The Noonday Demon

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The Noonday Demon Page 33

by Solomon, Andrew


  Drinking is not a simple matter: it has divergent motivations and effects on various people in disparate places. Raising the taxes on alcoholic beverages in Scandinavian countries is believed to keep a lid on suicide rates. I have read many studies that say that being an alcoholic is depressing, but I do not believe that all alcoholics are depressed. The relationship between depression and alcohol is a matter of temperament and context, two highly variable attributes. I definitely drink more when I am anxious—in ordinary anxiety-producing social interactions or when a little bit of depression-style anxiety comes sweeping across me—and I have found myself disturbingly reliant on alcohol during rough times. My tolerance goes up and down and my response is inconsistent; I have taken alcohol and felt the tension lift, but I have also had a bit to drink and felt perilously suicidal, and overwhelmed, and weak, and afraid. I know that I shouldn’t drink when I’m feeling depressed, and if I stay at home, I don’t drink; but in social situations it’s hard to say no, and harder yet to tread that line between alleviating fretfullness and inviting despondency. I often get it wrong.

  Acute drinking will of course lead to headaches and feelings of inefficiency or incompetence, as well as indigestion. Serious alcoholism over a protracted time may lead to cognitive impairment or even to psychosis, as well as to severe physical ailments such as cirrhosis; alcoholics tend to die younger than nondrinkers. Withdrawal from chronic alcohol use may include delirium tremens, which can be fatal. Ninety percent of Americans now living have consumed alcohol at some stage during their life. In the United States, about 10 percent of men and 5 percent of women develop physiological alcohol addiction—which means that they will experience elevated heart rate, delirium tremens, and agitation if they attempt to give up drinking. The physiological mechanism of alcohol in the brain is not fully understood; nor is the physiological basis for consumption, though serotonin seems to affect one’s ability to resist the temptation to drink. It appears that alcohol at high doses has an adverse effect on neurotransmitters, possibly via certain GABA receptors, which are also the target for Valium. Continued drinking seriously affects memory and appears to cause permanent damage to the ability to order new experiences, incorporating them into a through line of recollection. This means that one loses the essential shape of one’s own history; life is remembered in spots and episodes rather than as a coherent narrative.

  There are many models for treating alcoholism apart from depression, but when the two conditions exist together, psychodynamic therapies appear to be most effective. Alcoholics Anonymous and other twelve-step programs provide supportive settings in which people can share both their experiences of alcoholism and their experiences of depression. Other group therapies and even short-term institutionalization are also highly productive at addressing alcoholism and depression as if they spring from a single cause. For many people, this works whether there is a single cause or not. Practitioners at Columbia University use an individual cognitive-behavioral therapy in the interests of relapse prevention. The program is written down and can be practiced in the same way by any clinician. “It is very much a ‘here and now’ form of therapy,” David McDowell explains. The typical treatment course begins with a week or two to address the person’s cravings and then goes on to elucidate an individual’s triggers for relapse and to figure out how to deal with them.

  Alcoholism has more recently been treated with Antabuse, a drug that alters alcohol metabolism and diminishes tolerance for alcohol. It is a sort of self-discipline extender. People who wake up full of determination but find their will weakening at noonday often take Antabuse to enforce their decision not to drink. People in detox are usually highly ambivalent, and Antabuse helps them to seize on the desire for freedom rather than the desire for an addictive substance. One doctor who works with high-powered substance abusers, mostly doctors and lawyers, has them write and sign and give to him letters of resignation to their licensing board; if they relapse, he mails the letters. Some of those who work on addiction have been using drugs that block the effects of substances of abuse, thus destroying motivation for abuse. Naltrexone, for example, is a narcotic antagonist that blocks the effects of heroin. It also prevents alcohol from exerting an influence on endorphins, so destroying the most common motives for drinking. If you’re on Naltrexone, you aren’t going to get any form of pleasure out of the substances you abuse. The drug has been successful in helping people to break the patterns of addiction because it undermines motivational desire.

