is more likely to receive widespread community support. Clearly, the spread of the DARE program in the schools is based partly on the fact that it demonstrates and encourages cooperation between the police and the schools, as well as encourages parental involvement. Community-based programs can bring other resources to bear. For example, the city council and local businesses can be involved in sponsoring alcohol-free parties, developing recreational facilities, and arranging field trips so that, when the school-based program talks about alternatives, the alternatives are available. The public media can be enlisted not only to publicize public meetings and programs but also to present drug- and alcohol-related information that reinforces what is learned in the other programs.
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Mind / Body Connection Integrating Treatment and Prevention with Pregnancy Services Does your community provide needed services and compassionate support for pregnant women who use alcohol and drugs? An emerging consensus views alcohol, tobacco, and other drug use during pregnancy as a community problem. During this period when women anticipate major life change, prevention initiatives can enhance their motivation to have a healthy baby. And, for women with substance-abuse problems, pregnancy provides a similarly strong motivation to seek help. Fear of blame, legal intervention, and loss of child custody prevent many women from getting help. To counteract these barriers to services, prevention initiatives should promote services that are safe and confidential. Services should be not only physically accessible but also culturally accessible. Efforts that recognize the importance of relationships to women can call on the support of family members and others for alcohol-free and other drug-free pregnancies. Prevention strategies that combine information with options for change have shown promising results in reducing drug use during pregnancy. Find out if women in your area have access to an integrated system of alcohol, tobacco, and other drug treatment and maternal and child health care.
Communities Mobilizing for Change on Alcohol is one of SAMHSA’s model prevention programs (see page 421). The program works for change in alcohol ordinances in the community and alcohol policies of schools, universities, and civic organizations. It encourages parents, faith organizations, the police, city government, and all businesses and organizations within the community to promote the idea of limiting alcohol availability for 13- to 18year-olds. The program was studied in 15 communities over a five-year period and resulted in decreased alcohol sales to minors, decreases in friends providing alcohol to minors, and
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and to notify employees of the consequences of violating company policy regarding drug use. The ultimate goal is not to catch drug users and fire them but to prevent drug use by making it clear that it is not condoned.
What Should We Be Doing?
Community-based programs work best when they have widespread community support. This anti-tobacco mural is tied to the values of a local community and focuses on the traditional sacred origins of tobacco use among Native Americans.
decreases in self-reported drinking in the targeted age group.
Prevention in the Workplace As a part of its efforts to reduce the demand for drugs, the federal government has encouraged private employers, especially those who do business with the government, to adopt policies to prevent drug use by their employees. The most consistent feature of these programs is random urine screens. In 1989, rules went into effect requiring all companies and organizations that obtain grants or contracts from the federal government to adopt a “drug-free workplace” plan. The exact nature of the plan is up to the company, but guidelines were produced by the Department of Labor. Modeled after the Education Department’s What Works book, the Labor Department’s is called What Works: Workplaces Without Drugs.21 At a minimum, the Labor Department expects employers to state clearly that drug use on the job is unacceptable
By now you have picked up some ideas for things to do to reduce drug use, as well as some things to avoid doing. But the answer as to what needs to be done in a particular situation depends on the motivations for doing it. Most states require drug- and alcohol-abuse prevention education as part of a health curriculum, for example. If that is the primary motive for doing something, and if there doesn’t seem to be a particular problem with substance abuse in the schools, then the best thing would be to adopt one of the modern school-based programs that have been developed for this purpose, to make sure the teachers and other participants are properly trained in it, and to go ahead. In selecting from among the curricula, a sensible, balanced approach that combines some factual information with social skills training, perhaps integrated into the more general themes of health, personal values, and decision making, would be appropriate. The ones mentioned in the section “Programs That Work” fit this general description, and each deserves a careful look. Above all, avoid sensational scare stories, preachy approaches from the teacher to the student, and untrained personnel developing their own curricula. Another good thing to avoid is the inadvertent demonstration of how to do things you don’t want students to do. If, on the other hand, there is a public outcry about the “epidemic” of drugs and alcohol abuse in the community, speakers have inflamed passions, and there is a widespread fervor to do something about it, this presents both a danger and an opportunity. The danger is that this passionate group might attack and undermine the efforts already being made in the schools, substituting scary, preachy,
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negative approaches, which can have negative consequences. The opportunity lies in the possibility that this energy can be organized into a community planning effort, out of which could develop cooperation, increased parent understanding, a focus on family communication, interest in the lives of the community’s young people, and increased recreational and creative opportunities. The key to making this happen is convincing the aroused citizenry of the possibly negative consequences of doing what seems obvious and selling them on the idea of studying what needs to be done. A good place to start is by visiting the Web site of the Center for Substance Abuse Prevention (www.samhsa.gov/ csap). This agency produces updated materials for groups interested in developing drug- and alcohol-abuse prevention programs, provides technical assistance and training to communities interested in developing programs, and offers Community Partnership Grants. (A list of CSAP model programs is shown in the Drugs in Depth box on page 421.)
Summary •
We can distinguish between education programs with the goal of imparting knowledge and prevention programs aimed at modifying drug-using behavior.
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Most of the research over the past 30 years has failed to demonstrate that prevention programs can produce clear, meaningful, long-lasting effects on drug-using behavior.
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The affective education programs of the 1970s have been criticized for being too value-free.
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Based on the success of the social influence model in reducing cigarette smoking, a variety of school-based prevention programs have used the same techniques with illicit drugs.
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The DARE program has been adopted rapidly and widely, despite research showing limited impact on drug-using behavior.
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Current school-based approaches use refusal skills, countering advertising, public commitments, and teen leaders. Several of these programs have been demonstrated to be effective.
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Other nonschool programs are peer-based through after-school groups or activities, parent-based through parent and family training, or community-based.
Review Questions 1. What is the distinction between secondary and tertiary prevention? 2. What is the knowledge-attitudes-behavior model, and what information first called it into question? 3. Explain what is meant by “value-free” values clarification programs, and why they fell out of favor in the 1980s. 4. When the Drug-Free Schools programs began in 1986, the emphasis shifted away from curriculum to what? 5. What were the five successful components of the social influence model for smoking prevention? 6. In Project ALERT, what was the impact of using teen leaders to assist the instructors? 7. What distinguishes DARE from other similar programs based on the social influence model? 8. What do ALERT and Life Skills Training have in common, besides their effectiveness? 9. What are some of the “parenting” skills that might be taught and practiced in a prevention program? 10. What is the most common component of “drug-free workplace” plans?
References 1.
2.
National Institute on Drug Abuse. Drug Abuse Prevention for the General Population. Washington, DC: U.S. Department of Health and Human Services, 1997. Goodstadt, M. S. “School-based Drug Education in North America: What Is Wrong? What Can Be Done?” Journal of School Health 56 (1986), pp. 278–81.
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Swisher, J. D., and others. “Drug Education: Pushing or Preventing?” Peabody Journal of Education 49 (1971), pp. 68–75. Swisher, J. D., and others. “A Comparison of Four Approaches to Drug Abuse Prevention at the College Level.” Journal of College Student Personnel 14 (1973), pp. 231–35. Blum, R. H., E. Blum, and E. Garfield. Drug Education: Results and Recommendations. Lexington, MA: D.C. Heath, 1976. Swisher, J. D. “Prevention Issues.” In R. I. DuPont, A. Goldstein, J. O’Donnell, eds. Handbook on Drug Abuse. Washington, DC: NIDA, U.S. Government Printing Office, 1979. Schaps, E., and others. The Napa Drug Abuse Prevention Project: Research Findings. Washington, DC: DHHS Publication No. (ADM) 84-1339, U.S. Government Printing Office, 1984. “Prevention Research.” In Drug Abuse and Drug Abuse Research. Washington, DC: DHHS Publication No. (ADM) 85-1372, U.S. Government Printing Office, 1984. U.S. Department of Education. What Works: Schools without Drugs. Washington, DC: 1987. Evans, R. I. “Smoking in Children: Developing a Social Psychological Strategy of Deterrence.” Preventive Medicine 5 (1976), pp. 122–27. Flay, B. R. “What We Know About the Social Influences Approach to Smoking Prevention: Review and Recommendations.” In C. S. Bell and R. Battjes, eds. Prevention Research: Deterring Drug Abuse Among Children and Adolescents. Washington, DC: NIDA Research Monograph 63, DHHS Publication No. (ADM) 85-1334, U.S. Government Printing Office, 1985. McCarthy, W. J. “The Cognitive Developmental Model and Other Alternatives to the Social Skills Deficit Model of Smoking Onset.” In C. S. Bell and R. Battjes, eds. Preven-
13.
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tion Research: Deterring Drug Abuse Among Children and Adolescents. Washington, DC: NIDA Research Monograph 63, DHHS Publication No. (ADM) 85-1334, U.S. Government Printing Office, 1985. Albaum, G., and others. “Smoking Behavior, Information Sources, and Consumption Value of Teenagers: Implications for Public Policy and Other Intervention Failures.” Journal of Consumer Affairs 36 (2002), pp. 50–76. Ennett, S. T., and others. “Long-term Evaluation of Drug Abuse Resistance Education.” Addictive Behaviors 19 (1994), p. 113. Ennett, S. T., and others. “How Effective Is Drug Abuse Resistance Education? A Meta-analysis of Project DARE Outcome Evaluations.” American Journal of Public Health 84 (1994), p. 1394. West, S. L., and K. K. O’Neal. “Project D.A.R.E. Outcome Effectiveness Revisited.” American Journal of Public Health 94 (2004), pp. 1027–30. Ellickson, P. L., and R. M. Bell. “Drug Prevention in Junior High: A Multi-site Longitudinal Test.” Science 247 (1990), pp. 1299–1305. Botvin, G. J., and S. P. Schinke. “Effectiveness of Culturally Focused and Generic Skills Training Approaches to Alcohol and Drug Abuse Prevention Among Minority Adolescents: Two-Year Follow-up Results.” Psychology of Addictive Behaviors 9 (1995), p. 183. “Parent Education.” In Prevention Plus: Involving Schools, Parents, and the Community in Alcohol and Drug Education. Washington, DC: DHHS Publication No. (ADM) 84-1256, U.S. Government Printing Office, 1984. National Institute on Drug Abuse. Drug Abuse Prevention for At-risk Groups. Washington, DC: U.S. Department of Health and Human Services, 1997. U.S. Department of Labor. What Works: Workplaces Without Drugs. Washington, DC: 1989.
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Do Your Goals and Behaviors Match? If you are a parent, think about your own family for a moment. Several of the risk and protective factors mentioned in Chapter 2 are related to family, and some of the effective prevention strategies target family activities. Consider the following questions (they can be answered either from the perspective of a child or a parent). 1. Is the interaction between the parent(s) and child generally positive? 2. Do the parents provide attention and praise to the child? 3. Is discipline consistent and usually effective and never involves physical punishment? 4. Is the child able to communicate his or her feelings to the parent(s)?
5. Does the child feel comfortable discussing rules and consequences, especially when it comes to the use of substances or other inappropriate behavior? 6. Does the family spend time together doing things every week? 7. Is the family capable of planning and organizing family activities? If the answer to most of these questions is yes, then your family is probably functioning pretty well. If the answer to most of them is no, then think about what steps you can take to change this situation. That might include scheduling some time with a family therapist or counselor.
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Treating Substance Abuse and Dependence Objectives After you have studied this chapter, you should be able to: • Discuss different types of treatment goals for substance abuse and how those goals relate to one’s belief about the nature of substance abuse. • Describe the influence of Alcoholics Anonymous on substance abuse treatment programs for alcohol and for other substances. • Explain how motivational interviewing is used in conjunction with the notion of stages of change to better prepare people for treatment.
Every year, hundreds of thousands of Americans undergo treatment for substance abuse and dependence. The word treatment conjures up images of hospitals, nurses, and physicians, but traditional medical approaches form only a small part of the overall treatment picture. As we will see, the variety of treatment approaches reflects the variety of substance abuse problems, as well as the variety of theories about substance abuse. The various treatment approaches are often used in combination.
Behavioral/ Psychosocial Treatments
• List the benefits and limitations of using contingency management to maintain abstinence. • Explain why drugs are sometimes used during the initial detoxification phase of treatment. • Discuss the three drugs that are available for use in treating alcohol dependence. • Describe the various forms of nicotine-replacement therapies and the use of Zyban in nicotine dependence treatment. • Explain both antagonist and substitution treatment for opioid dependence and list the most commonly used medication for substitution. • Describe the status of development of medications for treating cocaine dependence and cannabis dependence. • Explain why, despite the well-known failure rates in substance abuse treatment, the book still concludes that these treatments are effective.
Many early theories of substance dependence were based primarily on studying alcoholdependent individuals, so it should come
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Learning objectives Glossary flashcards Web activities and links Self-scoring chapter quiz Audio chapter summaries Video clips
However, most behavioral/psychosocial treatment programs today are not designed for a particular substance, but treat a variety of types of substance dependence. Below, we present some behavioral/psychosocial treatment approaches often used in helping individuals deal with their substance abuse problems.
Defining Treatment Goals The particular theoretical view one has of substance abuse influences not only the treatment approaches one is likely to take but also the goals of treatment. For example, if one accepts the increasingly predominant view of alcohol dependence as a biological disease, which someone either “has” or does not have and which has an inevitable progression to more and more drinking, then the only acceptable treatment goal is total abstinence. Other experts view alcohol dependence as representing one end of a continuum of drinking, with no clear dividing line. For some of these theorists, a possible beneficial outcome of treatment is controlled social drinking. Likewise, if one views opioid dependence as inherently evil, undermining the physical and mental health of its victims (a common view until fairly recently), then abstinence from opioids is the only acceptable goal. Americans seem to have accepted dependence on the legal opioid methadone as preferable to heroin dependence, so the goal has changed from eliminating opioid use to eliminating
heroin use. The case with cigarette smoking is similar; some programs have focused on cutting down on smoking, whereas most programs aim for complete abstinence. When we look for indicators of a treatment program’s success, if we find that some people are still using, but using less, should we claim any benefit? Or should we assume, as some do, that any decreases will be temporary and that, unless the person quits entirely, there has been no real improvement? Although the answer depends on your goals, the DSM-IV-TR can provide a useful guide for answering this question. Researchers have begun to estimate the cost savings resulting from increased employment and decreased crime after treatment, and to compare these savings with the cost of treatment itself, to develop a cost/benefit analysis of the effectiveness of treatment.
Alcoholics Anonymous The formation of Alcoholics Anonymous (AA) in 1935 can now be seen as an important milestone in treatment. This group, which has total abstinence as a goal, has given support to the disease model of alcohol dependence. One of the basic tenets of this group is that the “alcoholic” is biologically different from others and therefore can never safely drink any alcohol. Central to this disease model is the idea that the disease takes away the person’s control of his or her own drinking behavior and therefore removes the blame for the problem. AA members are quick to point out that removing blame for the disease does not remove responsibility for dealing with it. By analogy, we would not blame diabetics for being diabetic, but we do expect diabetics to control their diets, take their medication, and so on. Thus, the alcohol-dependent person is seen as having the responsibility for managing the disease on a day-by-day basis but need not feel guilty about being different. The major approach used by AA has been group support and a buddy system. The members of AA help each other through difficult periods and encourage each other in their sobriety.
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Drugs in the Media Celebrity Rehab It seems that every few weeks another well-known celebrity is caught in some kind of public misbehavior, followed by the explanation that the famous person is suffering from a substance-use disorder and will be entering a treatment program. Mel Gibson, Amy Winehouse, Drew Barrymore, Gary Busey, Britney Spears, Lindsay Lohan, Paris Hilton, and other film actors and music stars have made public confessions of their substance abuse and have gone to expensive residential treatment programs. This has become such a part of our culture that the cable channel VH1 began a reality TV series in 2008 called “Celebrity Rehab with Dr. Drew.” Eight somewhat less well known celebrities checked in for treatment with Dr. Drew Pinsky and his staff and were followed for 10 episodes until they “graduated.” Whether or not
Although AA has been described as a loose affiliation of local groups, each with its own character, they have in common adherence to a method. Nevertheless, formal evaluations of the success of AA have been few and have not been very positive. For example, studies of court-ordered referrals to AA or to other types
The major approach of Alcoholics Anonymous, founded in 1935, is group support and a buddy system.
these individuals will be successful in abstaining from future substance use, the series itself was apparently successful enough that a second season is planned. One question that most people raise when they hear about these famous people going into “rehab” is whether they are trying to blame their misbehavior on a substance rather than taking responsibility for their actions. Do you think that being under the influence of a drug or alcohol excuses people’s misconduct, or in some way diminishes their guilt? Do you suspect that sometimes a person who goes away to an expensive and sometimes luxurious “rehab” facility is just taking the easy way out? Finally, do those famous repeat offenders who keep going back to rehab give substance-abuse treatment itself a worse reputation than it deserves?
of interventions have not shown AA to be more effective. However, AA was developed by and for people who have made a personal decision to stop drinking and who want to affiliate with others who have made that decision, and it might not be the most appropriate approach for individuals who are coerced into attending meetings as an alternative to jail. More appropriate (and more difficult and expensive) evaluations of AA should be done to determine which types of drinkers are most likely to benefit from this organization’s program. This point is particularly important because many treatment programs, such as the Betty Ford Center, Hazelden, and Phoenix House, rely mostly on the 12-step model of AA (see Drugs in Depth). Moreover, a wide variety
abstinence: no alcohol or drug use at all. controlled drinking: the idea that alcohol abusers may be able to drink under control. Alcoholics Anonymous: a worldwide organization of self-help groups based on alcohol abusers helping each other achieve and maintain sobriety.
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DSM-IV-TR Psychiatric Diagnosis of Substance Disorders Diagnostic Criteria for Substance Dependence A maladaptive pattern of substance use, leading to clinically significant impairment or distress, as manifested by three (or more) of the following, occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of the substance to achieve intoxication or desired effect b. Markedly diminished effect with continued use of the same amount of the substance 2. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome for the substance b. The same (or a closely related) substance is taken to relieve or avoid withdrawal symptoms 3. The substance is often taken in larger amounts or over a longer period than was intended. 4. There is a persistent desire or unsuccessful efforts to cut down or control substance use. 5. A great deal of time is spent in activities necessary to obtain the substance.
of other self-help groups, including Cocaine Anonymous (CA), Narcotics Anonymous (NA), and Gamblers Anonymous (GA), have modeled the AA treatment approach.
Motivational Enhancement Therapy For many years, the predominant theories on why people seek treatment for substance abuse were based on the anecdotal experiences of alcohol-dependent individuals. According to the conventional wisdom, most substance abusers use the defense mechanism of denial and are obstinately unwilling to admit either that their substance use is unusual or that it has serious consequences for themselves or others. In this context,
6. Important social, occupational, or recreational activities are given up or reduced because of substance use. 7. The substance use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the substance. Diagnostic Criteria for Substance Abuse A. A maladaptive pattern of substance use leading to clinically significant impairment or distress, as manifested by one (or more) of the following, occurring within a 12-month period: 1. Recurrent substance use resulting in failure to fulfill major role obligations at work, school, or home. 2. Recurrent substance use in situations in which it is physically hazardous. 3. Recurrent substance-related legal problems. 4. Continued substance use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of the substance. B. The symptoms have never met the criteria for substance dependence for this class of substance.
only when the abuser “hits bottom”—that is, suffers sufficient consequences that the reality of the problem finally sinks in—will he or she be ready to seek help. The obvious problem with this perspective is that grave consequences (e.g., death) may occur before the abuser’s perception of “hitting bottom.” One relatively new treatment approach, motivational enhancement therapy, attempts to shift the focus away from denial and toward motivation to change.1 The idea is that targeting the abuser’s degree of motivation to quit substance use could enhance the effectiveness of treatment. Hence, ambivalent or less ready substance abusers should first receive motivational interviewing. During this nonconfrontational process, an assessment of the substance-using
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Drugs in the Media The 12 Steps of Alcoholics Anonymous 1. 2. 3. 4. 5. 6. 7. 8. 9.
We admitted we were powerless over alcohol— that our lives had become unmanageable. Came to believe that a Power greater than ourselves could restore us to sanity. Made a decision to turn our will and our lives over to the care of God as we understood Him. Made a searching and fearless moral inventory of ourselves. Admitted to God, to ourselves, and to another human being the exact nature of our wrongs. Were entirely ready to have God remove all these defects of character. Humbly asked Him to remove our shortcomings. Made a list of all persons we had harmed and became willing to make amends to them all. Made direct amends to such people wherever possible, except when to do so would injure them or others.
behavior and its consequences is completed to determine the abuser’s current stage of change because, according to this view, to help someone move from one stage to another through motivational interviewing, you need to know where he or she is in the decision-making process. In the precontemplation stage, the individual does not recognize that a problem exists. In the contemplation stage, the individual believes that a problem might exist and gives some consideration to the possibility of changing her or his behavior. In the preparation stage, the individual decides to change and makes plans to do so. In the action stage, the individual takes active steps toward change, such as entering treatment. Finally, the maintenance stage involves activities intended to maintain the change. The motivational interviewer attempts to help the client focus on the concerns and problem behavior but does not directly tell the client what to do. Ideally, if the therapist knows which stage of change the client is in, the discussion can be guided appropriately to help move the client to the next stage. Although this approach has been demonstrated
10. Continued to take moral inventory and when we were wrong promptly admitted it. 11. Sought through prayer and meditation to improve our conscious contact with God as we understood Him, praying only for knowledge of His will for us and the power to carry that out. 12. Having had a spiritual awakening as the result of these steps, we tried to carry this message to alcoholics, and to practice these principles in all our affairs. Source: The Twelve Steps are reprinted with permission of Alcoholics Anonymous World Services, Inc. Permission to reprint the Twelve Steps does not mean that AA has reviewed or approved the contents of this publication, nor that AA agrees with the views expressed herein. AA is a program of recovery from alcoholism only— use of the Twelve Steps in connection with programs and activities which are patterned after AA, but which address other problems, or in any other non-AA context, does not imply otherwise.
to decrease substance use,2 it is probably best conceptualized as a preparation for other therapies rather than as a stand-alone treatment.
