by Lance Dodes
One of the principal sources of confusion was that people mixed up physical addiction with the underlying nature of addiction. Even though both may be present in the same person at the same time, they actually have nothing to do with each other. Physical addiction is a simple physiological phenomenon that can happen to anybody. Our bodies react to certain drugs by adapting to them, changing to accommodate their presence. This phenomenon is called tolerance. Dramatic things can happen when people stop taking a drug to which they have become tolerant. Because the body is “prepared” to deal with the drug, when the drug is removed, a reaction occurs. The body pushes back, compensating for a drug that isn’t there.
This is known as a withdrawal syndrome—a set of physiological symptoms that are always expressed in the exact opposite direction from the effects of the drug. Since nearly every drug capable of producing physical addiction is a sedative (also known as a central nervous system depressant, or “downer”), the withdrawal syndrome is physiological overexcitement. In the case of alcohol, this starts with shaking (“the shakes”), but can proceed to full-blown seizures. Withdrawal from other drugs looks different. Narcotic withdrawal, for instance, commonly involves goose bumps and severe gastrointestinal discomfort. Interestingly, since seizures aren’t present for narcotic withdrawal, it’s actually medically safer to withdraw from heroin than from alcohol.
How do we know that this physical addiction has nothing to do with the true nature of addiction? One clue is that many addictions have no physical component at all. Examples include the addictive use of marijuana or LSD, which don’t produce a tolerance response, and all the non-drug addictions such as compulsive gambling, eating, shopping, and sex. A second clue is that it’s common to develop a physical addiction but never have a true addiction. Everyone who is hospitalized and given high enough doses of morphine over a period of enough time to treat pain—for example as part of treatment for cancer—will become physically addicted. But when these people are discharged, they generally don’t run out and find the local drug pusher. One more way to be sure that physical addiction and true addiction are separate things: we know from vast experience that, even after detoxification, when there is no more physical addiction, true addicts are not “cured” of their need to use alcohol or other drugs. Many return to use months or even years after detox.
THE BEGINNING OF MODERN UNDERSTANDING
Starting in the 1960s, experts in human psychology began to take an interest in addiction for the first time. Rather than viewing the behavior as a form of pleasure seeking, they theorized that taking drugs was something people did to manage intolerable feelings, almost like self-prescribing a medication. Thus was born the now-famous “self-medication hypothesis” of drug use.
Over time, other ideas about the psychology of addiction were developed, expanding and improving on this early insight. In the decades of my practice with patients with addictions, I noted that addiction as a behavior was very much like another common psychological symptom: compulsions, a category that includes other common unwished-for acts like having to arrange papers parallel to each other on a desk or having to excessively clean house. Many of these compulsions aren’t nearly as dangerous or destructive as addictions, of course; maddening as they might be, they are unlikely to result in a car accident or drunken brawl or do damage to vital organs. But even though the consequences may be less severe, these compulsive behaviors might share psychological roots with addictions. After all, by definition, compulsions are driven behaviors that people cannot stop themselves from doing, even when they want to. And so the question arose: what if addiction is just the name we give to compulsions that involve drugs?
(A word of clarification is needed here. There are compulsive behaviors that are not primarily psychological in origin: those described by the diagnosis obsessive-compulsive disorder, or OCD. The compulsions produced in OCD typically respond to medications such as Prozac and its SSRI cousins. In contrast, psychologically based compulsive behaviors do not respond to the Prozac group, since they have a psychological cause. Unlike the OCD symptoms, these compulsions are triggered by emotional factors and can be treated in psychotherapy. Depression is another example of a symptom that can have two separate causes. There is biochemical depression, which is caused by low levels of neurotransmitters and treatable by medication. And there is psychological depression, which does not respond to antidepressants but is treatable by psychotherapy.)
The idea that drug addictions (including alcoholism) are just compulsions focused on drugs had good support. In the early 1970s, researcher Lee Robins and her group looked at heroin addiction in soldiers who had returned from Vietnam.1 Many soldiers had used heroin extensively and in high doses during the war. In fact, the abuse was so widespread that when they returned to the States, soldiers were routinely screened for heroin addiction. Those who had a physical addiction to the drug were detoxified before returning to their homes.
At the same time soldiers were using so much heroin overseas, there was an explosion of heroin use in the United States (this is when the term “hooked on drugs” first arose). Yet there was a fascinating difference between these two cohorts of drug users. The stateside addicts had virtually no success maintaining abstinence after they were done with detox, which was what had led to the widespread fear that the nation was becoming irrevocably “hooked.” But Robins found, to the surprise of many, that just six months after coming home, over 90 percent of the veterans had quit using heroin. This seemed like an impossible result. After all, if heroin was so addictive, how could its fabled power fade immediately for some people and linger for others?
A logical question arose: were the stateside heroin addicts and the soldiers using the same drug? It turned out that, if anything, there was evidence that the heroin available in Vietnam was actually more powerful than its stateside counterpart. So there had to be something about the people that was different.