  The earliest written reference to marijuana is in a Chinese text on herbal remedies of the fifteenth century B.C., but the stuff did not become common in the West until Napoleon’s army brought it back from Egypt. Like alcohol, marijuana interferes with REM sleep. The brain has a specific receptor that responds to at least one of the many chemicals contained in marijuana smoke, which taps into the pleasure-reward circuitry of the brain. Marijuana is antimotivational and in this mimics symptoms of depression. Withdrawal is unpleasant but not agonizing (as with heroin), nor potentially life-threatening (as with alcohol), nor protracted (as with cocaine), and so the drug is often described as nonaddictive. Marijuana slows you down and may be used as an antianxiety drug; agitated depression may in fact be helped by marijuana. Since marijuana is not legally available, it is hard to control quantities and proportions ingested; and because the smoked or pyrolyzed dry leaf has about four hundred identifiable compounds, the effects of most of which are unknown, the effects are not pure. Occasional use of marijuana by a nonaddicted person to take the edge off a highly agitated depression is not an unreasonable mode of self-treatment. Though much work is now being done on medical uses for marijuana, these studies have not, so far, focused on its use for psychiatric complaints. Regular marijuana use becomes antimotivational and “has real neuro-cognitive changes which might as well be physiologically permanent if you’re high all the time,” McDowell says. Marijuana also, of course, carries all the toxicity of cigarettes, causing significant damage to the lungs.

  Hard drugs are those that cause high morbidity: caffeine is a stimulant and so is crack, but crack is classed as a hard drug because it is much more addictive and because it has a more sudden effect on the brain. Hard drugs are the most likely to become depressing—in part because they are super-illegal and acquiring them can mess up your life, in part because they are expensive, in part because they are usually impure, in part because people who abuse them tend to abuse alcohol too, in part because of the way they operate on your central nervous system. The relatives of people who abuse stimulants have high rates of depression. This would seem to indicate that a genetic predisposition toward depression may precede use of cocaine and other stimulants. Only about 15 percent of people who try cocaine become addicted to it, but for those who are prone, cocaine is the most addictive drug there is. Some lab rats will consistently choose cocaine-type stimulants over food or sex and, if they are given unlimited access, will use these stimulants until they die of exhaustion.

  Cocaine is an expensive antidepressant that causes an intense crash, which usually hits rock bottom about forty-eight to seventy-two hours after the high. “It’s a dirty drug that affects everything,” David McDowell says. “And it’s constantly depleting your neurotransmitter stores, so that you come crashing down.” The crash is characterized by intense feelings of agitation, depression, and fatigue. It would appear that the rush of dopamine that is released when one is experiencing the amphetamine or cocaine high actually depletes stores of dopamine, resulting in reduced dopamine levels in the brain. Herbert Kleber of Columbia says, “If the crash were bad enough, no one would use cocaine; and if the crash were mild enough, it wouldn’t matter that people use it. It’s that particular cocaine crash that does all the negative reinforcing, that gets people desperate.” The more addicted you get, the less pleasure you experience, and the more pain follows on the heels of pleasure. Cocaine and amphetamines seem to adversely affect many neurotransmitter systems, not only dopamine but also norepine
phrine and serotonin. In some people, nonetheless, acute craving for the drugs can last for decades after giving them up.

