The Noonday Demon (40 page)

D
epression and substance abuse form a cycle. People who are depressed abuse substances in a bid to free themselves of their depression. People who abuse substances disrupt their lives to the point that they become depressed by the damage. Do people who are “genetically inclined” to alcoholism become drinkers and then experience depression as a consequence of consuming a substance; or do people who are genetically inclined to depression use drink as a form of self-medication? The answer to both questions is yes. Falling serotonin appears to play a significant role in reinforcing alcoholism, so that an escalating depression might cause organic escalation of alcoholism. In fact there is an inverse relationship between serotonin levels in the nervous system and alcohol consumption. Self-medication with illicit drugs is frequently counterproductive: while licit antidepressant meds start off with side effects and build up to desirable effects, the substances of abuse usually start with desirable effects and build up to side effects. The decision to take Prozac instead of cocaine is a version of the strategy of deferred gratification, and the decision to take cocaine instead of antidepressants is predicated on a yearning for immediate gratification.

All substances of abuse—nicotine, alcohol, marijuana, cocaine, heroin, and about twenty others currently known—have major effects on the dopamine system. Some people have a genetic predisposition to use these substances. Substances of abuse act on the brain in three stages. The first stage is in the forebrain and affects cognition; this in turn excites fibers leading to the most primitive areas of the brain—the ones we have in common with reptiles—and these, finally, send tingling messages to many other parts of the brain, frequently affecting the dopamine system. Cocaine, for example, seems to block dopamine uptake, so that more dopamine is floating around in the brain; morphine causes the release of dopamine. Other neurotransmitters are also involved; alcohol affects serotonin,
and several substances seem to raise levels of enkephalin. The brain, however, is self-regulating and tends to sustain constant levels of stimulation; if you keep flooding it with dopamine, it will develop resistance so that it will require more and more dopamine to trigger a response. It either increases the number of dopamine receptors or decreases the sensitivity of existing dopamine receptors. This is why addicts need escalating quantities of their substance of abuse; it is also why people in recovery, who are no longer stimulating the excessive release of dopamine through substances, usually feel flat and greyed out and depressed: their natural dopamine levels are, by the standards of their adapted brains, extremely low. When the brain adjusts itself anew, withdrawal is complete.

Most people, if they take enough of an abusable substance for long enough, will become addicted to it. A third of all people who ever smoke a cigarette go on to develop a nicotine addiction; about a quarter of those who try heroin become dependent on it; about a sixth of those who try alcohol become dependent on that. The speed with which substances cross the blood-brain barrier and so intoxicate the user is often determined by the way the substance is ingested, with injection being fastest, inhalation next, and oral consumption slowest. Of course the speed also varies from substance to substance and will determine how rapidly reinforcing the substance is. “The question of who tries a substance once is pretty random,” David McDowell, director of the Substance Treatment and Research Service of Columbia University, says. “It has to do with where someone is and what his social climate is. But the follow-up is anything but random. Some people who try a substance go on with their lives and never give it another thought; some get hooked almost immediately.” For substance abusers as for depressives, a genetic predisposition interacts with external experience; people are born with a capacity to become substance abusers and, once they have abused a given substance for long enough, will become addicted to it. Depressed people who tend toward alcoholism will usually begin chronic heavy drinking about five years after the first major depressive episode; those who tend toward cocaine will on average start abusing it chronically about seven years after such an episode. No test exists at present to show who can use what substances with what levels of risk, though attempts to formulate such tests, mostly on the basis of certain enzyme levels in the bloodstream, are under way. It is not yet possible to see whether a physiological transformation in depressed people makes them more vulnerable to substance abuse, or whether the increased vulnerability is primarily psychological.

