CHAPTER 5
Gateway Drugs: Alcohol, Marijuana, and Cocaine
In this chapter, I review the drugs that usually initiate addiction—alcohol, marijuana, and cocaine—and focus on where they come from, how they have been used and abused, and how their use damages the body, mind, and spirit.
The introduction to the brain in Chapter 4 focused on the synapse, the tiny gap between nerve cells that is open to blood-supplied chemicals. Now we look at the most commonly used drugs of abuse to see how they affect the brain. This is called the drug’s mode of action. It is the science of psychopharmacology. In this chapter we explore the three most widely used intoxicating drugs: alcohol, marijuana, and cocaine. These three drugs are called the gateway drugs because they commonly form the gateways into the use of other, less commonly used drugs of abuse. Most drug users begin with alcohol and then, if they are to progress further into addiction, proceed to use marijuana and, later, cocaine. In Chapter 6 we explore the use of heroin and several other dangerous drugs of abuse, including LSD, Ecstasy, and PCP. (See Drug Facts on page 465 for a short summary of the most commonly abused drugs.)
The most important drugs of abuse are alcohol, marijuana, cocaine, and heroin. The first three of these drugs are the focus of this chapter, and heroin is discussed in Chapter 6. During the twentieth century, at an accelerating tempo, chemists have created an awesome number of molecules that are not found in nature but that have the capacity to produce brain reward and, therefore, addiction. Synthetic stimulants, including amphetamines and methamphetamines, and synthetic depressants, including the barbiturates, have been widely used in medicine for more than half a century. Synthetic stimulant drugs have much in common with cocaine. Synthetic depressants have much in common with alcohol.
Although thousands of chemicals can function in the brain as drugs, in the sense that they produce pleasure and intoxication, most drug problems throughout the world are caused by alcohol, marijuana, cocaine, and heroin, four relatively old and familiar drugs, and by a few other drugs that are closely related to them. Of these four drugs, only alcohol is swallowed and only alcohol use is legal anywhere in the world, and even alcohol use is not legal in the United States for people under the age of twenty-one. All four of these drugs are easily produced with little chemical sophistication from natural agricultural products available throughout the world.
Alcohol and Other Depressants
Alcohol, a liquid, is swallowed. It is not smoked, snorted, or injected as many other drugs are taken into the body. Alcohol, although the simplest psychoactive chemical, produces highly complex effects on the brain and the body. Alcohol changes the neurons’ membrane and opens the chloride and potassium channels at the synapse. Epinephrine concentrations in the blood rise after alcohol use, accounting for the raised heart rate and blood pressure following alcohol use. Alcohol affects the gamma-aminobutyric acid (GABA) system, producing quieting of the brain and temporarily reducing worry and tension. GABA is one of the brain’s principal neurotransmitters, being particularly involved in the inhibition of stimulation. The GABA system suppresses the locus coeruleus, blocking intense anxiety and panic. That is why the benzodiazepines, which reinforce the GABA system, are effective in suppressing panic attacks. Alcohol does this much less well because it is short-acting, so that the initial quieting of the GABA neurotransmitter system and the locus coeruleus is rapidly replaced by overstimulation of these brain mechanisms as the blood alcohol level declines in the hours immediately after a drinking episode ends. Alcohol also affects the dopamine, norepinephrine, and serotonin neurotransmitter systems in the brain.
The effects of alcohol vary with dose levels. Some effects are even reversed with chronic alcohol use. Because alcohol is rapidly metabolized, withdrawal effects, which are opposite to the effects of intoxication, are seen a few hours after alcohol use stops. Although acute alcohol use has a quieting effect that reduces anxiety, the alcohol withdrawal effect is the opposite, with brain excitation and anxiety being prominent features. Alcohol withdrawal causes insomnia and sometimes epileptic seizures, expressions of pathological brain excitation following alcohol’s initial brain quieting.
Because alcohol, like cocaine, heroin, and nicotine, is a short-acting substance, the heavy alcohol user is continually exposed to alternating intoxication and withdrawal effects that produce long-term disruption of brain functions. Alcohol can promote sleep shortly after use, but a few hours later, when the acute effects are replaced by withdrawal effects, the alcohol withdrawal actually creates anxiety and sleeplessness as well as nightmares. Following everyday drinking, especially drinking throughout the day (the way cigarette smokers consume nicotine), if drinking abruptly stops, the drinker can go into a severe withdrawal syndrome known as delirium tremens (DTs). This is a potentially fatal disease, including high fever, hallucinations (such as seeing pink elephants on the walls), and epileptic seizures. DTs are more commonly seen in maintenance drinking than in binge drinking.
Numbing the Brain
Alcohol is a depressant drug. Moderate use of alcohol leads to relaxation and lessening of inhibitions. Alcohol first affects the higher functions of the brain, including those managing self-observation and self-criticism. For this reason, drinkers feel relaxed and uninhibited, even as they sometimes say and do things that they later find embarrassing. Anger is often released after even relatively small doses of alcohol. It is common to find that routine evening alcohol drinkers, even when drinking fairly small amounts, become hard to live with as the evening wears on and they drink more and more. This is not normal drinking. Reasonable social drinking produces no negative effects at all. When evening drinking produces changed moods and behaviors, such as anger and irritability, it means that the line has been crossed into alcohol abuse. It signals the need for an intervention leading to treatment as described in Chapter 10.
In higher doses, alcohol can produce lack of coordination and digestive upsets, particularly vomiting, since alcohol irritates the lining of the stomach and triggers the brain’s vomiting mechanism. Alcohol’s role in body heat loss can be deceptively dangerous in situations in which hypothermia, or loss of normal body heat, may develop. Alcohol at first swallow gives a warm glow as blood flows to the skin, but the resulting heat loss, masked by alcohol’s anesthetic effects, can have dire consequences that may prove fatal in cold environments. In even larger doses, alcohol can cause blackouts, periods when the alcohol user looks and acts more or less normal, although intoxicated. After blackouts, however, alcohol users have no memories of what happened to them during the blackout period. Blackouts are an early and relatively common symptom of excessive drinking.
Loss of consciousness after drinking large amounts of alcohol—”passing out”—can be extremely dangerous if vomiting occurs while the drinker is unconscious, because the vomited stomach contents can be inhaled into the lungs of the intoxicated person, producing asphyxiation or life-threatening pneumonia as stomach acid literally digests vulnerable lung tissues. Long-term use of alcohol leads to liver damage, internal bleeding, and, ultimately, brain damage. Alcohol use is highly correlated with the abuse of other drugs and with many types of cancer. Because many heavy drinkers also smoke cigarettes, the fact that heavy alcohol use multiplies the cancer risks of smoking is especially serious. The tetrahydrocannabinol in marijuana suppresses vomiting. Because many marijuana smokers also drink heavily, and because vomiting after heavy drinking can save the drinker’s life by eliminating alcohol from the stomach, marijuana smoking can raise the risk of a fatal alcohol overdose.
The United States government’s report, Alcohol and Health, from the Department of Health and Human Services summarizes the effects of alcohol on the body this way: “The range of medical consequences of alcohol abuse is both immense and complex—virtually no part of the body is spared the effects of excessive alcohol consumption.” The catalog of ill effects of drinking begins with the liver, the body’s chemical factory, which is hit first by alcohol taken into the body through the stomach. The liver is the primary place where alcohol is metabolized (broken down) into carbon dioxide and water. Damage to the liver from drinking, which usually becomes severe after ten or more years of heavy drinking, comes in three types: fatty liver, where yellow fat replaces normal red liver tissue; alcoholic hepatitis, when the liver is acutely inflamed and often seriously malfunctioning, with jaundice (the skin and the whites of the eyes turn yellow) as a common symptom; and finally, cirrhosis of the liver. Both fatty liver and alcoholic hepatitis may be reversible if the person stops drinking, but relapses to drinking can be disastrous to the liver.
With both fatty liver and alcoholic hepatitis, the liver is often enlarged, extending below the ribs on the right side of the body into the abdomen. The third sort of alcohol-caused damage is the chronic state following both fatty liver and alcoholic hepatitis, cirrhosis of the liver. In this end-stage disease, the fatty tissue and the normal liver tissue are both replaced by white scar tissue. This liver disease is not reversible, although when the person stops drinking, the cirrhosis (scarring) process may not progress further. The cirrhotic liver is small and does not work well to clean the blood, so jaundice, severe blood poisoning, and blockage of the blood supply from the intestines are common symptoms of this progressive and fatal disease. Chronic liver disease, including cirrhosis, is the ninth leading cause of death in the United States, reflecting a high level of alcohol abuse.
In the gastrointestinal tract, alcohol is a severe irritant, causing inflammation of the esophagus and stomach, often worsening peptic ulcer disease. Excessive drinking is a major cause of acute and chronic inflammation of the pancreas. Acute pancreatitis is one of the most painful of all diseases, producing an unrelenting knifelike pain in the middle abdomen between the rib cage and the belly button. This is an acute, recurrent disease that can be fatal. Heavy long-term drinking is often combined with nutritional diseases, leading to a variety of brain degenerations, including paralysis of nerves and memory deficits, many of which are not reversible once drinking stops.
Alcohol abuse also leads to anemia (loss of red blood cells) and a variety of cardiovascular diseases, including high blood pressure and stroke, as well as increased risk of heart attacks. Alcohol can also lead to degeneration of the heart muscle with the result that the heart no longer pumps efficiently. Chronic alcohol abuse is a significant contributor to cancer of the mouth, esophagus, stomach, larynx, liver, and lung. (See Chapter 9 for guidelines on how much alcohol is too much.)
The alcohol blocker Antabuse (disulfiram), introduced into medical practice in 1948, temporarily poisons the liver enzyme needed to metabolize alcohol to carbon dioxide and water. It allows the buildup of acetaldehyde, an intermediary metabolic product, in the drinker’s body. Acetaldehyde is toxic and causes flushing of the skin, headaches, stomachaches, and elevated blood pressure. If a person drinks a lot of alcohol, Antabuse can even cause death. The alcoholic seeking motivation to avoid alcohol use needs to take Antabuse only once a day, usually in the morning when the determination not to drink is relatively high. Later in the day, when temptation to drink typically rises, the drinker is protected by Antabuse because of the fear of illness or death from drinking alcohol after using Antabuse. Because Antabuse poisons enzymes in the body for quite a while, the person must stop Antabuse use for one to two weeks before drinking alcohol; otherwise, disturbing and potentially dangerous symptoms are likely to result from drinking alcohol.
There are two serious problems with the use of Antabuse to treat alcoholism. The first is that it is specific for alcohol, which makes it possible for alcoholics to use other drugs and get high even when they take Antabuse. For example, they can use closely related medicines such as Xanax and Valium, or they can take quite different substances such as cocaine or marijuana and get high despite taking Antabuse. The second problem is that alcoholics can simply stop taking Antabuse. The people most familiar with alcoholism, those in Alcoholics Anonymous, generally take a dim view of treating alcoholism with Antabuse because it does not deal with the alcoholic as a whole person.
