Cornered (14 page)

So who are the real addicts? According to the tobacco industry, as Dr. Terry said, “It is generally accepted among psychiatrists that addiction to potent drugs is based upon serious personality defects from underlying psychologic or psychiatric disorders which may become manifest in other ways if the drugs are removed.” America's 50 million smokers surely could not be put into this category. The basic problem with these conclusions is that they are at least thirty years out of date. Medical science has moved on.

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S
ECONDS AFTER
a smoker inhales, the nicotine is absorbed into the bloodstream and sets up a biological chain reaction in the brain. Nicotine acts like a neurotransmitter, the natural chemical messengers in the brain that send information from one nerve cell to the next. Nerve signals travel electrically and at junctions between the nerve cells must cross gaps called synapses. The natural neurotransmitters are released by the nerve cell on one side of the gap and dock on the other side with a receptor protein. In the instant of pleasure, the signal from one of these messengers, acetylcholine, triggers the release of another messenger, dopamine, which stimulates nerve cells involved with pleasure. Nicotine mimics acetylcholine and grabs some of the nerve sites normally used by it. So a gulp of tobacco smoke containing nicotine triggers a rush of pleasurable dopamine.

The natural messenger, acetylcholine, is absorbed by its receptor protein and then promptly released and reabsorbed by the nerve cell that set it free. But nicotine gets stuck on the protein, preventing the receptor from working again for a while. Thus, nicotine gives a quick buzz, after which the stimulation declines gradually until the receptors are freed again.

The brain cells quickly adapt to having sites blocked by nicotine by generating more sites. When the nicotine eventually unblocks these sites, there are then more sites available than normal and the result is overstimulation, which causes a person to become irritable and cranky—a symptom of nicotine withdrawal. When smokers say smoking “relaxes” them, what they are actually saying is that the new nicotine “hit” from a fresh cigarette is treating their nicotine withdrawal symptoms.

The paradox of the nicotine “fix” is that it can be either a “high” or a “low”: nicotine can act as a stimulant, increasing attentiveness, heart rate, and blood pressure, but it can also act as a depressant, inhibiting the flow of information between nerve cells.

As the nervous system adapts to nicotine, a smoker slowly increases the number of cigarettes smoked and hence the level of nicotine in the blood—until the number of sites stimulated and blocked by nicotine is balanced by the new sites made available by the neurotransmitters. The smoker has reached a “target level,” which he then needs to maintain by keeping up his level of nicotine.

When the smoker goes to sleep, the nicotine level drops dramatically—about forty-five minutes after a cigarette is smoked the concentration of nicotine in the blood is half what it was—which is why smokers often talk about the first cigarette in the morning being the best. The length of time between a smoker waking up and his first cigarette is a measure of the severity of his dependence. More than one-third of smokers reach for their first cigarette within ten minutes of waking; nearly two-thirds within the first half hour. When a smoker stops smoking, it takes one or two weeks for his brain chemistry to return to normal. Some studies suggest long-term smoking can make near-permanent changes in the brain.

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S
O
,
WHY DID
the 1964 Surgeon General's report say smoking was a nicotine “habit,” not an “addiction”? At the time, the two nongovernmental authorities then charged with classifying drugs—the World Health Organization and the American Psychiatric Association—used two categories, “habituating” and “addicting.” Drug “addiction,” said the WHO, was a state of periodic or chronic intoxication produced by the repeated consumption of a drug that creates an overpowering need, or compulsion, to increase the dose and a psychological dependence, with detrimental effect on the individual and society. Included in this group were the opiates and barbiturates. “Habituation,” on the other hand, was a desire but not a compulsion, with little or no tendency to increase the dose, some degree of dependence but no withdrawal symptoms, and with possible detrimental effects on the individual but not on society. Cocaine, amphetamines, and nicotine were included in this group.

In the 1964 report, the section dealing with nicotine addictiveness was a mere five pages out of a 387-page review of the scientific literature on smoking and health. Dr. Terry had made a point of inviting the tobacco companies to submit names of experts so that the report should be seen to be fair. The addiction section was written by Maurice Seevers, chairman of the pharmacology department at the University of Michigan, whose name had been put forward to the Surgeon General by the tobacco companies.

Seevers was an expert on habit-forming drugs. From the start, he dismayed some of his colleagues on the committee writing the report by refusing to label nicotine an addictive substance, but they had to concede they did not have his expertise. As one of them acknowledged subsequently, he was “one tough hombre,” who would not even concede that the issue of the effects of nicotine was controversial.