What was this difference? The soldiers used heroin because they were at war, with all its unthinkable horrors. Heroin helped them to deal with this external reality; once that reality evaporated, they no longer needed the drug. But the stateside addicts used heroin for completely different reasons—because it served an emotional purpose for them, just like any other compulsive behavior. Their war was in a sense internal; their drug use was driven by enduring psychological issues, not temporary circumstantial ones. These were the true addicts, the ones who couldn’t quit.
The Robins study became a landmark in the recognition of the idea that compulsive drug use has nothing fundamentally to do with the physical action of the drug; it has to do with the psychology of its use. This was clear evidence that addiction was more about something in people’s minds, not something in the chemicals they used. Thinking about this now, it seems obvious—as I said, large numbers of people develop physical dependencies on prescribed drugs every year and do not go on to become addicts once the prescription runs out.
In case further evidence was warranted, another massive natural experiment around the same time drove the point home. In 1970, the surgeon general mandated that all cigarette packs carry a warning label about the dangers of smoking; in 1985, this label was hardened with specific mentions of lung cancer, heart disease, and emphysema. When these warnings appeared, millions of people stopped smoking, even though they had been physically addicted to the nicotine in cigarettes.2 Just like the soldiers in Vietnam, many had been smoking for reasons other than a psychological compulsion—enjoyment, for one—which meant they could relatively easily decide to stop when they realized it was dangerous for them to smoke.
Once again, even for a drug known to cause physical addiction like heroin or nicotine, taking it in very high quantities for a long time could not cause people to become addicts if they also didn’t have a psychological need to use the drug.
By the mid-1980s, the self-medication concept had become largely solidified among clinicians and researchers studying addiction.3 And soon a new piece of ev
idence began to gain recognition: people often switched between drug addictions and non-drug addictions. As many as 75 percent of compulsive gamblers have some alcohol abuse history, for example.4 Many people switch between the addictive use of drugs and non-chemical addictions such as Internet use and shopping. This would be inexplicable if addiction were about drugs or their effects. Yet it makes perfect sense when addiction is viewed through the prism of function: it is clearly doing something for these people emotionally. And in this sense, almost any behavior will do.
RISE OF THE BIOLOGISTS
But just as a consensus was beginning to develop around the psychology of addiction, a new hypothesis entered the fray. A group of scientists at the National Institute on Drug Abuse (NIDA) began to publish a series of studies in the first decade of this century devoted to the neurobiology of addiction. They eventually declared that they had discovered the biological basis of addiction.
The NIDA scientists have been tremendously successful from a public relations standpoint. Journalists who rely on big announcements to drive interest have repeated the NIDA’s bold claims ad nauseam, and as a result many lay people now believe the idea that addiction is an issue of brain chemistry. The power of this idea is its aura of rigor. Neurobiology is often described as hard science—the researchers use the very latest imaging tools and technologies, and their literature comes complete with numbers and beautiful images of the brain “lighting up.” Compared with the “soft science” of psychology, these stories feel far more modern and accurate. But are they?
Here is what the researchers found. They began by addicting rats to heroin. Then they showed those rats “cues” that had been present at the time they received heroin and were therefore associated with the drug—a play on Pavlov, with heroin instead of biscuits. Soon these cues excited the rats even when the drug wasn’t present, confirming that the researchers had successfully created a “conditioned reflex.” Then the NIDA researchers did something new: they examined the rats’ brains. And what they discovered was that these brains had actually changed as a result of exposure to the drug. Specifically, their brains secreted more of a neurotransmitter called dopamine in response to the cues, which triggered the “reward” or “pleasure” pathway of the brain. They then noted something else: this brain change, called upregulation, since it involved an excessive response to a stimulus, was permanent. Once the rats’ brains had become upregulated, they would never return to normal. The researchers concluded from this evidence that addiction must therefore be a “chronic brain disease” caused by taking significant amounts of a drug. And even though these tests did not involve people, the researchers announced that they had discovered the cause of addiction in humans.5
This conclusion was problematic in several ways, but the biggest by far was that it fits virtually nothing we know about human addiction. For example, recall the Vietnam veterans study once again. Those soldiers had taken significant quantities of heroin over a long period of time, far more than enough to create a physical addiction to the drug. If we subscribed to the “chronic brain disease” theory, then those soldiers should have undergone a permanent brain change that rendered them addicts forever. In fact, only a small percentage of these users became addicted at any time after their return.6 The same thing happened when those warning labels appeared on cigarette packs: millions quit, despite the fact that their usage patterns should have upregulated them into a lifetime of subservience to tobacco. People stopped smoking because they realized that smoking is dangerous, and because they could stop. None of this fits the profile of a chronic brain disease.