Antabuse treatment does not lead to long-term recovery. At best, Antabuse provides a relatively brief period when the alcoholic can get alcohol out of his or her brain and make some long-term decisions about getting well. I have found that Antabuse does not lead to recovery unless the alcoholic attends meetings of AA or NA. If Antabuse is used with psychotherapy, I have rarely seen it lead to prolonged, stable recovery from addiction. In fact, like psychotherapy for addicted people, it can become a “cover” for continued addiction as alcoholics delude those around them into a false sense that the problem of alcohol addiction is under control.
In 1995 the Food and Drug Administration (FDA) approved the use of naltrexone (ReVia) as a part of a comprehensive treatment of alcohol dependence. Naltrexone works by blocking the opioid receptor system that may play a role in the reinforcement of alcohol use. In two studies, the use of this medicine reduced craving for alcohol and relapse by about 50% during the twelve weeks of the studies. Although it is too early to know the ultimate place of this medicine, which had previously been used to treat heroin addicts (see page 185), in the treatment of alcohol dependence, naltrexone appears to offer new hope for at least some alcoholics. Equally importantly, the introduction of naltrexone underlines the importance of the new brain biology in the treatment of addictive disease.
Measuring Alcohol Intoxication
Acute intoxication after drinking results from alcohol traveling from the stomach and the intestines through the bloodstream past the liver and finally to the brain. The level of alcohol in the blood is called the blood alcohol concentration (BAC). To understand the relationship of drinking to the BAC, you need to know that all alcoholic beverages contain the same ethyl alcohol. The only important differences between one form of alcohol and any other for health are the concentration of alcohol in the drink. The other substances in the drink, mostly flavorings to disguise the generally unpleasant taste of alcohol, have little or no health effects. One twelve-ounce can of beer contains about 0.5 ounce of pure ethyl alcohol. About five ounces of wine and about 1.5 ounces of distilled spirits (whiskey, rum, or vodka, for example) also contain about 0.5 ounce of pure alcohol. Each of these amounts of alcohol is considered equal to one drink. Thus, three beers are equal to about fifteen ounces of wine, or about half a bottle of wine. This is also equal to three ordinary mixed drinks, assuming each drink contains about one 1.5-ounce-sized jigger of distilled spirits.
When a person drinks alcohol, the alcohol is distributed more or less evenly throughout the person’s body. Larger people (e.g., those who weigh more) have bigger bodies in which to dilute the alcohol they drink, and therefore their BAC is lower after each drink they take than is the BAC in people who weigh less. Many other factors influence BAC levels. For example, women generally metabolize alcohol less rapidly than men do, so their BACs tend to be higher even when they weigh the same. The biggest factors governing BAC, however, are not gender or weight, but how much a person drinks and how long after the drink is consumed the BAC is checked. This is because the liver is efficient at metabolizing alcohol. The liver can break down one drink of alcohol (0.5 ounce) into carbon dioxide and water in about an hour and a half.
A 160-pound man who drinks a great deal of alcohol in an hour has a BAC about as follows: after two drinks, 0.02%; three drinks, 0.05%; and four drinks, 0.07%. A 120-pound woman has a BAC after two drinks of 0.04%; three drinks, 0.06%, and four drinks, 0.09% (see Figure 5–1). The liver drops the BAC by about 0.015% per hour after drinking stops. It is unusual for normal social drinkers to get their BAC to over 0.05%. If a person were to drink one or two drinks over the course of a two-hour period, a typical social drinking pattern, the BAC would never be greater than about 0.03%. Assuming that the person then had dinner with one glass of wine, by the end of the evening, approximately four hours from the start of the first drink, the BAC would be 0.03% or less. If that same person drank five drinks in one hour—not many nonalcoholics can do that, even if they try—the BAC would be about 0.07% five hours later if the person had no more to drink after that time.
Several years ago I worked with a group of judges who were away at a retreat, so no one was driving after dinner. We set up a Breathalyzer and had them check their BACs at various times during the cocktail hour, during dinner, and then at the end of dinner. They were amazed at how low their BACs were even when they felt somewhat intoxicated immediately after drinking. None had even one reading of 0.08% or higher. They were surprised because the legal limit for driving in much of the United States today is 0.10%. When they had seen people in their courts with BACs in excess of this number, they assumed that they had had one or two drinks in the evening before being picked up by the police, because that is what the drunk drivers told them. The average number of drinks consumed by people picked up for drunk driving by the police is about thirteen in the five hours before their arrest. Such drinking cannot be defined as “social” or “responsible” drinking.
Figure 5–1
Number of drinks and blood alcohol concentration (BAC) in one hour of drinking.
SOURCE. U.S. Department of Transportation, National Highway Traffic Safety Administration. Improving Understanding of Alcohol Impairment and BAC Levels, and Their Relationship to Highway Accidents (DOT, hs-807-433). Washington, DC, U.S. Department of Transportation, 1989.
In a recent study of new alcohol testing equipment, several of my colleagues gave alcohol to experienced alcohol-drinking college students who were at least twenty-one years old. We gave them as many drinks as they felt comfortable drinking in a safe setting, a hotel hospitality room. Over a three-hour period these students drank three to five drinks each. None of them got a BAC of more than 0.05% at any time of the study. We asked the students how they would have felt if we had asked them to drink enough alcohol to get to a BAC of 0.10%. None felt they could have done that without feeling ill. As it was, one woman felt so drunk that she feared for how she would have driven a car right after drinking.
We did not let any of these students leave the test site until their BACs returned to below 0.02%, which took about two hours after they stopped drinking. This experiment was a confirmation that the current standard for impairment on the highway of 0.10% or even 0.08% is substantially too high. Normal social drinkers, even when they drink more than they feel comfortable drinking, do not get BACs into this range. When someone has a BAC of 0.08% or higher, that person is a heavy drinker who has drunk a large amount of alcohol immediately before the test.
Although the amount of alcohol consumed and the time over which it is consumed are the major determinants of the BAC, the presence or absence of food in the stomach is another important factor in determining BACs because food absorbs alcohol and slows absorption, thus giving the liver more time to break down the alcohol. Social drinkers often drink small amounts of alcohol usually with food to keep their BACs low because they do not like the intoxication caused by high BACs.
The effect produced by any level of BAC is different for different people. Inexperienced drinkers are often profoundly impaired with BACs of 0.05% or so, whereas experienced heavy drinkers can appear normal with BACs of 0.10% or higher. This is not because the livers of experienced drinkers are better at metabolizing the alcohol, but because their brains have learned to function reasonably with alcohol present. This is called state-dependent learning. It means the person has become accustomed to functioning with a drug in the brain. This is mostly a learning effect, not a metabolic effect. Young and inexperienced drinkers have severe behavioral effects far below the legal cutoff of 0.10% for drunkenness on the highway. Although heavy drinkers can appear normal in routine settings, they, like inexperienced drinkers, are not safe behind the wheels of cars if they have a BAC above about 0.04%.
The levels set for legal limits on the highways are averages and may not reflect the actual levels of impairment from alcohol seen in individuals, because there is so much variation in alcohol’s effects. Even more variable is the effect of impairment from alcohol and other drugs in relation to specific tasks. When people are expected to do something routine they can often do it with a fairly high BAC, but when they are confronted with a divided attention task (e.g., adjusting their radio while still keeping track of what is happening on the highway in front of them) and when they are confronted by an unfamiliar experience (e.g., a biker unexpectedly entering the highway from a driveway), they are often profoundly impaired even with relatively low BACs.
One important paradox of chronic, heavy drinking is that alcoholics and other heavy drinkers can generally “hold their liquor,” meaning that they show relatively minor effects from heavy drinking. But when their livers become adversely affected by their drinking, as often happens after years of heavy drinking, their livers do not metabolize the alcohol (or any other chemical) effectively. Then their alcohol sensitivity goes up, not only compared with their own previous prodigious abilities to drink but even compared with inexperienced drinkers. Alcoholics can be drunk and stay drunk for hours after one or two beers once their livers are damaged. This saves them a lot of money, but it is a terrible prognostic sign. Usually such increased sensitivity to alcohol means that death from irreversible liver failure is close at hand.
Any alcohol in the bloodstream is associated with impaired performance. For that reason, the U.S. Department of Transportation has set 0.02% as the maximum allowable level for commercial drivers. As recently as ten years ago, some states had legal BAC levels as high as 0.15% for all drivers. Today, in states across the country, the permissible level of alcohol in the blood for driving is falling. The best social policy is to keep the nation’s roads and highways drug and alcohol free. That means that, as a practical matter, the maximum permissible BAC should be 0.02% or less. In the United States we are now watching the social contract with respect to alcohol drinking change from the standard that one should not drive “drunk” to a better standard that a person should not drive within several hours after drinking alcohol.
My simple standard, outlined in more detail on pages 288–92, is that one should not drink more than two to three drinks in any twenty-four-hour period and that one should not drive within four hours of the last drink. This will ensure that the BAC is well below 0.02% before driving. Heavy drinkers do not know how much they drink, so they often state, sometimes with complete innocence, that they only had “a few beers,” when their BAC is 0.10% or higher.
I am reminded of a minister who was arrested for driving while impaired (DWI). Her BAC was 0.12%. She told me that she had had “no more than three drinks the entire evening.” She was so upset with the arresting police officer that she argued with him and finally hit him, leading to an additional criminal charge of striking an officer. This was totally out of character for this generally calm and self-controlled woman. She was shocked when I reviewed with her the facts about BACs. She too suffered from denial, once more making the point that addiction distorts the thinking of all people.
In contrast to heavy drinkers who regularly understate their use of alcohol and its impairing effects on them, including their ability to drive a car, many inexperienced drinkers and most ordinary social drinkers not only feel impaired after one or two drinks, but they are afraid to drive for fear that they will be picked up by the police for drunk driving. This is a socially useful fear because it contributes to their drinking less, especially when they will be driving. However, in one sense, it is an unrealistic fear. Even if such people had an automobile accident and were taken by a police officer for a blood alcohol test, they would be passed as not impaired by alcohol because their BACs would be so low, far below the current minimum standard of 0.08% and even below the future standard of 0.04%. On the other hand, most of these inexperienced drinkers are impaired by low doses of alcohol, so their fears are well founded. No alcohol use before driving, which is the universal standard in Europe today, is the best policy.
The Alcohol Paradox: Safest and Most Destructive
Alcohol holds the apparently paradoxical position of being legal for adults in North America and throughout the non-Muslim world and at the same time being the world’s most devastating drug. Alcohol is relatively safe, compared with most illegal drugs, but its wide use and relative social acceptance produce high social and medical costs. Why is alcohol so much more widely used than any other abused chemical, and why, despite its apparently safe use by many people, does alcohol cause more problems (in terms both of health and behavior) than all other intoxicating drugs combined?
The basic picture of addiction explains these apparent paradoxes. Alcohol is the most easily manufactured intoxicating drug, being made by simple fermentation of sugar. For this reason, alcohol production was discovered in virtually all early human societies (except the Eskimos, who lacked a supply of carbohydrates, including sugar). Alcohol is used orally, which somewhat limits its reinforcing properties. Until the discovery of distillation in the modern era, alcohol concentration was limited to that produced by wine (about 11%) or beer (about 5%) through natural fermentation.