  Continued use of cocaine exacerbates depressive symptoms. A ten-week course of antidepressants will often get someone who wants to get off cocaine through the extended aftermath of the drug crash, but depending on underlying conditions and neurological damage, depression may require permanent treatment. Regular use of cocaine or amphetamines may do permanent damage to the dopamine systems of the brain, giving one a permanent physiological depressed baseline. Cocaine is one of a number of drugs that might be called long-term depression augmenters. It seems to alter the functioning of the anxiety mechanisms of the brain by altering levels of corticotropin releasing factor (CRF). Whether, or when, the brain has enough plasticity to recover from such changes is not clear. Some brains seem to be able to compensate better than others. A brain on antidepressants, a brain that has a capacity to sink into severe depression, is a delicately balanced organ. Parts of the brain that are involved in addiction and drugs of abuse are also involved in the regulation of moods, and they are germane to affective disorder. Depleting the dopamine reserves and mucking around with CRF in such a brain is inviting disaster. If you have any inclination whatsoever toward depression, don’t use cocaine: no matter how good you may feel during the initial rush, you will feel terrible afterward, much more terrible than can possibly be worth it.

  I had taken cocaine and found it charmless when I was in college. I tried it again a decade later and it was a totally different experience—perhaps because of aging; perhaps because of a brain more vulnerable in the aftermath of my depression; perhaps because of the antidepressants I take. It gives me a kind of blissful energy and a sexual exuberance and a feeling of superhero power that are quite fantastic. I get to the point of being unable to string together a sentence and I don’t care if I never string together a sentence again. I realize that the solutions to everything are simple and straightforward. Being high on cocaine breaks up your memory enough so that the past can’t haunt the future. The chemical happiness of a good hit of cocaine feels completely uncircumstantial. I can remember sitting around with a numb nose, thinking that if I could freeze life in that second, I would do so and stay there forever. I almost never use the drug, but the idea that I would never want it is ridiculous. I fell in love with cocaine in those first minutes of rush. The specter of imbalancing my brain and the devastating hangover are all that keep me away from the cocaine high.

  Opiates, another class of much abused substances, are extremely dangerous in part because of how they are consumed; and they are depressants, which means that they do not do great things for depression. On the other hand, they don’t lead to the kind of desperate crash that cocaine will bring about. A quarter to half of opiate abusers are depressive. Opiates, including opium, heroin, and prescription drugs such as Demerol, are to the mind what the fetal position is to the body. Opiates blot out time, so that you cannot remember where your thoughts come from, cannot tell whether they are new or old, cannot get them to interact with one another. The world closes in around you. Your eyes can process only one object at a time, and your mind can hold just one thought at a time, and you don’t really care what you do because the present has become unfocused and piecemeal the way memories are usually unfocused and piecemeal. The opiate high lasts for hours. It is an experience of perfect not-wanting. I have never taken heroin, but I have smoked opium, and only on opium have I ever felt that I simply don’t want anything: to scratch my head, to eat, to sleep, to get up, to lie down, to make plans, to be truly great, to remember friends. It is a nonintimate drug; it kills my sex drive and cuts me off from other people, so that I lie shallow-eyed, staring off into diagonal space. It provokes a happy listlessness, an idleness that driven people can’t experience any other way. It also entails a kind of short-term absence of memory (Did I say anything to that person? Do I know which one that is?) that, when it’s brief, constitutes a high—and, were it further protracted, would be suggestive of Alzheimer’s disease. Writing this, I can recall how opium set my brain free and made me balloon man, floating serenely through the air. Opiates are classed as depressants, but their effect is not simple suppression of feelings; it is a species of joy that comes of having your feelings suppressed. On opiates, you can give anxious depression the slip. An opiate high feels like the prelapsarian version of life, when doing nothing at all was quite sufficient.

  People who have come off heroin and other opiates and are being maintained either drug-free or on methadone suffer a high rate of depression. Neurologists say this is because of organic damage to the brain. Psychologists say this is because these people were depressive in the first place and depression led them to addiction. Either way, your mood prognosis after extended abuse of opiates is not good. The opiate withdrawal period is particularly gruesome; the cravings are strong, and depression weakens will, making it much harder to withdraw. On the other hand, heroin is not as highly addictive as the “war on drugs” rhetoric would suggest. During the Vietnam War, most of the ground troops used heroin, and there was fear that upon their return, the United States would have to fight a terrible battle with the drug. In fact, studies indicate that most veterans of Vietnam have used heroin at least once since their return, but only a small proportion of them have a continuing addiction.

