The Sober Truth (13 page)

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 evidence 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.

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.

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.