Thus, almost all human populations have a long history of alcohol use and relatively well-developed cultural means of limiting alcohol’s problems. Nevertheless, the introduction of distilled spirits had profoundly destructive effects in all societies when it first occurred, as described in Chapter 2.
Alcohol is the world’s most abused drug because it is the world’s most socially tolerated drug. Alcohol was used by 113 million Americans in 1998, whereas only 11 million used marijuana, the second most widely used intoxicating drug. Alcohol is more widely tolerated than any other drug, not because it is safe but because it is somewhat safer than most of the other drugs. Even more important, alcohol is more familiar than other drugs to most people in all parts of the world. Alcohol produces the most harm of any intoxicating drug because it is the most widely used drug.
When the social costs of alcohol use are related to the extent of use, it is the least problem-generating intoxicating drug on a per-use basis. But because alcohol use is so extensive, it produces the highest total social costs of any drug. Alcohol is generally the first drug that young people use. It is thus the ultimate gateway drug.
When any family, community, or nation attempts to deal with the problems of intoxicating drugs, alcohol must be a central focus of those efforts. The United States ranks midway between the high-consumption wine-drinking nations of southern Europe and such low-consumption nations as Algeria, Morocco, and Thailand.
When I speak to sophisticated North American high school and college students, some of whom oppose the restrictions of the twenty-one-year-old legal drinking age for alcohol, I can count on one of the students to bring up the fact that there is no minimum legal drinking age in Europe. Anyone of any age can buy and use alcohol. According to these skeptical students, the youth of Europe have far fewer problems with alcohol than do their North American peers. This argument appears to go easily to the next step. It is the prohibition of youthful drinking in North America—and the “mistrust” that underlies it—that causes teenage drinking problems. How could the solution to this problem be simpler? Eliminate the drinking age and, presto, there will be fewer youthful drinking problems in North America! The logic here is as breathtaking as I have found it to be commonplace. Writ larger, this is a central argument used by advocates of fully legal drugs. In this misguided view, it is the prohibition of drugs that causes drug problems. Therefore, get rid of the prohibition and we can solve our alcohol and drug problems.
Before responding to this critique of current North American alcohol and drug policies, we need to have a few facts. Prohibition in North America came about because of the problems created by the use of addicting substances, not the other way around. The biggest cause of problems with alcohol and other drugs is not prohibition. It is the effects of the drugs themselves. In every situation, in every nation, prohibition reduces drug use and legalization raises drug use. It is both unbelievable and totally without foundation in experience anywhere in the world that legalizing drug use, or any other act of increasing acceptance of drug use, would have any effect other than increasing drug use and increasing the problems caused by that drug use. Reducing the drinking age or, even worse, eliminating it entirely would increase youthful use of alcohol, not reduce it.
Problems such as teenage drunk driving deaths would go up if alcohol use by youth were legalized in North America. The national experience during a decade in which the American drinking age for alcohol was reduced to eighteen (roughly 1974 to 1984) was a clear lesson on this point. Drunk driving deaths for teenagers rose. When the legal drinking age was returned to twenty-one, where it had been in the United States since 1933, teenage drunk driving deaths fell.
There is an important point buried in this common question: Why is it that Europe does not have legal drinking ages and yet has fewer adolescent drinking problems than now occur in the United States? The answer is that most European communities have fewer automobiles, and those they have are less likely to be driven by teenagers. Additionally, Europeans have had far tighter family and community controls over teenagers than do communities in the United States. European communities have not had the tradition of youthful peer group drunkenness and illegal drug use that has become commonplace in North America over the last three decades. Europe has a driving age of eighteen, in contrast to the usual North American age of sixteen or, in some places, even fifteen.
The global cultural drift is toward the American model of teenage use of alcohol and other drugs. Today European youth are experiencing increasing levels of abuse of illicit drugs and alcohol. It is not difficult to predict that within a decade or less there will be far tighter legal and other formal controls on youthful drinking in Europe than exist today. Exchange students with whom I have talked make this point clearly. They see far more unsupervised peer drinking and drug use in the United States than in Europe, and they also see increasing evidence of the American pattern emerging in Europe. There are sound historical and biological reasons to restrict drinking of alcohol and smoking of cigarettes for teenagers.
When societies have tight controls over adolescent behavior, based on widely observed family and community values, it is less important to place legal controls over drinking and drug use by teenagers. To the extent that any community moves toward the modern high-risk approach to the teenage years—with looser adult supervision and greater socializing among adolescent peers—then there is a greater need for legal and other formal limitations on adolescent behaviors that are clearly destructive both to the youths themselves and to their communities.
As one forty-five-year-old woman patient of mine who grew up in the South American country of Colombia said:
When I grew up, I was under my parents’ watchful eyes every minute of the day. Now my teenage daughter, who is growing up in the United States, is free to go and come as she pleases, without the close, continuous oversight I had. She has risks that I never had. I do not begrudge her this freedom. I want her to have it, as I wanted it for myself. But I also see how hazardous it is for her and her friends.
It is not just alcohol; of course, drugs and sex also play big roles in the high-risk modern teenage lifestyle.
North American youth who want to adopt the European system for the alcohol drinking age might think twice about trading positions with their European peers who cannot drive until the age of eighteen , and who face during their entire lives a highway standard that calls for no alcohol in the blood of drivers of any age. Europeans are generally not as tough as North Americans on the drinking age issue, but they are a lot tougher when it comes to drinking behind the wheel of an automobile, for both youth and adults.
Alcohol as Medicine
In the heyday of patent medicines at the end of the nineteenth century, drugs of abuse were common ingredients in concoctions sold for virtually every imaginable ache or pain. This was no accident. Drugs of abuse produce powerful effects on the brain, including the effect of reward. They suppress pain. The brain is organized so that pleasure and pain are reciprocals. What produces pain reduces pleasure; what produces pleasure reduces pain. Many of the most powerful painkillers are abused drugs. In addition, some pleasure-producing drugs also cause physical dependence, which keeps the customer coming back, the way nicotine dependence sustains the sales of cigarettes.
Alcohol was a mainstay of patent medicines 100 years ago. In an era of growing hostility to nonmedical alcohol use, especially alcohol use by women, patent medicines were a relatively available source of the euphoric and analgesic effects of alcohol. Before the Pure Food and Drug Act of 1906 required labeling of all substances sold as medicines, the buyers of patent medicines had no way of knowing that alcohol was a major ingredient in the products they bought.
Today, alcohol is used commonly in over-the-counter medicines as a liquid in which to dissolve other substances. The amount of alcohol contained in these products is usually small, although it can cause problems, especially for alcoholics. Alcohol itself is not thought of as a medicine today. It is not prescribed by physicians, largely because alcohol lacks any specific medical benefit, and because it is likely to be abused. There were three primary indications for the past use of alcohol as a medicine: it was used as a painkiller, as a sleep-inducer, and as an antianxiety agent. Today there are safer medicines for all these indications. Nevertheless, recovering alcoholics, especially those taking the alcohol-blocking agent Antabuse, should read the labels of over-the-counter medicines carefully because some use alcohol as a solvent. The increasingly common label on over-the-counter preparations, “alcohol free,” is a reminder of the history of alcohol’s past role as a medicine.
Other Depressants
In the same way that stimulant drugs stimulate the central nervous system generally, so the depressant drugs depress the brain generally. These drugs work in a variety of ways to slow down brain processes. In medicine, depressants can calm someone who is pathologically stimulated (as in an anxiety disorder or epilepsy). These can be desirable effects, as can depressant use as part of anesthesia before surgery. Depressants also can reduce fear and cause amnesia as part of surgical anesthesia.
The depressants are used in medicine to treat anxiety and insomnia. The barbiturates were the most commonly used depressants until the 1960s, when the benzodiazepines replaced them in medical practice. Alcohol has many effects similar to those of the barbiturates and the benzodiazepines, but because it has no medical use and is by far the most widely used intoxicant in the world, it is treated separately in this chapter. Alcohol has a far shorter duration of action than either the barbiturates or the benzodiazepines, underscoring the role of pharmacology in determining abuse liability.
THE WHIPSAW: INTOXICATION AND WITHDRAWAL. In overdose situations, depressants can suppress the brain so profoundly that consciousness is lost and breathing stops. During the first half of the twentieth century, the barbiturates were widely used in outpatient medicine to treat insomnia and anxiety. They were a common cause of deaths from suicide throughout the industrial world. When depressants are abruptly discontinued after prolonged, everyday use, there is an overshooting of opposite effects associated with withdrawal—a pathological brain stimulation. When chronic nonmedical use of a stimulant is stopped abruptly, the drug abuser is exhausted and often sleeps for long periods of time. In contrast, when chronic nonmedical use of a depressant is abruptly stopped, the drug abuser often is pathologically stimulated. Anxiety, insomnia, and even epileptic seizures are common depressant withdrawal effects. Stimulant users after use of the drugs appear wired or uptight, whereas depressant users appear slowed down, drunk, or sleepy immediately after drug use.
For both stimulants and depressants, the effects of drug use are reversed during the hours or days after everyday use stops, during the withdrawal period. Therefore, depressants cause mental depression immediately after use but rebound or withdrawal stimulation after the depressant use stops. One of the most common signs of cocaine use in the workplace is sleepiness and lethargy, the withdrawal symptoms following acute overstimulation by cocaine.
Marijuana
Marijuana, or pot, is a plant product, like tobacco, and it is usually smoked, although it can also be swallowed. Marijuana is not injected or snorted as cocaine and heroin often are. Marijuana, unlike alcohol, cocaine, and heroin, is not a specific single chemical. Marijuana is a crude drug, a complex chemical slush. All four of the most commonly abused drugs in the world are simple agriculturally produced substances with long histories. Before the last half of the nineteenth century, these drugs were used by people in relatively simple and traditional ways. For example, cocaine was used by chewing the coca leaf, and opiates were consumed as opium, the dried sap of the opium poppy. Since the advent of modern chemistry, however, cocaine has been purified and has totally displaced coca leaf chewing, except for a few South Americans living in the Andes Mountains who continue to chew coca leaves. In the twentieth century, heroin has replaced opium use throughout the world.
In contrast, marijuana is still widely used as a crude agricultural drug of abuse. The leaves and flowering tops of the plant Cannabis sativa typically are smoked. This plant comes in three forms: the drug plant, the hemp plant, and the intermediate plant. The common hemp plant contains little drug, but the drug plant contains large concentrations of psychoactive chemicals. Cannabis is available to drug users in three forms. Marijuana is the leaves and stems of the plant. It looks like common dried spice or herb leaves, much like dried parsley. Hashish is the resin of the cannabis plant. Hashish resin is dried and compressed into balls, cakes, or cookielike shapes. Hash oil is the concentrated chemicals in the hashish. It looks like motor oil.