  Hallucinogens and the “club drugs” (ecstasy/MDMA, Special K/ketamine, GHB) make up another class of substances of abuse. Perhaps my personal favorite (and least favorite) drug of all is ecstasy, which I have taken only four times. I saved one relationship that was in trouble when I took E and said a lot of things I felt but hadn’t been able to say. I got another year out of that relationship, and I wonder whether with another dose of E every six months I might have ended up in a happy marriage. I’m kind of a passionate idealist under the best of circumstances, and when I have taken E, I realize that I can save the world and I get excited about doing it. I begin by communicating enormous love to everyone within reach. The solutions to all my problems become clear. Unfortunately, the solutions I devise usually turn out, when I come back down, to be rather unsatisfactory. It would not solve all my problems (or theirs) for me to marry into the British royal family, nor would there be any expedient way of accomplishing that objective. It would not be a good idea to title this book Poems from the Dark Side or The Little Golden Book of Depression. I do not have the qualifications to become a professional ski instructor in Argentina or anywhere else. But though the lucidity is false, the feeling of lucidity is lovely. Ecstasy also gives me an unbelievable three-day hangover during which my jaw aches, my mouth is dry, and my head feels like the French Revolution. I don’t tend to get bad hangovers from alcohol or any other drugs, but my down stretch after ecstasy was enough to keep me from using it regularly.

  Reading the clinical pharmacology of ecstasy makes my stomach turn. The idea that I ever allowed such a substance to enter my body appalls me. At the doses used for recreational purposes (between a hundred and a hundred fifty milligrams), ecstasy damages brain serotonin axons—the part of the nerve cell that reaches out to other cells—in monkeys and other mammals. The evidence strongly suggests that it does the same thing in humans. The drug essentially causes an explosion of serotonin and dopamine, releasing big stores of these substances and then damaging the cells where they were stored. Furthermore, it prevents the synthesis of more serotonin. Regular users of ecstasy have lower serotonin levels than other people, sometimes as much as 35 percent lower. Researchers have reported a number of episodes of a single dose of ecstasy triggering permanent psychiatric illness—sometimes immediately, and sometimes years later. Depressed people are in no position to be lowering their serotonin levels and should therefore give this drug the widest possible berth. “If you take a lot of it over an extended time, you may destroy your capacity to feel happiness; it can cause in the long term the adverse effects that cocaine causes in the short term,” David McDowell of Columbia says of the drug. “Fre
shmen love it; sophomores like it; juniors worry about it; and seniors are afraid of it. Alcohol can become your best friend, but ecstasy can’t. My real fear is that a lot of people who have used a lot of ecstasy in the past two decades are going to think they’re fine, and then when they turn fifty, they’re going to plummet. Depressed patients who use the drug? I say to them, ‘In twenty years, do you want to be on three medications or on ten?’ ”

  The benzodiazepines (or benzos)—Valium, Xanax, Klonopin—and their cousins (Ambien and Sonata) are perhaps the most confusing drugs of all: they are addictive and they are useful for psychiatric complaints. They are very effective against anxiety, but because there is a lot of cross-tolerance between them and barbiturates or alcohol, they should not usually be prescribed for people likely to abuse those substances. The benzos are a valid short-term way of dealing with something that needs both an immediate and a long-term solution. The idea is to get on other medications that will allow you to taper off the benzos and then to use them only for regulatory purposes, to help on days when one particularly requires help. To take the benzos daily long-term is ill-advised and dangerous. The benzos that are most often sold on the street are short-acting ones, roofies, called the “date-rape drug” because they induce a temporary miasma in which someone cannot necessarily assert or defend herself. In general, however, the benzos are abused by people for whom they have been prescribed. You should always think twice before you take a benzo, and if you find yourself needing escalating doses, you should figure out why. Covering up symptoms with benzos is like taking antacids for stomach cancer.

 

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