Chapter 5

Steadying the Ark

We walk the streets and share the stairwells with them. In the winters, we catch their colds, or perhaps give them ours. From the other side of the elevator, we hear the music that leaks from the edges of their headphones. We may have been where they are, and returned. Or perhaps we may yet be among them. Many of us will yet learn to carry the burden of a psychiatric disorder.

Evidence is mounting that people with a variety of psychiatric problems such as depression, hyperactivity, anxiety, and eating disorders are at increased risk for smoking. Additionally, the high rate of smoking among patients with schizophrenia is well established. Persons with these disorders may need to get professional treatment for the disorder before they can successfully quit smoking. This also may mean that researchers will need to develop new smoking treatments tailored for persons with specific psychiatric problems.

The rest of us who smoke may have little notion of the extra problems faced by smokers whose smoking is tied to a psychiatric problem. For them, quitting tobacco may involve nothing more than enduring withdrawal symptoms and adjusting behaviors; it may mean the exacerbation of their psychiatric symptoms, such that what is now a manageable condition can worsen and become unpredictable. The nicotine in the bodily system of a smoker affects how some psychiatric medications work. When the smoker stops using nicotine, the medications work less effectively or predictably. Whatever symptoms nicotine has affected, either directly or indirectly, can change.

Also, smokers whose symptoms have been masked or moderated by nicotine may find that quitting smoking causes symptoms to appear. A smoker prone to depression may find that quitting smoking results in the recurrence of depressive symptoms. A person with an anxiety disorder may find that no longer using nicotine results in a groundswell of anxiety symptoms. A smoker with schizophrenia may find that her antipsychotic medication becomes more potent when she quits smoking. Some schizophrenia symptoms may suddenly worsen when a smoker with schizophrenia quits. Many smokers who try to quit find the experience noxious, uncontrollable, and unpredictable. They are not sure what is happening inside them, or why. As a result, they continue to smoke.

Smoking is commonplace among people with several psychiatric conditions, including depression, schizophrenia, and substance abuse. Patients in treatment for these problems can quit smoking without serious impact on their ongoing treatment if their medications are managed within the framework of smoking cessation. The most disturbing symptoms of their psychosis or their depression could remain controlled. They do not need tobacco to stay rational or to feel healthy.

Nicotine produces a range of effects on human emotions. Scientists have proposed various neural and physiological mechanisms for nicotine's effects, which vary according to the place in the brain where nicotine is absorbed, the amount that is absorbed, and the rate of absorption. In addition, a smoker's state, such as being agitated, rested, active, or quiescent, determines the effect of nicotine. Depending on how it is taken into the body, nicotine can be either sedating or stimulating. Used in subtly different ways, it can have dramatically different effects; it can help an anxious person relax and can provide an emotional lift for a person who is depressed.

Mood and Nicotine

Evidence abounds that tobacco use affects mood. Tobacco companies themselves tout the "pleasure" of smoking, not just in sensation, but in emotional effect. The reality is that even if smokers don't necessarily like the fact that they smoke, they seem to like to smoke. Nicotine may not be an intoxicant, but it does appear to be a euphoriant, or a substance providing feelings of euphoria. The research team of Cynthia and Ovide Pomerleau of the University of Michigan demonstrated this in a 1992 study showing that different amounts of nicotine produced varying euphoriant effects. Smokers reported fewer euphoriant sensations when they used an ultra-low-nicotine cigarette rather than a medium-nicotine cigarette or their usual brand. When subjects smoked a high-nicotine cigarette, they reported at least one euphoria sensation that started about 2.5 minutes after the cigarette was lit. The Pomerleaus suggested that the effects, documented in relation to the subjects' blood plasma levels of nicotine, reflected what is called a dose-response relationship. In other words, the higher the level of nicotine, the more pronounced the euphoria, at least to a point. The phenomenon was particularly observable when subjects had been abstinent from tobacco overnight. It was also more pronounced in the smokers reporting a greater dependence on nicotine.