The major cause of the high of marijuana is delta-9-tetrahydrocannabinol (THC), which is found in relatively high concentrations (roughly 1% to 6%) in the marijuana used by drug abusers. Hashish contains similar concentrations of THC, but hash oil can be 20% or more pure THC. Marijuana and hashish contain over 420 different chemicals, which fall into eighteen different chemical families. Of these chemicals, THC is the major one that produces the high. THC is one of sixty-one chemicals in marijuana that are cannabinoids, or chemicals found only in the marijuana plant. Another common cannabinoid is cannabidiol, which, like all of the cannabinoids, is biologically active, meaning it affects the body of the marijuana user even though cannabidiol does not cause a high.
Once the marijuana is smoked, users inhale more than 2,000 different chemicals into their lungs to be taken in their bloodstreams to all the cells of their bodies. In terms of the complexity of the chemical exposure for the users, marijuana is unlike alcohol, cocaine, or heroin because it is a crude, not a pure drug.
THC is highly soluble in fats, so it rapidly passes the blood-brain barrier. This property, combined with THC’s insolubility in water, results in the unusually long retention of THC in the brain and other fat-containing tissues of the body. THC is trapped in the body’s organs that use fatty building blocks, such as the brain and the reproductive glands. It is not quickly carried away by the water-based bloodstream as are water-soluble drugs. This means that THC persists in the brain and reproductive organs for days or even weeks after the drug was last used.
THC increases the heart rate and raises the blood pressure by stimulating the norepinephrine (NE) neurotransmitter system. THC can cause panic attacks and trigger agoraphobia among vulnerable people, presumably by this same mechanism. Other physical effects of marijuana use include increased hunger (called “the munchies” by marijuana users) and thirst, bloodshot eyes, and dilated pupils.
In high doses, THC can produce short-term or prolonged psychosis, supporting the view that the serotonin system of neurotransmitters also is affected by marijuana. It is possible that THC affects both the acetylcholine and GABA systems in the brain. The retained THC continues to affect the brain long after the marijuana high has passed. A study of young heavy marijuana smokers showed that their memory was still impaired six weeks after they stopped smoking the drug.
Marijuana smoke contains more tar and cancer-causing chemicals than even cigarette smoke. One marijuana cigarette has as much cancer-causing tar as seventeen tobacco cigarettes. Marijuana smoke, like tobacco smoke, causes bronchitis, inflammation of the airways in the lungs, and chronic respiratory illnesses. THC also affects most other systems of the body. It reduces normal hormone function in both males and females, reducing fertility and causing miscarriages. Both alcohol use and marijuana use during pregnancy can produce the fetal alcohol syndrome, a specific congenital abnormality often associated with impulsive behavior and lifelong mental retardation.
The Dumb High
The most striking effects of marijuana are on the user’s brain. With occasional use, marijuana produces sedation and slightly altered mental processes. Learning is slowed, and concentration and short-term memory are hampered. Reaction times are slower and perceptions of time and distance are distorted, making driving and other safety-related behaviors especially hazardous after marijuana use. Users are commonly unaware of their impairments after using small doses of marijuana. Larger doses can precipitate acute anxiety or panic, or schizophrenic episodes, particularly for novice marijuana users and for people subject to these mental health disorders. Long-term effects of marijuana use are still being researched, but there is growing evidence of permanent brain cell and chromosomal damage as well as the impairment of logical thinking. Some long-term users of marijuana show prolonged, perhaps lifelong, deficits in memory and motivation as well as irritability.
Although marijuana was not the first drug in the modern drug epidemic—a dubious distinction that belongs to the hallucinogens, especially naturally occurring mescaline and psilocybin as well as synthetic LSD—marijuana by 1970 became the central drug in the modern North American drug abuse epidemic. Because marijuana does not produce respiratory depression or other acute effects associated with overdose death (as heroin, barbiturates, and even alcohol do), and because withdrawal was not observed when chronic marijuana users refrained from use for a few days, marijuana had the aura of a safe high, the requirement for a new gateway drug. In the 1970s, marijuana mistakenly was the model for a “soft” drug as heroin was the model for a “hard” drug.
One of the more remarkable aspects of the marijuana story has been the difficulty scientists have had in understanding how marijuana works in the brain. Only in 1987 was the THC receptor in the brain identified, and not until 1992 was the naturally occurring neurotransmitter that fits this brain lock identified. The THC receptors, widely distributed throughout the brain, have been found in particular abundance in the cerebellum and the hippocampus, two primitive brain areas involved with motor functions, learning, and memory. These areas are connected to the pleasure centers of the brain, but it remains unknown what the natural brain function is for these receptors.
Experiments on rats have shown that THC causes impairments of short-term memory, which is similar to the effects produced when hippocampi in the rats’ brains are damaged. Long-term marijuana use causes irreversible cell destruction in these same hippocampal brain regions. This may explain why people who have used a lot of marijuana for many years find that their memory is permanently impaired, just as heavy and prolonged alcohol use can permanently damage the users’ livers as well as their brains and nerves.
Prolonged and even permanent changes after long-term marijuana use need to be kept in perspective. Whenever long-term drug users stop drug use, the damage to their bodies stops. The body often develops ways of compensating, partially or in some cases totally, for the harm done by the earlier drug use. The permanence of the damage done by any drug should never become an excuse not to quit drug use. Damage to the brain and other parts of the body should be a reason never to start and, if a person has started, an even more compelling reason to quit the drug use. This fact of life applies to marijuana as it does to all nonmedical drug use.
One of the claims made for marijuana by enthusiastic supporters of this drug is that, unlike alcohol, marijuana does not cause a hangover after heavy use. The scientific basis for this common observation is not reassuring. Alcohol is quickly eliminated from the body, usually within a few hours after drinking stops. The withdrawal or hangover experience after alcohol use reflects the brain’s attempt to get along without the presence of the chemical. This does not occur for marijuana because THC stays in the brain for days after use of the drug stops. The fact that marijuana does not cause a hangover the way alcohol commonly does after heavy use is not an advantage at all. Marijuana stays in the brain for a long time so that the brain is still experiencing the effects from pot smoking days after the drug use has stopped, in contrast to alcohol use.
The Careless Drug
Marijuana makes users stupid and lazy. It is the “careless drug,” because pot users often lose the capacity to care. In the most extreme form, this is called the amotivational syndrome, meaning that chronic pot smokers become listless and apathetic, not just when using the drug but all of the time. This tragic state is called “burnout” by drug abusers themselves. Unlike cocaine, which often quickly brings users to their knees, marijuana claims its victims in a slower and more cruel fashion. It robs many of them of their desire to grow and improve, often making heavy users settle for what is left over in life. For this reason, marijuana is the most insidious drug. Its effects are both profound and subtle.
Heroin use encourages criminality, as heroin addicts steal and rob to get money to keep getting high. Cocaine makes users unstable and aggressive, as their brains get stuck on “go.” Marijuana makes its users lose their purpose and their will, as well as their memory and motivation. Marijuana smokers do not often come into treatment for their addiction simply because neither they nor those around them can differentiate their true selves from the effects of their drug use. They commonly just sink lower and lower in their performance and in their goals in life as their pot smoking continues. Their hopes and lives literally go up in marijuana smoke.
It is no coincidence that the terrible 1987 train crash at Chase, Maryland, which claimed seventeen lives, was caused by an engineer high on pot. He looked fine to his co-workers that day, but he drove his train through four warning signals into the path of a high-speed Amtrak passenger train. He performed his important and potentially dangerous job with an attitude of carelessness that I have come to recognize as the common result of marijuana use. Based on my experience with marijuana users, when I learned that an employee in a paper mill reached in to grab a piece of wood through a fast-moving belt, in total violation of the basic safety rules of the company, I suspected that his carelessness was the result of marijuana use. A drug test conducted while the employee was in the hospital confirmed my fears. That man lost the use of his right arm as a result of his injury. That was a hard way to learn about the so-called safe high of marijuana.
Marijuana as Medicine
Marijuana, like opium, coca leaves, and alcohol, has a long history as a folk medicine used to treat an endless variety of human miseries. Prescientific cultures, lacking modern purified, potent medicines, relied on commonly available natural psychoactive substances to reduce human suffering. The abused drugs, because of their effects on the brain’s pleasure/pain centers, were attractive in this role. In addition, incorporating these abusable substances into folk medicines rather than making them available for personally controlled pleasure ensured that their use within the community would be controlled not merely by the user but by culturally responsible therapists. Thus, the use of folk medicines was not for recreational purposes but for medical purposes with strict cultural controls.
Until the middle of the nineteenth century, there were few chemically pure medicines, so the use of complex natural substances, such as opium and cannabis, was common. In the last half of the nineteenth century, modern chemistry purified chemicals used as medicines so that morphine was extracted from opium and cocaine was extracted from the coca leaf. Only in the late 1960s was purified THC extracted from marijuana leaves and resin and identified as the chemical that causes the high and many of the other effects of marijuana use.
Modern medicine, beginning in the first two decades of the twentieth century, for the first time brought chemical science to the ancient art of medical therapeutics. Physicians from then on did not use unpurified and unstable natural products as medicines. They used chemically purified and stable pharmaceuticals to treat specifically diagnosed medical illnesses. For severe pain, for example, physicians prescribed morphine or, in more recent years, synthetic opiate substitutes, rather than prescribing a mixture of alcohol and opium, called laudanum, as occurred in the nineteenth century and earlier. By using a chemical that was pure and stable, physicians knew precisely what their patients were taking and could give their patients these substances free of a hodgepodge of inactive and potentially harmful substances. Physicians could be sure that the specific therapeutic substance was present in a known, controllable dose.
Marijuana, with over 420 chemicals, let alone marijuana smoke, with over 2,000 different chemicals, many of which are known to be harmful to the user’s health, is not an attractive modern medicine. Nevertheless, marijuana smoke does have powerful effects on the brain and other parts of the body. Modern biomedical research into the effects of smoked marijuana has identified many effects, some of which may be found to have therapeutic potentials to treat specific illnesses.
Several years ago, dronabinol (Marinol), a synthetic THC, was approved by the FDA as a medicine in both capsule and suppository forms to treat the severe nausea and vomiting sometimes caused by cancer chemotherapy. When patients are treated with powerful medicines to kill cancer cells in their bodies, the medicines also are toxic to other rapidly dividing cells in the body, including those in the gastrointestinal tract and those that make both red and white blood cells. Some of these anticancer medicines also stimulate the brain’s vomiting center. Nausea and vomiting after cancer chemotherapy are both extremely unpleasant and potentially dangerous, especially for people who are already seriously ill.
Doctors discovered that THC reduces nausea and vomiting for such patients. This led to strong political pressure from the promarijuana lobby to approve marijuana for medical treatment as a compassionate response to the suffering of cancer patients. Marijuana, or even purified THC, was not and never has been proposed as a treatment for cancer. The only proposed use for marijuana or THC in the treatment of cancer patients is to treat the nausea and vomiting associated with the use of chemotherapy.
Oncologists, the medical specialists who treat cancer, studied THC and found that it was helpful for some patients but that it had many unwanted side effects, including making it unsafe to drive a car and sometimes causing psychosis. Most cancer patients who were not previously drug addicted found the effects of THC to be extremely unpleasant. Oncologists did not want to use smoked crude marijuana as a medicine because it contained so many chemicals, some of which actually caused cancer and suppressed the immune system, and because the dose of THC reaching the patient could not be controlled accurately with smoking. In recent years, new synthetic medicines, unrelated to THC or marijuana, have been developed that have made THC obsolete in the treatment of nausea and vomiting from chemotherapy. Ondansetron (Zofran) is one example of these new, more effective, far safer, and more powerful antinausea medicines.