Most depressed substance abusers have two linked illnesses running concurrently, each of which requires treatment and each of which exacerbates
the other. These illnesses interact within the dopamine system. The popular idea that you have to get a person off substances before you pay attention to his depression is faintly ludicrous: you are asking someone who tamps down his misery to let that misery blossom before you do anything about it. The idea that you can ignore addiction and treat depression as the primary illness, helping someone feel so good that he won’t want substances anymore, overlooks the reality of physical dependence. “If there’s anything we’ve learned in the addiction field,” says Herbert Kleber, who was for some years deputy drug czar for the United States and who now heads Columbia University’s Center for Addiction and Substance Abuse, “it’s that once you get addicted—it doesn’t matter how you got there—you have a disease with a life of its own. If you treat a depressed alcoholic with an antidepressant, you produce a nondepressed alcoholic.” Taking away the original motivation for abusing substances does not free someone who has developed a pattern of substance abuse.

Theoreticians are keen to separate mood state and substance dependency. Some straightforward measures—family history of depression, for example—can identify a primary depression, and a family history of substance abuse may point to a primary substance problem. Beyond this, the terms get vague. Alcoholism causes the symptoms of depression. The mainstream therapeutic philosophy at present holds that substance abuse should be treated first, and that after a person has been “clean” or “sober” for about a month, his emotional condition should be assessed. If the person is feeling good, the addiction was probably the cause of the depression, and so lifting the addiction has lifted the depression. This is all well and good in principle, but in fact the upheaval caused by withdrawal is enormous. Someone who feels great at the end of a month off substances is probably suffused with pride at his self-control and is experiencing adjusted levels of all kinds of hormones, neurotransmitters, peptides, enzymes, and so on; such a person is not necessarily free of either his alcoholism or his depression. Someone who is depressed at the end of a month off substances may be depressed for life-related reasons that reflect neither the emotional state that first led him into substance abuse nor an underlying emotional state now laid bare. The notion that someone can be restored to a condition of purity, this idea that substances mask an abuser’s true self, is perfectly ludicrous. Furthermore, withdrawal-related mood problems may make their first appearance only after a sober month or two. It takes many months for the body to achieve optimal recovery from long-term substance abuse; some brain alteration “appears to be permanent,” according to Kleber, and some has a life of at least a year or two. Positron-emission tomography (PET) scans show the
effects of various substances of abuse on the brain, and they show limited recovery even at the three-month point. There are persisting lesions, and chronic abusers of substances often suffer permanent memory damage.

If it is sadistic to begin by taking depressed substance abusers off their substances, then does it make sense to begin by giving them medication? The use of antidepressants on depressed alcoholics will cause some alleviation of their desire for drink if depression is a primary motive for their alcoholism. This mode of testing—to begin by alleviating the depression—is more generous than the stripping away of substances to reveal a person with or without a “real depression.” Antidepressant treatment is undeniably useful in reducing substance abuse; recent studies have shown that putting alcoholics on SSRIs increases the chances that they will be able to come off alcohol. Clearly, depression can be significantly ameliorated with psychodynamic therapy, or just with attention—and the close attention paid to people who participate in studies can have a beneficial effect on substance use quite apart from the protocol of the study. Depressed alcoholics tend to be terribly isolated, and interrupting that isolation often alleviates some depressive symptoms.

“There’s a certain judgmental quality in trying to get technical about what illness is primary and what is secondary, trying to apportion blame to self-indulgence or mental illness,” says Elinore McCance-Katz of Albert Einstein College of Medicine. “As someone who treats people with addiction problems and mental health problems, however, I do want to know because it may be predictive of how they’re going to do in the future; it’s going to be helpful to me in terms of how I educate and work with them; it’s going to be helpful to me in terms of what medications I may treat them with and for how long. But the bottom line is that if they have both disorders, both disorders have to be treated.” It is sometimes the case that self-medicators are using substances to control agitated depression that might, unchecked, include suicidal wishes or acts. If you get such a person off the alcohol without making plans to control the depression in some better way, you run a severe risk of creating a suicide. “When depression is not diagnosed because of the lack of abstinence,” David McDowell of Columbia says, “maintaining abstinence may hinge upon treating the depression.” In other words, if you’re depressed, you may not be able to cope with the stress of detoxifying.