Contingency Management A behavioral approach to treating substance abuse that has received substantial attention in recent years is contingency management. This approach has produced consistent reductions in substance-using behaviors among diverse substance-abusing populations.3 In this approach, individuals receive immediate rewards (e.g., vouchers redeemable for goods or services) for providing drug-free urine samples, and the value of the rewards is increased with consecutive drug-free urine samples. However, rewards are withheld if the client’s
stages of change: a model for decision making consisting of precontemplation, contemplation, preparation, action, and maintenance.
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Targeting Prevention Avoiding Relapse Relapse Avoiding One important type of substance-abuse prevention involves those who have been in treatment and are trying to avoid relapsing, or going back to their previously abusive behavior. Think about the messages these people receive each day from public media (such as television, movies, newspapers, and the Web) and from other individuals. Which of these messages support relapse prevention and which tend to encourage relapse? Have a conversation with a friend, relative, or classmate who has been in treatment for substance abuse and has had to deal with the problem of relapse prevention. Ask what was helpful for him or her and what made it more difficult to avoid substance abuse.
urine sample is positive for an illicit drug. In addition to receiving rewards, clients participate in counseling sessions weekly, where they learn a variety of skills to help them minimize substance use. A weakness of contingency management is the cost of the rewards, which could preclude the use of this procedure by small, less well-funded treatment programs.
Relapse Prevention Another behavioral strategy is called relapse prevention, an approach that uses cognitivetherapy techniques with behavioral-skills training. Individuals learn to identify and change behaviors that may lead to continued drug use, such as going out to bars or associating with users. Relapse prevention has been shown to be more effective at decreasing substance use than most standard psychotherapies, and the beneficial effects persist for as long as a year following treatment.4 This approach is criticized for placing greater demands on the patients compared to other substance-abuse treatments, and it may be particularly challenging for individuals who have cognitive limitations.5
Pharmacotherapies (Medication Treatments) Substance abuse and dependence are increasingly viewed as “brain diseases,” much like, for example, Parkinson’s disease. But the overwhelming majority of individuals who use substances do not become dependent, whereas virtually all of the individuals who lose greater than 80 percent of nigrostriatal dopamine neurons will exhibit symptoms of Parkinson’s disease. Nevertheless, an intense amount of research efforts have focused on developing medications to treat substance abuse and dependence. The rationale is that as we increase our understanding of brain mechanisms mediating substance abuse, we should be better able to use medications to target these mechanisms, thereby blocking the reinforcing effects of drugs of abuse (i.e., the “magic bullet approach”). Despite the enthusiasm accompanying medication development efforts, most experts do not believe that pharmacotherapies alone will cure a chronic, relapsing disorder such as substance abuse, in part, because the problem of substance abuse is expressed behaviorally. Thus, a major hope is that pharmacotherapies will provide a window of opportunity by relieving withdrawal symptoms, for example, so that behavioral/ psychosocial treatments can be used. Below we describe some medications that have been used to help substance abusers deal with withdrawal symptoms and maintain abstinence. The focus of our discussion will be limited to alcohol, nicotine, the opioids, cocaine, and cannabis. These substances were selected for their public health importance and because a large amount of research has been conducted regarding their use.
Detoxification and Maintenance Phase Pharmacological interventions are typically initiated at two different phases of the dependence cycle: detoxification and maintenance. Detoxification can be viewed as an initial and immediate goal during which medications are administered to alleviate unpleasant
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withdrawal symptoms that may appear following abrupt cessation of drug use (e.g., the nicotine patch and nicotine gum have been used to treat individuals experiencing cigarette smoking abstinence symptoms). Medications used in the detoxification phase are also sometimes used in the maintenance phase (e.g., nicotine replacement medications). Thus, the distinction between a detoxification medication and a maintenance medication is sometimes less clear. Maintenance on pharmacological agents can be viewed as a longer-term strategy used to help the dependent individual avoid relapsing to the abused drug. Three major maintenance strategies are used. First, agonist or substitution therapy is used to induce cross-tolerance to the abused drug. Methadone, a long-acting μ-opioid agonist, for heroin dependence, and nicotine replacement medications for tobacco dependence have been used as agonist maintenance treatments to prevent relapse and cravings in individuals attempting to maintain abstinence. Agonist maintenance agents typically have safer routes of administration and/ or diminished psychoactive effects. Second, antagonist therapy is used to produce extinction by preventing the user from experiencing the reinforcing effects of the abused drug (e.g., the opioid antagonist naltrexone, which selectively blocks opioid effects). Finally, punishment therapy is used to produce an aversive reaction following ingestion of the abused drug. Disulfiram (Antabuse) for the treatment of alcohol dependence is an example of punishment therapy. Disulfiram inhibits aldehyde dehydrogenase, a major enzyme involved in alcohol metabolism, which, in the presence of alcohol, can produce unpleasant symptoms including headache, vomiting, and breathing difficulties.
Alcohol Pharmacotherapies have become increasingly important in the treatment of alcohol dependence, in part, because of the serious nature of
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the acute alcohol withdrawal syndrome. This syndrome is typically characterized by tremors, tachycardia (rapid heartbeat), hypertension, perfuse sweating, insomnia, hallucinations, and seizures. Medical risks associated with the alcohol withdrawal process often require an inpatient medical setting. During detoxification, two of the central tasks for the clinician are to reduce autonomic hyperactivity and to prevent the development of seizures. For several reasons, administration of a benzodiazepine during alcohol detoxification is the standard treatment approach. There is a high degree of cross-tolerance between alcohol and the benzodiazepines. Because benzodiazepines can serve as substitutes for alcohol and generally have longer half-lives than alcohol, the withdrawal process can be safely completed. Benzodiazepines, by potentiating the inhibitory actions of GABA on the central nervous system, significantly decrease the risk of seizures during detoxification. In addition, the increased autonomic arousal that occurs during alcohol withdrawal is similar to the initiation of the “stress response” (i.e., increased heart rate, blood pressure, respiration, and anxiety). This suggests the mechanisms that mediate the stress response may also play a role in alcohol withdrawal symptoms. Because it is well documented that increased GABAergic transmission markedly diminishes the stress response,6 it is not surprising that benzodiazepines are also effective in attenuating the autonomic hyperactivity that accompanies alcohol withdrawal symptoms. Some clinicians might be wary about the potential for abuse associated with the use of some rapid-acting benzodiazepines (e.g., alprazolam), particularly in alcohol-abusing populations.7 Thus, benzodiazepines with a slower onset of action such as clonazepam or oxazepam may be more suitable in this population. Three medications have received Food and Drug Administration (FDA) approval for the treatment of alcohol abuse and dependence: disulfiram (Antabuse), naltrexone, and acamprosate (calcium acetylhomotaurinate). All of these medications are used during the main-
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tenance phase. Typically, these medications are used for weeks or months, but indefinite maintenance for years is unusual with these approaches. Nearly a half century ago it was discovered that ingestion of disulfiram in the presence of alcohol resulted in an unpleasant reaction, including facial flushing, accelerated pulse, throbbing headache, nausea, and vomiting.8 As stated above, these symptoms occur as a result of the increased amount of acetaldehyde in the body following inhibition of aldehyde dehydrogenase by disulfiram. Since this initial observation, several studies have assessed disulfiram as a pharmacotherapeutic option in treating alcohol-use disorders. In general, disulfiram has not been shown to be effective in achieving abstinence or delaying relapse; most individuals simply do not take the medication. Naltrexone was developed as an opioid antagonist and has been used in the treatment of opioid dependence. In the early 1990s, data from two large studies of naltrexone for the treatment of alcohol dependence showed that the medication substantially reduced days of alcohol drinking per week, the rate of relapse among those who drank, and alcohol craving.9 The precise mechanism of action for naltrexone-related reductions in alcohol drinking is not fully understood, but it has been suggested that the medication blocks opioid receptors, thereby preventing the release of alcohol-induced dopamine, which in turn blocks the reinforcing effects of alcohol.10 Although great fanfare accompanied the approval of naltrexone and many alcoholdependent individuals were treated with this medication, it has not had a big impact on overall treatment success. The latest medication to receive approval for the treatment of alcohol-use disorders is acamprosate, a compound that bears a structural resemblance to GABA. Acamprosate exerts at least two actions that have been proposed to be important for its clinical utility in treating alcohol dependence: normalizing basal GABA concentrations, which are proposed to
be disrupted in alcohol-dependent individuals, and blocking the glutamate increases observed during alcohol withdrawal.11 In several studies, acamprosate has been shown to be effective in decreasing alcohol relapse. But, because the medication only recently received FDA approval, the impact of its availability on treating alcohol-use disorder in broader clinical populations has yet to be determined.
Nicotine More than 98 percent of tobacco users are cigarette smokers. Despite the declining social acceptability and rates of cigarette smoking, a substantial proportion of individuals remains dependent. Tobacco smoke contains as many as 4,000 chemical constituents, but nicotine is thought to be the primary component responsible for the maintenance of continued use. When most smokers attempt to quit, they experience withdrawal symptoms, such as anxiety, depression, dysphoria, irritability, decreased concentration, insomnia, increased food intake, and cigarette craving. Pharmacotherapies have been used primarily to attenuate these symptoms. Five nicotine-replacement therapies have received FDA-approval for treating nicotine dependence: transdermal nicotine patch, nicotine gum, nicotine nasal spray, nicotine vapor inhaler, and nicotine lozenge. Before initiating nicotine-replacement treatments, smokers are advised to discontinue the use of other nicotine-containing products because of concerns about nicotine toxicity that might result from concurrent use of nicotine-containing products (e.g., cigarettes in combination with the nicotine patch). All of these treatments have been demonstrated to increase quit rates in controlled clinical studies.12 These studies have been conducted under fairly strict conditions, with a prescribed quitting period, several visits to the clinic to assess progress, and the usual trappings of a clinical research study, often including the collection of saliva or other samples to detect tobacco use. That’s a far cry from buying nicotine gum at the corner store, with
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no plan for quitting, no follow-up interviews, and no monitoring. Thus, it is not surprising that the average person might have great difficulties quitting even with the aid of nicotinereplacement medications. In 1997, the FDA approved bupropion (Zyban), the first non-nicotine pharmacotherapy for smoking cessation. Bupropion is also used in the treatment of depression, where it is referred to as Wellbutrin. Although the neurochemical mechanisms that underlie bupropion’s therapeutic effects have yet to be definitively determined, the mechanism of action most commonly attributed to bupropion is inhibition of dopamine and norepinephrine reuptake and, to a lesser extent, blockade of acetylcholine receptors.13 Unlike nicotine-replacement therapies, there is no absolute requirement for the smoker to abstain from the
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use of nicotine-containing products. Bupropion has been shown to gradually decrease cigarette craving and use in some clinical trials. Because nicotine-replacement medications and bupropion have been demonstrated to decrease cigarette smoking when administered alone, it has been suggested that greater treatment success might be achieved if the two strategies were combined. Unfortunately, data from a recent investigation indicated that the addition of bupropion treatment to nicotine-replacement therapy did not significantly increase smoking cessation rates.14 In May 2006, the FDA approved the latest smoking cessation medication. Varenicline is a partial nicotinic-receptor agonist, meaning that, even at large doses, it does not produce the full response of nicotine. As a result of its properties, it should be able to reduce symptoms of withdrawal and craving, while blocking the effects of nicotine should the smoker relapse. Varenicline was found to be more effective than placebo or bupropion and is a viable option for smoking cessation therapy.15
Opioids
Zyban (bupropion) was the first non-nicotine pharmacotherapy for smoking cessation. The drug, also used to treat depression, appears to gradually reduce cravings for cigarettes.
Historically, anticholinergic drugs, such as belladonna, were used in the treatment of opioid dependence.16 The idea was that anticholinergics would produce a state of delirium for several days, after which the dependent person would emerge cured of dependence without remembering the dreadful experience of the withdrawal process. A more recent version of this approach is “rapid opioid detoxification.” Opioid-dependent individuals are anesthetized and, while unconscious, are given an opioid antagonist, so that withdrawal will occur while they are unconscious. After 24 hours the patient is released and enters a period of counseling, combined with continued opioid antagonist treatment. This procedure has been vehemently criticized because it increases the risk of problems during the withdrawal process and because aftercare (behavioral/psychosocial treatment) is often deemphasized.
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Drug withdrawal can have unpleasant and potentially dangerous symptoms. Drugs may be administered to reduce withdrawal symptoms.
Although opioid withdrawal is not life threatening, symptoms such as nausea, vomiting, diarrhea, aches, and pain can be unpleasant. Medications are administered to minimize discomfort. Methadone (Dolophine), an opioid analgesic developed in Germany during World War II, is commonly used
in this capacity. It has a long duration of action, which means that it needs to be taken less frequently to prevent withdrawal symptoms. Another medication that has been shown to decrease opioid withdrawal symptoms is buprenorphine, a partial opioid agonist. Buprenorphine has a relatively large margin of safety and a low overdose potential. In addition, it has a long duration of action and blocks the effects of other opioid agonists such as heroin. As a result of these features, both methadone and buprenorphine are FDA-approved opioid-dependence medications. These medications are used not only during detoxification, but during maintenance as well. Methadone maintenance, the most common form of treatment for opioid dependence, may continue for months or years. The duration of buprenorphine maintenance might be similar, but because the medication has only recently received approval, this is not yet known. One major concern in the treatment of opioid dependence is opioid-induced overdose,
Table 18.1 Medications Used to Treat Substance Abuse and Dependence Substance
Treatment Medication
Proposed Mechanism(s) of Action
Alcohol
Benzodiazepines Disulfiram Naltrexone Acamprosate
Increase the activity of GABA Inhibits aldehyde dehydrogenase Opioid receptor antagonist Normalizes basal GABA concentrations; blocks alcohol-withdrawal-induced glutamate increases
Nicotine
Nicotine replacements Bupropion Varenicline
Full agonists at nicotine receptors Inhibits the reuptake of dopamine and norepinephrine; acetylcholine receptors antagonist Partial nicotine-receptor agonist
Opioids
Methadone Buprenorphine Naltrexone
Full agonist at opioid receptors Partial agonist at opioid receptors Opioid receptor antagonist
Cocaine
Modafinil*
Increases the activity of dopamine, norepinephrine, and glutamate; decreases the release of GABA
Cannabis
Dronabinol*
Full agonist at cannabinoid receptors
*Not FDA approved to treat substance abuse or dependence.
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which could lead to a coma and eventual death via respiratory depression. Because the shortacting opioid antagonist naloxone has a greater affinity for brain opioid receptors than do most opioid agonists, including heroin, it is often used for treating opioid overdose. Following its administration, naloxone displaces the opioid agonist from the receptors, and thereby rapidly reverses the overdose. This observation led to speculations about the use of opioid antagonists in treating opioid dependence. That is, if a user takes heroin, for example, while being maintained on an opioid antagonist, the effects of heroin would not be felt. This rationale provided the basis for the approval of the longacting opioid antagonist naltrexone for treating opioid dependence. Although naltrexone therapy has been shown to be effective in the treatment of opioid dependence, this therapy appears to be appropriate for only highly motivated individuals because most opioid abusers enrolled in naltrexone therapy prematurely discontinue treatment. To circumvent compliance problems, a new depot formulation of naltrexone, which requires one administration per month, is being studied as a potential opioiddependence treatment medication. Initial findings are encouraging, as depot naltrexone has been demonstrated to block heroin-related effects for up to six weeks.17 An interesting problem arises if a patient on naltrexone is involved in an accident and requires some pain relief. Current practice is to give high doses of hydromorphone (Dilaudid) to overcome the antagonism. This should be done only in a hospital and with extreme caution.
Cocaine Although a cocaine withdrawal syndrome does not appear to be a major feature of cocaine dependence,18 some investigators have documented symptoms of depression, nervousness, dysphoria, anhedonia, fatigue, irritability, sleep and activity disturbances, and craving for cocaine.19 Behavioral and mood changes that accompany cocaine withdrawal might be related
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to a decrease in the activity of monoamine neurotransmitters, which play an important role in movement and mood regulation. Accordingly, medications that increase monoaminergic activity may be useful in treating withdrawal symptoms and thereby prevent relapse. A plethora of medications, ranging from selective agonists of monoamine neurotransmitters to agents that simultaneously enhance the activity of multiple neurotransmitters, have been evaluated according to this theory. Unfortunately, to date, the vast majority of medications assessed have not been effective at treating cocaine withdrawal symptoms or dependence.20 The situation is not completely bleak, however, as recent data from investigations of modafinil (Chapter 6) suggest that the medication is useful in treating cocaine dependence.21 In these studies, cocaine use and cocaine-related subjective effects (e.g., euphoria and craving) were markedly reduced when cocaine abusers were taking modafinil compared with placebo. While the mechanisms underlying modafinil’s therapeutic actions are unknown, the drug appears to increase the activity of several neurotransmitters (e.g., dopamine, norepinephrine, and glutamate) and decrease the release of GABA.22 Although modafinil is not FDA approved for the treatment of cocaine abuse or dependence, some physicians may use the medication for this purpose off-label. There are no medications approved to treat cocaine abuse or dependence.
Cannabis Most users of cannabis consume the drug infrequently without apparent negative consequences. A small proportion, however, experience problems related to frequent cannabis use.
anhedonia [an hee doeⴕ nee ya]: lack of emotional response; especially an inability to experience joy or pleasure. off-label: use of prescription drug to treat a condition for which the drug has not received U.S. FDA approval.
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Mind/Body Connection The Nature of Dependence Is drug dependence strictly a matter of neurotransmitters and neural adaptation, as seems increasingly to be the accepted viewpoint, or will it ultimately be impossible to understand such a complex set of behaviors by reducing the problem to its biochemical correlates? This has been a huge and ongoing debate among proponents of the various views of drug dependence, but currently the research funding and most of the information seen in the popular media favor biological approaches to understanding these problems. This chapter’s focus on drug treatments for substance dependence seems to be based on an implied acceptance that some biochemical imbalance is at the heart of people who are seemingly unable to exert control over their own drug-using behavior. However, many, including proponents of the Alcoholics Anonymous philosophy, believe that substance dependence is a “spiritual” disorder— essentially that an individual human is not recognizing the need to draw upon either God or
An estimated 1 in 11 cannabis users will become dependent.23 Rates of cannabis dependence in several countries have increased substantially over the past decade as well as the number of individuals seeking treatment. Many individuals seeking treatment for cannabis dependence reported experiencing withdrawal symptoms and that these symptoms made it more difficult to maintain abstinence. As a result, efforts to develop medication for cannabis dependence have primarily focused on relieving withdrawal symptoms. Cannabis withdrawal is characterized by symptoms of irritability, anxiety, sleep disruptions, and aches.24 A growing number of medications have been tested for efficacy in relieving these symptoms, but only one has been demonstrated to be effective—oral ⌬9-THC (dronabinol). The primary reason for evaluating the effects of dronabinol on cannabis withdrawal was based on the idea of substituting a longer-acting pharmaco-
some other source of spiritual strength to help win the struggle with the bottle or needle or pill. For these people, drug treatments, especially of the substitution/maintenance type, are often seen as a crutch that does not address the individual’s basic problem and cannot therefore be of much long-term benefit. To others, substance abuse and dependence can be approached through behavioral techniques such as contingency management or through a variety of psychosocial approaches such as group therapy. For them, medication might be seen as a temporary aid in assisting the person to “reprogram” his or her thinking, routines, and social interactions, but it is ultimately these changes in relationships, attitudes, and activities that are the key to longer-term success. How do you feel about the evidence showing that former heroin users can often be maintained for years on methadone, a legal substitute, while they attend school, work, and otherwise enjoy more productive and less dangerous lives than if they had continued to use heroin?
logically equivalent drug for the abused substance, stabilizing the individual on that drug, and then gradually withdrawing the substituted drug, thus decreasing the likelihood of precipitating abstinence symptoms. It was recently demonstrated that dronabinol markedly reduced symptoms associated with cannabis abstinence including self-reported ratings of cannabis craving, anxiety, misery, and sleep disturbance. The medication also reversed the withdrawal-associated psychomotor performance decrements as well as the anorexia and weight loss associated with cannabis withdrawal. These results indicate that moderate doses of oral dronabinol might be beneficial in the treatment of cannabis dependence.25 To date, no medications are approved for the treatment of cannabis dependence although dronabinol is sometimes used off-label for this purpose. Table 18.1 summarizes medical treatments for substance abuse.
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Treatment: The Big Picture in the United States In each state, the agency that has primary responsibility for public funding of substance abuse treatment programs submits annual reports to the U.S. Substance Abuse and Mental Health Services Administration (SAMHSA). Between 1996 and 2006, the data from more than 1.8 million admissions each year for substance abuse were compiled into the Treatment Episode Data Set.26 In 2006, four substances accounted for about 90 percent of these admissions: alcohol (40 percent), opioids (18 percent), marijuana (16 percent), and cocaine (14 percent). Of those who reported opioids as their primary drug of abuse, 77 percent were heroin users, and 72 percent of those who reported cocaine as the primary drug were crack cocaine smokers. The average age of those admitted with marijuana as the primary drug was 24 years. In 2006, 50 percent of the substance-abuse clients were treated as outpatients, 13 percent as hospital inpatients (detoxification), and 17 percent in a residential setting. These data suggest that the bulk of our substance-abuse treatment should focus on developing more effective interventions for alcohol, opioid, marijuana, and cocaine abuse that can be delivered on an outpatient basis. As reviewed previously, most recent research efforts to develop pharmacotherapies to treat substance abuse have been aimed at decreasing the use of these substances (and nicotine). But, without effective outpatient behavioral/psychosocial interventions, the overall success of pharmacotherapies alone to treat substance abuse is likely to be unimpressive. This is because substance abusers may show poor medication compliance, even on medications that have been demonstrated to be effective at decreasing substance use (e.g., disulfiram for alcohol dependence and naltrexone for opioid dependence). Moreover, substance abusers often present with additional mental disorders and multiple other functional impairments. Thus, behavioral/psychosocial treatments are needed to address these issues so that overall treatment success is enhanced.