Marijuana has been proposed as a treatment for the wasting (loss of appetite and loss of weight, which can be life threatening) in AIDS because of marijuana’s well-known tendency to produce “the munchies,” or the desire to eat high-calorie foods. Not only is there no solid scientific evidence that marijuana or THC helps AIDS patients, but marijuana’s well-known ability to depress the immune system and to cause cancer makes it extremely unattractive as a medicine for AIDS sufferers, who are literally dying from damaged immune systems. The fact that marijuana can cause some AIDS sufferers to feel high and therefore less upset is no more a reason to use marijuana as medicine for these sick patients than it is to give them alcohol or cocaine.
Marijuana has been proposed as a treatment for asthma, but, although THC does dilate the bronchi (which are closed down by asthma attacks) in the short run, the irritants in marijuana smoke actually cause lung pathology, including long-term bronchial constriction, after prolonged use. Therefore, marijuana is not likely to gain favor as an asthma treatment.
It has been proposed that marijuana can be used to treat glaucoma. THC does reduce the pressure in the eye for a few hours, as do many other substances, including alcohol. However, glaucoma is a twenty-four-hour-a-day disease, so a person who is treated for glaucoma with marijuana has to smoke pot or take THC pills around the clock. Worse still, marijuana and THC are weak in their effects on pressure in the eyeball, so the person with glaucoma has to use not only around-the-clock marijuana smoke or THC but also routine glaucoma medicines. No controlled scientific studies have shown that THC or marijuana add anything useful to the other medicines routinely used in the treatment of glaucoma, all of which last longer, produce fewer unwanted side effects, and are more powerful in their effects in reducing eye pressure than is marijuana, or THC.
Marijuana has been proposed as a treatment for the spasticity of multiple sclerosis. No controlled studies have been conducted to show that THC helps with this serious problem, although cannabidiol, a nonpsychotropic cannabinoid found in marijuana, may prove effective. These preliminary results showing benefit from the use of cannabidiol have not been confirmed in controlled studies.
The National Institutes of Health recently completed a review of all the proposed medical uses of marijuana and THC and concluded that there was no longer any basis for the government to have a compassionate program to supply marijuana to sufferers from any illness whatsoever. None of the medical uses for marijuana so far proposed met even the minimal standards of safety and efficacy required of a proposed medicine. Thus, although THC capsules and suppositories remain available to doctors treating cancer patients for nausea and vomiting, there is no other approved use for THC, and there is no approved use for smoked marijuana as a medicine to treat any illness. When THC and marijuana have been used in experimental settings to treat various illnesses, doctors have found that the psychoactive effects—the high and the mental clouding—are unpleasant to most patients, except those who were previously drug abusers. Marijuana and THC are poorly tolerated and exceedingly unattractive to most medical patients.
Meanwhile, the promarijuana lobby has not been satisfied with the approval of purified, synthetic THC because they want to focus on very sick patients using smoked marijuana, the crude drug, as medicine. They want the public to see smoked marijuana as medicine—as a way of rehabilitating the negative image of marijuana. Promarijuana apologists insist on the use of crude, smoked marijuana, not THC or other purified chemicals for medical treatments. The marijuana-as-medicine controversy has become a political issue in North America.
The FDA and the National Institutes of Health oppose such proposals, as do the National Institute on Drug Abuse and the Drug Enforcement Administration. Virtually all of the medical organizations that speak up for the welfare of the patients in each of the proposed areas where marijuana might be used are also opposed to marijuana as medicine. Most of the proponents of marijuana as medicine are the same people who want to normalize and/or legalize illicit drugs, especially marijuana.
It is useful to remember that all abused drugs have powerful effects on the body. It may someday be discovered that one or more of the individual chemicals in some of the commonly abused drugs will play a uniquely useful role in the medical treatments of some illnesses. The biomedical research now going on into the effects of abused drugs may identify important therapeutic effects of some of these specific chemicals.
Even the most antidrug activist needs to recall the nature of the modern social contract for drug use. It specifies that, under the careful supervision of a physician, abused drugs will be available in medical treatments of illnesses other than addiction. Thus, medical use is not an enemy of drug abuse prevention, as long as the medical use of potentially addictive medicines meets the standards set for other medicines and as long as the use is properly controlled to protect both the patient being treated and the community from the potential harm such medicines can cause when they leak out of the medical care system.
To this contract for medical treatments with abused drugs, I add one additional element. Substances that are of high abuse potential and substances that are currently widely used nonmedically in the society should be required to meet a higher standard than substances not widely abused. Not only should they be shown as safe and effective in specific medical applications, the standard that any medicine must meet, but they should also meet the standard that they provide a significant benefit not currently available from nonabused or less abused medicines.
Thus, before THC or heroin, two widely abused substances, are introduced as medicines, they should be shown to offer specific benefits not available with less socially risky substances. Although it is possible that in the future some of the chemicals in abused drugs will meet this higher standard, none does so today Certainly, smoked marijuana will never be approved as a medicine, any more than smoked tobacco or, for that matter, alcohol, will be approved as an acceptable modern medicine.
The marijuana-as-medicine advocates have several advantages in the current political debates over medical use. The prodrug lobby is large and powerful in North America, and it has now concentrated on this issue because it has proved powerless in its earlier, more frontal assault on the prohibition against marijuana. To sharpen their attacks on prohibition and to gain supporters, promarijuana advocates have focused on the most feared illnesses that induce the greatest sympathy for their sufferers, such as terminal cancer, AIDS, and multiple sclerosis. They have exploited the widespread conviction that the government agencies that control the approval of medicines are too slow and too tradition-bound to approve many medicines that can help suffering patients with these illnesses, especially potential medicines that are controversial because they are abused drugs.
Finally, this lobby has capitalized on the interest in traditional medicines and on alternatives to modern scientific medicines, both of which have enjoyed a new vogue in recent years. Folk medicines have an appeal to many North Americans who fear modern science. Thus, the fact that marijuana was used for centuries as a folk medicine is seen, in this highly romanticized view, as evidence that it should be available today as a prescribed or an over-the-counter remedy.
Recall the free-for-all days of the end of the nineteenth century when patent medicines did contain abused drugs. Although the promarijuana lobby can score some points today by talking about folk medicines in ancient China, the patent medicine debacle of a hundred years ago not only is closer to home but virtually impossible to romanticize. Americans tried the experiment of using cocaine, heroin, alcohol, and other abused drugs as folk medicines, as over-the-counter products, at the beginning of the twentieth century. It was an unmitigated disaster. We do not need to repeat that experiment at the end of the twentieth century.
The way medicines are approved in the United States today not only favors medicines that are developed and sponsored by large, sophisticated pharmaceutical companies, but the current path to approval by the FDA requires the issuing of a potentially lucrative patent that permits the recovery of the large costs of gaining approval. Because no one can patent ancient drug substances such as opium and marijuana, there is no money in such remedies for modern pharmaceutical companies.
Government agencies that often sponsor biomedical research, including research into the effects of abused drugs, seldom promote specific medicines, and when they do they have a hard time gaining FDA approval. Thus, if any of the chemicals in abused drugs were to show promise as more effective medicines than the medicines currently in use, it would not be easy to get approval within the current system. On the other hand, patents can be granted for specific chemicals in these crude, traditional drugs.
Today, more than seventy chemicals found in marijuana or related to chemicals found in marijuana smoke are under active investigation by pharmaceutical companies in all parts of the world. The normal profit motive will reinforce the desire of these companies to find more effective medicines for serious illnesses. It is possible that someday, perhaps soon, one or more of these chemicals will become widely useful in the modern treatment of a disease. If so, we can all be grateful for one more benefit from the modern scientific study of abused drugs, because that study will have been the basis of the new medicine.
A persistent fantasy of mine is that someday there will be a clear-cut positive medical use from one of the chemicals in marijuana, and I will be able to join with my longtime foes in the drug prohibition battles and support approval for the medical use of the substance. This would please me greatly because it would add credibility to my claim all these years that I do not oppose the medical uses of these substances on a political or even a moral basis, but simply because none of the chemicals in marijuana has met the minimum standard of showing promise that it is better for the treatment of any illnesses than currently available medicines. When I see that evidence, I look forward to joining in the battle on the side of the medical use of these chemicals. So far I have waited twenty years without having that opportunity.
Despite the apparently compelling evidence that smoked marijuana is unacceptable as a modern medicine for any condition, the promarijuana lobby has convinced many well-meaning people that drug prohibition zealots (as they often characterize me) are keeping suffering, sick people from the relief that smoked marijuana could provide. In state after state, voters have passed initiatives supporting medical marijuana since 1996, including Maine in 1999. It remains to be seen how this political success will be translated into practical outcomes since there is no legal supply of marijuana and since the Federal Food and Drug Administration (FDA) and the Drug Enforcement Administration (DEA) have control over the use of abused drugs in medical practice. Both the FDA and DEA have strongly opposed medical marijuana—unless the chemicals in marijuana smoke were to go through routine approval for safety and efficacy, which it has not done.
Cocaine and Other Stimulants
Substances that stimulate the brain come from many natural and synthetic sources. Naturally occurring brain stimulants include cocaine (from the leaves of the South American coca plant), cathine and cathinone (derived from the khat plant of northeastern Africa and the Arabian peninsula), nicotine (from tobacco leaves), and caffeine (from coffee beans and tea leaves). Synthetic brain stimulants include amphetamine and its chemical cousins, such as methamphetamine, 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA). This is a diverse catalog of substances with diverse histories and diverse effects in all parts of the world. The most powerful stimulant effects are produced by cocaine and the amphetamines, whereas MDA and MDMA are powerful hallucinogens that are closely related chemically.
Cocaine and the amphetamines are among the best understood drugs of abuse. Cocaine can be smoked (“crack” or “free-base”), snorted up the nose, or injected intravenously. It can also be taken by mouth and swallowed. Amphetamines, in contrast to cocaine, are commonly used by mouth, but they are also injected or smoked (“ice”). The related hallucinogens, MDA and MDMA, are taken by mouth. These drugs all stimulate the central nervous system, increasing the heart rate and blood pressure. Stimulant drugs mimic the alarm function of the sympathetic nervous system, the NE neurotransmitter system of the brain. In moderate doses, the stimulant drugs suppress appetite and increase alertness, effects that some drug users find extremely attractive. Other effects of stimulants are to reduce pain, to bolster feelings of confidence and competence, and to produce sustained high-energy levels that obliterate fatigue. Cocaine and amphetamines have profound effects on the heart and on the brain. Epileptic seizures and heart stoppage are possible following nonmedical stimulant use, and both can cause sudden death. Seizures and sudden heart stoppage are possible outcomes of cocaine use, especially when the drug is smoked or injected intravenously.