Scientists have been aware for decades of what is called nicotine's paradoxical effects that vary according to dose and means of delivery. At the low doses of cigarette smoking, nicotine appears to be a likable substance in those who have used it long enough not to be affected by its toxic effects. Although cigarettes are not rated as pleasurable as alcohol or other drugs, nicotine rates well on "drug-liking" and euphoria rating scales. In these studies, a subject is given nicotine without knowing which of several substances it might be, or when it will be administered, and then is asked to report how much he or she likes it, or to note when he or she feels euphoric. Other research has shown that intravenous infusion of nicotine produces a "rush" somewhat similar to that of cocaine or morphine, although shorter in duration. Similarly, the administration of a drug that blocks nicotine's effects, the drug antagonist mecamylamine, also attenuates subjects' nicotine-liking scores.

Nothing to Smile About

Fundamental to understanding these effects is a comprehension of the overall anatomy of the brain, which is shaped somewhat like the meat of a walnut. Its two halves are connected by several bundles of fibers that allow the two sides, with their respective specialized functions, to communicate. The brain functions, however, as a unitary whole, not as two competing sides (left-brain/right-brain theories and arguments with oneself notwithstanding). Although certain tasks, such as comprehending written language, are relegated to specific parts of one side of the brain, the information is rapidly transmitted to other areas of the brain as well. Streams of information continually travel throughout the brain, needing neither a passport nor luggage to go from one side to the other. The intact brain is, indeed, one organ.

Nonetheless, parts of the brain are specialized. As the brain develops before birth, through early childhood, and into adolescence, cells migrate to predetermined locations throughout the brain, developing into intricate structures with distinct functions. Not only are functions focused to allow primary processing in specific areas of the brain, but the two hemispheres of the brain approach information processing differently. The right hemisphere, as a whole, tends to process information more holistically and conceptually. The left hemisphere tends toward a more step-by-step, analytic interpretation. If our brain is intact, we rely on neither one side nor the other, but rather on the interaction and synthesis of both. Having two sides to our brains not only affords us a developmental spare in case one side is damaged, but also allows us a richness of interpretation, as information is analyzed in different but complementary ways.

Emotions are believed by many scientists to be based in what is called a lateralized function, a function that is mediated primarily on one side of the brain. While emotion does not originate entirely in either hemisphere of the brain, studies of localization of emotional processing in the brain have shown that the hemispheres play different roles in our emotional comprehension and expression. We read others' emotions with parts of our brain that, for most people, are located in the right hemisphere. We examine what we have read with input from the left hemisphere. We apparently use right-hemisphere capacities to generate emotionally expressive output, although without the left hemisphere, that output might be limited to mere sound and fury.

One relatively noninvasive, inexpensive way of watching the brain work is with the technology of the electroencephalograph, or EEG. This procedure monitors and allows measurement of the brain's electrical activity. A dense array of EEG electrodes located all over the scalp can be mathematically and visually transformed to provide a picture of the brain's functioning. EEG and related research and diagnostic techniques provide a way of observing the brain's electrochemical activity in process.

EEG studies of the brain's response to the administration of nicotine show a fairly consistent picture. Nicotine use is associated with relatively greater right-hemisphere EEG changes than left-hemisphere changes. Since the brain's neurotransmitter systems are somewhat different in the two hemispheres, and since a given drug binds to receptor sites according to patterns specific to one side of the brain or the other, the finding that nicotine does not affect both sides of the brain in the same way is no surprise. As for what this implies, that issue may be best addressed by looking at nicotine in other contexts.

Nicotine's effects may be linked to a person's state when using the substance. For example, when research subjects are relatively unaroused (referring here to alertness and vigilance, not to matters sexual), a modest dose of nicotine makes them more alert and increases the activation of their brain's cortex, or outer layer of gray matter.

However, nonhuman animals given nicotine when they are aroused or stressed experience a decrease in certain EEG measures and in behavioral signs of arousal. This raises the question, does nicotine act as a modulator of emotions? The answer is less clear when the question is considered in humans. Apparently, the effects of nicotine vary not only according to one's state of arousal, but also according to the complexity of one's emotional and arousal state.