Correlations are manipulated to try to construct a system of diagnosis in a field where knowing the origin of the illness is only a small piece of knowing how to treat it. One recent study, for example, looked at sleep patterns and determined that shortened latency for rapid eye movement (REM) sleep (the length of time before one enters the first REM stage
after falling asleep) indicated that depression was the primary illness, while a protracted latency for REM sleep indicated that alcoholism was the primary illness. Some clinicians claim that early-onset alcoholism is more likely to be the consequence of depression than is later-onset alcoholism. Some tests measure metabolites of serotonin, or levels of cortisol and other hormones, and hope to demonstrate through these measurements the presence of a “real” depression—but since much real depression does not manifest itself in such metabolites, the tests are of limited utility. An incredibly broad range of statistics is available, but it seems that about a third of all substance abusers suffer from some kind of depressive disorder; and it is evident that a high number of depressives abuse substances. Substance abuse frequently begins in early adolescence, at a stage at which people with a predisposition for depression may not yet have developed the complaint. Abuse may begin as a defense against a developing depressive tendency. Sometimes, depression makes someone who has been a user of an addictive substance into an addict. “People who are taking things because they’re anxious or because they’re depressed are much more likely to develop a real dependence,” Kleber says. People who have recovered from substance abuse are far more likely to relapse when they’re depressed than otherwise. R. E. Meyer has proposed five possible relationships between substance abuse and depression. Depression may be the cause of substance abuse; depression may be the result of substance abuse; depression may alter or exaggerate substance abuse; depression may coexist with substance abuse without affecting it; depression and substance abuse may be two symptoms of a single problem.

It is extremely confusing that substance use, withdrawal from substance use, and depression have overlapping symptoms. Depressants such as alcohol and heroin relieve anxiety and aggravate depression; stimulants such as cocaine relieve depression and aggravate anxiety. Patients with depression who abuse stimulants may have behavior that appears schizophrenic, though that behavior will remit with
either
a discontinuation of substance use or a successful treatment of the depression. In other words, the symptoms of the combination are worse than the combined symptoms of the two component diseases. In dual-diagnosis cases, the alcoholism is often more severe than average alcoholism, and the depression is also often more severely symptomatic than average depression. Fortunately, people with dual diagnosis are more likely to seek help than those with either problem alone. They are also, however, more likely to relapse. Though substance abuse and depression may be separate problems, unquestionably each of them has physiological consequences in the brain that may severely exacerbate the others. Some substances (cocaine,
sedatives, hypnotics, and anxiolytics) that do not cause depression when they are being used do affect the brain in such a way that they cause depression during withdrawal; some substances (amphetamines, opioids, hallucinogens) cause depression as part of their immediate intoxicating effect. Some (cocaine, ecstasy) cause a high and then a compensatory low. This is not a tidy matter. All of these substances, and alcohol in particular, will exacerbate suicidality. All of them blur minds enough to disrupt compliance with prescription regimens, which can create real chaos for people ostensibly on sustained antidepressant treatment.

All of this being said, depression remits more or less permanently in some people after they detoxify themselves, and the correct treatment for such people is abstinence. Other people’s interest in drugs and alcohol simply peters out when their depression is brought under control, and the correct treatment for such people is antidepressant medication and therapy. Most substance abusers, like most depressives, require psychosocial intervention, but this is not invariably the case. Unfortunately, clinicians still have inadequate understanding of how many antidepressant medications may interact with substances of abuse. Alcohol accelerates the absorption of medications, and this rapid absorption significantly raises the side effects of drugs. Tricyclic antidepressants, an older form of treatment, may in combination with cocaine cause significant stress to the heart. It is important, when prescribing antidepressants to a substance abuser who has gone sober, to assume that that person could return to his substance of choice, and to exercise caution in prescribing drugs that may in combination with substances cause significant harm. In some instances, psychodynamic therapy may be the safest way initially to address depression in substance abusers.