Crack cocaine, the smokable form of cocaine, is more fat soluble than the older cocaine hydrochloride, which is snorted. Because of this higher fat solubility, crack cocaine penetrates the blood-brain barrier more quickly and then leaves the brain more quickly than powdered cocaine. Thus, crack or freebase cocaine is especially addicting, both because it produces a more rapid high and because it produces a faster and more intense crash following use.
Cocaine users may experience “coke bugs,” an uncomfortable sensation that bugs are burrowing under their skin. These feelings can be so intense that cocaine users become obsessed, developing the delusion that there are actually bugs under their skin. They seek to dig out the bugs with their fingernails, creating terrible, but characteristic, sores on their arms, legs, and other parts of their bodies.
As with all abused drugs, limiting use of cocaine or an amphetamine to occasional small amounts becomes increasingly difficult as the addict loses control of the drug use while addiction deepens. The stimulants are among the most reinforcing of all drugs, making them the most powerfully addicting drugs. When drug addicts abuse stimulants, especially when they inject or smoke stimulants, they quickly lose control of their drug use and of their lives.
Stimulant Addiction: The Quickest Bottom
No other drugs bring users to their knees, forcing them to seek help, as fast or as powerfully as do the stimulants. Many recovering addicts harbor dreams that they can learn in the future to drink alcohol socially or use marijuana or opiates with some moderation. Few stimulant users, once they have become addicted, believe they can ever again use these drugs under any semblance of control. When they do relapse, as they often do, to stimulant use after a period of abstinence, it is seldom with the hope that their stimulant use will be controlled. Addicts relapse knowing that the ending of the stimulant-using episode will be disastrous. The lure of the stimulant high is so powerful that they simply do not, at the time, count the costs to themselves and others. For most cocaine addicts, their “bottoms” rise up and hit them between the eyes within weeks or months of starting to smoke or shoot the drug.
Long-term effects, and effects of larger doses of stimulants, include heart palpitations, anxiety and panic attacks, extreme irritability, insomnia, seizures, paranoid psychosis, and death. The fact that this list of consequences, widely understood by stimulant abusers, does not discourage stimulant use for millions of people speaks eloquently to the grip that stimulants have on the lives of many drug addicts.
Cocaine
Cocaine is a simple chemical derived from the coca leaves grown in the Andes Mountains of South America. It is the only naturally occurring local anesthetic. Although cocaine promotes the release of dopamine (DA) into the synapse in the brain, its major action is to block the reuptake of DA from the synapse by the presynaptic axon, especially in the areas of the brain associated with sensations of pleasure. DA cannot be retrieved effectively by the axon of cocaine users, so it accumulates in the synapse. Because the cocaine-affected neurons govern pleasure and general brain stimulation, cocaine use produces euphoria, an exaggerated sense of well-being, and heightened feelings of energy. The cocaine user’s appetite disappears, and sleep becomes impossible for several hours after use. Cocaine use locks the brain into the “go” mode.
An enzyme that is present in the brain’s DA synapses metabolizes the DA abnormally caught in the synapse of the cocaine user. The axon is able to make new DA only very slowly Because most DA normally is picked up and recycled by the axon, this slow, gradual metabolic process of making new DA is not a problem for the brain in the absence of cocaine use. The metabolism of DA by this enzyme and the production of new DA by the axon are normally in balance. However, with repeated cocaine use, DA is depleted from the axon and finally within the synapse itself as the normally occurring enzyme eats up the DA trapped in the synapse. This DA destruction occurs because of the increased exposure of DA to the enzyme caused by the cocaine-induced, abnormally prolonged presence of DA in the synapse.
The effects from a single use of cocaine last less than an hour, so cocaine users typically take the drug in “runs,” meaning they take repeated doses of cocaine every few minutes over periods of hours or days. The longer a cocaine run lasts, the less pleasure the cocaine user experiences with each use of the drug, as DA is progressively more depleted in the axon and later in the synapse. DA depletion leads to the crash that characteristically ends a cocaine run.
Cocaine does not produce either the physical dependence or the withdrawal that fits the model addiction based on heroin addiction. Cocaine users do not use the drug every single day, around the clock, the way heroin addicts (as well as cigarette smokers and maintenance drinkers) do. When people stop cocaine use, they do not have a clearly defined withdrawal syndrome, although they predictably are depleted and exhausted. This fact misled experts on addiction for many years into thinking that cocaine use was not addicting. Today it is clear that after cocaine users take their drug in runs, the typical user feels tired and depressed, often intensely so. When cocaine use stops, users have a hard time adjusting to their lives and finding pleasure from any activity at all.
THE “WHITE LADY” TURNS DEEP BLUE. Heroin is often called “boy,” and cocaine is often called “girl.” The events at the synapse explain why cocaine users feel depressed and exhausted at the end of a run of drug use, an experience called the “coke blues.” Cocaine users not only feel terrible after a run of cocaine use, but they find they are unable to experience life’s normal pleasures. Their brain’s DA pleasure system has been overstimulated and exhausted by cocaine use. The brain requires weeks or even months to reestablish a normal equilibrium in the DA synapses. After years of work with chronic cocaine users, I am concerned that after prolonged heavy abuse, the DA system of some chronic users may never again function normally, producing a lifelong state of diminished ability to experience normal pleasures.
Cocaine is available to drug abusers in North America today in two forms. The white, snowlike powdered form of cocaine was the first to be used widely in the late 1970s by celebrities and the risk-taking upper class, especially those associated with the fields of sports and entertainment. Because of the association of cocaine use with people on the fast track and its initial high cost, powdered cocaine took on an aura of sophistication, becoming known as the champagne of illegal drugs. Sports figures and risk-taking businesspeople found cocaine attractive for its energizing qualities and promotion of the feeling of omnipotence. Crack cocaine, which became widely available in the United States after 1985, is composed of small pellets, or “rocks,” which are smoked by heating with a flame to produce vapors that are inhaled like tobacco or marijuana smoke.
Although cocaine was initially seductive, heavy cocaine users frequently became paranoid and developed severe psychosis after repeated use. Perceptions became distorted, judgment was altered, and careers and families were destroyed as cocaine addiction deepened. The high cost of cocaine meant that many of the worst effects of chronic use were financial, as people literally put their financial security, and that of their families, up their noses.
COCAINE COMPULSION. Cocaine is the only drug that gives users good feelings when initially used but mostly uncomfortable feelings when subsequently used. With most drugs of abuse, including alcohol, marijuana, and heroin, people who begin using these drugs experience euphoria during their initial honeymoon stage of drug use. As their addiction deepens, they are more likely to report that they feel “normal” after they use the drug than to report that they feel euphoria. With cocaine, this dismal pattern is exaggerated as long-time cocaine users not only report that they no longer feel high after cocaine use, but they report that cocaine use makes them feel paranoid and frightened. Despite the bad feelings, the compulsion to use cocaine not only persists but grows stronger over time with repeated use of the drug.
One young man described to me using cocaine alone in his apartment and pulling down the shades and double locking his door. He then crawled around on the floor, alone and terrified, fearing that the police would look in his window or break in his door. Despite these dreadful feelings, he kept using cocaine, spending thousands of dollars for this experience. This amazed him and gave both of us a new understanding of the word compulsion when it comes to repeated cocaine use.
Many chronic stimulant abusers describe an irresistible compulsion to use their drugs again if they have access to stimulants. This compulsion is not based only on the desire to get high or to feel pleasure. They know from repeated experience that they will never again feel the intense pleasure they found with their initial doses of the stimulant. Nevertheless, they are compelled by a dark inner force from their selfish, addicted brains, a force that they have great difficulty describing, much less escaping. Their primitive brain systems have a hunger that they cannot resist. Watching this phenomenon in my patients who abuse stimulants has been my closest encounter with the full power of the addicted selfish brain. This dreadful experience can only be compared to the brain force experienced by obsessive-compulsive patients to repeat their rituals: It defies language, logic, and common human experience. This force to repeatedly use stimulants simply dominates and obliterates the otherwise sensible person’s willpower.
Cocaine use rose rapidly in the United States in the late 1970s and early 1980s among affluent drug users, most of whom were previously heavy users of alcohol and marijuana. Cocaine had been used extensively in the earlier American drug epidemic at the end of the nineteenth century as an over-the-counter medicine. Cocaine has been popular with intravenous heroin users since the 1920s, when hard-core addicts often injected cocaine along with heroin, in what was called a “speedball.” The mixture of a stimulant with a depressant is a common pattern among drug abusers who are disturbed by the negative effects of one class of drugs alone. Heroin users, for example, often feel uncomfortably sedated or lethargic, so they add cocaine or other stimulants to their drug menu. Cocaine users often feel wired or uptight, so they often lace their cocaine with depressants, such as heroin, or even medicines, such as barbiturates or benzodiazepines, to blunt the unpleasant effects of their stimulant abuse.
When cocaine use took off in North America in the early 1980s, these earlier negative experiences were forgotten as cocaine was seen to be the new marijuana, the safe step beyond marijuana for people willing to use illegal drugs nonmedically to get high.
A HISTORICAL TURNING POINT IN THE AMERICAN DRUG ABUSE EPIDEMIC. Len Bias, the University of Maryland basketball superstar, died on June 19, 1986, of a cocaine overdose following his signing of a multimillion-dollar professional contract with the Boston Celtics. This event ended the widespread feelings of euphoria about cocaine as the safe champagne of abused drugs. America’s amnesia about cocaine’s dangers ended overnight when Bias died. Although other celebrities had died of drug overdoses, no other event in America’s drug abuse history had such impact as the death of this American prince at the height of his powers. The media played the death at top volume for months. Many Americans participated in the national outrage and mourning over the death of this attractive, talented young man. In this sense at least, his death was not in vain, as it galvanized a major national response not only to cocaine but to all illicit drug use.
This was the most public drug abuse death in history. Bias’s death produced a massive reaction, whereas earlier deaths of such media figures as Elvis Presley, Jimmy Hendrix, and John Belushi did not, in part because all of them were seen as jaded by their celebrity, whereas Bias was a college student when he died. In addition, Bias’s death occurred when crack cocaine had recently hit North America like a destructive hurricane. The United States was also entering an election season, which added a political dimension to the public reaction, as representatives of both parties tried to outdo each other in their responses to the drug abuse epidemic.
Bias’s death not only changed the nation’s thinking about cocaine, but it also dispelled many lingering myths about drug abuse. For two decades, so-called drug experts had told the public that people use drugs because they suffer from low self-esteem or from some mental disturbance. Others claimed that drug use reflected failures in family life or economic disadvantage. Bias died in a college dormitory a few hours after he left his loving father. He was not depressed. He was certainly not financially or educationally disadvantaged. The one aspect of his story that did reinforce a stereotypical—and wrong—view of addiction was that Bias was black. As noted in Chapter 3, 80% of the users of illicit drugs in the United States are white. With that one exception, this most public of all drug deaths is a useful standard against which to gauge any theory of why people use illegal drugs. The simple answer, repeated throughout this book, is that users like the feelings that drugs produce, and they believe they can get away with that use, that chemical high.