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Is Treatment Effective? There is a widespread belief that substanceabuse treatment is often ineffective. We’ve all heard of well-known athletes who have been in treatment programs and later are found to be using illegal drugs, and we might know an alcohol abuser who went into treatment and later began drinking again. Treatment doesn’t work for every client every time, especially if our expectation is that one treatment exposure will eliminate the use of the substance for the rest of the person’s life. Substance dependence is often a chronic illness that shares many characteristics with other chronic illnesses such as diabetes, hypertension, and asthma. There are no reliable “cures,” and all of these conditions may require continuing care throughout the patient’s life. An important question is whether substanceabuse treatment programs have any beneficial effect—and, if they do, are their effects worth the cost? In general, people who go into treatment fare better than those who do not, as measured by reduced crime, increased employment, and better health. A report by the California Department of Alcohol and Drug Programs concluded that, on average, seven dollars are saved for every dollar invested in the treatment of alcohol
Drug treatment doesn’t work for every person every time, but overall, treatment does reduce drug use, reduce associated criminal activity, and increase employment. By continuing to participate in outpatient drug rehabilitation meetings, these teens increase the likelihood that their substance-abuse treatment will be a success over the long term.
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and other drug abuse.27 Alcohol and other drug use was reduced by about two-fifths after treatment; treatment for crack cocaine, powder cocaine, and methamphetamine use was equally effective as for alcohol; and criminal activity declined by about two-thirds after treatment. One report reviewed 53 studies of the effectiveness of substance-abuse treatments for adolescents. Overall, most of the treated adolescents had significant reductions in substance use and problems in other life areas in the year following treatment, and an average of 32 percent remained abstinent at the end of a year. Successful program completion, involvement in outpatient therapy, and the inclusion of the family therapy as one treatment component all appeared to predict success.28 Overall, substance abuse treatment does work. It saves lives, saves money, and is, therefore, a worthwhile investment.
•
Zyban (bupropion) may be used alone or in combination with various forms of nicotine-replacement therapy to aid smoking cessation.
•
Methadone is the drug most commonly used to treat opioid dependence, although buprenorphine is now also available for use in substitution/maintenance treatment. Naltrexone blocks the effects of any opioids the user might take, but it has not been as effective as methadone in helping people to abstain from heroin or other abused opioids. Rapid opioid detoxification is a short-term method to avoid experiencing withdrawal symptoms.
•
Although recent findings with modafinil have been encouraging, no medication has yet been developed specifically for treatment of cocaine dependence.
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Cannabis withdrawal symptoms can be relieved by the use of dronabinol, which shows promise as a treatment for cannabis dependence.
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Overall, substance-abuse treatment programs are considered to be effective because they do help many people to abstain, sometimes only for a few months, but often for many years. The benefits far exceed the cost of providing the programs.
Summary •
Treatment for substance abuse and dependence may include both behavioral/ psychosocial approaches and the use of various medications.
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Many of today’s psychosocial treatment programs are heavily influenced by the philosophy developed by Alcoholics Anonymous. These are often referred to as 12-step programs.
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Motivational interviewing is usually used in conjunction with stages of change theory, to help move people from one stage to another in the process of quitting.
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Medications are often used to ease withdrawal during detoxification. Maintaining abstinence may be assisted by either agonist substitution or by antagonist treatment.
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Antabuse (disulfiram) interferes with alcohol metabolism to produce illness if the patient uses alcohol. Naltrexone and acamprosate are also available to assist in preventing relapse.
Review Questions 1. List at least 8 of the 12 steps of Alcoholics Anonymous. 2. What are the four “stages of change” listed in the text? 3. Describe the kinds of contingencies used in contingency management: What happens if the client has several “clean” urine samples in a row? What happens if the client fails one of the urine sample tests? 4. Give one example for each: agonist/substitution therapy, antagonist therapy, and punishment therapy.
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5. What drugs are typically used to reduce withdrawal symptoms during alcohol detoxification? 6. Compare and contrast the use of disulfiram (Antabuse) versus either naltrexone or acamprosate for alcohol dependence. 7. List four of the five types of available nicotinereplacement therapy. 8. How are methadone and buprenorphine similar to each other and different from naltrexone as treatments for opioid dependence? 9. The effort to develop drugs to treat cocaine dependence has targeted which neurotransmitter systems? 10. How big a problem is cannabis dependence, and what seems to be the most promising drug treatment currently being studied?
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Rollnick, S., and W. R. Miller. “What Is Motivational Interviewing?” Behavioural and Cognitive Psychotherapy 23 (1995), pp. 325–34. Polcin, D. L., G. P. Galloway, J. Palmer, and W. Mains. “The Case for High-Dose Motivational Enhancement Therapy.” Substance Use and Misuse 39 (2004), pp. 331–43. Higgins, S. T., S. H. Heil, and J. P. Lussier. “Clinical Implications of Reinforcement as a Determinant of Substance Use Disorders. Annual Review of Psychology 55 (2004), pp. 431–61. Carroll, K. M., B. J. Rounsaville, C. Nich, L. T. Gordon, P. W. Wirtz, and F. Gawin. “One-year Follow-up of Psychotherapy and Pharmacotherapy for Cocaine Dependence. Delayed Emergence of Psychotherapy Effects.” Archives of General Psychiatry 51 (1994), pp. 989–97. Aharonovich, E., E. Nunes, and D. Hasin. “Cognitive Impairment, Retention and Abstinence Among Cocaine Abusers in Cognitive-behavioral Treatment.” Drug and Alcohol Dependence 71 (2003), pp. 207–11. Chrousos, G. P., and P. W. Gold. “The Concepts of Stress and Stress System Disorders: Overview of Physical and Behavioral Homeostasis.” Journal of the American Medical Association 267 (1992), pp. 1244–52. Woods, J. H., J. L. Katz, and G. Winger. “Benzodiazepines: Use, Abuse, and Consequences.” Pharmacology Review 44 (1992), pp. 151–347. Hald, J., E. Jacobsen, and V. Larsen. “The Sensitizing Effect of Tetraethylthiuram Disulfide (Antabuse) to Ethyl Alcohol.” Acta Pharmocologica et Toxicologica 4 (1948), pp. 285–96. O’Malley, S. S., and others. “Naltrexone and Coping Skills Therapy for Alcohol Dependence: A Controlled Study.” Archives of General Psychiatry 49 (1992), pp. 894–98; and Volpicelli, J., and others. “Naltrexone in the Treatment of
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Alcohol Dependence.” Archives of General Psychiatry 49 (1992), pp. 867–80. Sinclair, J. D. “Evidence About the Use of Naltrexone and for Different Ways of Using It in the Treatment of Alcoholism.” Alcohol 36 (2001), pp. 2–10. Dahchour, A., and P. De Witte. “Ethanol and Amino Acids in the Central Nervous System: Assessment of the Pharmacological Actions of Acamprosate.” Progress in Neurobiology 60 (2000), pp. 343–62. George, T. P., and S. S. O’Malley. “Current Pharmacological Treatments for Nicotine Dependence. Trends in Pharmacological Sciences 25 (2004), pp. 42–48. Ascher, J. A., and others. “Bupropion: A Review of Its Mechanism of Antidepressant Activity.” Journal of Clinical Psychiatry 56 (1995), pp. 395–401; and Slemmer, J. E., B. R. Martin, and M. I. Damaj. “Bupropion Is a Nicotinic Antagonist.” Journal of Pharmacology Experimental Therapies 295 (2000), pp. 321–27. Simon, J. A., C. Duncan, T. P. Carmody, and E. S. Hudes. “Bupropion for Smoking Cessation: A Randomized Trial.” Archives of Internal Medicine 164 (2004), pp. 1797–1803. Stack, N. M. “Smoking Cessation: An Overview of Treatment Options with a Focus on Varenicline.” Pharmacotherapy 27 (2007), pp. 1550–57. Latimer, D., and J. Goldberg. Flowers in the Blood: The Story of Opium. New York: Arno Press, 1981. Comer, S. D., and others. “Depot Naltrexone: Long-lasting Antagonism of the Effects of Heroin in Humans.” Psychopharmacology, 159 (2002), pp. 351–60. Foltin, R. W., and M. W. Fischman. “A Laboratory Model of Cocaine Withdrawal in Humans: Intravenous Cocaine.” Experimental and Clinical Psychopharmacology 5 (1997), pp. 404–11. Gawin, F. H., and H. D. Kleber. “Abstinence Symptomatology and Psychiatric Diagnosis in Cocaine Abusers. Clinical Observations.” Archives of General Psychiatry 43 (1986), pp. 107–13. Hart, C. L. and W. J. Lynch “Developing Pharmacotherapies for Cannabis and Cocaine Use Disorders.” Current Neuropharmacology 3 (2005), pp. 95–114. Dackis, C. A, and others. “A Double-blind, Placebocontrolled Trial of Modafinil for Cocaine Dependence.” Neuropsychopharmacology 30 (2005), pp. 205–11; and Hart, C. L., and others. “Smoked Cocaine Self-Administration is Decreased by Modafinil.” Neuropsychopharmacology 33 (2008), pp. 761–68. Wisor, J. P. and K. S. Eriksson “Dopaminergic-adrenergic Interactions in the Wake Promoting Mechanism of Modafinil.” Neuroscience 132 (2005), pp. 1027–34; Madras, B. K., and others. “Modafinil Occupies Dopamine and Norepinephrine Transporters In Vivo and Modulates the Transporters and Trace Amine Activity In Vitro.” Journal of Pharmacology and Experimental Therapeutics 319 (2006), pp. 561–69; and Ferraro, L., and others. “The Vigilance Promoting Drug Modafinil Increases Extracellular Glutamate Levels in the Medial Preoptic Area and the Posterior Hypothalamus of the Conscious Rat: Prevention by Local GABAA Receptor Blockade.” Neuropsychopharmacology 20 (1999), pp. 346–56. Anthony, J. C., L. A. Warner, and R. C. Kessler. “Comparative Epidemiology of Dependence on Tobacco, Alcohol, Controlled Substances, and Inhalants: Basic Findings
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from the National Comorbidity Survey.” Experimental and Clinical Psychopharmacology 2 (1994), pp. 244–68. Hart, C. L. “Increasing Treatment Options for Cannabis Dependence: A Review of Potential Pharmacotherapies.” Drug and Alcohol Dependence 80 (2005), pp. 147–59. Lichtman, A. H., J. Fisher, and B. R. Martin. “Precipitated Cannabinoid Withdrawal Is Reversed by Delta(9)-tetrahydrocannabinol or Clonidine.” Pharmacology, Biochemistry and Behavior 69 (2001), pp. 181–88. Substance Abuse and Mental Health Services Administration. Treatment Episode Data Set (TEDS). Highlights--
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Back Matter
Appendix
Appendix A: Drug Names
A
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Drug Names
A
B
Abilify (aripiprazole): a typical antipsychotic.
belladonna: poisonous anticholinergic plant.
acamprosate (Campral): treatment for alcohol dependence.
Benzedrine: amphetamine. CNS stimulant and sympathomimetic. Brand name no longer used.
acetaminophen: OTC analgesic. Similar to aspirin in its effects.
benzodiazepines: class of sedative-hypnotics that includes diazepam (Valium).
acetophenazine: Tindal. Antipsychotic.
benztropine: Cogentin. Anticholinergic used to control extrapyramidal symptoms.
acetylsalicylic acid: aspirin. OTC analgesic. alprazolam: Xanax. Benzodiazepine sedative.
black tar: a type of illicit heroin.
Amanita muscaria: hallucinogenic mushroom.
bromide: group of salts with sedative properties.
Ambien: zolpidem. Non-benzodiazepine sedativehypnotic.
buprenorphine (Subutex): opioid used as a maintenance treatment for heroin users.
amitriptyline: Elavil, Endep. Tricyclic antidepressant.
bupropion: Wellbutrin. Atypical antidepressant. Also Zyban, to reduce craving during tobacco cessation.
amobarbital: Amytal. Barbiturate sedative-hypnotic. amoxapine: Asendin. Tricyclic antidepressant. amphetamine: Benzedrine. CNS stimulant and sympathomimetic. Amytal: amobarbital. Barbiturate sedativehypnotic. Anavar: oxandrolone. Anabolic steroid. angel dust: street name for PCP. Antabuse: disulfiram. Alters metabolism of alcohol; used to treat alcohol dependence.
butabarbital: Butisol. Barbiturate sedativehypnotic. Butisol: butabarbital. Barbiturate sedative-hypnotic.
C caffeine: mild stimulant found in coffee and in OTC preparations. cannabis: the marijuana plant.
aprobarbital: Alurate. Barbiturate sedativehypnotic.
carbamazepine: Tegretol. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Artane: trihexyphenidyl. Anticholinergic used to control extrapyramidal symptoms.
Catapres: clonidine. Antihypertensive drug shown to reduce narcotic withdrawal symptoms.
Asendin: amoxapine. Tricyclic antidepressant.
Celexa: citalopram. Atypical antidepressant.
aspirin: acetylsalicylic acid. OTC analgesic.
chloral hydrate: Noctec. Nonbarbiturate sedativehypnotic.
Ativan: lorazepam. Benzodiazepine sedative. atropine: anticholinergic. Aventyl: nortriptyline. Tricyclic antidepressant. ayahuasca: a combination of two plants, one of which contains DMT. Hallucinogen.
chlordiazepoxide: Librium. Benzodiazepine sedative. chlorpheniramine maleate: OTC antihistamine. chlorpromazine: Thorazine. Antipsychotic.
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Appendix A: Drug Names
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chlorprothixene: Taractan. Antipsychotic.
dextromethorphan: OTC cough suppressant.
Cibalith: lithium citrate. Salt used in treating mania and bipolar affective disorders.
diazepam: Valium. Benzodiazepine sedative.
Citalopram: Celexa. Atypical antidepressant. clenbuterol: an alpha-2 adrenergic agonist developed to treat asthma, but used by athletes to build muscle. clonidine: Catapres. Antihyperintensive drug shown to reduce narcotic withdrawal symptoms. clorazepate: Tranxene. Benzodiazepine sedative. clozapine: Clozaril. Atypical antipsychotic. Clozaril: clozapine. Atypical antipsychotic. cocaine: CNS stimulant and local anesthetic. codeine: opioid analgesic found in opium. Cogentin: benztropine. Anticholinergic used to control extrapyramidal symptoms.
diethylpropion: Tenuate, Tepanil. Amphetaminelike appetite suppressant. dihydrocodeine: opioid analgesic. Dilaudid: hydromorphone. Opioid analgesic. diphenhydramine: antihistamine. disulfiram: Antabuse. Alters metabolism of alcohol; used to treat alcoholism. DMT: dimethyltryptamine. Hallucinogen. Dolophine: methadone. Opioid analgesic. DOM: hallucinogen. doxepin: Sinequan. Tricyclic antidepressant. dronabinol: Marinol. Prescription form of delta-9tetrahydrocannabinol.
Compazine: prochlorperazine. Antipsychotic. creatine: natural substance found in meat and fish that might have anabolic properties and is used by athletes.
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Cylert: pemoline. Stimulant used to treat ADD with hyperactivity.
Elavil: amitriptyline. Tricyclic antidepressant.
Effexor: venlafaxine. Antidepressant (SSRI). Endep: amitriptyline. Tricyclic antidepressant. endorphin: endogenous substance with effects similar to those of the opioid analgesics.
D Dalmane: flurazepam. Benzodiazepine hypnotic. Darvon: propoxyphene. Opioid analgesic. Datura: genus of plants, many of which are anticholinergic.
enkephalin: endogenous substance with effects similar to those of the opioid analgesics. ephedrine: sympathomimetic used to treat asthma. Equanil: meprobamate. Nonbarbiturate sedativehypnotic.
Demerol: meperidine. Opioid analgesic.
Eskalith: lithium carbonate. Salt used in treating mania and bipolar affective disorders.
Depakene: valproic acid. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
eszopiclone: Lunesta. Non-benzodiazepine sedative-hypnotic.
desipramine: Norpramin, Pertofrane. Tricyclic antidepressant. Desoxyn: methamphetamine. CNS stimulant and sympathomimetic.
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Desyrel: trazodone. Atypical antidepressant.
fenfluramine: Pondimin. Appetite suppressant, removed from the market in 1997.
Dexedrine: dextroamphetamine. CNS stimulant and sympathomimetic. dexfenfluramine: Redux. Appetite suppressant, removed from the market in 1997. dextroamphetamine: Dexedrine. CNS stimulant and sympathomimetic.
fentanyl: Sublimaze. Potent synthetic analgesic. flunitrazepam: Rohypnol. Benzodiazepine hypnotic, not sold in the U.S. Known as a “date-rape” drug. fluoxetine: Prozac. Antidepressant (SSRI).
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www.mhhe.com/hart13e fluphenazine: Permitil, Prolixin. Antipsychotic.
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flurazepam: Dalmane. Benzodiazepine hypnotic.
Klonopin: Clonazepam. Benzodiazepine sedativehypnotic, also used as an anticonvulsant.
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GEOdon: Ziprasidone. Atypical antipsychotic.
LAAM: L-alpha-acetyl-methadol. Long-lasting synthetic opioid used in maintenance treatment of narcotic addicts.
GHB: gamma hydroxybutyrate. CNS depressant, produced naturally in small amounts in the human brain. Has been used recreationally and, in combination with alcohol, has some reputation as a “date-rape” drug. Ginkgo biloba: a dietary supplement believed by some to increase blood circulation.
Lamictal: lamotrigine. Anticonvulsant also used as a mood stabilizer in bipolar disorder. lamotrigine: Lamictal. Anticonvulsant also used as a mood stabilizer in bipolar disorder. laudanum: tincture (alcohol solution) of opium. Lexapro: escitalopram. Atypical antidepressant.
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Librium: chlordiazepoxide. Benzodiazepine sedative. Lithane: lithium carbonate.
Haldol: haloperidol. Antipsychotic.
lithium carbonate, lithium citrate: salts used in treating mania and bipolar affective disorders.
haloperidol: Haldol. Antipsychotic.
Lithobid: lithium carbonate.
henbane: poisonous anticholinergic plant.
lorazepam: Ativan. Benzodiazepine sedative.
heroin: Diacetylmorphine Narcotic analgesic.
Lortab: acetaminophen-hydrocodone combination. Analgesic.
Halcion: triazolam. Benzodiazepine hypnotic.
hydrocodone: Opioid analgesic. hydromorphone: Dilaudid. Opioid analgesic.
loxapine: Loxitane. Antipsychotic. Loxitane: loxapine. Antipsychotic. LSD: lysergic acid diethylamide. Hallucinogen.
I ibogaine: hallucinogen, also proposed to reduce craving in drug addicts. ibuprofen: analgesic and anti-inflammatory.
Ludiomil: maprotiline. Tricyclic antidepressant. Luminal: phenobarbital. Barbiturate sedativehypnotic. Lunesta: eszopiclone. Non-benzodiazepine sedativehypnotic.
imipramine: Janimine, Tofranil. Tricyclic antidepressant. isocarboxazid: Marplan. MAO inhibitor used as antidepressant.
M mandrake: anticholinergic plant.
J Janimine: imipramine. Tricyclic antidepressant.
maprotiline: Ludiomil. Tricyclic antidepressant. Marijuana: Common name for the cannabis plant and for its dried leaves. Marinol: dronabinol. Prescription form of delta-9tetrahydrocannabinol.
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Marplan: isocarboxazid. MAO inhibitor used as antidepressant.
Ketalar: ketamine. Dissociative anesthetic.
Mazanor: mazindol. Appetite suppressant.
ketamine: Ketalar. Dissociative anesthetic.
mazinodol: Mazanor, Sanorex. Appetite suppressant.
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MDA: hallucinogen.
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MDMA: hallucinogen. Mebaral: mephobarbital. Barbiturate sedative-hypnotic.
olanzepine: Zyprex. Atypical antipsychotic.
Mellaril: thioridazine. Antipsychotic.
opium: opioid analgesic.
meperidine: Demerol. Opioid analgesic.
oxandrolone: Anavar. Anabolic steroid.
mephobarbital: Mebaral. Barbiturate sedativehypnotic.
oxazepam: Serax. Benzodiazepine sedative.
meprobamate: Equanil, Miltown. Nonbarbiturate sedative-hypnotic.
oxycodone: Percodan. Opioid analgesic. OxyContin: continuous-release form of oxycodone. oxymorphone: Numorphan. Opioid analgesic.
mescaline: hallucinogen found in peyote cactus. mesoridazine: Serentil. Antipsychotic. methadone: Dolophine. Narcotic analgesic.
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methamphetamine: Desoxyn, Methedrine. CNS stimulant and sympathomimetic.
Pamelor: nortriptyline. Tricyclic antidepressant.
methaqualone: Quaalude, Sopor. Nonbarbiturate sedative-hypnotic.
paraldehyde: nonbarbiturate sedative-hypnotic.
methylphenidate: Ritalin. Stimulant used to treat ADD with hyperactivity.
Parnate: tranylcypromine. MAO inhibitor used as antidepressant.
Metrazol: pentylenetetrazol. Convulsant formerly used in convulsive therapy.
paroxetine: Paxil. Antidepressant (SSRI).
