Authors: Richard Kluger
The relative worthlessness of such efforts was pointed up in a January 1968 article, “Smoking and Kids: Why Are We Failing?,” in the house organ of the U.S. Clearinghouse on Smoking and Health. According to its author,
Encyclopaedia Britannica
science editor Anslie H. Drummond, Jr., the difficulty with motivational inquiries into youngsters’ behavior was that they often responded as they thought adults wanted them to; more to the point with regard to smoking, they often were unable to identify the real reasons for taking up such a notorious custom—and even if they could, they might not choose to disclose it. But clearer to Drummond was the reason young people were unswayed by adult alarms over their imperiled futures if they smoked: “For the great majority, there is virtually nothing in their lives to help them integrate the meaning of lung cancer and death … .” Neither their smoking friends nor smoking parents had yet fallen victim to the habit, and if smoking grandparents
had, the resulting diseases were common to older people and thus not readily blamed on or thought to be exclusively due to tobacco. By contrast, the perceived gratifications of smoking were immediate as well as mild and thus far more manageable when compared to other quick-acting but disabling drugs like euphoria-inducing cocaine or the mind-blurring, reflex-slowing sedatives, marijuana and alcohol, all fraught with antisocial implications. Their very mildness and perceived function as both stimulant and relaxant made cigarettes as useful to youngsters as to adults, and their cheapness, easy availability, and naughtiness made them still more so.
Perhaps the world’s leading investigator into smokers’ motives was M. A. H. Russell of the Addiction Research Unit at London’s Institute of Psychiatry, who in the May 8, 1971, issue of the
British Medical Journal
delineated five types of smokers. Least caught up in the habit were “psychosocial” smokers who affected the use in adolescence or as a prop in social situations as adults, with a correspondingly low intake of nicotine. “Indulgent” smokers undertook the habit mostly for sensual or sensory rewards, of which the taste, smell, and “kick” at the back of the throat from inhaling were the most obvious. A third category used cigarettes largely for “tranquilization,” in particular the calming effects of oral gratification “and the occupation of the hands to relieve anxiety and tension.” Others favored smoking for its “stimulation” in sustaining the performance of or allaying fatigue from monotonous tasks like long-distance driving or for enhancing alertness, perseverance, and creativity in demanding cerebral tasks like writing or meeting a deadline in a hectic commercial transaction. Finally, there were plain and simple “addictive” smokers who lit up every twenty or thirty minutes primarily to avoid the dreaded symptoms of withdrawal. Russell did not notably elucidate just why and how smokers in each category derived their rewards or to what extent the categories overlapped. What mattered most, in Russell’s view, was that “people who smoke at all sooner or later become regular, dependent smokers”—and only about 15 percent of them quit before reaching sixty.
A parallel avenue of sociological investigation was the hypothesis, favored by tobacco industry apologists like Wakeham, that smokers were basically different sorts of people from nonsmokers and may have been programmed that way from birth by a genetic code regulating the production of certain enzymes that governed emotional disposition and behavioral choices. Given that more than one-third of all U.S. adults smoked, could any valid generalization be offered about a “smoker’s personality”? Surely all kinds of people smoked. But investigators throughout the ’Sixties and ’Seventies by and large corroborated certain tendencies apparent to any close observer of the smoke-wreathed human animal. Most smokers seemed to be moré stressed and inordinately driven than nonsmokers, more impulsive and demonstrative and less in control of
their emotions, conduct, and social and occupational environments. Many if not most smokers held a more fatalistic view of life than nonindulgers: your being could be snuffed out the next instant for any of a hundred reasons, thus take what pleasures you can from life without unduly fretting over the risk. In disproportionate numbers smokers felt saddened, if not cheated, by the hand fate had dealt them: impoverishment, too few brains or too little learning, inadequate social or professional opportunity, and/or loveless marriage. None of these explanations, though, especially a possible genetic predisposition to smoke, served to exonerate the cigarette itself from its lethal effects. Indeed, those most vulnerable to the habit were the ones best advised to try to flee from its ravages before it was too late.