After Len Bias’s death, many Americans reassessed cocaine, finding it to be much more addictive and dangerous than originally thought. In fact, cocaine’s popular image shifted almost overnight from “soft,” like marijuana, to “the most addictive” of all drugs, “worse than heroin.” Most of the media coverage of cocaine, which had been accepting if not approving before 1986, turned unrelentingly hostile to cocaine use in subsequent years. Suddenly, gone from the mass media were the latter-day Timothy Learys, who touted the virtues of cocaine use to gullible Americans. Prevention and intervention efforts aimed at cocaine use began after 1986 to target an audience that previously had dismissed the incipient dangers of cocaine use, especially youth who were frequent users of alcohol and marijuana.
Len Bias’s death also helped dispel the idea that drug addiction was a result of poverty, poor family life, or lack of education, or that it represented a self-destructive or even suicidal act. Bias died in a college dormitory on the brink of a fabulously lucrative career. He used cocaine that fateful night to celebrate, to party, with his friends.
CRACK: THE ULTIMATE ADDICTION. Crack is a smokable form of cocaine that was first widely used in about 1985, beginning in East and West Coast urban areas. Cocaine hydrochloride was the standard form of cocaine from the end of the nineteenth century until the early 1980s. It could be snorted or injected, a pattern of use that was also seen with heroin use over the same period of time. In the 1980s, a new technique for using cocaine was developed that involved creating what was called freebase, a chemical form of cocaine that was more fat soluble than the hydrochloride and that had a lower vaporization temperature (98°C versus 195°C for cocaine hydrochloride). At first, freebase cocaine had to be made with ether extraction from the hydrochloride, a process that was dangerous because ether is explosive. The terrible fire that burned the comedian Richard Pryor reflected this older technique of freebase manufacture.
In the mid-1980s, a new technique was developed to manufacture freebase: baking soda and water were used to make gray “cracks” or “rocks” of cocaine freebase. This was an easier and safer technique to create a smokable form of cocaine. After smoking crack, the cocaine hits the user’s brain at very high levels within eight seconds, by far the fastest and most powerful way to get a drug high. Even intravenous use takes twice as long, or about sixteen seconds, to reach the brain. Peak effects occur within fifteen minutes of using cocaine by smoking or injecting and within thirty minutes by snorting the drug. The high of the cocaine is gone within an hour, although impairment of thinking can last for days or even weeks after high-dose use of cocaine.
The rapid acceptance of crack cocaine by novice and veteran drug abusers can be attributed to several factors. Cocaine is a highly addictive drug. The first rush after using cocaine produces such a strong sense of pleasure that many one-time users are strongly motivated to recapture those feelings. Smoking drugs—modeled on the experience of smoking tobacco cigarettes and marijuana—is an acceptable activity for many people today. Especially with the recent media attention to the dangers of intravenous drug use, even many dedicated drug abusers have become more wary of needles and injected drugs than they were before the appearance of AIDS. Thus, those seeking intense drug highs, caused by rapidly rising high brain levels of abused drugs, have been attracted to drug smoking.
Even as heavy drug abusers began to avoid intravenous drug use as being too dangerous and as marking depraved addiction, they mistakenly considered smoking a more normal or safe way to use drugs. Although drug smoking does not spread HIV infection, it is as addicting as injecting intravenously because it delivers rapidly rising and high doses of the drug to the brain. All drug abuse lowers inhibitions and promotes antisocial behavior. Therefore, even when drug abusers do not inject drugs, they are at increased risk of HIV infection because of other high-risk behaviors, especially promiscuous sexual activities.
Women are more inclined to smoke rather than inject drugs, making crack cocaine smoking more attractive than intravenous cocaine use to female drug abusers. Women have long been especially attracted to stimulant use compared with other classes of drugs. Crack use by pregnant women has resulted in the tragically common phenomenon of the crack baby, the infant born addicted to cocaine with congenital problems and developmental handicaps.
Marketing tactics of drug dealers have influenced the spread of crack cocaine use. Distributors package crack in relatively small units, making the purchase more attractive and affordable to adolescents and those with lower incomes. Buying powdered cocaine used to mean spending several hundred dollars at a time. Buying crack after 1985 meant coming up with only $5 to $10. The entry cost for the cocaine market fell dramatically in the late 1980s. Just as Milton Hershey took an expensive luxury item, chocolate, and introduced the nickel chocolate bar in the early 1900s, making chocolate, for the first time, affordable for nearly everyone, the same market shift occurred for cocaine in the late 1980s. Cheap crack largely replaced expensive powdered cocaine as the dominant form of the drug.
The profits of cocaine dealers skyrocketed as a result of this change, recruiting new users and sellers with an explosive rate of growth. In America’s cities, the problems of crack cocaine use and crime became thoroughly and disastrously intertwined in recent years, not only because crack users stole property and sold drugs to buy their crack, but because cocaine use itself made people aggressive and paranoid. Crack cocaine in the late 1980s overcame individuals, families, and whole communities with a ferocity never seen before with any other drug habit. Crack cocaine effectively dashed any hope of drug proponents peddling their permissive ideas to the American public about illicit drugs. The question that drug legalizers could not answer became “What about crack? How would you handle that drug if illicit drugs were made legal?” They could not answer because this drug habit was so disastrous to virtually everyone using crack and to those around them.
Cocaine as Medicine
When cocaine was first available to physicians in the 1880s, it was used to treat many conditions, including depression and drug abuse. Sigmund Freud tried cocaine and found it miraculous, recommending it to a good friend and to his fiancée. Within a few years, cocaine was found to have two characteristics that made it useful in medicine. It was a local anesthetic agent, and it stopped blood flowing locally. Ultimately, cocaine found a limited medical use as a local anesthetic, which continues to this day, in minor surgery and in surgery involving bloody procedures, such as hemorrhoidectomies and tonsillectomies.
However, in the last fifty years, a wide variety of synthetic medicines have been developed, such as novocaine, which have fewer disturbing side effects on the brain and the heart than does cocaine. These new synthetics have virtually replaced cocaine in modern medical practice. Nevertheless, cocaine remains available in the American pharmacopeia for a few medical uses. Cocaine is not available to treat depression or drug abuse, however. The late twentieth-century prodrug lobby, which has shown much enthusiasm for the medical uses of marijuana and heroin, has yet to show any interest in either alcohol or cocaine as medical treatments.
Stimulants
AMPHETAMINES and METHAMPHETAMINE. The synthetic stimulants mimic the effects of cocaine by inhibiting DA reuptake, but their major effect is to release DA into the synapse. In addition, amphetamines and methamphetamine are direct catecholamine agonists. They fit the DA and NE locks on the dendrites. The synthetic stimulants turn on the receiving dendrites in this DA neurotransmitter system just as cocaine does, especially in the brain’s pleasure centers. The synthetic stimulants also inhibit enzymes that break down DA and NE in the neuron. The combination of direct action at the receptor site and inhibition of the enzymes that metabolize DA causes synthetic stimulants to produce effects over a longer time than does cocaine. Therefore, depletion effects, such as depression and lack of pleasure, after synthetic stimulant use are even more prolonged and intense than the depletion effects of cocaine use.
LIFE ON A RUN. A run of stimulant use, whether cocaine or methamphetamine, ends with a reversal of the user’s initial experience— euphoria is followed by depression, energy by exhaustion, pleasure by malaise. The major difference between cocaine and synthetic stimulants is that the synthetic stimulants produce effects for many hours after a single use rather than for only a few minutes, as does cocaine. Synthetic stimulants are often used orally, especially early in an addict’s career of drug abuse, whereas cocaine is usually snorted or smoked. Experienced synthetic stimulant users, like other serious drug abusers, usually move from oral use to smoking (a concentrated form of methamphetamine that can be smoked is called “ice”) or to intravenous injection to produce more rapid and higher peaks of the drug in their brains. The eager pleasure centers of their brains, once turned on to the intensely rewarding stimulant drug high, demand these rapidly achieved high levels of the drug.
In the 1930s and 1940s, stimulants were widely used orally in everyday medical practice, especially to treat obesity and depression. They were even sold over the counter without a prescription to long-distance truck drivers and others subject to fatigue. Synthetic stimulants were met with widespread enthusiasm, as cocaine and heroin had been at the end of the nineteenth century when they were introduced. However, within a few years it was widely recognized that the benefits of stimulant use, which appeared to be quick and powerful, were not sustained over time and that stimulant users quickly developed a dependence on the medicines that was hard to break.
Dedicated and unrepentant users of illicit drugs often make fun of antidrug slogans designed to discourage nonmedical drug use. They love to mock Reefer Madness, the antimarijuana film made in the late 1930s, for example. But when it comes to the stimulants, the drug culture itself came up with one of the most powerful of all antidrug slogans, “Speed Kills.” That slogan grew out of the devastating experience in the late 1960s with the use of intravenous amphetamines and methamphetamine. Intravenous stimulant use not only made its users paranoid and sick, but it literally killed them with the violence that their drug use unleashed. “Speed Kills” also refers to a deeper truth about drug use in general and stimulant use in particular. It is a dream killer, a killer of the soul and a killer of hope.
Today the synthetic stimulants have two approved medical uses: to treat hyperactivity or attention-deficit disorder, especially in children, and to treat the rare sleep disorder narcolepsy. In modern medical treatments of these disorders, stimulants are used orally at low and stable doses with few, if any, problems, as long as the patient was not an alcoholic or a drug addict before these medicines were prescribed. In the treatment of both hyperactivity and narcolepsy, the euphoria experienced by high-dose stimulant users for obesity and depression is not seen. Tolerance to the beneficial effects does not develop even after long-term use. Thus, these medicines have become generally accepted but only in the treatment of these two specific and relatively uncommon illnesses.
More recently in the United States, some sophisticated psychopharmacologists are finding new medical uses for the stimulants, including rediscovering their role in the treatment of obesity and depression. Stimulants are also now more widely used to treat adult attention-deficit disorder. These new stimulant uses may trigger conflicts with drug enforcement officials because of the high abuse potential of these drugs.
KHAT. The khat (or qat) plant is a bush with fleshy brownish-green leaves with serrated edges and a glossy top. It has been cultivated and used as a stimulant for centuries in the northeast corner of Africa and the Arabian peninsula in ways that are similar to the use of coca leaves in the Andes or the use of coffee in much of the rest of the world. Khat is typically chewed for hours at a time in social settings, usually by men, often producing animated conversations such as those that might occur at a coffeehouse. Cathinone, the psychoactive ingredient of khat, is an alkaloid with a chemical structure similar to amphetamine. Some people from khat-using parts of the world who have emigrated to other places have gone to considerable trouble and expense to continue to obtain khat. Because the material is psychoactive only while the twigs are fresh and green, it rapidly loses its value, much as coca leaves do.
Although relatively few problems have been reported in Africa or Arabia with traditional khat chewing, cases of amphetamine-like paranoid psychoses have been seen in other countries where people have used large amounts of the drug. In the reported cases, the psychotic symptoms disappeared within five hours after the khat chewing stopped. Effects from persistent khat use include stained gums and teeth, constipation, elevated blood pressure, and impotence.