Miltown: meprobamate. Nonbarbiturate sedativehypnotic.
PCP: phencyclidine, angel dust. Hallucinogen.
paregoric: tincture (alcohol solution) of opium.
Paxil: paroxetine. Antidepressant (SSRI).
mirtazapine: Remeron. Atypical antidepressant.
pemoline: Cylert. Stimulant used to treat ADD with hyperactivity.
Moban: molindone. Antipsychotic.
pentazocine: Talwin. Opioid analgesic.
modafinil: Provigil. Atypical CNS stimulant.
pentobarbital: Nembutal. Barbiturate sedativehypnotic.
molindone: Moban. Antipsychotic. morphine: opioid analgesic.
pentylenetetrazol: Metrazol. Convulsant formerly used in convulsive therapy.
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Percodan: oxycodone. Opioid analgesic.
naloxone: Narcan. Opioid antagonist.
perphenazine: Trilafon. Antipsychotic.
naltrexone: Trexan, reVIA. Opioid antagonist. Used in treating alcoholism.
Pertofrane: desipramine. Tricyclic antidepressant.
Nardil: phenelzine. MAO inhibitor used as antidepressant. Navane: thiothixene. Antipsychotic. Nembutal: pentobarbital. Barbiturate sedativehypnotic.
Permitil: fluphenazine. Antipsychotic.
peyote: cactus containing mescaline (hallucinogenic). phencyclidine: PCP, angel dust. Hallucinogen. phendimetrazine: amphetamine-like appetite suppressant.
Norpramin: desipramine. Tricyclic antidepressant.
phenelzine: Nardil. MAO inhibitor used as antidepressant.
nortriptyline: Aventyl, Pamelor. Tricyclic antidepressant.
phenmetrazine: Preludin. Amphetamine-like appetite suppressant.
Novocain: Procaine. Local anesthetic.
phenobarbital: Luminal. Barbiturate sedative-hypnotic.
Numorphan: oxymorphone. Opioid analgesic.
phentermine: Amphetamine-like appetite suppressant.
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phenylpropanolamine (PPA): OTC appetite suppressant.
secobarbital: Seconal. Barbiturate sedative-hypnotic.
Pondimin: fenfluramine. Appetite suppressant, removed from the market in 1997.
Serax: oxazepam. Benzodiazepine sedative.
Seconal: secobarbital. Barbiturate sedative-hypnotic. Serentil: mesoridazine. Antipsychotic.
Preludin: phenmetrazine. Amphetamine-like appetite suppressant.
Sernyl: former brand name for PCP.
prochlorperazine: Compazine. Antipsychotic.
sertraline: Zoloft. Antidepressant (SSRI).
Prolixin: fluphenazine. Antipsychotic.
Sinequan: doxepin. Tricyclic antidepressant.
propoxyphene: Darvon. Narcotic analgesic.
Sonata: zaleplon. Non-benzodiazepine sedativehypnotic.
protriptyline: Vivactil. Tricyclic antidepressant. Prozac: fluoxetine. Antidepressant (SSRI). pseudoephedrine: OTC sympathomimetic. psilocybin: hallucinogen from the Mexican psilocybe mushroom.
Sopor: methaqualone. Non-barbiturate sedativehypnotic. Steroids: Various important hormones and their chemical derivatives. Usually refers to the anabolic steroids used by athletes and body builders. stanozolol: Winstrol. Anabolic steroid.
Q
Stelazine: trufluoperazine. Antipsychotic. Sublimaze: fentanyl. Potent synthetic analgesic.
Quaalude: methaqualone. Non-barbiturate sedativehypnotic.
T R Redux: dexfenfluramine. Appetite suppressant, removed from the market in 1997.
Talwin: pentazocine. Opioid analgesic. Taractan: chlorprothixene. Antipsychotic.
Remeron: mirtazapine. Atypical antidepressant.
Tegretol: carbamazepine. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Restoril: temazepam. Benzodiazepine hypnotic.
temazepam: Restoril. Benzodiazepine hypnotic.
reVIA: naltrexone. Opioid antagonist used in treating alcohol dependence.
Tenuate: diethylpropion. Amphetamine-like appetite suppressant.
Risperdal: risperidone. Atypical antipsychotic.
Tepanil: diethylpropion. Amphetamine-like appetite suppressant.
risperidone: Risperdal. Atypical antipsychotic. Ritalin: methylphenidate. Stimulant used to treat ADHD. Rohypnol: flunitrazepam. Benzodiazepine hypnotic, not sold in the U.S., known as a “date-rape” drug.
Teslac: testolactone. Anabolic steroid. testolactone: Teslac. Anabolic steroid. theophylline: mild stimulant found in tea; used to treat asthma. thioridazine: Mellaril. Antipsychotic.
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thiothixene: Navane. Antipsychotic. Thorazine: chlorpromazine. Antipsychotic.
Saint John’s wort: a dietary supplement used by some to treat depression.
Tindal: acetophenazine. Antipsychotic.
SAMe: S-adenosyl-L-methionine. Dietary supplement proposed as a possible treatment for depression.
Tofranil: imipramine. Tricyclic antidepressant.
Sanorex: mazindol. Appetite suppressant.
tranylcypromine: Parnate. MAO inhibitor used as an antidepressant.
scopolamine: anticholinergic.
TMA: indole hallucinogen. Tranxene: clorazepate. Benzodiazepine sedative.
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Drug Names
trazodone: Desyrel. Atypical antidepressant. Trexan: naltrexone. Opioid antagonist.
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triazolam: Halcion. Benzodiazepine hypnotic.
Wellbutrin: bupropion. Atypical antidepressant.
trifluoperazine: Stelazine. Antipsychotic.
Winstrol: stanozolol. Anabolic steroid.
trihexyphenidyl: Artane. Anticholinergic used to control extrapyramidal symptoms. Trilafon: perphenazine. Antipsychotic.
X
2-CB: catechol hallucinogen.
Xanax: alprazolam. Benzodiazepine sedative.
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Z
Valium: diazepam. Benzodiazepine sedative.
zaleplon: Sonata. Non-benzodiazepine sedativehypnotic.
valproic acid: Depakene. Anticonvulsant also used as a mood stabilizer in bipolar disorder.
Ziprasidone: Gedon. Atypical antipsychotic.
Varenicline: Chantix. To redce nicotine intake and craving during tobacco cessation. Partial nicotine agonist.
Zoloft: Sertraline. Antidepressant (SSRI).
venlafaxine: Effexor. Antidepressant (SSRI).
zolpidem: Ambien. Non-benzodiazepine sedativehypnotic.
Vesprin: triflupromazine. Antipsychotic. Vicodin: Hydrocodone-acetaminophen conbination. Analgesic. Vivactil: protriptyline. Tricyclic antidepressant.
Zyban: bupropion.To reduce craving during tobacco cessation.
Zyprexa: olanzepine. Atypical antipsychotic.
Hart−Ksir−Ray: Drugs, Society and Human Behavior, 13th Edition
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Appendix
Appendix B: Resources for Information and Assistance
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Federal Government Agencies National Clearinghouse for Alcohol and Drug Information Office of Substance Abuse Prevention (OSAP) P.O. Box 2345 Rockville, MD 20847-2345 Local: (240) 221-4019 T0ll-free: 1-800-729-6686 http://ncadi.samhsa.gov Drugs & Crime Data Center Bureau of Justice Statistics 810 Seventh Street, NW Washington, DC 20531 (202) 307-0765 www.ojp.usdoj.gov/bjs/
Alcohol Alcohol Research Information Service 430 Lanthrop Street Lansing, MI 48912 (517) 485-9900 www.mondaymorningreport.org [email protected] Alcoholics Anonymous World Services P.O. Box 459 New York, NY 10163 (212) 870-3400 www.alcoholics-anonymous.org American Council on Alcoholism 1000 E. Indian School Rd. Phoenix, AZ 85014 Toll-free: 1-800-527-5344 www.aca-usa.org
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Resources for Information and Assistance American Health and Temperance Society 6830 Eastern Ave, NW Washington, DC 20012 (202) 722-6736 BACCHUS of the U.S.(Boost Alcohol Consciousness Concerning the Health of University Students) P.O. Box 100430 Denver, CO 80250-0430 (303) 871-0901 www.bacchusgamma.org Licensed Beverage Information Council 1250 I St., Suite 900 NW Washington, DC 20005 (202) 682-8800 MADD (Mothers Against Drunk Driving) 511 E. John Carpenter Frwy, Suite 700 Irving, TX 75062 Local: (214) 744-6233 Info: 1-800-GET-MADD Help Line: 1-877-MADD-HELP www.madd.org National Alcohol Hotline 24-hr, 7 day/wk 1-800-ALCOHOL National Council on Alcoholism and Drug Dependence 244 E. 58th St. 4th Floor New York, NY 10022 (212)269-7797 Hope-Line: 1-800-NCA-CALL www.ncadd.org
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Appendix B Resources for Information and Assistance
RID (Remove Intoxicated Drivers) P.O. Box 520 Schenectady, NY 12301 (518) 372-0034 Toll-free: 1-888-283-5144 www.rid-usa.org
Smoking ASH (Action on Smoking and Health) 2013 H Street, NW Washington, DC 20006 www.no-smoking.org or www.ash.org Smoking Control Advocacy Resource Center 1730 Rhode Island Ave, Suite 600, NW Washington, DC 20036 (202) 659-8475 Tobacco Institute 2025 M Street, NW Washington, DC 20036 (202) 367-1176 www.tobaccoinstitute.com
Drugs Alcohol and Drug Problems Association of North America 307 N. Main St. Black Walnut, MO 63301 (can’t find phone number- site being built) www.adpana.com American Council for Drug Education 164 W. 74th St. New York, NY 10023 1-800-488-DRUG www.acde.org Do It Now Foundation PO Box 27568 Tempe, AZ 85285-7568 (480)736-0599 www.doitnow.org Drug Policy Foundation changed to: Drug Policy Alliance Network
70 W. 36th St, 16th Floor New York, NY 10018 (212) 613-8020 www.drugpolicy.org Summit Oaks Hospital 19 Prospect St. Box 100 Summit, NJ 07901 (908) 522-0914 I-800-COCAINE www.summitoakshospital.com Narcotic Educational Foundation of America 28245 Avenue Crocker, Suite 230 Santan Clarita, CA 91355-1201 (661)775-1648 Toll-free: (877) 775-NARC www.cnoa.org/NEFA.htm National Drug Information Center of Families in Action, Inc. changed to: National Families in Action 2957 Clairmont Road NE, Suite 150 Atlanta, GA 30329 (404) 248-9676 www.nationalfamilies.org NIDA (National Institute on Drug Abuse) National Institutes of Health 6001 Executive Boulevard, Room 5213 Bethesda, MD 20892-9561 (301) 443-1124 www.nida.nih.gov NORML (National Organization for the Reform of Marijuana Laws) 1600 K St NW, Suite 501 Washington, DC 20006-2832 (202)483-5500 www.norml.org PRIDE (Parent Resource Institute for Drug Education) 50 Hurt Plaza, Suite 210 Atlanta, GA 30303 (404) 577-4500 www.prideusa.org
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Appendix B: Resources for Information and Assistance
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Appendix B Resources for Information and Assistance
Drug Information on the Internet Much information, opinion, misinformation, and discussion about drugs is available on the Internet. It is possible to learn about the latest drug fads, to get involved in arguments about drug policy, and occasionally even to learn some solid facts by browsing on the Internet. But be warned that there is no quality control on many of these
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computer sites—they represent the ultimate in free expression! You’re liable to find such things as a bogus recipe for making LSD from Foster’s beer, warnings about water addiction, and other foolishness mixed in with potentially useful information, so take care. Links to some relevant Internet sites are found on the Online Learning Center.
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Glossary A abstinence Refraining completely from the use of alcohol or another drug. Complete abstinence from alcohol means no drinking at all. Abstinence syndrome: see withdrawal syndrome. abstinence violation effect The tendency of a person who has been abstaining (as from alcohol), and “slips,” to go on and indulge fully, because the rule of abstinence has been broken. acetaldehyde The chemical product of the first step in the liver’s metabolism of alcohol. It is normally present only in small amounts because it is rapidly converted to acetic acid. acetaminophen An aspirinlike analgesic and antipyretic. acetylcholine Neurotransmitter found in the parasympathetic branch and in the cerebral cortex. acetylsalicylic acid The chemical known as aspirin; an over-the-counter drug that relieves pain and reduces fever and inflammation. action potential A brief electrical signal transmitted along a neuron’s axon. active metabolites Pharmacologically active chemicals formed when enzymes in the body act on a drug. acute In general, “sharp.” In medicine, “rapid.” Referring to drugs, the short-term effects or effects of a single administration, as opposed to chronic, or longterm, effects of administration. additive effects When the effects of two different drugs add up to produce a greater effect than either drug alone. As contrasted with antagonistic effects, in which one drug reduces the effect of another, or synergistic effects, in which one drug greatly amplifies the effect of another. adenosine A chemical believed to be a neurotransmitter in the CNS, primarily at inhibitory receptors. Caffeine might act by antagonizing the normal action of adenosine on its receptors.
one example is learning how to achieve certain “feelings” (of excitement or belonging to a group) without using drugs. agonist A substance that facilitates or mimics the effects of a neurotransmitter on the postsynaptic cell. AIDS Acquired immunodeficiency syndrome, a disease in which the body’s immune system breaks down, leading eventually to death. Because the disease is spread through the mixing of body fluids, it is more prevalent in intravenous drug users who share needles. The infectious agent is the human immunodeficiency virus (HIV). alcohol Generally refers to grain alcohol, or ethanol, as opposed to other types of alcohol (for example, wood or isopropyl alcohol), which are too toxic to be drinkable. alcohol abuse In the DSM-IV-TR, defined as a pattern of pathological alcohol use that causes impairment of social or occupational functioning. Compare with alcohol dependence. alcohol dehydrogenase The enzyme that metabolizes almost all of the alcohol consumed by an individual. It is found primarily in the liver. alcohol dependence In the DSM-IV-TR, alcohol dependence is considered a more serious disorder than alcohol abuse, in that dependence includes either tolerance or withdrawal symptoms. alcoholic personality Personality traits, such as immaturity and dependency, that are frequently found in alcoholics in treatment. Many of these consistent traits might be a result of years of heavy drinking rather than a cause of alcoholism. Alcoholics Anonymous (AA) A worldwide organization of self-help groups based on alcoholics helping each other achieve and maintain sobriety.
ADHD Attention deficit hyperactivity disorder, a learning disability. Terminology of the DSM-IV-TR.
alcoholism The word has many definitions and therefore is not a precise term. Definitions might refer to pathological drinking behavior (e.g., remaining drunk for two days), to impaired functioning (e.g., frequently missing work), or to physical dependence. See also alcohol abuse and alcohol dependence.
affective education In general, education that focuses on emotional content or emotional reactions, in contrast to cognitive content. In drug education,
alternatives (to drugs) Assuming that there are motives for drug use, such as the need to be accepted by a group, many prevention and treatment programs
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teach alternative methods for satisfying these motives; may include activities such as relaxation or dancing. Alzheimer’s disease A progressive neurological disease that occurs primarily in the elderly. It causes loss of memory and then progressively impairs more aspects of intellectual and social functioning. Large acetylcholine-containing neurons of the brain are damaged in this disease. Amanita muscaria The fly agaric mushroom, widely used in ancient times for its hallucinogenic properties. amotivational syndrome A hypothesized loss of motivation that has been attributed to chronic marijuana use. amphetamine A synthetic CNS stimulant and sympathomimetic. anabolic Promoting constructive metabolism; building tissue. anabolic steroids Substances that increase anabolic (constructive) metabolism, one of the functions of male sex hormones. The result is increased muscle mass. analgesic Pain-relieving. An analgesic drug produces a selective reduction of pain, whereas an anesthetic reduces all sensation. anandamide A naturally occurring brain chemical with marijuana-like properties. androgenic Masculinizing. anesthetic Sense-deadening. An anesthetic drug reduces all sensation, whereas an analgesic drug reduces pain. angel dust A street name for phencyclidine (PCP) when sprinkled on plant material. anhedonia Lack of emotional response; especially an inability to experience joy or pleasure. animism The belief that objects and plants contain spirits that move and direct them.
antecedents In the context of Chapter 1, behaviors or individual characteristics that can be measured before drug use and might therefore be somewhat predictive of drug use. These are not necessarily causes of the subsequent drug use. anticonvulsant A drug that prevents or reduces epileptic seizures. antidepressant A group of drugs used in treating depressive disorders. The MAO inhibitors, the tricyclics, and the SSRIs are the major examples. antihistamines A group of drugs that act by antagonizing the actions of histamine at its receptors. Used in cold and sinus remedies and in OTC sedatives and sleep aids. anti-inflammatory Reducing the local swelling, inflammation, and soreness caused by injury or infection. Aspirin has anti-inflammatory properties. antipsychotics A group of drugs used to treat psychotic disorders, such as schizophrenia. Also called neuroleptics or major tranquilizers. antipyretic Fever-reducing. Aspirin is a commonly used antipyretic. antitussive Cough-reducing. Narcotics have this effect. OTC antitussives generally contain dextromethorphan. anxiety disorders Mental disorders characterized by excessive worry, fears, avoidance, or a sense of impending danger. At pathological levels, these disorders can be debilitating. anxiolytics Drugs, such as Valium, used in the treatment of anxiety disorders. Literally, “anxiety-dissolving.” aphrodisiac Any substance that is said to promote sexual desire. aspirin Originally Bayer’s brand name for acetylsalicylic acid, now a generic name for that chemical. assassin The story is that this term for a hired killer is derived from a hashish-using cult, the hashshiyya. ataxia Loss of coordinated movement; for example, the staggering gait of someone who has consumed a large amount of alcohol.
Antabuse Brand name for disulfiram, a drug that interferes with the normal metabolism of alcohol, so that a person who drinks alcohol after taking disulfiram will become quite ill. Antabuse interferes with the enzyme aldehyde dehydrogenase, so that there is a buildup of acetaldehyde, the first metabolic product of alcohol.
attention-deficit hyperactivity disorder A learning disability accompanied by hyperactivity. More common in male children. This DSM-IV-TR diagnostic category replaces hyperkinetic syndrome and minimal brain dysfunction.
antagonist A substance that prevents the effects of a neurotransmitter on the postsynaptic cell.
autonomic nervous system The branch of the peripheral nervous system that regulates the visceral,
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www.mhhe.com/hart13e or automatic (“involuntary”) functions of the body, such as heart rate and intestinal motility. In contrast to the somatic, or voluntary, nervous system. axon A region of a neuron that extends from the cell body and is responsible for conducting the electrical signal to the presynaptic terminals. B BAC Blood alcohol concentration, also called blood alcohol level (BAL). The proportion of blood that consists of alcohol. For example, a person with a BAC of 0.10 percent has alcohol constituting one-tenth of 1 percent of the blood and is legally intoxicated in all states.
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and electrical attractions between a specific molecule and its receptor, so that there is a much higher probability that the receptor will be occupied by its proper molecule than by other molecules. biopsychosocial A theory or perspective that relies on the interaction of biological, individual psychological, and social variables. bipolar disorder One of the major mood disorders. Periods of mania and periods of depression have occurred in the same individual. Also called manicdepressive illness.
balanced placebo A research design in which alcohol is compared with a placebo beverage, and subjects either believe they are drinking alcohol or believe they are not.
blackout A period of time during which a person was behaving, but of which the person has no memory. The most common cause of this phenomenon is excessive alcohol consumption, and blackouts are considered to indicate pathological drinking.
barbiturate A major class of sedative-hypnotic drugs, including amobarbital and sodium pentothal.
black tar A type of illicit heroin usually imported from Mexico.
basal ganglia A subcortical brain structure containing large numbers of dopamine synapses. Responsible for maintaining proper muscle tone as a part of the extrapyramidal motor system. Damage to the basal ganglia, as in Parkinson’s disease, produces muscular rigidity and tremors.
blood alcohol concentration A measure of the concentration of alcohol in the blood, expressed in grams per 100 ml (percentage).
behavioral tolerance Repeated use of a drug can lead to a diminished effect of the drug (tolerance). When the diminished effect occurs because the individual has learned to compensate for the effect of the drug, it is called behavioral tolerance. For example, a novice drinker might be unable to walk with a BAC of 0.20 percent, whereas someone who has practiced walking while intoxicated would be able to walk fairly well at the same BAC. behavioral toxicity Refers to the fact that a drug can be toxic because it impairs behavior and amplifies the danger level of many activities. The effect of alcohol on driving is an example. benzodiazepine The group of drugs that includes Valium (diazepam) and Librium (chlordiazepoxide). They are used as anxiolytics or sedatives, and some types are used as sleeping pills. bhang A preparation of cannabis (marijuana) that consists of the whole plant, dried and powdered. The weakest of the forms commonly used in India. binding The interaction between a molecule and a receptor for that molecule. Although the molecules float onto and off the receptor, there are chemical
blood-brain barrier Refers to the fact that many substances, including drugs, that can circulate freely in the blood do not readily enter the brain tissue. The major structural feature of this barrier is the tightly jointed epithelial cells lining blood capillaries in the brain. Drug molecules cannot pass between the cells but must instead go through their membranes. Small molecules and molecules that are lipid- (fat-) soluble cross the barrier easily. Obviously, all psychoactive drugs must be capable of crossing the blood-brain barrier. brain stem The medulla oblongata, pons, and midbrain. Located between the spinal cord and the forebrain, and generally considered to contain the “oldest” (in an evolutionary sense) and most primitive control centers for such basic functions as breathing, swallowing, and so on. brand name The name given to a drug by a particular manufacturer and licensed only to that manufacturer. For example, Valium is a brand name for diazepam. Other companies may sell diazepam, but HoffmanLaRoche, Inc., owns the name Valium. C caffeinism Excessive use of caffeine. Camellia sinesis The plant from which tea is made.