Oddities and Entities

Some studies do show that nicotine has a dampening effect when used during a state of heightened arousal. Other studies show that nicotine increases arousal even when the user is already highly aroused. Yet other studies show that nicotine's effects depend on the baseline rate of behavior. These varied findings may reflect differences in research paradigms, and the difficulty of studying such subtle and transient things as emotions.

In contrast to all those models, nicotine researcher David Gilbert proposed that smoking can lead to "simultaneous increases in subjective alertness" as well as to increased EEG arousal, and can still decrease stress. He and others have concluded that stress and arousal may be "orthogonal dimensions," or separate entities.

Gilbert reported in a 1995 article that extroverted smokers responded to smoking with diminished drowsiness and decreased slower-wave EEG activity. (The slower our EEG waves, the drowsier and less alert we feel.) Smokers testing as more neurotic and depressed responded to nicotine with increased drowsiness and slower-wave EEG activity. Higher rates of baseline depression symptoms were associated with right-hemisphere EEG activity in the frontal lobes of the brain, a pattern characteristic of depressed persons. Smoking normalized this left-right asymmetry between the hemispheres of the brain.

The complexity of nicotine use is obvious in these varying ways of examining the relationship between mood and tobacco use. To some, it may seem that these multiple approaches are analogous to the tale of the blind men describing an elephant. The important fact is not that the descriptions illustrate different aspects of the elephant, but that the elephant is indeed there. However it is described, the connection between nicotine use and emotional functioning does appear to be as real as an elephant, and for many smokers it looms as large.

Depression and Nicotine

Depression is everywhere throughout the world. About 3 percent of those in the United States will, sometime in their life, experience a depression severe enough to be classed as a Major Depressive Disorder, using the nomenclature of mental health professionals. To meet criteria for such an episode, a depression must involve more than merely feeling down or blue. Someone whose sleep patterns are disturbed, who has lost interest in activities that used to be pleasurable, or who has gained or lost weight without consciously trying may be depressed. Someone who feels hopeless, who wishes he or she were dead, or has planned suicide may be severely depressed, and most likely could benefit from professional help.

As distressing and serious as these symptoms sound, they are well documented and remarkably similar in cultures all over the world. Women tend to experience them with greater prevalence than men. Children and adolescents experience them. Good people and bad people experience them. Research suggests that some people are genetically predisposed to developing depression, although many internal and external factors apparently can trigger depression. For example, some women experience depression while pregnant, others experience it after having a baby, and yet others are depressed at not being able to have a baby. Sometimes depression seems to focus on an issue, but just as often it does not. Depression is treatable by medication, sometimes by psychotherapy, sometimes both; and sometimes it stubbornly persists until it spontaneously wears itself out. For some people, it never abates.

Nor is it always evident at diagnosable, clinically relevant levels. Many people live out their lives with a subclinical level of depression as nagging and wearing as a persistent infection or a low fever. This dysphoria (also termed dysthymia) casts a subtle gloom over their lives. For those who are chronically depressed, battling varying degrees of dysphoria becomes the struggle of a lifetime. The current widespread availability of antidepressants is a godsend for many depressed persons, although others are neither helped nor satisfied by medications.

Some people find that potentially dangerous and addictive substances offer relief from the flatness and bleakness of depression. Often, that relief becomes a trap.

Enter tobacco.

Psychiatry research articles published several years ago began to raise the possibility that depression might be a cause of smoking, although the research did not contradict the notion that depression might have a role in maintaining smoking. Naomi Breslau and colleagues Marlyne Kilbey and Patricia Andreski examined whether smokers with a history of depression were at increased risk for developing severe nicotine dependence. Conversely, they asked in a 1993 paper, were those with a history of nicotine dependence at greater risk for depression? The answers, based on interviews with young adults, were yes and yes. This could imply causality, they said, but more likely it pointed to a mutual cause of both smoking and depression.

Breslau also noted in a 1995 report that dependent smokers had increased odds for alcohol and illegal drug use disorders, for major depression, and for anxiety disorders. The presence of major depression and an anxiety disorder were both associated with nicotine dependence. Persons with a history of conduct problems in youth had increased odds for developing nicotine dependence. She explained that smoking and depression are "bi-directional," in that both conditions increase the odds for the onset of the other. This suggested that both were caused by some as-yet-unidentified common predisposition, such as neuroticism, but that neither smoking nor depression causes the other.