Many smokers convinced themselves that a tobacco-free life would be unendurable; cigarettes served them with wonderfully protean versatility as both stimulant and relaxant. But how, psychologists pondered now, could the very same substance provide those diametrically opposed uses, especially when most observable bodily responses to smoking resembled the patterns of emotional arousal,
e.g.
, about a 15 percent increase in heartbeat rate, a jump of ten to twenty points in blood pressure resulting from a narrowing of the peripheral blood vessels? These phenomena acted to produce a surge of energy associated with the body’s fight-or-flight reflex at moments of high anxiety and were thus useful to smokers, rescuing them from depression, boredom, or fatigue—in short, nicotine served as an “upper,” like an amphetamine; how could it also trigger stress-relieving reactions by the body?
To find out, scientists began taking a more intensive look at the interplay of blood, nerves, and muscle tissue chemically activated by nicotine. A picture was assembled of how nerve cells formed a body-wide transmission system that could be both readily activated and deactivated by the particular properties of nicotine. When chemically charged, each nerve cell sent an impulse down its length to a fibrous extension, or axon, and relayed it to a receiver station, or dendrite, on the next nerve cell; the junction of these two, the synapse, is a microscopic gap that is crossed by the conversion of the nerve’s electric impulse into a chemical secretion that serves as a neurotransmitter as it binds chemically on the surface of the dendrite, if it is receptive to the particular compound bearing its message, thus stimulating a chain reaction. These neurotransmitters vary in nature and do their work selectively in the reactions they trigger. Nicotine was found to act in a way imitative of one of the body’s most important natural neurotransmitters—acetylcholine (ACT), a compound that is active as a stimulant where nerves and muscles meet and also serves to release other neurotransmitters, in particular those that travel to the adrenal glands near the kidneys. When aroused by neural receptors sensitive to ACT or nicotine, these glands release adrenaline with its highly stimulating effects on the circulatory
and muscular systems, in the process raising the metabolic uptake of the body’s fuels,
i.e.
, causing it to burn its food supply faster. A comparable, transient increase in brain-wave activity was also observed.
But there was nothing automatic about this neurological transmission process once it began; it had to be repeated, and so each nicotine-receptive dendrite, after dispatching the impulse, released a protein that broke up the key-and-lock bond between neurotransmitter and receptor, allowing some of the chemical compound to be taken back by the axon terminal in the adjacent nerve cell for further use and thus clearing the connection for the next impulse. Nicotine, as it happens, forms a stronger and longer-lasting bond at the junction point between nerve cells, and though the chemical secretion it activates is readily cleared away when small doses are relayed, the transmission site grows clogged when a lot of nicotine is taken up by the lungs and blood and floods the neural chain. The eventual effect of this process, some investigators found, is to block and finally halt the stimulating effects of nicotine entirely, thus slowing muscular activity, the heart in particular, and with it the delivery of oxygen throughout the body and brain—in short, causing a sedative effect. Thus, scientists have speculated that smokers consciously or subconsciously vary their nicotine dosage to mesh with their biorhythm and stress levels as the day wears on.
Nicotine, then, came to be understood through the work of many investigators, most prominent among them UCLA psychiatrist Murray Jarvik and Columbia psychologist Stanley Schachter, as possessing a dual or “biphasic” nature, initially stimulating but giving way upon heavier dosage to a depressant effect after inhibition of the neural release mechanism. And the more frequently the smoker found himself able to achieve the physiological reaction desired—at, say, 200 puffs a day—the more thoroughly he conditioned himself to want these effects and trained his body to tolerate them. Eventually one in four smokers pays with his or her life for this systemic fooling of nature.
II
AMONG
the several dozen scientists gathered on the Caribbean island of St. Martin early in 1972 for a seminar, sponsored by the tobacco industry, on why people smoke was Duke-trained psychologist William L. Dunn, who had joined the research staff of Philip Morris eleven years earlier, when Helmut Wakeham saw value in probing the behavior of smokers. In a report to his company on the consensus among the psychologists at St. Martin, Dunn offered a stunningly simple answer to the profound question of why so many millions were driven to such self-destructive folly: “The primary incentive to cigarette smoking is the immediate salutary effect of inhaled smoke upon body
function.” The cigarette, he wrote, ought properly to be conceived of “not as a product but as a package. The product is nicotine. … Think of the cigarette pack as a storage container for a day’s supply of nicotine.” An integral part of the product’s appeal, he went on, was its convenience—it was unobtrusively portable, instantly accessible, easily prepared for use and discard, its rate of consumption readily metered to dispense the desired level of nicotine; its psychoactive ingredients reached the brain rapidly—within seconds—and its acute effects lasted no more than thirty minutes. Here was the ideal mild stimulant-sedative.