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Cannabis Genus of plants known as marijuana or hemp. Includes C. indica and C. sativa.
comatose A state of unconsciousness from which the individual cannot be aroused.
carbon monoxide A poisonous gas found in cigarette smoke.
congeners In general, members of the same group. With respect to alcohol, the term refers to other chemicals (alcohols and oils) that are produced in the process of making a particular alcoholic beverage.
catheter A piece of plastic or rubber tubing that is inserted or implanted into a vein or other structure. central nervous system Brain and spinal cord. charas A preparation of cannabis, or marijuana, that is similar to hashish. The most potent form of marijuana commonly used in India. chemical name For a drug, the name that is descriptive of its chemical structure. For example, the chemical name sodium chloride is associated with the generic name table salt, of which there may be several brand names, such as Morton’s. chipper An individual who uses heroin occasionally. chlorpheniramine maleate A common over-thecounter antihistamine found in cold products. chronic Occurring over time. Chronic drug use is long-term use; chronic drug effects are persistent effects produced by long-term use. chronic obstructive lung disease A group of disorders that includes emphysema and chronic bronchitis. Cigarette smoking is a major cause of these disorders. cirrhosis A serious, largely irreversible, and frequently deadly disease of the liver. Usually caused by chronic heavy alcohol use. club drugs Drugs associated with use at all-night dance parties, known as “raves,” held in dance clubs, abandoned warehouses, and increasingly in more traditional nightclubs as the rave-party generation moves into its 20s. The drugs most commonly included in this group include the hallucinogen MDMA and the depressants GHB and Rohypnol. coca The plant Erythroxylon coca, from which cocaine is derived. Also refers to the leaves of this plant. cocaethylene A potent stimulant formed when cocaine and alcohol are used together. cocaine A CNS stimulant and local anesthetic; the primary active chemical in coca. cocaine hydrochloride The most common form of pure cocaine; it is stable and water soluble. coca paste A crude, smokable extract derived from the coca leaf in the process of making cocaine. codeine A narcotic chemical present in opium.
controlled drinking The concept that individuals who have been drinking pathologically can be taught to drink in a controlled, nonpathological manner. controlled substance A term coined for the 1970 federal law that revised previous laws regulating narcotics and dangerous drugs. Heroin and cocaine are examples of controlled substances. correlate A variable that is statistically related to some other variable, such as drug use. crack Street name for a smokable form of cocaine. Also called rock. crank Street name for illicitly manufactured methamphetamine. crystal meth Street term for a form of methamphetamine crystals, also called ice. cumulative effects Drug effects that increase with repeated administrations, usually due to the buildup of the drug in the body. CYP450 Cytochrome P450 refers to a group of enzymes found in the liver that are responsible for metabolizing foreign chemicals, including most drugs.
D DARE Drug Abuse Resistance Education, the most popular prevention program in schools. date-rape drug A substance given to someone without her knowledge to cause unconsciousness in order to have nonconsensual sex. Rohypnol and GHB have become known for such use. A 1996 U.S. law provides serious penalties for using drugs in this manner. Datura A plant genus that includes many species used for their hallucinogenic properties. These plants contain anticholinergic chemicals. DAWN Drug Abuse Warning Network, a federal government system for reporting drug-related medical emergencies and deaths. DEA United States Drug Enforcement Administration, a branch of the Department of Justice.
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www.mhhe.com/hart13e delirium tremens Alcohol withdrawal symptoms, including tremors and hallucinations. demand reduction Efforts to control drug use by reducing the demand for drugs, as opposed to efforts aimed at reducing the supply of drugs. Demand reduction efforts include education and prevention programs, as well as increased punishments for drug users. dendrite Treelike region of a neuron that extends from the cell body and contains in its membrane receptors that recognize and respond to specific chemical signals. depolarized When the membrane potential is less polarized. depressant Any of a large group of drugs that generally slow activity in the CNS and at high doses induce sleep. Includes alcohol, the barbiturates, and other sedative-hypnotic drugs. depression A major type of mood disorder. detoxification The process of allowing the body to rid itself of a large amount of alcohol or another drug. Often the first step in a treatment program. deviance Behavior that is different from established social norms and that social groups take steps to change. dextromethorphan An over-the-counter cough control ingredient. diagnosis The process of identifying the nature of an illness. A subject of great controversy for mental disorders. distillation The process by which alcohol is separated from a weak alcohol solution to form more concentrated distilled spirits. The weak solution is heated, and the alcohol vapors are collected and condensed to a liquid form. dopamine A neurotransmitter found in the basal ganglia and other regions of the brain. dose-response curve A graph showing the relationship between the size of a drug dose and the size of the response (or the proportion of subjects showing the response). double-blind procedure A type of experiment in which the patients and those evaluating them do not know which patients are receiving a placebo and which are receiving the test drug. dronabinol The generic name for prescription THC in oil in a gelatin capsule.
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drug Any substance, natural or artificial, other than food, that by its chemical nature alters structure or function in the living organism. drug abuse The use of a drug in such a manner or in such amounts or in situations such that the drug use causes problems or greatly increases the chance of problems occurring. drug dependence A state in which a person uses a drug so frequently and consistently that the individual appears to need the drug to function. This may take the form of physical dependence, or behavioral signs may predominate (e.g., unsuccessful attempts to stop or reduce drug use). drug disposition tolerance The reduced effect of a drug, which can result from more rapid metabolism or excretion of the drug. drug misuse The use of prescribed drugs in greater amounts than, or for purposes other than, those prescribed by a physician or dentist. DSM-IV-TR Diagnostic and Statistical Manual of Mental Disorders, fourth edition text revised, published by the American Psychiatric Association. It has become a standard for naming and distinguishing among mental disorders.
E Ecstasy Street name for the hallucinogen MDMA. Also called “XTC.” ECT Electroconvulsive therapy, or electroconvulsive shock treatment. A procedure in which an electrical current is passed through the head, resulting in an epileptic-like seizure. Although this treatment is now used infrequently, it is still considered to be the most effective and rapid treatment for severe depression. ED50 The effective dose for half the subjects in a drug test. effective dose The dose of a drug that produces a certain effect in some percentage of the subjects. For example, an ED50 produces the effect in 50 percent of the subjects. Note that the dose will depend on the effect that is monitored. emphysema A chronic lung disease in which tissue deterioration results in increased air retention and reduced exchange of gases. The result is difficulty breathing and shortness of breath. An example of a chronic obstructive lung disease, often caused by smoking.
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endorphins Morphine-like chemicals that occur naturally in the brains and pituitary glands of humans and other animals. There are several proper endorphins, and the term is also used generically to refer to both the endorphins and the enkephalins. enkephalins Morphine-like chemicals that occur naturally in the brains and adrenal glands of humans and other animals. The enkephalins are smaller molecules than the endorphins. enzyme A large, organic molecule that works to speed up or help along a specific chemical reaction. Enzymes are found in brain cells, where they are needed for most steps in the synthesis of neurotransmitter molecules. They are also found in the liver, where they are needed for the metabolism of many drug molecules. ephedrine A drug derived from the Chinese medicinal herb ma huang and used to relieve breathing difficulty in asthma. A sympathomimetic from which amphetamine was derived. epilepsy A disorder of the nervous system in which recurring periods of abnormal electrical activity in the brain produce temporary malfunction. There might or might not be loss of consciousness or uncontrolled motor movements (seizures). ergogenic Energy-producing. Refers to drugs or other methods (e.g., blood doping) designed to enhance an athlete’s performance. ergotism A disease caused by eating grain infected with the ergot fungus. There are both psychological and physical manifestations. F FAS Fetal alcohol syndrome. FDA United States Food and Drug Administration. fen-phen A combination of two prescription weightcontrol medications, fenfluramine and phentermine. No longer prescribed due to concerns with toxicity to heart valves. fermentation The process by which sugars are converted into grain alcohol through the action of yeasts. fetal alcohol effect Individual developmental abnormalities associated with the mother’s alcohol use during pregnancy. fetal alcohol syndrome Facial and developmental abnormalities associated with the mother’s alcohol use during pregnancy.
flashback An experience reported by some users of LSD in which portions of the LSD experience recur at a later time without the use of the drug. fly agaric mushroom Amanita muscaria, a hallucinogenic mushroom that is also considered poisonous. freebase In general, when a chemical salt is separated into its basic and acidic components, the basic component is referred to as the free base. Most psychoactive drugs are bases that normally exist in a salt form. Specifically, the salt cocaine hydrochloride can be chemically extracted to form the cocaine free base, which is volatile and can therefore be smoked. functional disorder A mental disorder for which there is no known organic cause. Schizophrenia is a form of psychosis that is considered to be a functional disorder. G GABA An inhibitory neurotransmitter found in most brain regions; gamma-aminobutyric acid. gamma hydroxybutyrate (GHB) CNS depressant, produced naturally in small amounts in the human brain; has been used recreationally and, in combination with alcohol, has some reputation as a date-rape drug; chemically related to GABA. ganja A preparation of cannabis (marijuana) in which the most potent parts of the plant are used. gateway substances Substances, such as alcohol, tobacco, and sometimes marijuana, that most users of illicit substances will have tried before their first use of cocaine, heroin, or other less widely used illicit drugs. generic name For drugs, a name that specifies a particular chemical without being chemically descriptive or referring to a brand name. As an example, the chemical name sodium chloride is associated with the generic name table salt, of which there may be several brand names, such as Morton’s. glia Brain cells that provide firmness and structure to the brain, get nutrients into the system, eliminate waste, form myelin, and create the blood-brain barrier. glutamate An excitatory neurotransmitter found in most brain regions. GRAE “Generally recognized as effective”; a term defined by the FDA with reference to the ingredients found in OTC drugs (see also GRAS).
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www.mhhe.com/hart13e GRAHL “Generally recognized as honestly labeled” (see also GRAE and GRAS). grain neutral spirits Ethyl alcohol distilled to a purity of 190 proof (95 percent). grand mal An epileptic seizure that results in convulsive motor movements and loss of consciousness. GRAS “Generally recognized as safe”; a term defined by the FDA with reference to food additives and the ingredients found in OTC drugs. H hallucinogen A drug, such as LSD or mescaline, that produces profound alterations in perception. hashish A potent preparation of concentrated resin from the Cannabis plant. hash oil A slang term for oil of cannabis, a liquid extract from the marijuana plant. henbane A poisonous plant containing anticholinergic chemicals and sometimes used for its hallucinogenic properties. Hyoscyamus niger. heroin Originally Bayer’s name for diacetylmorphine, a potent narcotic analgesic synthesized from morphine. HIV Human immunodeficiency virus. The infectious agent responsible for AIDS. homeostasis A state of physiological balance maintained by various regulatory mechanisms; body functions such as blood pressure and temperature must be maintained within a certain range.
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I ibogaine A hallucinogen that has been shown to reduce self-administration of cocaine and morphine in rats and is proposed to reduce craving in drug addicts. ibuprofen An aspirin-like analgesic and antiinflammatory. ice The street name for crystals of methamphetamine hydrochloride. illicit drug A drug that is unlawful to possess or use. IND Approval to conduct clinical investigations on a new drug, filed with the FDA after animal tests are complete. indole A type of chemical structure. The neurotransmitter serotonin and the hallucinogen LSD both contain an indole nucleus. inhalants Any of a variety of volatile solvents or other products that can be inhaled to produce intoxication. insomnia Inability to sleep. The most common complaint is difficulty falling asleep. Often treated with a hypnotic drug. intramuscular A type of injection in which the drug is administered into a muscle. intravenous (IV) A type of injection in which the drug is administered into a vein. L
hooka A water pipe, often with more than one mouthpiece. Used to smoke tobacco or marijuana.
laissez-faire A theory that government should not interfere with business or other activities.
human growth hormone A pituitary hormone responsible for some types of giantism.
LD50 The lethal dose for half the animals in a test.
hyperactive Refers to a disorder characterized by short attention span and a high level of motor activity. The DSM-IV-TR term is attention-deficit hyperactivity disorder. hyperpolarized When the membrane potential is more negative. hypnotic Sleep-inducing. For drugs, refers to sleeping preparations. hypodermic syringe A device to which a hollow needle can be attached, so that solutions can be injected through the skin. hypothalamus A group of nuclei found at the base of the brain, just above the pituitary gland.
lethal dose The dose of a drug that produces a lethal effect in some percentage of the animals on which it is tested. For example, LD50 is the dose that would kill 50 percent of the animals to which it was given. leukoplakia A whitening and thickening of the mucous tissues of the mouth. The use of chewing tobacco is associated with an increase in leukoplakia, considered to be a “precancerous” tissue change. limbic system A system of various brain structures that are involved in emotional responses. lipid solubility The tendency of a chemical to dissolve in oils or fats, as opposed to in water. lipophilic The extent to which chemicals can be dissolved in oils and fats.
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lithium A highly reactive metallic element, atomic number 3. Its salts are used in the treatment of mania and bipolar disorder. longitudinal study A study done over a period of time (months or years). look-alikes Drugs sold legally, usually through the mail, that are made to look like controlled, prescriptiononly drugs. The most common types contain caffeine and resemble amphetamine capsules or tablets.
bodies in the midbrain and their terminals in the forebrain, on various structures associated with the limbic system. Believed by some theorists to be important in explaining the therapeutic effects of antipsychotic medications. Also believed by some theorists to be important for many types of behavioral reinforcers. metabolism (of drugs) The breakdown or inactivation of drug molecules by enzymes, often in the liver. metabolite A product of enzyme action on a drug.
M ma huang A Chinese herb containing ephedrine, which is a sympathomimetic drug from which 0 amphetamine was derived. major depression A serious mental disorder characterized by a depressed mood. A specific diagnostic term in the DSM-IV-TR. malting The process of wetting a grain and allowing it to sprout, to maximize its sugar content before fermentation to produce an alcoholic beverage. mandrake Mandragora officinarum, a plant having a branched root that contains anticholinergic chemicals. Now classed among the other anticholinergic hallucinogens, this plant was widely believed to have aphrodisiac properties. marijuana Also spelled marihuana; dried leaves of the Cannabis plant. Marinol The brand name for prescription THC in oil in a gelatin capsule. MDMA Methylenedioxy methamphetamine, a catechol hallucinogen related to MDA. Called “Ecstasy” or “XTC” on the street. medial forebrain bundle A group of neuron fibers that projects from the midbrain to the forebrain, passing near the hypothalamus. Now known to contain several chemically and anatomically distinct pathways, including dopamine and norepinephrine pathways. medical model With reference to mental disorders, a model that assumes that abnormal behaviors are symptoms resulting from a disease. mental illness A term that, to some theorists, implies acceptance of a medical model of mental disorders. mescaline The active hallucinogenic chemical in the peyote cactus. mesolimbic dopamine pathway A group of dopamine-containing neurons that have their cell
metabolize To break down or inactivate a neurotransmitter (or a drug) through enzymatic action. methadone A long-lasting synthetic opioid; commonly used in the long-term treatment for opioid dependence. methadone maintenance A program for treatment of narcotic addicts in which the synthetic drug methadone is provided to the addicts in an oral dosage form, so that they can maintain their addiction legally. methylphenidate A stimulant used in treating ADHD; brand name Ritalin. Mexican brown A form of heroin that first appeared on American streets in the mid-1970s. Because the heroin is made from the hydrochloride salt of morphine, it is brown in its pure form. moist snuff A type of oral smokeless tobacco that is popular among young American men. A “pinch” of this finely chopped, moistened, flavored tobacco is held in the mouth, often between the lower lip and the gum. monoamine A class of chemicals characterized by a single amine group; monoamine transmitters include dopamine, norepinephrine, and serotonin. monoamine oxidase (MAO) inhibitor A drug that acts by inhibiting the enzyme monoamine oxidase (MAO). Used as an antidepressant. mood disorder Mental disorders characterized by depressed or manic symptoms. morphine A narcotic; the primary active chemical in opium. Heroin is made from morphine. morphinism An older term used to describe dependence on the use of morphine. motivational interviewing A technique for encouraging alcoholics or addicts to seek treatment by first assessing their degree of dependence and then discussing the assessment results. Direct confrontation is avoided.
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www.mhhe.com/hart13e N naloxone An opioid antagonist used in treating alcoholism. narcolepsy A form of sleep disorder characterized by bouts of muscular weakness and falling asleep suddenly and involuntarily. The most common treatment employs stimulant drugs such as amphetamine to maintain wakefulness during the day. narcotic Opioid (in pharmacology terms), or a drug that is produced or sold illegally (in legal terms); in the United States, a “controlled substance.” narcotic antagonists Drugs that can block the actions of narcotics. Native American Church A religious organization active among American Indians, in which the hallucinogenic peyote cactus is used in conjunction with Christian religious themes. NDA In FDA procedures, a New Drug Application. This application, demonstrating both safety and effectiveness of a new drug in both animal and human experiments, must be submitted by a drug company to the FDA before a new drug can be marketed. neuroleptic A general term for the antipsychotic drugs (also called major tranquilizers). neuron Brain cell that analyzes and transmits information via chemical and electrical signals. neurotransmitter A chemical messenger that is released by one neuron and that alters the electrical activity in another neuron; its effects are brief and local.
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nonspecific effects Effects of a drug that are not changed by changing the chemical makeup of the drug. Also referred to as placebo effects. norepinephrine A neurotransmitter that might be important for regulating waking and appetite. NORML National Organization for the Reform of Marijuana Laws. NSAIDs Nonsteroidal anti-inflammatory drugs, such as ibuprofen and naproxen. nucleus accumbens A collection of neurons in the forebrain thought to play an important role in emotional reactions to events. nucleus basalis A group of large cell bodies found just below the basal ganglia and containing acetylcholine. These cells send terminations widely to the cerebral cortex. In Alzheimer’s disease, there is a loss of these neurons and a reduction in the amount of acetylcholine in the cortex. O off-label Use of a prescription drug to treat a condition for which the drug has no received U.S. FDA approval. opioid One of a group of drugs similar to morphine, used medically primarily for their analgesic effects. Opioids include drugs derived from opium and synthetic drugs with opium-like effects.
Nicotiana Any of several types of tobacco plant, including N. tobacum and N. rustica.
opioid antagonist Any of several drugs that are capable of blocking the effects of opioids. Used in emergency medicine to treat overdose and in some addiction treatment programs to block the effect of any illicit opioid that might be taken. Nalorphine and naltrexone are examples.
nicotine The chemical contained in tobacco that is responsible for its psychoactive effects and for tobacco dependence.
opium A sticky raw substance obtained from the seed pods of the opium poppy and containing the narcotic chemicals morphine and codeine.
nigrostriatal dopamine pathway A group of dopamine-containing neurons that have their cell bodies in the substantia nigra of the midbrain and their terminals in the corpus striatum (basal ganglia), which is part of the extrapyramidal motor system. It is this pathway that deteriorates in Parkinson’s disease and on which antipsychotic drugs act to produce side effects resembling Parkinson’s disease.
organic disorder For mental disorders, those with a known physical cause (e.g., psychosis caused by long-term alcohol use).
nitrosamines A group of organic chemicals, many of which are highly carcinogenic. At least four are found only in tobacco, and these might account for much of the cancer-causing property of tobacco.
OTC Over-the-counter. OTC drugs are those drugs that can be purchased without a prescription. P Papaver somniferum The opium poppy. paraphernalia In general, the equipment used in some activity. Drug paraphernalia include such items as syringes, pipes, scales, or mirrors.
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parasympathetic The branch of the autonomic nervous system that has acetylcholine as its neurotransmitter and, for example, slows the heart rate and activates the intestine. Parkinson’s disease A degenerative disease of the extrapyramidal motor system, specifically involving damage to the nigrostriatal dopamine system. Early symptoms include muscular rigidity, tremors, a shuffling gait, and a masklike face. Occurs primarily in the elderly. passive smoking The inhalation of tobacco smoke from the air by nonsmokers. patent medicines Proprietary medicines. Originally referred to medicines that were, in fact, treated as inventions and patented in Great Britain. In America, the term came to refer to medicines sold directly to the public. PCP Phenycyclidine; 1-(1-phenylcyclohexl) piperidine. A drug with hallucinogenic properties that was originallly developed as an anesthetic; it is not legally available for human use. This hallucinogen is often referred to as angel dust. PDR Physician’s Desk Reference, a book listing all prescription drugs and giving prescribing information about each. Updated yearly. pekoe A grade of tea. peptide A class of chemicals made up of sequences of amino acids. Enkephalins are small peptides containing only five amino acids, whereas large proteins may contain hundreds.
placebo An inactive drug, often used in experiments to control for nonspecific effects of drug administration. postsynaptic Refers to structures associated with the neural membrane on the receiving side of a synapse. potency Measured by the amount of a drug required to produce a given effect. precursor Something that precedes something else. In biochemistry, a precursor molecule may be acted upon by an enzyme and changed into a different molecule. For example, the dietary amino acid tryptophan is the precursor for the neurotransmitter serotonin. prodrugs Drugs that are administered in an inactive form and become effective after they are chemically modified in the body by enzymes. Prohibition The period 1920–1933, during which the sale of alcoholic beverages was prohibited in the United States. proof A measure of a beverage’s alcohol content; twice the alcohol percentage. proprietary A medicine that is marketed directly to the public. Also called OTC, patent, or nonprescription medicines. prostaglandins Local hormones, some of which are synthesized in response to cell injury and are important for initiating pain signals. Aspirin and similar drugs inhibit the formation of prostaglandins.
peyote A hallucinogenic cactus containing the chemical mescaline.
protective factors Behaviors, attitudes, or situations that correlate with low rates of deviant behavior, including use of illicit drugs. Examples include commitment to school, religiosity, and having parents who communicate opposition to drug use.
phantastica Hallucinogens that create a world of fantasy.
protein binding The combining of drug molecules with blood proteins.
pharmacodynamic tolerance Reduced effectiveness of a drug resulting from altered nervous system sensitivity.
psilocybin The active hallucinogenic chemical in Psilocybe mushrooms.
phenothiazines A group of chemicals that includes several antipsychotic medications.
psychedelic Another name for hallucinogenic drugs. Has a somewhat positive connotation of mind viewing or mind clearing.
phenylpropanolamine (PPA) Until 2000, an active ingredient in OTC weight-control products.
psychoactive A term used to describe drugs that have their principal effect on the CNS.
physical dependence Defined by the presence of a consistent set of symptoms when use of a drug is stopped. These withdrawal symptoms imply that homeostatic mechanisms of the body had made adjustments to counteract the drug’s effects and without the drug the system is thrown out of balance.
psychological dependence Behavioral dependence, indicated by a high rate of drug use, craving for the drug, and a tendency to relapse after stopping use. psychopharmacology Science that studies the behavioral effects of drugs.