A 1998 article by Breslau and her colleagues concluded that depression contributes to daily smoking across the life span, and that the influence of depression on smoking begins in adolescence. The investigators followed more than 1,000 young adult smokers for five years to collect the data reported in Archives of General Psychiatry. Their data did not support the notion that depression led to the initiation of smoking by their subjects. They did suggest, however, that attempts to "self-medicate depressed mood" could explain the subjects' movement toward daily smoking.

The researchers also indicated that smokers were at greater risk for developing major depression, but they did not attribute this to smoking. Rather, they looked toward what they termed "shared etiologies," or causes that both depression and smoking have in common, such as social environment, personality, and coping styles. They explained that early conduct problems appeared to be related to both smoking and depression, and that these associations accounted in part for the connection between depression and smoking.

Their study contradicted earlier cross-sectional reports that depression made smoking cessation more difficult. Instead, Breslau and her co-authors found no indication that depression influenced cessation.

Kenneth Kendler and his colleagues worked with a group of twins to evaluate whether smoking and depression are causally related. After controlling for factors such as personal and family smoking and depression history, they concluded that the relationship between smoking and depression occurred "solely" from familial factors that predisposed people to both conditions. In women, they explained, the relationship between smoking and depression was not causal but came primarily from factors that could be genetic, related to family environment, or both. Their study was the first published report to document a strong association between smoking and future depressive episodes.

The risk for suicide also has been associated with smoking. A physician at the University of California at Davis, Bruce Leistikow, combined numerous studies into one overall analysis to identify a link between suicide and smoking. Previous research had shown that smokers had elevated rates of suicidal thoughts, attempts, and completions. As with the findings linking depression and smoking, Leistikow's meta-analysis did not indicate that smoking causes suicide, but did demonstrate a significant connection. In published studies, higher rates of smoking have been associated with higher rates of suicide. Former smokers had lower suicide rates than current smokers.

Such links between emotions and nicotine use have other manifestations as well. Smokers who report high levels of negative emotions such as depression are less likely to quit using tobacco. High levels of such feelings also can statistically predict smoking, as well as the use of other substances of possible abuse. Smokers accurately expect that using tobacco will curb their negative emotional feelings. Not only that, but negative emotions can trigger a relapse to smoking among ex-smokers; the more negative the emotion, the greater the likelihood of actually relapsing, rather than just being tempted.

Even if depression doesn't necessarily lead to smoking, or vice versa, evidence is plentiful that the two do co-occur with some frequency. Researcher Sharon Hall and colleagues, examining this intertwining, explained in 1993 that smoking is perceived as reducing negative emotional state and stress, and enhancing mood. Nicotine also is a means of focusing attention away from disturbing stimuli or interference, and providing stimulation during boredom or inactivity. Similarly, nicotine withdrawal can result in negative, unpleasant feelings that peak one to two weeks after cessation and return to a baseline state about one month after the smoker stops. The uncomfortable sensations of depression, anxiety, restlessness, nervousness, irritability, impatience, anger, and aggression experienced by some quitting smokers may be more than just withdrawal symptoms: They may be "the emergence of preexisting psychopathology." In other words, smoking may help curb those symptoms; but when the smoking stops, the symptoms return.

Depressed people tend to engage in fewer pleasurable activities than do nondepressed people. They also experience more relationship problems, are less inclined to anticipate positive events, are more inclined to anticipate negative events, and may experience distorted thinking when they feel at their worst. As a result, they also may have less contact with the people, circumstances, and beliefs that might help them lift the depression. In this condition, the quick relief obtained from nicotine's mild euphoriant and anxiety-reducing effects is highly reinforcing. As Hall and colleagues pointed out, "Pharmacologically, it stimulates the organism."

No wonder so many of us organisms keep smoking.