This marvel, of course, had a serious short-term catch to it: you could not condition yourself to enjoy its multiple uses and then just take it or leave it. You had to keep taking it, every forty minutes or so, depending on one’s level of addiction, or suffer the consequences of withdrawal. The symptoms, varying with the duration of one’s abstinence, included edginess, irritability, hostility, depression, mood swings among all or several of these, oral fixation, craving, headache, constipation, and weight gain. However real the sedating effects of heavy smoking, they in fact merely masked the keen distress that would otherwise have affected the smoker if he quit. Nor could the conditioned customer easily reduce his or her tar and nicotine intake. A report on smoker psychology that Dunn himself co-authored in March 1977 said, “We find that our smokers [were] smoking cigarettes in 1972 that delivered significantly less tar and nicotine than in 1968. At the same time they were smoking more cigarettes as well as more of the rod [farther down the tobacco portion] from each cigarette. These findings suggest … that a tar and nicotine quota mechanism may be operative. That is, they may be smoking more … to compensate for the decreases in the tar and nicotine delivery of their cigarettes.” In a deposition for a product liability suit ten years later, Dunn claimed that Philip Morris scientists had not concluded that the compensation theory was valid—and not surprisingly, for if they had, as Dunn’s paper suggests they in fact did, it would have gone a long way toward demonstrating the pointlessness, if not downright deceit, of the industry’s efforts to modify its product.
No doubt secondary to smoking’s effects on the body’s chemistry—but nonetheless a large part of its appeal—were the infinite forms of gratification arising from the sensuous nature of the act, starting with the gently crackling removal of the cellophane wrap and moving on to the tweezerlike extraction of the cigarette, the staccato tapping of it against the wrist or a firm surface, the becalming insertion into the mouth, the magical burst of flame, the searing intake to fill the void within, the rasp on the tracheal tissue on the way down, and finally the glorious expulsion of aromatic clouds to fill one’s entire immediate surround. Then there was the ongoing busyness of the hands and mouth, using the little white cylinder as a wonderfully communicative device and personality surrogate: the languorous drag that bespoke of knowing cool, the leaning
this way or that to flick an ash, the dismissive snuffing out of the deliciously reduced thing.
As far back as the 1950s, students of smoking behavior were reading psychic states into these manipulative and exhibitionist patterns
(e.g.
, handling a cigarette in a delicate or arty manner was thought to conceal a sense of inferiority). The cigarette was the all-purpose sublimation. That it continued to be so understood by smokers themselves was well captured by one who knew the price of this indulgence, New Haven surgeon-author Richard Selzer, who wrote in his 1976 book,
Mortal Lessons:
“[L]et no meddlesome man caution me against the extravagance, the injuriousness, of tobacco … . To deny me my smoke is to extinguish me as utterly as would death itself… . Smoking is good for the dumpish heart, lights up the gloomies… .”
III
WHILE
many of smoking’s perceived blessings were subjective, a few could be measured with clinical objectivity, such as the use of cigarettes to suppress the appetite and reduce weight. Nicotine had been shown to lower the level of insulin in the bloodstream and thus ease the smoker’s craving for sweets. The nicotine-triggered effects of adrenaline on the stomach’s musculature produced a transient effect of fullness that could somewhat allay the pangs of hunger. A Temple University study had determined that smokers, who on average weighed seven pounds less than nonsmokers, were lighter not because they ate less but because smoking had intensified their metabolic rate; a month after quitting, a cohort of ex-smokers showed an 8 percent drop in oxygen consumption and a 5 percent slowing of their heartbeat. By the late 1980s, researchers were finding that smokers experienced a disproportionately high expenditure of energy when they were engaged in light activity as opposed to when they were at rest. Just why this was so was unclear, but the association of smoking and slimness had an undeniable basis in fact.