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www.mhhe.com/hart13e psychosis A type of mental disorder characterized by a loss of contact with reality and by deterioration in social and intellectual functioning. psychotomimetic Another name for hallucinogenic drugs. Has a negative connotation of mimicking psychosis. Q quid A piece of something to be chewed, such as a wad of chewing tobacco. R receptors Specialized cell structures that recognize and respond to signals from specific chemicals (neurotransmitters or drugs). reinforcement The process of strengthening a behavioral tendency by presenting a stimulus contingent on the behavior. For example, the tendency to obtain and take a drug might be strengthened by the stimulus properties of the drug that occur after it is taken, thus leading to psychological dependence.
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sedative A drug used to relax, tranquilize, or calm a person, reducing stress and excitement. semipermeable Allowing some, but not all, chemicals to pass. serotonin A neurotransmitter found in the raphe nuclei that might be important for impulsivity and depression. shisha Sweetened, flavored tobacco for use in a hooka. side effects Unintended drug effects that accompany the desired therapeutic effect. sidestream smoke Smoke that comes from the ash of a cigarette or cigar. sinsemilla A process for growing marijuana that is especially potent in its psychological effects because of a high THC content; from the Spanish for “without seeds.” smokeless tobacco Various forms of chewing tobacco and snuff. social influence model A prevention model adapted from successful smoking-prevention programs.
reuptake One process by which neurotransmitter chemicals are removed from synapses. The chemical is taken back up into the cell from which it was released.
somatic system The part of the nervous system that controls the voluntary, skeletal muscles, such as the large muscles of the arms and legs.
Reye’s syndrome A rare brain infection that occurs almost exclusively in children and adolescents. There is some evidence that it is more likely to occur in children who have been given aspirin during a bout of flu or chicken pox.
specific effects Those effects of a drug that depend on the amount and type of chemical contained in the drug.
risk factors Behaviors, attitudes, or situations that correlate with, and might indicate the development of, a deviance-prone lifestyle that includes drug or alcohol abuse. Examples are early alcohol intoxification, absence from school, and perceived peer approval of drug use. rock Another street name for crack, a smokable form of cocaine. Rohypnol (flunitrazepam) A benzodiazepine hypnotic; not sold legally in the United States and known as the “date-rape drug.” S safety margin Dose range between an acceptable level of effectiveness and the lowest toxic dose. salicylate A class of chemicals that includes aspirin. schizophrenia A chronic psychotic disorder for which the cause is unknown.
speed A street term used at one time for cocaine, then for injectable amphetamine, and later for all types of amphetamine. Probably shortened from speedball. SSRI Selective serotonin reuptake inhibitor; a class of antidepressants that includes Prozac. stages of change Theoretical description of the cognitive stages through which an addict would go in moving from active use to treatment and abstinence: precontemplation, contemplation, preparation, action, and maintenance. stimulant Any of a group of drugs that has the effect of reversing mental and physical fatigue. subcutaneous Under the skin. A form of injection in which the needle penetrates through the skin (about 3/8 inch) but does not enter a muscle or vein. sympathetic nervous system The branch of the autonomic nervous system that contains norepinephrine as its neurotransmitter and, for example, increases heart rate and blood pressure.
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sympathomimetic Any drug that stimulates the sympathetic branch of the autonomic nervous system—for example, amphetamine. symptom In medical terms, an abnormality that indicates a disease. When applied to abnormal behavior, seems to imply a medical model in which an unseen disease causes the abnormal behavior. synapse The space between neurons. synesthesia A phenomenon in which the different senses become blended or mixed—for example, a sound is “seen.” Might be reported by a person taking hallucinogens.
time course Timing of the onset, duration, and termination of a drug’s effect in the body. tolerance The reduced effectiveness of a drug after repeated administration. toxic Poisonous, dangerous. transporter Mechanism in the nerve terminal membrane responsible for removing neurotransmitter molecules from the synapse by taking them back into the neuron. tricyclics A group of chemicals used in treating depression.
synthesis The formation of a chemical compound. For example, some neurotransmitter chemicals must be synthesized within the neuron by the action of enzymes on precursors.
truth serum Any drugs used to “loosen the tongue,” in association with either psychotherapy or interrogation. Although people might speak more freely after receiving some drugs, there is no guarantee that anything they say is true.
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tachyphylaxis A rapid form of tolerance in which a second dose of a drug has a smaller effect than a first dose taken only a short time before.
uptake The process by which a cell expends energy to concentrate certain chemicals within itself. For example, precursor substances to be synthesized into neurotransmitters must be taken up by the neuron.
tar With regard to tobacco, a complex mixture of chemicals found in cigarette smoke. After water, gases, and nicotine are removed from the smoke, the remaining residue is considered to be tar. tardive dyskinesia Movement disorders that appear after several weeks or months of treatment with antipsychotic drugs and that usually become worse if use of the drug is discontinued. temperance With reference to alcohol, temperance originally meant avoiding hard liquor and consuming beer and wine in moderation. Eventually the temperance movement adopted complete abstinence as its goal and prohibition as the means. tetrahydrocannabinol The most active of the many chemicals found in cannabis (marijuana). THC Tetrahydrocannabinol.
V values clarification A type of affective education that avoids reference to drugs but focuses on helping students recognize and express their own feelings and beliefs. W Wernicke-Korsakoff syndrome Chronic mental impairments produced by heavy alcohol use over a long period of time. withdrawal syndrome The set of symptoms that occur reliably when someone stops taking a drug; also called abstinence syndrome.
theobromine A mild stimulant similar to caffeine and found in chocolate; a xanthine.
X
theophylline A mild stimulant similar to caffeine and found in tea; a xanthine.
xanthine The chemical class that includes caffeine, theobromine, and theophylline.
therapeutic index (TI) Ratio of the lethal dose to the effective dose for half the animals in an experiment (LD50/ED50).
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Credits Photo Credits Chapter 1 p. 2, Ryan McVay/Getty Images; p. 3L, Emma Lee/Life File/Getty Images; p. 3R, Getty Images; p. 5, Brand X Pictures; p. 11, © The McGraw-Hill Companies, Inc./Gary He, photographer; p. 17, © Brand X Pictures/ PunchStock; p. 19, © BananaStock/PunchStock Chapter 2 p. 25, Brand X Pictures; p. 28, Photodisc Collection/Getty Images; p. 30, © Annie Griffiths Belt/ Corbis; p. 34, McGraw-Hill Companies, Inc./Gary He, photographer; p. 37, © The McGraw-Hill Companies, Inc./Jill Braaten, photographer; p. 40, © Mikael Karlsson Chapter 3 p. 51, National Library of Medicine; p. 54L, Library of Congress Prints and Photographs Division (09335u); p. 54R, Library of Congress Prints and Photographs Division (3C03376U); p. 59, PhotoLink/Getty Images; p. 61, © The McGraw-Hill Companies, Inc./Jill Braaten, photographer; p. 67, © Royalty-Free/Corbis; p. 74, © Thorne Anderson/Corbis Chapter 4 p. 80, Jim Wehtje/Getty Images;
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p. 250, IMS Communications Ltd./Capstone Design/FlatEarth Images; p. 252, Stockdisc/PunchStock Chapter 11 p. 257, © Ingram Publishing/ SuperStock; p. 258, Ryan McVay/Getty Images; p. 260T, C. Sherburne/PhotoLink/ Getty Images; p. 260B, Jules Frazier/Getty Images; p. 261, S. Meltzer/PhotoLink/ Getty Images; p. 262, PhotoLink/Getty Images; p. 263, Library of Congress Prints and Photographs Division (3A25022U); p. 264, Spike Mafford/Getty Images; p. 265, L. Hobbs/PhotoLink/Getty Images; p. 266, © Royalty-Free/Corbis; p. 267, Library of Congress Prints and Photographs Division (3G12222U); p. 269, © The McGraw-Hill Companies/Jill Braaten, photographer; p. 272, © The McGrawHill Companies/Lars Niki, photographer; p. 273, Ryan McVay/Getty Images Chapter 12 p. 279, © Brand X Pictures/ Punchstock; p. 281, © The McGraw-Hill Companies, Inc./Jill Braaten, photographer;
p. 286, Mitch Hrdlicka/Getty Images; p. 287, © McGraw-Hill Companies/Suzie Ross, Photographer; p. 288, © Royalty-Free/Corbis; p. 297, © The McGraw-Hill Companies, Inc./Christopher Kerrigan, photographer Chapter 13 p. 306, © Botonica/JupiterImages; p. 311, © Steven L. Raymer/Getty Images/National Geographic; p. 312, Drug Enforcement Administration; p. 317, Medioimages/ PictureQuest; p. 325, Photodisc Green/Doug Menuez/Getty Images Chapter 14 p. 331, Drug Enforcement Administration; p. 338, © Bettmann/Corbis; p. 340, Drug Enforcement Administration; p. 343, © IT Stock/ age footstock; p. 345, Courtesy of the author; p. 346, US Fish & Wildlife; p. 348, © Stapleton Collection/ Corbis; p. 350, Drug Enforcement Administration; p. 356, © Steven P. Lynch; p. 358, © Ingram Publishing/AGE Fotostock Chapter 15 p. 365, Drug Enforcement Administration;
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Index A AA. See Alcoholics Anonymous abortion, spontaneous, 222, 246, 274 abstinence, 430 abstinence violation effect, 226 acamprosate, 435, 436 acetaldehyde, 208, 209 acetaminophen, 295, 298 acetic acid, 208 acetylcholine, 85 pathways, 90 acetylsalicylic acid, 292 acquired immune deficiency syndrome (AIDS), 31 alcohol and, 220 action potential, 84–85 addiction, 6, 34 Check Yourself, 47 heroin, 326 introduction of, 199 addictive personality, 38–39 adenosine, 270 S-adenosyl-L-methionine, 285 ADH. See antidiuretic hormone ADHD. See attention-deficit hyperactivity disorder administration inhalation, 114 injection, 113–114 oral, 111, 113 topical, 114 “Advantages of Substituting the Morphia Habit for the Incurably Alcoholic,” 314 advertising, countering, 417–418 Advisory Committee on Smoking and Health, 238 Afghanistan, 74 agonist, 95 maintenance agents, 435 agoraphobia, 174 agranulocytosis, 179 Agriculture Department, U.S., 56
AIDS. See acquired immune deficiency syndrome Air Surgeons Bulletin, 137 alcohol. See also specific alcoholic beverages absorption, 206 abstinence violation effect and, 226 AIDS and, 220 actions mechanisms of, 209 advertising, 194 as anesthetic, 209 anxiety and, 210 behavioral effects of, 210–216 binge drinking, 205 blackouts from, 215 brain damage and, 218–219 cancer and, 220 cognitive factors regarding, 226 college students and, 206 consumption of, per capita, 198 controlled social drinking of, 430 crime and, 42, 215–216 cultural influence on, 203 death from, 216 dehydrogenase, 208 demonization of, 198 dependence, 39, 40, 222–226, 227 detoxification, 222 disease and, 218, 224 distillation, 193–194, 226 distribution, 206–208 dose-response curves for, 107f driving under influence of, 212–213 Drug Abuse Warning Network and, 28 drug tolerance and, 209 erotic films and, 214, 215 fluid balance and, 216 GABA and, 209 gender and, 205–206, 227 genetics and, 226, 227 as “Good Creature of God,” 198
hallucinations from, 223–224 heart and, 219–220 homicide and, 215 hormonal effects and, 216 immune system and, 220 liver response to, 209 metabolizing, 208–209 minimum age to purchase, 202 morality and, 199 myopia, 211–212, 215, 227 opium v., 310 overdose, 216 penile tumescence and, 214 peripheral circulation and, 216 pharmacology, 206–209 pharmacotherapies for, 435–436 physiological effects of, 216 placebo effects and, 211 poisoning, 216 pregnancy and, 222 problem, 198–203 regulation after 1933, 202 relapse, 224 removal of, 208 sexual assault and, 215 sexual behavior and, 214–215 as social excuse, 226 social stress and, 204–205 suicide and, 216 tax, 201, 202–203 tension and, 204–205 time-out, 211–212 toxicity, 216–221 traffic fatalities involving, 212–213, 227 trends in, 12f trends in, U.S., 203–204, 204f vomiting from, 217 withdrawal syndrome, 222–224 alcohol content, blood (BAC), 206, 207t behavior change and, 210–211, 211t estimating, 208, 227 intake and, 208f
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alcohol effect, fetal, 222 alcohol syndrome, fetal (FAS), 221–222, 223, 227 animal research on, 221 criteria for, 221 diagnosing, 222 gender and, 223 alcoholic dementia, 218 family, 39 hepatitis, 219 personality, 225 Alcoholics Anonymous, 224 Alcoholics Anonymous (AA), 38, 430–432 buddy system, 431 court-ordered referrals to, 431 evaluations of, 431 religion and, 225 twelve step program, 431, 433 aldehyde dehydrogenase, 208 allergy medications, 300 Alpert, Richard, 337–338 dismissal of, 338 alpha-methyltryptamine (AMT), 346 alprazolam, 435 alt.psychoactives newsgroup, 299 Alzheimer’s disease, 90 AMA. See American Medical Association Amanita muscaria, 358–360 Ambien, 162 ambrosia, 358 Amendment, 18th, 200–201 repeal of, 202 Amendment, 21st, 202 American football, 394–395 American Medical Association (AMA), 371 American Psychiatric Association, 36 American Revolution, 263 amino acids, 401 amotivational syndrome, 383 amphetamines, 136–148, 148. See also specific amphetamines absorption, 141 action mechanism of, 141 acute toxicity, 147 in American football, 394–395
appetite-depressant effect of, 137 in athletics, 147, 394 in baseball, 396 beneficial uses of, 141–147 calming effect of, 144 chemical structure of, 140–141 chronic toxicity, 147–148 compulsive/repetitive actions and, 148 concern over, 147–148 dependence potential of, 148 depression and, 141–142 development of, 136–137 early uses for, 136–137 effectiveness of, 397 elimination, 141 euphoria from, 141 history of, 136–140 hyperactive children and, 143–144 in 1960’s, 137–139 legal use of, 143 longterm behavioral consequences of, 147 mood and, 142 Olympics and, 394 paranoid psychosis from, 148 paranoid psychotic reactions to, 137 patent for, 136 pharmacology of, 140–141 tablet, 137 violence and, 147 wartime uses of, 137 weight control and, 142–143 AMT. See alpha-methyltryptamine analgesic-antipyretics, 298 analgesics, 269t, 291–296 ingredients in, 296t anandamide, 374 angel dust, 354 anhedonia, 439 Anheuser-Busch, 195 animal research, 25, 59 benzodiazepine, 164 on beta-2 agonists, 403 on fetal alcohol syndrome, 221 opioid, 322 PCP, 352 on serotonin, 90
animism, 331–332 ANS. See nervous system, autonomic Anslinger, Harry, 63, 75, 369–370 Antabuse, 435 antagonist, 95 opioid, 320 therapy, 435 antianxiety drugs, 173 anticonvulsants, 186 hypnotics as, 163 antidepressants, 105, 173, 180–184 action mechanism of, 184 effectiveness of, 106 lag period, 184 sales of, 182 stimulants and, 117 suicide and, 182 antidiuretic hormone (ADH), 216 Anti-Doping Agency, U.S., 395 Anti-Drug Abuse Acts of 1986/1988, 65–69, 130–131 antihistamine, 290, 298 effectiveness of, 299 antipsychotics, 104, 177–180 action mechanism of, 178–179 agranulocytosis and, 179 allergic reactions to, 179 atypical, 178t conventional, 178t introduction of, 188 long-term effectiveness of, 180 photosensitivity and, 179 side effects of, 179–180 treatment effects of, 178 anxiety, 172 alcohol and, 210 disorders, 173, 174 Aqua-Dots, 169 The Arabian Nights, 369 army LSD research, 337 Artificial Paradises (Baudelaire), 369 As Good as It Gets, 173 aspirin, 291–295 action mechanism of, 294–295 anti-inflammatory properties of, 293 antipyretic properties of, 292–293 bleeding time and, 293
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www.mhhe.com/ray13e continued gastrointestinal bleeding and, 294 side effects of, 293 therapeutic dose of, 293 therapeutic use of, 292–293 Assassins, cult of, 371 Association Against Prohibition, 201 ataxia, 107 athletics amphetamines and, 147, 394 banned substances in, 393 caffeine in, 393 cocaine in, 393 historical drug use in, 392–397 international drug testing in, 394 stimulants in, 392–393 atomoxetine, 144 Atropa belladonna, 355 attention-deficit hyperactivity disorder (ADHD), 144 diagnostic criteria for, 145 symptoms of, 146 Avicenna, 309 axon, 83 ayahuasca, 346 B BAC. See alcohol content, blood BALCO Laboratories, 395–396 Balzac, Honoré de, 272 barbital, 154 barbiturates, 153, 154–156. See also specific barbiturates action mechanism, 159 dependence, 156, 163–164 fast-acting, 155 groupings of, 156t short-acting, 155 suicide and, 156 tolerance, 156 basal ganglia, 87 baseball, 396 Baudelaire, Charles, 369 Bayer Laboratories, 291–292 A Beautiful Mind, 173 Bechler, Steve, 282, 398 beer, 194–196 ale, 195 lager, 195 largest selling brands, 195t
© The McGraw−Hill Companies, 2009
INDEX malt liquor, 195 behavior, chemical theories of, 96 belladonna, 355–356, 437 pupil dilation and, 356 Benzedrine, 136 Benzocaine, 290 benzodiazepines, 153, 157–159, 173, 224, 435 animal research and, 164 overdose of, 158 physical dependence of, 158 benzopyrene, 383 beta-2 agonists, 403 Betty Ford Center, 431 Beverly, Robert, 358 bhang, 368 The Bible, 356–357 bipolar disorder, 175 relapses of, 185 Birney’s Catarrh Cure, 53 Biruni, 309 black market steroids, 401 Black Mass, 356 black tar heroin, 318 black tea, 264 blackouts, 215 blockers, 95 starch, 290 blood alcohol content. See alcohol content, blood (BAC) blood proteins, 115 blood-borne diseases, 30–32 blood-brain barrier, 82, 115 in infants, 115 B&M External Remedy, 57 bodybuilding, 404 Bonds, Barry, 395 Boston Tea Party, 263 bourbon, 198 Bourne, Peter, 130 brain alcohol and damage to, 218–219 association areas of, 86 chemical pathways in, 89–91 drugs and, 91–96 major structures of, 86–89, 88f marijuana and damage to, 384 stem, 88 brain-scanning techniques, 38, 96–97 limitations of, 97
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brand names, 102, 119 brandy, 193, 197 Brecher, E.M., 4 British East India Company, 311 bromides, 154 bronchodilation, 375 Buddha, 357 bufotenin, 360 buprenorphine, 438 bupropion, 252, 437 Bureau of International Narcotics and Law Enforcement Affairs, 73 Bureau of Narcotics, 63 Burke, Ken, 127 Bush, George W., 71, 225 C Cade, John, 184 caffeine, 404 action mechanism of, 270 in analgesics, 269t in athletics, 393 behavioral effects of, 272–274 in beverages/food, 266t cancer and, 274 Check Yourself, 277 concern over, 274–275 death from, 275 dependence, 270, 271 in diuretics, 269t headaches and, 272, 273 heart disease and, 274–275 hyperactivity and, 273 panic attacks and, 273 as performance enhancer, 398 pharmacology of, 270–274 physiological effects of, 271–272 reproductive effects and, 274 sobering up with, 274 in soft drinks, 268t in stimulants, 269t time course of, 270 tolerance, 270 caffeinism, 275 calcified lime, 125 calcium acetylhomotaurinate, 435 Camels, 236–237 Caminiti, Ken, 395 camphor, 177 cancan, 259