Schizophrenia and Nicotine

Persons with schizophrenia are more likely than not to be smokers. Between 50 and 90 percent (the rate varies, depending on diagnostic criteria) of those with this debilitating psychiatric condition smoke. Unlike the common misperception that schizophrenia refers to having a dual personality, this disorder actually relates to psychotic or delusional thoughts, social withdrawal, and inability to function adequately in daily life. Untreated, those with schizophrenia might exhibit bizarre behavior and might be unable to experience pleasure. Two questions relate to the high prevalence of smoking among those with schizophrenia: Why do the majority of them smoke, and what happens when they stop?

As it turns out, many persons with schizophrenia not only smoke, they sometimes smoke to excess. Some patients, according to a 1986 report by Darrell G. Kirch and colleagues, used tobacco to the point of nausea, and developed water intoxication from reduced secretion of an antidiuretic hormone as a result of the excessive nicotine use. One reason for this overuse may be that nicotine appears to normalize a mental "gating" mechanism that typically malfunctions in those with schizophrenia. Lawrence E. Adler and his associates at the University of Colorado Health Sciences Center reported in a series of articles in the early 1990s that the administration of nicotine temporarily helped correct a sensory gating abnormality in which those with schizophrenia are hypervigilant in responding to sensory input that a person with normal functioning would ignore, such as background traffic noise. The administration of nicotine normalized a brainwave indicator of this gating defect in both smokers and nonsmokers. Nicotine temporarily and briefly overrode the brain defect that is characteristic of schizophrenia, thus giving patients a brief period of calm.

The inability of many persons with schizophrenia to filter out irrelevant stimuli apparently is an inherited trait that predisposes them to developing schizophrenia. The brain defect is not, by itself, sufficient to cause schizophrenia. Healthy siblings of some patients with schizophrenia also have the inherited trait, but they do not have schizophrenia. The gene that appears responsible for this condition is linked to a brain receptor that filters incoming information. Nicotine stimulates that brain receptor. Therefore, schizophrenic persons who use tobacco are briefly turning on this receptor and thus getting temporary respite from the information overload common to their condition.

This landmark genetic work is described in reports by Sherry Leonard and Robert Freedman at the University of Colorado School of Medicine and their colleagues. Scientists have not yet found the gene mutation that causes this condition; nonetheless, the gene discovery itself opens the possibility of new treatments that target this receptor.

Another clue as to the effects of nicotine in patients with schizophrenia comes from a finding that smokers using antipsychotic medication experienced less of a disorder called akathesia, a restlessness and inability to sit down that is a side effect of the medication, than did nonsmokers using the same medication. Schizophrenic patients who smoked experienced fewer involuntary movements and reported less jitteriness over the course of a four-week study in which they used fixed doses of antipsychotic medication. Using the medication resulted in increased involuntary movements in nonsmoking patients with schizophrenia.

The researcher conducting the study, Nicholas Caskey, hypothesized that people with schizophrenia may smoke partially to reduce the unpleasant side effects of antipsychotic medication. Nicotine may have some beneficial effect in lowering some of the side effects, particularly akathesia and abnormal movements. Even if this turns out to be the case, patients with schizophrenia would be better off using a less dangerous source of nicotine than cigarettes (for example, nicotine gum or patch).

Smokers with schizophrenia do find that they can quit using tobacco without an increase in their psychiatric symptoms. However, quitting tobacco might worsen a movement disorder called tardive dyskinesia, which is also a side effect of some antipsychotic medications.

Caffeine, Alcohol, and Nicotine

Caffeine, alcohol, and tobacco are the drugs most commonly used throughout the world. They are also commonly used together.

Most smokers are used to having coffee and tobacco together. In fact, smokers drink more coffee than nonsmokers. Exactly why this is the case isn't yet clear, although scientists have found some curious relationships between caffeine and nicotine. A smoker who also uses caffeine (which is to say, the majority of smokers) might find it easier to strategize quitting smoking if he or she understands that the two are connected.

The relationship between caffeine use and nicotine consumption is probably at least partially behavioral. Coffee consumption and cigarette smoking are so frequently done together that either can serve as a cue that triggers the other, but smoking most often follows coffee consumption, not vice versa.