And we have an even larger sample to disprove the neurobiological model: alcoholism itself. Close to 100 percent of adults in America drink alcohol. Many people drink in large quantities for many years, especially when they’re younger. Many such people drink enough to become physically dependent. Yet despite enormous exposure over many years, the vast majority of younger heavy drinkers never become alcoholics. If the “chronic brain disease” theory were correct, they all would be.
And consider once more the millions of people whose prescription drug use for temporary or chronic pain produces powerful tolerance and withdrawal. The vast majority of these people do not go on to become addicts; the chronic brain disease theory should see them upregulated into a life of permanent addiction.
What happened is that the NIDA researchers made a critical, and critically false, assumption. Knowing that all mammals share essentially the same reward system in the brain, they assumed that humans exposed to drugs in high doses over long periods would develop the same response: given heavy enough exposure, people would run around helplessly seeking the drug like rats in a cage. But what they overlooked was precisely what makes humans different from rats. On top of our pleasure pathway, we have a very large “higher” brain. We humans almost always do things not just because we are physically excited by them, but because of a very complex mechanism we possess that rats do not. This mechanism is psychology.
As evidence, consider that unlike rats, humans often become calmer at the moment they decide to have a drink, or choose to call their dealer, or plan a trip to the casino. Tranquil hours may pass between decision and delivery. The fact that the mere act of deciding seems to calm our nerves suggests that this act has some psychological significance to us. (More on this in a moment.)
There is another essential fact about human addiction that has gone ignored by the NIDA team: humans regularly perform addictive acts in response to being emotionally upset. A broken relationship, a stinging defeat, a painful incident that causes guilt or shame—these are common precipitants of addictive acts in humans. We are complex creatures who are governed as much by our thoughts and feelings as by our reptilian pleasure pathways. To reduce human addiction to the physiological excitement of rats is to dismiss everything that makes us human.
Finally, what the rat researchers call automatic behavior—running around seeking heroin upon exposure to cues in their environment—is a conditioned reflex with a neurobiological basis, similar to seeking behavior—when people are in physical withdrawal and need to get to their drug. But this automatic behavior has simply nothing to do with addiction, and should never have been called addiction to begin with.
THE GENETICISTS
Closely related to the neurobiologists are the geneticists, who are often the sources for mass media reports announcing the good news that we have finally found the gene for alcoholism. (People seem to find this gene so often that one wonders how they manage to keep losing it.) Confusion has arisen because of some findings that suggest that for some people with alcoholism, there is some genetic “loading”; that is, a degree to which the diagnosis correlates with genetic inheritance. But this should not be taken as evidence that there is a gene for alcoholism or addiction or that addiction is somehow a genetic disorder.
The problem comes down to confusion between causation and correlation once again. Statistically, it is likely that many genes, possibly hundreds or thousands of them, may play some role in increasing the susceptibility to addiction. This has led some researchers to refer to susceptibility genes. But nobody has ever discovered any of these genes, despite the fact that they have been repeatedly sleuthed by our most sophisticated chromosomal techniques. I reviewed the best-known genetic studies in my book The Heart of Addiction, but I’d like to repeat just one salient point here.7
One of the most popular tools in genetics is the identical-twin study—popular because it allows researchers to study two different people with exactly the same genes. Twin studies have revealed that if one twin has alcoholism, it is more likely than not (greater than 50 percent chance) that the other twin does not have alcoholism. This would be an impossible finding in the case of a true genetic disease, of course. It’s true that evidence shows that if one twin is an alcoholic, the other has about a 40 percent chance of having alcoholism too, which is higher than the general population.8 But when we consider that the identical twins in these
studies were raised simultaneously by the same parents, at the same time, in the same environment, and typically have very similar experiences growing up, the increased correlation (called concordance in genetic studies) is to be expected.
In fact, there is probably some genetic influence on addictions, but this shouldn’t be surprising. Many human conditions, like peptic ulcer disease or hypertension, have some genetic loading, meaning that genes confer some degree of increased susceptibility without the condition being directly heritable. Given the way addiction works psychologically, it could be possible that some decreased biological tolerance of certain emotions could lead to a variety of symptoms, including addiction. But nobody in human history has ever walked into a bar because a gene told them to.
THE PSYCHOLOGY OF ADDICTION
Now let us return to the compulsion model. The idea fits neatly with much that has been written about addiction for centuries. People have understood the basic nature of compulsions for a long time, even before modern psychology. William Shakespeare provided an especially clear example in Macbeth: Lady Macbeth demonstrates literature’s most quotable compulsion when she wails “Out, damned spot!” while ceaselessly washing her hands. The “spot” that she imagines is the blood of people she has murdered, of course, and her compulsive behavior is universally comprehensible in human terms: a symbolic gesture to undo her guilt. Because she can’t actually reverse the murders, the compulsion becomes a stand-in for the act itself: cleanse the hands if you can’t raise the dead. In psychology, there is a word for an action like this that substitutes for a more direct behavior: a displacement.