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cancer, 220 alcohol and, 220 caffeine and, 274 cigarette smoking and, 238 cannabinoids, 373 Cannibas, 365. See also marijuana absorption, 373–374 abuse potential of, 375–376 action mechanism of, 374 active ingredient in, 378 behavioral effects of, 375–378 buyers clubs, 380 distribution, 373–374 elimination, 373–374 history of, 368–373 history of, early, 368–369 in 19th century, 369 medical uses of, 378–381 new science of psychology and, 369 pharmacology of, 373–378 pharmacotherapies, 439 physiological effects of, 374–375 preparations from, 366–368 romantic literature and, 369 Cannibas indica, 366 Cannibas ruderalis, 366 Cannibas sativa, 366 carbamazepine, 60 carbohydrates, 401 Carter, Jimmy, 386 Carter, Rosalynn, 386 cataplexy, 168 catheters, 35 2-CB, 252 CCK. See cholecystokinin “Celebrity Rehab with Dr. Drew,” 431 cell body, 83 Center for Substance Abuse Prevention (CSAP), 421 cereal grains, 193 cerebellum, 374 cerebral atrophy, 384 cerebral cortex, 86 subdivisions of, 87f cerebral trauma, 115 Cerletti, Ugo, 177 champagne, 196 Chantix, 252 charas, 366
Check Yourself addiction, 47 caffeine, 277 consequences, 77 daily mood changes, 189–190 drinking problem, 229 goals/behaviors, 23, 427 hallucinogens, 363 how do drugs work?, 121 memory, 389 natural body cycle, 99 over-the-counter drugs, 303 run the race, 407 sensation-seeking scale, 151 street slang, 329 tobacco awareness, 255 toxicity, 49 Cheek, J. O., 260 Chemical Diversion and Trafficking Act, 67 chemical names, 102 chewing gum, nicotine, 252 chloral hydrate, 154 chlordiazepoxide, 157, 159 chlorpheniramine maleate, 298 chlorpromazine, 177, 350 introduction of, 186 chocolate, 264–266 European introduction of, 265 health warnings, 265 legends surrounding, 264 liquor, 265 milk, 266 preparation of, 265 cholecystokinin (CCK), 290 Chute, Anthony, 233 cigar bars, 243 cigarette smoking, 236–237. See also specific brands in adolescents, 417 advertising of, 238 cancer and, 238 cognitive developmental approach to, 418 current use of, 241 decline in, 253 facial malformations and father’s, 247 filter, 237, 238
hidden costs of, 251 lawsuits regarding, 238–239 low academic performance and, 14 oral gratification from, 250 passive, 244–246 pregnancy and, 246–247 quitting, 251–252 reducing, 416 safer, 240–241 sales of, 239f sidestream smoke from, 245 worldwide, 246 cigars, 236, 242–243 cirrhosis, 219, 220f Civil War, 52 Claviceps purpurea, 333–334 clenbuterol, 403 Clinton, Bill, 12, 13 Clinton, Hilary Rodham, 146 clonidine, 323 clozapine, 179 Le Club de Hachischins, 369 CNS. See nervous system, central coca, 124 paste, 129 wine, 125 Coca-Cola, 125, 266–268 misbranding of, 267 as tonic, 267 trial of, 1911, 267 cocaethylene, 117, 133 cocaine, 54–55, 67, 124–136, 148, 267 absorption, 132 action mechanism of, 132 acute toxicity of, 133 in athletics, 393 beneficial uses of, 132–133 chemical structure of, 132f chronic toxicity of, 133–134 concern for, 133 contemporary legal controls on, 130–132 dangers, 128 dependence potential of, 133–134 early legal controls on, 128–129 early psychiatric uses of, 126–128 elimination of, 132 fame and, 130
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www.mhhe.com/ray13e continued forms of, 129–130 freebasing, 130 friendship and, 135 future of, 135–136 heart muscle and, 133 history of, 124–125 hydrochloride, 129–130 introduction of, 136 as local anesthesia, 125–126, 132–133 media focus on, 130 minimum sentences for, 131 negative publicity for, 129 overuse of, 55 paranoid psychosis from, 133 patterns of use, 135 as performance enhancer, 398 pharmacotherapies, 439 pregnancy and, 134 price of, 74, 135 production of, 135 racial characteristics and, 131t as safe exhilarant, 127 supplies of illicit, 134–135 toxicity, 44 trends in, 12f wealth and, 130 withdrawal symptoms, physical, 134, 439 “Cocaine Lil,” 129 cocoa butter, 265 codeine, 312 antitussive properties of, 322 coffee, 257–261 arabica, 260 commercial roasting of, 260 decaffeinated, 261 economics of, 261 instant, 261 legends surrounding, 257–258 “nerves,” 271 robusta, 260 sexual excitability and, 258 specialty, 259 Cohoba snuff, 345 cold, common, 296–298 treatment of, 298–300 Coleman, Tom, 126 perjury charges, 127 Coleridge, Samuel Taylor, 309 college students
© The McGraw−Hill Companies, 2009
INDEX alcohol and, 206 drug use and, 20 Collier’s, 53 Columbus, Christopher, 232–233 coma, induced, 176 comatose, 107 Communities Mobilizing for Change on Alcohol, 423 Compoz, 290 Comprehensive Drug Abuse Prevention and Control Act of 1970, 64–65 structure of, 64 compulsive behavior, 37 “The Confessions of an English Opium-Eater” (De Quincey), 309–310 congeners, 198, 217 conservatism, 384 Conte, Victor, 395 contingency management, 433–434 “continuum of care,” 412 Controlled Substances Act, 65, 75 Corona, 196 coronaviruses, 297 cotinine, 417 cough suppressants, opioid, 322 Council for Tobacco Research, 238, 243 The Count of Monte Cristo (Dumas), 369 crack, 67, 130 baby, 134 dependence, 66 minimum sentences for, 131 Craig, Elijah, 197 crank, 139 creatine, 403 creativity, 341, 342 crime, 26, 40–43, 44 alcohol and, 42, 215–216 “criminal type,” 41 crystal meth, 139 CSAP. See Center for Substance Abuse Prevention Csikszentmihalyi, Mihaly, 359 2-C-T7, 352 Cuforhedake Brane-Fude, 57 cumulative effects, 111 cyclazocine, 355 Cylert, 145–146
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D DARE. See Drug Abuse Resistance Education Daruma, 261 date-rape drugs, 67, 159, 160, 168 datura, 357–358 DAWN. See Drug Abuse Warning Network De Quincey, Thomas, 309–310 DEA. See Drug Enforcement Agency deactivation, 116–118, 120 death, 28–29, 29t alcohol related, 216 caffeine related, 275 heroin related, 315 nicotine, 248 tobacco related, 244f death penalty, 63 delirium tremens, 223 Delphi, temple at, 357 delta-9-tetrahydrocannabinol (THC), 71, 366 dendrites, 83 denial, 432 dependence, 6, 26, 32–36, 44 alcohol, 39, 40, 222–226, 227 amphetamine, 148 behavioral, 33–34 biological, 38 biopsychosocial perspective on, 40 caffeine, 270, 271 changing views of, 34–35 cocaine, 133–134 crack, 66 diagnostic criteria for, 36, 432 disease and, 40 family and, 39–40 marijuana, 381–382 medical models for, 34–35 medications used to treat, 440 nicotine, 249–251 potential, 37, 38t as spiritual disorder, 440 Valium, 164 views of, 37–40 dependence, physical, 33, 35–36 barbiturate, 156 opioid, 322–324
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dependence, psychological, 33–34, 35–36 barbiturate, 156, 163–164 benzodiazepine, 158 Librium, 163 opioid, 323–324 Valium, 163 Xanax, 164 depersonalization, 341 depressants, 103–104, 153, 169. See also specific depressants overdose of, 169 stimulants and, 117 depression, 175 Dexatrim, 289 Dexedrine, 141 dextromethorphan (DM), 298, 354 abuse of, 299 diacetylmorphine, 312 diagnosis, 171 diazepam, 158, 159, 223 Dickens, Charles, 296 Dietary Supplement Health and Education Act (DSHEA), 60, 281–282 dietary supplements, 60–61. See also specific dietary supplements dangerous, 283–284t health claims of, 281 diethylene glycol, 58 Dilaudid, 439 dimethyltryptamine (DMT), 345–346 Dionysius, 358 disease, 172 alcohol and, 218, 224 dependence and, 40 distilled spirits, 197–198 disulfiram, 435 diterpines, 275 diuretics, 269t DM. See dextromethorphan DMT. See dimethyltryptamine Dolophine, 438 DOM, 350 The Doors of Perception (Huxley), 349 dopamine, 38, 89–90, 92f precursor, 89
dose-response curve, 106 for alcohol, 107f dose-response relationships, 106–109 double-blind procedure, 106 dronabinol, 71, 379, 440 drug combinations, 29 czar, 69 du jour, 4 illicit, 6 law violations, 43, 44 misuse, 6 Drug Abuse Control Amendments of 1965, 64 Drug Abuse Resistance Education (DARE), 418–420 acceptance of, 419 additional programs, 420 beginnings of, 418–419 components of, 419 ineffectiveness of, 420 studies on, 419–420 Drug Abuse Warning Network (DAWN), 27, 30 alcohol and, 28 heroin in, 30 Drug Enforcement Agency (DEA), 64 drug use alternatives to, 415 antecedents of, 16–18 characteristics of, 32 college students and, 20 concern for, 3 correlates of, 13–20 dangers of, 29–30 deviant, 6, 20 education level and, 14–15 experimenting with, 414 extent of, 8–9 flagged, 414 gender and, 14–15 influences on, 20f initiation of, later, 16 knowledge, 413 models for, 19 motives for, 3, 18–20, 21 positive attitude towards, 413 prevention, 18, 411 progression of, 21
protective factors, 13–14 punitive approach to, 416 race and, 14–15 rate of, 21 reducing, 424 religion and, 14 risk factor, 13–14 social decisions about, 411 stereotypes, 15 trends in, 7, 9–13 trends in, social, 13 Drug-Induced Rape Prevention and Punishment Act, 160 drugs, over-the-counter (OTC), 286 Check Yourself, 303 choosing, 300–301 examples of, 288–291 ingredients in, 300t label standards for, 287 number of, 287 prescription drugs v., 287–288 regulation of, 286–287 sedative, 290–291 sleep aid, 290–291 stimulant, 288–289 weight-control, 289–290 drugs, prescription, 29 effectiveness of, 58–59 “free trial” offers of, 162 marketing new, 59–60 media coverage of, 53 off-label, 60 opioid, 318–319 over-the-counter drugs v., 287–288 preclinical investigations of, 59–60 purity of, 56–58 regulation of, 56–61 rules for, 57 safety of, 58 DSHEA. See Dietary Supplement Health and Education Act Dumas, Alexander, 369 Dutch East India Company, 262 E Ebers papyrus, 307 Eclipse, 241 economies, 7 Ecstasy. See MDMA
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www.mhhe.com/ray13e ECT. See electroconvulsive therapy ED. See effective dose Edgewood Arsenal, 337 Edison, Thomas, 236 education, 411 affective, 414–415 drug use and level of, 14–15 normative, 418 effective dose (ED), 108 electroconvulsive therapy (ECT), 177, 184 Elixir Sulfanilamide, 58 Ellis, Havelock, 349 emergency room, visits to, 27–28, 29t emphysema, 251 endorphins, 91, 320 energy drinks, 268–269 hype surrounding, 269 English East India Company, 262 enkephalins, 320–321 entactogens, 332 entheogens, 332 enzymes, 92 action of, 93f CYP450, 117, 118, 155 metabolic, 94f Enzyte, 285 ephedra, 61, 136, 282, 289, 404 ephedrine, 136, 141 as performance enhancer, 398 epilepsies, 163 E.R., 412 ergogenics, 394 ergotism, 334 erotic films, 214, 215 eszopiclone, 162 evil spirits, 7 Excedrin, 269, 273 F facial malformations, 247 fats, 401 burning, 404 fatty liver, 219 FDA. See Food and Drug Administration fear, 31 fentanyl, 319 fermentation, 192, 226 fetal alcohol syndrome. See alcohol syndrome, fetal (FAS)
© The McGraw−Hill Companies, 2009
INDEX fever, 300 “fight or flight” response, 86 Financial Crimes Enforcement Network, 73 flashbacks, 342 flow, 359 flowering orange pekoe tea, 263 flunitrazepam, 159 fluoxetine, 182, 188 fly agaric, 358–360 flying ointments, 356 Food and Drug Administration (FDA), 57 “Adverse Events Reporting” process of, 282 “Good Manufacturing Practices” regulations of, 282 Modernization Act, 60 Food, Drug and Cosmetic Act, 280, 287 foxy methoxy, 346, 352 freebasing cocaine, 130 Freud, Sigmund, 126–128, 130 G GABA, 90, 98, 119, 159 alcohol and, 209 subtypes, 93 Galen, 161, 307–308 gamma hydroxybutyrate (GHB), 155, 168–169 recreational dose of, 168 structure of, 168 gangrene, 334 ganja, 367 gaseous anesthetics, 166–167 gateway substances, 17–18, 21 interpretation of, 17 gender alcohol and, 205–206, 227 drug use and, 14–15 fetal alcohol syndrome and, 223 generalized anxiety disorder, 174 “generally recognized as effective” (GRAE), 287 “generally recognized as honestly labeled” (GRAHL), 287 “generally recognized as safe” (GRAS), 287
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generic names, 102 genetics, 16 GHB. See gamma hydroxybutyrate gin, 197 ginkgo biloba, 286 glial cells, 81–82 glue-sniffing, 167 glutamate, 90–91 goals, 410–411 “Good Friday Experiment,” 344 GRAE. See “generally recognized as effective” GRAHL. See “generally recognized as honestly labeled” grain neutral spirits, 197 grapefruit-juice, 103 GRAS. See “generally recognized as safe” green tea, 263 Griffiths, Roland, 344, 345 H habituation, 32 Hague Conference, 1912, 56 Haight-Ashbury district, 138 Halcion, 162 Haldol, 95, 104 Hallucinogen Persisting Perception Disorder, 342 hallucinogen research, government funding of, 345 hallucinogens, 104. See also specific hallucinogens amphetamine derivatives of, 350–352 anticholinergic, 355–360 Check Yourself, 363 deliriants, 352–355 hallucinogens, catechol, 346–352 structure of, 347f hallucinogens, indole, 333–346 structures of, 334f haloperidol, 95, 104 Halsted, W. S., 126 handwashing, 297 hangover, 217–218 products to prevent, 218 harmaline, 346 Harrison Act of 1914, 55–56, 61–63, 75, 129 Boggs amendment to, 63
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continued opioid abuse after, 314–318 opioid abuse before, 313–318 hash oil, 368 hashish, 366, 368 hashishiyya, 368 Hawaiian baby woodroses, 344 Hazelden, 4319 HDL. See high-density lipoproteins head shops, 68–69 headaches, 272, 273 The Health Consequences of Using Smokeless Tobacco, 242 heart muscle alcohol and, 219 cocaine and, 133 Heffter, Arthur, 348–349 Heineken, 196 henbane, 357 hepatitis B, 31 hepatitis C, 31 herbal tea, 264 Herbert, Bob, 126, 127 heroin, 312–313 abuse patterns with, 325–326 addiction, 326 banging, 325 black tar, 318 chippers, 326 cost of, 316, 318 currents use of, 318 death penalty and, 63 deaths, 315 in Drug Abuse Warning Network, 30 epidemics, 308 “French connection” for, 317 injection, 325 maturing out of, 326 Mexican brown, 318 misconceptions about, 326 overdose, 325 preconceptions about, 326 prohibition of, 41 purity of, 316, 318 smoking, 318 street slang, 329 toxicity, 44 variability of, 325 withdrawal symptoms of, 33, 326 Hicks, Thomas, 392 hidden messages, 417
high-density lipoproteins (HDL), 220 hippocampus, 374 Hippocrates, 96 The History and Present State of Virginia (Beverly), 357 “hitting bottom,” 432 HIV. See human immunodeficiency virus Hoa-tho, 378 Hoffman, Albert, 335–336, 360 Holmes, Sherlock, 128 Homeland Security, 67 homeostasis, 81 Homer, 307 homicide, 215 hookahs, 243 Hoover, J. Edgar, 63 hops, 194 hormones, 97 Hornbeck, Mark, 367 horny goat weed, 285 Hostetter’s Bitters, 53 Hotel Pimodan, 369 “How to Create a Nationwide Drug Epidemic” (Brecher), 4 HR 613, 210 Huckleberry Finn, 223–224 human growth hormone, 402 human immunodeficiency virus (HIV), 31, 32 humors, four, 96 Huxley, Aldous, 349 hydrocodone, 318 hydromorphone, 439 hypnotic drug therapy, 161 hypnotics, 153. See also specific hypnotics abuse patterns, 165 as anticonvulsants, 163 as anxiolytics, 160–161 beneficial uses of, 160–163 concern over, 163–165 nonbenzodiazepine, 159 toxicity of, 164–165 withdrawal, 164 hypothalamus, 88 I “I Get a Kick Out of You,” 129 ibotenic acid, 360
ibuprofen, 296 ice, 139 identification, 105, 119 impulsivity, 15, 39 IND. See “Notice of Claimed Investigational Exemption for a New Drug” inhalants, 153, 165–168, 413 examples of, 166 Inhalants: Kids in Danger, Adults in the Dark, 413 inhaler, nicotine, 252 injection heroin, 325 intramuscular, 113–114 intravenous, 113 subcutaneous, 113–114 “An Inquiry into the Effects of Ardent Spirits on the Mind and Body” (Rush), 199 insomnia, 161, 163 insulin, 176 intestinal disorders, 321 “Intoxicating Preparations Made with Cannabis,” 378 iron supplements, 401 J James, William, 349 Jamestown weed, 357–358 jaundice, 219 de Jerez, Rodrigo, 233 jimsonweed, 357–358 Johnson, Alan, 367 Johnson, Gary, 367 Jolt cola, 268 Jones-Miller Act, 62 The Jungle (Sinclair), 55 “Just Say No,” 12 K Kaldi, 258 Kefauver, Estes, 58 Kefauver-Harris amendments, 58–59, 286 Ketalar, 353 ketamine hydrochloride, 353 King, Rodney, 355 knockout drops, 154 Korsakoff’s psychosis, 218 “Kubla Khan” (Coleridge), 309
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www.mhhe.com/ray13e L labeling, 280 standards, 287 Laborit, Henri, 177 LaGuardia, Fiorello, 372 LaGuardia Report, 372 laissez-faire, 26, 52 The Lancet, 234 laudanum, 309 laughing gas, 166 LD. See lethal dose League of Spiritual Discovery, 338 Leary, Timothy, 337–338, 339, 373 arrest of, 338 dismissal of, 338 lethal dose (LD), 108 of nicotine, 248 leukoplakia, 242 Librium, 157–158 dependence, 163 Life Skills Training, 421 Liggett, 240–241 limbic system, 88 Linnaeus, 233 lipid solubility, 111 lipophilic molecules, 82 Lipton, Thomas, 264 liqueurs, 198 The Literary Digest, 370 lithium, 184–186, 188 limitations of, 185 noncompliance rate for, 185 liver cirrhosis, 219, 220f disorders, 219 fatty, 219 response to alcohol, 209 Lloyd, Edward, 259 Lloyds of London, 259 loose-leaf tobacco, 242 Louisiana Purchase Exposition, 264 lovastatin, 282–283 lozenges, nicotine, 252 LSD. See d-lysergic acid diethylamide “The LSD Controversy,” 341 Lunesta, 162 d-lysergic acid diethylamide (LSD), 333–344 absorption, 339
© The McGraw−Hill Companies, 2009
INDEX adverse reactions to, 341 army research with, 337 behavioral effects of, 339 beliefs about, 342–343 Central Intelligence Agency research with, 337 creativity and, 341, 342 depersonalization with, 341 discovery of, 335–337 early research, 335–337 emotions and, 340 experience, 340–341 flashbacks, 342 initial effects of, 340–341 large-scale production of, 337 panic reactions to, 342 peak of, 338–339 pharmacology, 339 in psychotherapy, 336 recreational use of, 337–339 therapeutic uses of, 336, 342–343 tolerance, 339 lysergsaurediethylamid, 335 M ma huang, 136, 289 Macbeth (Shakespeare), 160, 214 magnetic resonance imaging (MRI), 97 malaria therapy, 176 male enhancement, natural, 285 malt, 193 mandrake, 356–357 MAO. See monoamine oxidase inhibitors Mariani, Angelo, 125 marijuana, 5, 105, 365. See also Cannibas abuse, 381–382 academic performance and, 14f acute physiological effects of, 382 American society and, 384–386 amotivational syndrome and, 383 availability of, 9–10 blood pressure and, 375 brain damage and, 384 chronic lung exposure to, 382–383
475
cognitive processing and, 377 concentration and, 377 concern over, 381–384 cost of, 372 decriminalizing, 385–386 dependence, 381–382 driving ability and, 382 emotions and, 384 epidemiological studies on, 382 heart rate and, 375f high school seniors and, 385 immune system and, 383 inhibitory control and, 377 insanity and, 384 laboratory studies on, 382 memory and, 377 panic reactions to, 382 placebos and, 377 protective factors, 14f “pyramid of prejudice” towards, 371 reproductive effects of, 383 risk, 10, 14f spread of, 385 trends, 9–12, 10f, 12f use by age, 11f violence and, 371 visuospatial processing and, 377 withdrawal, 381–382 zero tolerance seizures and, 386 marijuana, medicinal, 69, 378–381 compassionate use of, 381 media on, 367 Marijuana Tax Act, 63, 371–373, 378 Marinol, 379 Maxwell House, 260 MBD. See minimal brain dysfunction McCarthy, Joseph, 63 MDA, 350 MDMA, 350–352, 359 studies on, 351 de Medici, Catherine, 233 medicine chest, 290 “The Men’s Answer to the Women’s Petition Against Coffee,” 258