High Anxiety

A common criticism of research studies of common life events such as coffee drinking is that the results are not necessarily generalizable beyond the laboratory. Ken Perkins at the University of Pittsburgh has worked around this limitation by having smokers use both nicotine and caffeine under conditions comparable to those in which they would normally be used. Studying research participants in settings of rest and casual physical activity, he reported in 1994 that the cardiovascular and self-reported subjective effects of nicotine and caffeine may be additive.

Several factors could account for the frequent combined use of nicotine and caffeine. One could offset the other, since caffeine can increase anxiety and arousal and nicotine can decrease both. It is also possible that stress or the consumption of alcohol could contribute to the relationship. Whatever the cause of the connection, severing the tie could result in unpleasant effects. Caffeine is metabolized faster when it is consumed by someone who also uses nicotine. When a smoker stops using nicotine, caffeine is metabolized more slowly, and thus remains in the body longer. If caffeine consumption levels are unchanged, this results in a greater accumulation of caffeine in the body, with the pattern of elevation lasting for as long as six months.

Just as it is common for a smoker to sip a cup of coffee before using tobacco, it is also common for smoking to accompany the use of alcohol. Nicotine and alcohol have separate and distinct effects, both emotional and physiological. Perkins and his colleagues reported in 1996 how men and women respond to nicotine and alcohol separately and together. Nicotine, taken by itself, increases a feeling of "head rush," dizziness, jitteriness, tension, arousal, decreased fatigue, and relaxation. Alcohol also brings feelings of "head rush," jitteriness, and dizziness, but adds feelings of intoxication. It has no other stimulant effects. Taken together, nicotine attenuates some of the sedating and intoxicating effects of alcohol, a finding that had been reported in several previous studies utilizing performance and EEG measures. Perkins and his colleagues also found that men and women responded differently to the combination of nicotine and alcohol. Men using both substances together experienced a reduction in dizziness, relaxation, tension, vigor, and arousal. In contrast, women using both substances experienced enhanced effects of both substances.

Smoking cessation was accompanied by an increase in wine consumption in a large group of male World War II veteran twins studied by investigators Dorit Carmelli and associates at SRI International in California. Following alcohol and tobacco use over a 16-year period of late adulthood, the investigators learned that continuing smokers also used increasing amounts of wine. Alcohol consumption did not change across time in nonsmokers.

Drown Your Sorrows

Carmelli's colleague Gary Swan and his collaborators in 1996 identified a genetic factor apparently underlying the joint use of tobacco, alcohol, and coffee. A report on research with 356 pairs of middle-aged twins, about half of them monozygotic (identical), concluded that the most parsimonious interpretation of the twins' use of tobacco, alcohol, and coffee was a "common genetic latent factor" that would explain the association between use of the substances. A 1997 report by the same team found similar results in an examination of self-report data from nearly 4,600 twin pairs.

Such relationships, however, are not necessarily predictive. A multi-site research team from the universities of Michigan, Minnesota, and Nebraska had hoped that a measure of their participants' alcohol intake would predict the amount of tobacco use approximately four years later. Instead, Faryle Nothwehr and colleagues found that not only did alcohol consumption not predict later tobacco use, but those who quit smoking were no more likely to reduce their alcohol use than were continuing smokers. Therefore, even though alcohol use and smoking are highly related, quitting smoking did not necessarily reduce alcohol consumption. Men in the study drank more alcohol and smoked more cigarettes than their women counterparts. Among nondrinkers, men were more likely than women to quit smoking. Surprisingly, drinkers and nondrinkers used about the same amount of cigarettes. Those who drank heavily smoked more than did lighter drinkers. And, not surprisingly, smokers used more alcohol than did nonsmokers.

The findings were concordant with a 1993 study in which Perkins and associates reported that middle-aged women who smoke or who used to smoke consume half again as much alcohol as do women who have never smoked. A history of using cigarettes also was associated with dietary and activity patterns that heightened the risk of some chronic diseases. Current smokers reported engaging in less physical activity than did never-smokers and ex-smokers. Quitting smoking was associated with more physical activity.

These connections between commonly used substances can be problematic for a smoker who wants to quit using tobacco, or an alcoholic who is attempting to quit drinking. It is commonly but perhaps inaccurately believed that cigarettes provide help for alcoholics dealing with the stress of abstinence from alcohol. However, it may be that because smoking and drinking so often go together, smoking could act as a trigger, prompting a recovering alcoholic to resume drinking.