A diplomat who served in the Somalian capital of Mogadishu during the United Nations peacekeeping mission in 1992 reported that most of the local gunmen were khat chewers who did whatever they needed to do to get their drug during the day (very much, he said, like American cocaine or heroin users), only to spend their evenings and nights talking together and chewing khat leaves. He told me that it was much safer to walk around the streets of Mogadishu in the evenings, when the gunmen were relatively happily occupied, than it was in the daytime, when they were seeking money to get their drug.
Although khat use is in a legal limbo in much of the world, it is an illegal drug in the United States, with importers of the drug being subject to arrest and imprisonment. It is likely that other parts of the world, including Europe, will make khat illegal in the future.
Case Histories
The triggering of panic disorder in vulnerable people is just one of the many ways drug abuse interacts with mental disorders. Drug abuse can trigger psychotic episodes in people with schizophrenia and bipolar disorder and, through the chronic intoxication resulting from repeated nonmedical drug use, it can lead to poor compliance with needed medical treatments of many mental disorders. In addition, some people with mental disorders use alcohol and other nonmedical drugs in a misguided effort to reduce their discomfort, in what has been called “self-medication,” leading to the compounding of the original psychiatric problem by the addition of a new problem, addiction.
In the case history below, Carrie’s disastrous and prolonged panic attack was triggered by stimulation of the NE neurotransmitter system in her brain. The psychosis caused by being high on marijuana and the delusional experiences with the clock and with her husband appearing to be the devil reinforced her panic reaction, leading to prolonged hospitalization and disability. All this resulted from one use of marijuana by a young woman who had never previously been mentally ill or seen a psychiatrist.
Carrie
Carrie was fifty-one when she rolled up her sleeve and showed me the scars on her left arm from the time when she put her arm through a window in a mad effort to get out of her home at the age of twenty-six. She had then been married for two years. She had grown up in Iowa in a family of teetotalers, vowing that she would not repeat the mistake of her parents, who she felt had sacrificed their social life to their decision not to drink alcohol: “I heard from lots of people in our community that they would have liked to have known my parents better, but the fact that my parents did not drink made their friends uncomfortable, so they just did not pursue the friendship.” As a teenager, she made herself drink alcohol to be social. She noted that shortly after she left college in the late 1960s, “all of a sudden marijuana was everywhere and I realized it was just like alcohol. If I did not use pot, I would lose many of my friends, just like my parents lost their friends.” She persuaded her husband to buy some pot and to set aside an evening for them to use it so that she could learn about this exciting new social drug.
About a year before her first use of marijuana, Carrie had experienced her initial panic attack while she was spending an evening with her mother-in-law, a woman who made Carrie uncomfortable. She commented that “although that first panic attack was upsetting, it was not a big deal and it passed fairly quickly.” On the evening, a year later, when Carrie first used marijuana, she took two or three puffs and sat back, waiting for the magical high. She felt a strange, growing discomfort along with a sense that time was distorted. She looked at the clock and saw the hands rapidly moving backward around and around the clock. Her husband looked to her suddenly like the devil. She had an overwhelming feeling that she had to get out of her own home. She panicked, smashing her arm through the front window in a bizarre effort to get out of the house. Her husband, frightened by her disturbed behavior, tried to hold her, which scared her more. He finally called the rescue squad, which took her to a hospital.
Carrie was admitted to a psychiatric hospital when her distress did not diminish in a few hours. She described to me how she paced the halls of the hospital, wringing her hands and sobbing uncontrollably about what had happened to her mind. She stayed in the hospital for six weeks and was reluctant to leave even then, fearing a return of the panic attacks after she was at home alone. She stayed on the medicine Stelazine for several years thereafter and had a hard time stopping it because she feared that the medicine was all that kept her from repeating the dreadful experience. Over the next twenty years, she continued to have anxiety and panic problems but in time came to recognize these as symptoms of agoraphobia with panic attacks that had been triggered by her one experience of marijuana use. She showed no signs of schizophrenia or other psychotic mental illness over those years.
Carrie does not know, and neither do I, if she would have had a terrible, prolonged panic problem if she had never used marijuana, but we both were sure that the “breakdown” in her life was set in motion by her single use of marijuana. As Carrie said to me: “Isn’t it ironic? Now I barely drink at all, and I certainly do not use any illegal drugs, including marijuana. But at that time I was going to do whatever it took to avoid what I considered to be my parents’ mistake in not using alcohol and drugs. What a high price I have paid, and my husband has paid, for that seemingly innocent decision.”
Frank
I have seen Frank once every month or two in psychotherapy for ten years. He is a drug addict who has never hit bottom. Early on, I told him that I doubted that he could get well until he does hit bottom. His reply was, "It’s only been twenty-five years that I have escaped a bottom. Maybe the next twenty-five will be different." Frank was a phenomenally awkward kid. He could not catch a ball or run, and he felt he was ugly. He had acne as a teenager and still did from time to time at the age of forty.
Frank had one great gift, however. He was good at math, and when computers came along, he became a genius with the most complex computer programs. He went to college at Cal Tech and did well academically, although he never dated. His way of relating to other young people was with drugs. He loved marijuana, and later he developed a major infatuation with cocaine. He got married at one point to a woman who did not care much for him but found him to be a steady meal ticket. They broke up when she inherited some money and no longer needed his financial support.
About fifteen years ago, Frank discovered sleeping pills when he was at a computer convention and could not sleep. A friend gave him a sleeping pill, and Frank found that it helped him sleep despite the excitement of the meeting. He was never without them after that. He got sleeping pills from me, even though he was an active addict, and he has stayed in therapy with me even though we both doubted that I was helping him with his drug problem. He also has seen other doctors in consultation while seeing me because I was concerned about my treatment of him, including his use of sleeping pills. He has never used more than the prescribed amount of the sleeping pills, and he has been honest with me about his use of medicines, even when it upset us both. He never drank, finding no pleasure in alcohol. In later years, he used marijuana only in social settings, mostly once or twice a month. He never used marijuana on weekdays, and never during or before work. He calculated that he had spent about $150 on marijuana in a typical year. He had a large supply of marijuana in his freezer, but he felt no compulsion to use it except when friends were over. Then he shared his marijuana with them.
Frank’s cocaine use was a different matter. When he had been married, he became frightened by his cocaine use. His wife was a heavy cocaine user, and Frank found that his life was thoroughly out of control because he had so much of the drug around. Once he left his wife, he was able to moderate substantially his cocaine use. He uses cocaine for about five to ten hours, approximately once every six to twelve weeks, mostly at national computer conventions, where he claimed that many of the people under the age of about forty used cocaine. After using cocaine, he felt awful and missed work for a day or two. He told me that, unlike marijuana, he could not keep cocaine around his house because he simply used it all up whenever he had any. He also never got a steady supplier of cocaine, fearing that it would then be too easy to get cocaine in larger quantities. He estimated that he had spent about $1,500 a year on cocaine when he used it. “If I had spent $10,000 or $20,000, I would have called that a bottom. But I could afford this much for cocaine, even if I knew it was dumb.”
Frank was impressed by the antidrug TV commercials that showed a man with a straw up his nose to snort cocaine. The man in the TV ad watched money pass by him, only to be sucked up his nose. Then he saw a $200 TV go by and get vacuumed up his nose. An elegant $100 dinner and theater evening went up his nose, an entire automobile, and then even a home. “These ads work for me; they make sense to me because I know I waste a lot of money on cocaine, while the TV ads that show addicts with fried brains don’t seem realistic,” Frank told me.
I did my best to get Frank to go into addiction treatment, but he refused. I tried to get him to go to AA and NA meetings. He went for a while and even tried Rational Recovery, an alternative nonspiritual mutual-aid program. He only went for a few meetings of Rational Recovery.
Frank became sexually involved with a woman who was addicted to alcohol. He was amazed by how hard it was for her to live a stable life without regular attendance at AA meetings and a strict adherence to the nonuse of alcohol and other drugs. He said, “If cocaine were as available to me as alcohol is to Judy, I would have to go to NA or Rational Recovery meetings every day, just the way she goes to AA meetings.” Here we see the role of the environment in the process of addiction. Neither Frank nor his girlfriend, Judy, were stable in their relationships with their drugs of abuse, but their problems were different because of the difference in exposure to the drug. They had another difference: Judy had an alcoholic mother, but Frank had no addicted relatives.
Frank also suffered from depression and social phobia, a morbid fear of social encounters. He used several antidepressants to help him cope with these problems. Frank and I talked a lot about his need to get on with his life, including improving his work-related skills. He did many things right in his life, including, for the first time in his life, buying a home of his own, “so I can pay a mortgage instead of rent.” This step into adulthood scared him a lot. Without too much access to cocaine, Frank became relatively stable for several years without any addiction treatment. He and I both knew that his stability was relative and fragile. Despite the absence of some risk factors experienced by his girlfriend, he had at least one foot on a banana peel, and we both knew it.
I wondered out loud to him one day what would happen if the contractor for whom he worked as a computer whiz started random drug tests. Frank’s reply was simple: “It would depend on how often they tested me. I didn’t use cocaine very often, so if they tested me once every year or two I would probably just keep on the way I was and take my chances. But if they tested more often, or if they tested me when I came back from missing work (often caused by his cocaine use), then I would quit using it. I don’t want to lose my job. I’m an addict but I’m not crazy. At that point I would have a reason to stop using cocaine, at least as long as I worked for a company that did drug tests.”
Frank also liked to tease me about suing me for malpractice because I encouraged him to buy his home: “When the bank comes after me, I will be at my attorney’s office.” I asked him about his sleeping pill use. “Oh,” replied Frank, “I won’t sue you for that. That was my idea.”
Frank got remarried to a woman who was fiercely antidrug. That marriage did for Frank what I could not do. His wife gave him a definite reason to quit marijuana and cocaine use. He told me that it was easy to stay clean because he did not want to lose his marriage or incur the wrath of his wife. He was convinced that, unlike his employer who never suspected his drug use, his wife would catch him if he used again. Surprisingly to me, Frank did not miss marijuana or cocaine once he put them behind him, but he also was clear that if he were around these drugs a lot, especially if he were married to a heavy user (as opposed to his antidrug wife), he would quickly slip back into heavy-duty use.
For years after I wrote this case history, Frank remained in psychotherapy with me. He still took sleeping pills, but less than he used to and never more than prescribed. He was recently in a conflict with another physician about his use of amphetamines for daytime sleepiness and Percodan, an opiate painkiller, for headaches. He had not used cocaine, marijuana, or any other illicit drug in many years saying, “I’ve become so right-wing on drugs I don’t even consider the possibility of using them again.” He noted he used illicit drugs “to get high, to become intoxicated” while he never used medicines for that effect. He clearly saw the difference between drugs and medicines, but he had a harder time seeing the difference between controlled (potentially addicting) medicines and noncontrolled medicines. He wanted me to accept that he had rid himself of marijuana and cocaine use over a long period of time without AA or NA. I accepted that achievement and respected him for it. I knew that AA and NA are not the only ways to get well from addiction to alcohol and other drugs, but I also knew from my experience over many years with hundreds, if not thousands, of patients that for most addicted people the Twelve Step programs are the best, although not the only, ways to stay well for a lifetime.