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mental disorders, 171–175 classification of, 172–175 diagnosis of, 188 medical model of, 171–172 in movies, 173 treatment of, 175–186 treatment of, before 1950, 175–177 treatment of, consequences of, 186–187 mental hospitals indefinite commitment to, 187 movement out of, 187 patients in, number of, 186f meprobamate, 156–157 Merchandise No. 5, 266–268 “Mescal: A Study of a Divine Plant” (Ellis), 349 mescal beans, 347–348 mescal buttons, 346–347 mescaline, 336, 346–350 discovery of, 348–349 early research on, 348–349 pharmacology of, 349–350 synthesizing, 349 mesolimbic dopamine pathway, 89 metabolic syndrome, 180 metabolite, 116 active, 118 methadone, 322, 430, 435, 438 methamphetamines, 82, 138, 139–140, 288 in community, 8 memory deficits and, 82 stovetop laboratories for, 139 treatment for, 140 methapyrilene, 290 methaqualone, 157 5-methoxy DIPT, 346 methyl donor, 285 methylene chloride, 261 methylphenidate, 144 methylxanthines, 270 Metrazol, 177 Mexican brown, 318 Mickey Finn, 154, 159 microbreweries, 195 Miles Nervine, 290 minerals, 401 minimal brain dysfunction (MBD), 144
misbranding, 55 of Coca-Cola, 267 miscarriage. See abortion, spontaneous Mitchell, Weir, 349 modafinil, 143, 439 moist snuff tobacco, 242 Monitoring the Future Project, 9, 135 monoamine oxidase inhibitors (MAO), 180–181, 250, 346 examples of, 181t limitations of, 181 monoamine theory of mood, 96 Montezuma, 264–265 mood disorder, 174–175 diagnosis of, 176 mood stabilizers, 184–186 moonwalking, 354 Moore, Joe, 126 morality, 199 morning glories, 344 Morpheus, 312 morphine, 311–312 commercial production of, 52 medical value of, 312 Morris, Philip, 236 motivational enhancement therapy, 432–433 action stage, 433 contemplation stage, 433 maintenance stage, 433 motivational interviewing, 432 precontemplation stage, 433 motor cortex, 86 Mountain Dew, 268 movies mental disorders in, 173 tobacco in, 234 Multidisciplinary Association for Psychedelic Studies, 337 “munchies,” 377 muscarine, 359 muscimol, 360 N nalorphine, 320 naloxone, 315, 320, 324 naltrexone, 320, 435, 439 development of, 436 Narcan, 324
narcolepsy, 137, 143, 168 narcosis therapy, 176 Narcotic Control Act of 1956, 63 narcotic farms, 63 Narcotics Division, 61 National Drug Control Policy, Office of, 69 National Drug Control Strategy, 73 The National Formulary, 57 National Organization for the Reform of Marijuana Laws (NORML), 385 National Prohibition Party, 200 National Survey on Drug Use and Health, 11, 135 Native American Church, 348 natural highs, 415 NDA. See new drug application needle exchange programs, 31 freaks, 324 habit, 324 sharing, 31–32 nerve cells, 81–82 nervous system, 81–83 somatic, 85 nervous system, autonomic (ANS), 85–86, 98 parasympathetic, 86 sympathetic, 86 nervous system, central (CNS), 86 overexcitement of, 119 Nestlé, 266 neuroleptic, 177 neurons, 83, 116 depolarized, 85 hyperpolarized, 85 regions of, 83f neurotransmission, 83–85 neurotransmitters, 84, 97–98 availability of, 116 lifecycle of, 91–94, 98 monoamine, 96 release of, 94f new drug application (NDA), 58 New England Journal of Medicine, 53 new science of psychology, 369 The New York Times, 351 “Negro Cocaine ‘Fiends’ are a New Southern Menace,” 129
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www.mhhe.com/ray13e “This Is Your Brain on Meth: A ‘Forest Fire’ of Damage,” 82 Nicot, Jean, 233 Nicotiana rustica, 234 Nicotiana tobacum, 234 nicotine, 105 absorption, 248 behavioral effects of, 249 chewing gum, 252 deactivation of, 248 death from, 248 dependence, 249–251 inhaler, 252 lethal dose of, 248 lozenges, 252 metabolizing, 248 pharmacology of, 247–251 pharmacotherapies, 436–437 physiological effects of, 248–249 poisoning, 248 reinforcement properties of, 250, 252 replacement therapy, 252, 436 skin patches, 252 structure of, 247f nigrostriatal dopamine pathway, 89, 98 nitrites, 167 nitrous oxide, 166, 354 traveling demonstrations of, 167 NoDoz, 269, 288 Nonprescription Drug Advisory Committee, 288 nonspecific effects, 105–106 nonsteroidal anti-inflammatory drugs (NSAIDs), 296 norepinephrine, 86, 92f, 94 pathways, 90 NORML. See National Organization for the Reform of Marijuana Laws “Notice of Claimed Investigational Exemption for a New Drug” (IND), 59 Novocaine, 133 NSAIDs. See nonsteroidal anti-inflammatory drugs nucleus accumbens, 89, 374 Nutt, Levi G., 62 Nytol, 290
© The McGraw−Hill Companies, 2009
INDEX O obsessive-compulsive disorder, 174 Odyssey (Homer), 307 Olson, Frank, 337 Olympics, 393 amphetamines in, 394 Omnibus Crime Control Act, 402 “On the Preparations of the Indian Hemp, or Gunjah,” 378 One Flew over the Cuckoo’s Nest, 173 oolong tea, 264 Operation Golden Flow, 317 opioid detoxification, rapid, 437 opioids, 104. See also specific opioids action mechanism of, 320–321 animal research on, 322 antagonists, 320 beneficial uses of, 321–322 chemical characteristics of, 319–320 concern over, 322–326 as cough suppressants, 322 cross-tolerance, 322 dependence, 322–324 before Harrison Act, 313–314 history of, 307–319 intestinal disorders and, 321 negative reinforcement of, 324 in 1980s, 317–318 in 1970s, 317–318 in 1960s, 316 pain relief from, 321 pharmacology of, 319–321 pharmacotherapies, 437–438 positive reinforcement of, 323 prescription, 318–319 prohibition, 62 tolerance, 322 toxicity of, 324–325 triad, 324–325 Vietnam War and, 316–317 withdrawal symptoms, 323t opium, 52, 307–311 alcohol v., 310 early history of, 307–309 in Greek medicine, 307–308 harvesting, 307 narcotic agents from, 319f
477
production of, increase in, 74 San Francisco ordinance on, 54 smuggling, 310–311 writers and, 309 Opium Wars, 53–54, 262, 310–311 orange pekoe tea, 263 Orlistat, 289 Orphan Drug Act, 60 Osler, William, 378 OTC. See drugs, over-the-counter outcomes, evaluating, 410–411 overdose alcohol, 216 benzodiazepine, 158 depressant, 169 heroin, 325 Oxford Group, 225 OxyContin, 318–319 P Pahnke, Walter, 344 pain, 291, 321 Pall Mall, 237 panic attacks caffeine and, 273 d-lysergic acid diethylamide and, 342 panic disorder, 174 Paracelsus, 309 paraldehyde, 154 paraphernalia, 68–69 Internet and, 69 prohibition of, 69 parent support groups, 422 parenting skills, 422 Parke-Davis Pharmaceutical Company, 128, 353 Parkinson’s disease, 87, 89, 95, 178, 434 patent medicines, 53, 54 patient, 171 PCP. See phenylcyclohexyl piperidine hydrochloride PDR. See Physician’s Desk Reference “Peace Pill,” 354 peer influence, 421 peer participation, 422 peer programs, 421–422 pekoe tea, 263
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Pemberton, J. C., 266 penile tumescence, 214 pentylenetetrazol, 177 People for the Ethical Treatment of Animals (PETA), 108 Perry, Rick, 127 personal skills, 415 personality disorders, 16, 39 personality variables, 15–16 PET. See positron emission tomography PETA. See People for the Ethical Treatment of Animals peyote, 346–350 as sacrament, 348 phantastica, 332 pharm parties, 27 pharmaceuticals. See drugs, prescription pharmacist(s) arrest of, 62 recommendations, 292 Pharmacology and Therapeutics, 313 pharmacotherapies, 434–440 alcohol, 435–436 Cannibas, 439 cocaine, 438–439 detoxification phase, 434–435 maintenance phase, 434–435 nicotine, 436–437 opioid, 437–438 phenacetin, 295 phenobarbital, 159 phenothiazines, 177, 178 phenylcyclohexyl piperidine hydrochloride (PCP), 352–353 as anesthetic, 353 animal research on, 352 folklore, 354–355 as “Peace Pill,” 354 recreational use of, 354–355 violence and, 354 phenylephrine, 288 phenylpropanolamine (PPA), 289 phenytoin, 378 Philip Morris, 250 Phoenix House, 431 photosensitivity, 179
Physician’s Desk Reference (PDR), 105 pipe dreams, 324 pituitary gland, 402 placebo, 105–106 alcohol and, 211 marijuana, 377 response, 106 steroids as, 400 plasma proteins, 115 Playboy Foundation, 385 Pliny, 357 poison arrow frogs, 248 poisoning alcohol, 216 nicotine, 248 Polo, Marco, 368 poppers, 167 Popular Science Monthly, 370, 371 Porter, Cole, 129 positron emission tomography (PET), 96–97, 97f post traumatic stress disorder, 174 postsynaptic cell, 93 potency, 109–110, 119 PPA. See phenylpropanolamine precursors, 67–68 dopamine, 89 uptake of, 91 pregnancy alcohol and, 222 cigarette smoking and, 246 cocaine and, 134 prevention programs and, 423 Premier, 241 Prescription Drug Marketing Act of 1988, 60 prescription drugs. See drugs, prescription pressure resistance, 415–416 presynaptic terminals, 83 prevention community programs for, 423–424 effectiveness of, 414 extracurricular approaches to, 422 family interaction approaches, 422 indicated, 412
informational programs for, 422 jealousy and, 423 knowledge-attitudes-behavior model of, 412–414 mistrust, 423 model programs, 421 parent support groups for, 422 parent/family programs for, 422–423 parenting skills and, 422 peer influence on, 421 peer participation in, 422 peer programs, 421–422 pregnancy and programs for, 423 primary, 411 prime-time programming, 412 programs that work, 420–421 relapse, 434 review of, 415–417 scare stories, 424 in schools, 412–421 secondary, 411–412 selective, 412 social influence model of, 417–418 teen leaders, 418, 419 tertiary, 412 types of, 411–412 universal, 412 value-free, 414–415 in workplace, 424 priest, 7 principles of psychoactive drugs, 4–5 prison Americans in, 68 costs, 73 treatment v., 62–63 problem behaviors, 14 procaine, 133 prodrugs, 118 Prohibition, 194, 195, 198, 200–202, 227 failure of, 201 as “noble experiment,” 201 Project ALERT, 420 proof, 194 propaganda, 411 Proposition 36, 65 prostaglandins, 294
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www.mhhe.com/ray13e Provigil, 143 Prozac, 90, 182, 188 pseudoephedrine, 288, 298 pseudoparkinsonism, 178–179, 180 psilocin, 344 psilocybe cubensis, 343 psilocybe mexicana, 343 psilocybin, 343–344 mystical experience and, 344 psychedelic, 332 “psychedelic 60s,” 333, 373 psychologist, 5, 183 Psychopharmacology, 345 psychosis, 173 functional, 174 organic, 174 psychotomimetics, 332 public commitment, 417, 419 punishment therapy, 435 Pure Food and Drugs Act, 1906, 55, 75, 314 pyschotherapeutic drugs, 104 Q Quaalude, 157 Quetzalcoatl, 264 Quiet World, 290 R race relations, 52 Raich, Angel, 380 Raich v Ashcroft, 380 Randall, Robert, 379 raves, 359 Reader’s Digest, 238 Reagan, Ronald, 12 receptors, 83, 93, 98, 116 blocking, 95 drug effects on, 95 Red Bull, 268–269 red yeast rice, 282–283 Reefer Madness, 41 reformism, 52 refusal skills, 415–416, 419 training, 417 regulation, 43 of alcohol after 1933, 202 local, 69 of over-the-counter drugs, 286–287
© The McGraw−Hill Companies, 2009
INDEX of prescription drugs, 56–61 state, 69 steroids, 400–402 tobacco, 238, 240 Reid, Samantha, 155 reinforcement, 19, 34, 36 negative, 324 nicotine and, 250, 252 opioid, 323–324 positive, 35 relapse alcohol, 224 prevention, 434 relaxation, 165 religion, 225 drug use and, 14 respiratory depression, 117 resting potential, 84 Reye’s syndrome, 294 Reynolds, 241 rhinoviruses, 297 Ricaurte, George, 351 Richardson, Benjamin, 154 Rig Veda, 358 rimonabant, 374 Ritalin, 144, 146 misuse of, 146 Robinson, F. M., 266 Robitussin, 299 rohypnol, 159, 160 Rolfe, John, 234 romantic literature, 369 Roosevelt, Theodore, 55 Rush, Benjamin, 199 rye whiskey, 198 S safety margin, 109 Saint Anthony’s Fire, 334–335 Saint John’s wort, 118, 279–280, 284–285 effectiveness of, 284–285 prescription drugs and, interactions with, 285 uses of, 284 Sakel, Manfred, 176 Salem witch trials, 335 salicylic acid, 291 salon.com, 412 salt-substitute poisonings, 185 salvia divinorum, 360
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Samantha Reid Foundation, 155 SAMHSA. See Substance Abuse and Mental Health Services Administration San Pedro cactus, 348 Sandoz Pharmaceutical Company, 336 scare stories, 424 scheduling, 64, 66–67, 69 summary, 66t schizophrenia, 89, 174, 185 diagnosis of, 175 negative symptoms of, 179 positive symptoms of, 179 schools drug-free, 416–417 prevention in, 412–421 store in, 415 Scientific America, 370 scopolamine, 290 Seagram, 194 secobarbital, 158 sedatives, 153 over-the-counter, 290–291 selective reuptake inhibitors, 182–184 examples of, 181t selective serotonin and norepinephrine reuptake inhibitors (SSNRIs), 182 selective serotonin reuptake inhibitors (SSRIs), 182 self-esteem building, 419 “sensation seeking,” 39 sentencing, 67 minimum, 131 Sentencing Commission, U.S., 131 Sernyl, 352 Sernylan, 353 serotonin, 88 animal research and, 90 pathways, 90 reuptake inhibitors, 90 Sertürner, Frederich, 312 sexual assault, 215 sexual behavior, 214–215 sexual excitability, 258 Shafer, Jack, 27 Shakespeare, William, 160, 214 shaman, 7, 332
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Shen Nung, 368, 378 Sherley amendment, 1912, 57 sherry, 197 shisha, 243 Shiva, 357 ShowerShock, 272 Sibutramine, 90 side effects, 109 antipsychotics, 179–180 aspirin, 293 SIDS. See sudden infant death syndrome Simpson, Tommy, 394 Sinclair, Upton, 55 sinsemilla, 368 sinus medications, 300 skin patches, nicotine, 252 skin popping, 114, 325 skydiving, 416 Slate, 27 Sleep-Eze, 290 sleeping pills, 138, 142, 161–162 over-the-counter, 290–291 smart pills, 145–147 The Snake Pit, 173 snuff, 233, 235 moist, 242 social failure, 415 social phobia, 174 social skills, 415 society, drug-free, 5 sodium bicarbonate, 401 soft drinks, 266–268 caffeine in, 268t Solanaceae, 355 Soma, 358 Sominex, 290 Sopor, 157 Special K, 353 specific phobia, 174 speed, 138 speedball, 129 SSNRIs. See selective serotonin and norepinephrine reuptake inhibitors SSRIs. See selective serotonin reuptake inhibitors stacking steroids, 399 Stallone, Sylvester, 402 Stamp Act of 1765, 263 Starbucks, 259
stereotypes, 15 steroids, 395 adverse effects on body, 400 anabolic, 394, 399 androgenic effects of, 399 black market, 401 entertainers and, 402 placebo effect of, 400 psychological effects of, 400 regulation, 400–402 research on, 399 stacking, 399 violence and, 400 Stewart, Larry, 127 Stickelmaier, Kate, 367 stimulants, 103. See also specific stimulants antidepressants and, 117 in athletics, 392–393 caffeine in, 269t depressants and, 117 molecular structures of, 140f over-the-counter, 288–289 as performance enhancers, 397–399 Stone, Edward, 291 STP, 350 Strattera, 144 Strengthening Families program, 422–423 strychnine, 392 subculture, deviant, 19 Substance Abuse and Mental Health Services Administration (SAMHSA), 299, 441 Sudafed, 288 sudden infant death syndrome (SIDS), 246 increased risk of, 247 suicide alcohol and, 216 antidepressants and, 182 barbiturates and, 156 methaqualone and, 157 “Suicide Tuesday,” 352 sulfa drugs, 58 Sullivan, John L., 236 Sunday, Billy, 201 Swarbick, Jack, 393 Sydenham, Thomas, 309 sympathomimetic, 136
nasal decongestants, 298 symptoms, 171 synapse, 92 synesthesia, 340 synthesis, 92 T tar, 240 tardive dyskinesia, 179–180 Task Force on Drug Abuse, 316 taurine, 269 Taylor, William, 400 tea, 261–264 bag, 264 black, 264 European record of, 262 fermentation of, 263 flavored, 264 flowering orange pekoe, 263 green, 263 herbal, 264 legends surrounding, 261 as medicinal plant, 262 oolong, 264 orange pekoe, 263 pekoe, 263 smuggling, 263 tax, 262, 263 Technique, 393 temperance movement, 199 teonanacatl, 343 testing, drug in athletics, 394 battles over, 396–397 false-positive results for, 72 federal employees, 70 federal support for, 70–72 hair, 72 methods, 71–72 military and, 70 private employers, 70 public schools, 70–71 transportation workers, 70 testosterone, 395 tetracycline, 113 tetrahydrogestrinone (THG), 395 thalidomide, 58 testing, 108 Thank You For Smoking, 234 THC. See delta-9-tetrahydrocannabinol
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www.mhhe.com/ray13e Theobroma, 264 Theobroma cacao, 265 theobromine, 266, 270 theophylline, 264, 270 therapeutic index (TI), 108 Theresa, Maria, 265 THG. See tetrahydrogestrinone thiamine, 218 ThinkGeek.com, 272 threshold, 106 TI. See therapeutic index time course, 110 time dependent factors, 110–111 tobacco attacking, 237–243 Check Yourself, 255 Chinese introduction to, 310 concern over, 243–247 deaths, 244f in early America, 235 early medical uses of, 233–234 European introduction of, 233, 252 health effects of, 243–244 history, 232–237 in movies, 234 nitrosamines, 242 as painkiller, 248 regulation of, 238, 240 shisha, 243 spread of, 234–235 surgeon general’s report on, 250 women and, 237 tobacco, chewing, 235–236, 241–242 advantages of, 242 loose-leaf, 242 moist snuff, 242 quid of, 242 tolerance, 33, 118, 120 barbiturate, 156 behavioral, 118–119 caffeine, 270 drug disposition, 118 LSD, 339 opioid, 322 pharmacodynamic, 119 pharmacokinetic, 118 Tour de France, 394 toxicity, 26 acute, 26–27, 28t
© The McGraw−Hill Companies, 2009
INDEX alcohol, 216–221 amphetamine, 147–148 behavioral, 28t categories of, 26–27 Check Yourself, 49 chronic, 26, 28t cocaine, 44, 133–134 heroin, 44 of hypnotics, 164–165 marijuana, 382–384 measuring, 108 monitoring the, 27 of opioids, 324–325 physiological, 26, 28t Trade and Revenue Act of 1767, 263 trafficking penalties, 65–66 Treasury Department, U.S., 56 treatment behavioral, 429–434 celebrity, 431 effectiveness of, 441–442 goals, 430 “magic bullet approach” to, 434 medication, 434–440 prison v., 62–63 psychosocial, 429–434 success of, 430 in United States, 441 Treatment Episode Data Set, 441 “tree of life,” 358 triazolam, 162 tricyclics, 181–182 examples of, 181t truth serum, 176 tuberculosis, 180 Tulia, Texas, 126–127 Twain, Mark, 247 tyramine, 181 U uisgebaugh, 197 Uniform Controlled Substances Act, 69 Unimed, Inc., 379 unipolar disorder, 185 United States Pharmacopoeia, 57, 102 “Unsubstantiated Claims and Documented Health
481
Hazards in the Dietary Supplement Marketplace,” 281 V vaccines, 7 Valium, 158 dependence, 164 values clarification, 414–415, 417 varenicline, 252, 437 vasopressin, 81, 216 Vaughn, William, 234 ventricular fibrillation, 133 Veronal, 154 Vick, Karl, 367 Vietnam War, 316–317 violence, 40–43 alcohol and, 215–216 amphetamines and, 147 marijuana and, 371 PCP and, 354 steroids and, 400 Vioxx, 295 visuospatial processing, 377 vitamins, 401 Vivarin, 288 vodka, 197–198 volatile solvents, 167–168 dangers from, 168 Volkow, Nora, 345 Volstead, Andrew, 200 vomiting center, 88 von Loewi, Otto, 86 von Meduna, Ladislas, 177 W Wafer, Billy, 127 war on drugs, 7 Washington, George, 51, 235 Wasson, Gordon, 343, 360 water, 401 WCTU. See Women’s Christian Temperance Union Wellbutrin, 437 Wernicke-Korsakoff syndrome, 218 What Works: Schools Without Drugs, 416 What Works: Workplaces Without Drugs, 424 whippets, 167 whiskey, 193 rye, 198
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INDEX
Whiskey Rebellion, 51 White, Tonya, 127 Wiley, Harvey, 56, 57 wine, 196–197 coca, 125 dry, 196 generic, 196 medicinal value of, 193 sparkling, 196 sweet, 196 varietal, 196 Winston, 237 de Wit, Harriet, 345 witches, 356 withdrawal symptoms, 33, 34, 118
alcohol, 222–224 amphetamine, 148 avoiding, 109 cocaine, 134, 439 elimination of, 34 heroin, 33, 326 hypnotics, 164 marijuana, 381–382 opioid, 323t reduction of, 34 Women’s Christian Temperance Union (WCTU), 200 “The Women’s Petition Against Coffee,” 258 Wood, Alexander, 312 workplace, “drug-free,” 424
Wright, Hamilton, 55–56 X Xanax, 161 dependence, 164 xanthines, 270 Xenical, 289 Xyrem, 168 Y yeast, 192–193, 226 yin-yang, 96 Z zolpidem, 162 Zyban, 252, 437
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