Quitting drinking is not always associated with quitting smoking; also, the use of either substance involves a known health risk. Richard Hurt and his colleagues at the Mayo Clinic studied a group of alcoholics who stopped drinking but did not stop smoking. A follow-up 20 years later found that almost half had died. Less than one-fifth of the general population normally would have died by that age. More than half of the deaths of the persons in treatment were due to tobacco-related disease. One-third died from alcohol-related disease.

Treatment Issues

Until the last few years, the mental health treatment community had little interest in promoting smoking cessation among patients with serious psychiatric disorders. In the words of researcher Michael Resnick, "Psychiatry is belatedly awakening to the seriousness of nicotine addiction." It is also belatedly realizing that psychiatric patients need, deserve, and can benefit from effective smoking cessation treatment.

The mental health community used to insist that psychiatric patients should not be given the additional challenge of quitting smoking, since it might disrupt treatment. They were perceived as being too fragile to quit, or as lacking sufficient insight to make them good candidates for quitting. In some psychiatric settings, it was considered beneficial for staff and patients to smoke together as a way to bridge communication barriers. Staff used cigarettes as a means of rewarding patients. Patients were expected to tolerate the environmental tobacco smoke in psychiatric units, even if it triggered a relapse in those who were ex-smokers.

When hospitals across the United States went smoke-free, many psychiatric units did not, as Resnick described the events. Typically, the rest of the hospital went smoke-free before the psychiatric unit did. When, in the late 1980s, hospitals began controlling and limiting smoking in psychiatric units, the results were encouraging. Chaos did not erupt. Staff, initially skeptical, became supportive. Some patients were given nicotine replacement treatment. Most patients were compliant. The air cleared. Staff no longer used cigarettes as reinforcement, patients and staff were no longer exposed to smoke, and hospitals could come completely into compliance with accreditation requirements that hospitals be smoke-free.

Providing effective smoking cessation programs for psychiatric patients requires that clinicians be familiar with both psychiatric treatment and addiction treatment. Many aspects of cessation treatment with these groups remain unexamined. Among these is the problem of convincing the patient to accept treatment and remain abstinent in a social environment outside the clinic that encourages or tolerates smoking. Psychiatric medications need to be considered and managed carefully, because of interactions with nicotine. No one yet knows which patients will be best suited for quitting on their own, when is the best time to offer cessation treatment, or exactly how to adjust treatment models to the needs of these patients. Despite those unknowns, current successes reported with psychiatric patients are encouraging.

At What Price?

Whatever effects nicotine has on a smoker require continual rejuvenation. Nicotine cannot fix or cure psychiatric symptoms. The euphoriant effect of smoking is not enormous, nor does it last long. It comes and goes within about 10 percent of the length of time that a cigarette lasts, the Pomerleaus estimate. What price do smokers pay for this temporary help, or this small effort toward emotional and mental steadiness?

As a smoker will tell you, it's the coping enhancement that makes tobacco so appealing, especially to people whose life problems and psychiatric symptoms are difficult to manage. For some smokers, tobacco is that nudge, that little indulgence that makes nightmares livable. Life has many such small regulators, however, such as tucking your cold toes under a snoozing dog, even when the rest of you can't get warm. Or petting your cat while you watch a sad movie. Or melting a piece of fine chocolate in your mouth while you mutter at your income tax forms. Independent of nicotine's addictive properties, it can be this sort of emotional stability, however small, however fleeting, that tobacco affords. It is one thing that keeps people smoking who have precious few other ways to cope. For many smokers, nicotine is also a glue that helps hold them together.

The price smokers pay for these gestures toward stability is, unfortunately, high. Their fate, however, is not without historical analog. It was the well intentioned, hapless Uzzah, we read in the Bible (2 Samuel 6:6-7), who drove a cart carrying the Ark of the Covenant from the house of Abinadab. When the ox stumbled at a threshing floor, Uzzah put forth his hand to steady the Ark.

For this, we learn, God struck him dead.