The key distinction, according to Seevers, was that hard-drug takers can harm society; nicotine only affects the individual. Seevers relied on the then generally accepted view of psychiatrists that addiction to potent drugs is based upon personality defects; true addicts are abnormal. A smoker in withdrawal from nicotine was not likely to become a burden on society. (Of course, he could find his fix at the local store. Seevers did not discuss the most obvious difference between hard drugs and tobacco—that the first are illegal, and tobacco is not.) Seevers's report did not explore another aspect of addiction: while some tobacco smokers were able to quit with seeming ease, others could not give up—much like any addict. Indeed, roughly two-thirds of current tobacco smokers have tried at least once, and one-third try in any given year. The relapse rate for tobacco use is remarkably similar to that of heroin. But apparently Seevers wanted a clear distinction between habit forming and addictiveness. The tobacco companies could not have wished for a better result.

The distinction was dropped shortly after Dr. Terry's report. To move the whole debate away from the moral and social issues associated with the term addiction, a new term, “dependence,” was adopted. The key change for the American Psychiatric Association was the new medical description of nicotine-withdrawal syndrome, which included the craving for the drug, irritability, frustration or anger, anxiety, difficulty concentrating, restlessness, decreased heart rate, and increased appetite or weight gain.

Twenty-four years later, the report of the then Surgeon General of the United States, Dr. C. Everett Koop, stated boldly that nicotine was addictive and the “pharmacologic and behavioral processes that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine.”

In the preface to his 639-page report, Dr. Koop wrote, “Some people may have difficulty in accepting the notion that tobacco is addicting because it is a legal product. The word ‘addiction' is strongly associated with illegal drugs such as cocaine and heroin. However … the [biological] processes that determine tobacco addiction are similar to those that determine addiction to other drugs, including illegal drugs.”

The central element of all forms of drug addiction, he said, was that the user's behavior is largely controlled by a psychoactive (mood changing) substance. Other criteria included compulsive use of the drug, repeated self-administration, “reinforcement” because of the drug's rewarding properties, and “tolerance,” whereby a given dose of a drug produces less effect or increasing doses are required to achieve a specified intensity of response. Finally, absence of the drug produces withdrawal symptoms. Nicotine was such a drug, the report concluded.

The industry immediately claimed the change was motivated by politics, not science. Dr. Koop had “moved the goal posts,” complained R. J. Reynolds. But the problem for the tobacco companies was that virtually the entire medical science and psychiatric community supported Koop's conclusions.

The tobacco companies were left with a handful of psychologists who had been promoting the idea that people smoked according to their personality or their genetic makeup and not because of a chemical addiction to nicotine. Extroverts smoke, introverts tend not to, was the message. To call nicotine addictive merely on medical science criteria of what happens to the brain was not a meaningful statement, merely a hypothesis, according to these researchers. In place of the “addiction hypothesis,” a small group of psychologists proposed what they called the “resource hypothesis”: that smokers use cigarettes primarily as a “tool” or “resource” that provides them with psychological benefits, such as increased mental alertness, reduced anxiety, and an ability to cope with stress.

The legal departments of the tobacco companies had often relied on the work of a British behavioral psychologist, Hans Eysenck, who argued that smoking and lung cancer were related to genetic makeup: that people were cancer-prone because of their genes, and their genes also somehow caused them to smoke. The companies also relied on the provocative writings of another English psychologist, David Warburton of the University of Reading. Attacking Koop's 1988 report, Warburton argued that nicotine fit only a few of the new criteria agreed upon by the American Psychiatric Association and the WHO. Koop, he charged, was ignoring “the discrepancies in his enthusiasm to find criteria to compare nicotine with heroin and cocaine use.”

Two R. J. Reynolds scientists, John Robinson and Walter Pritchard, working at the company's behavioral research and development center in Winston-Salem, North Carolina, joined the attack on Koop. They concentrated on the addiction criterion of intoxication—as their boss James Johnston would do at the Waxman hearings. If a drug did not result in intoxication, it could not be termed addictive, they said. Intoxication should be the key point in distinguishing between habituating and addicting drugs. They also argued that nicotine did not fit the “compulsive use” criterion since many smokers can do without a cigarette for long periods.

Most importantly, however, they said, “Common sense tells us that nicotine is
not
[their italics] like heroin, cocaine or any other ‘classic' addicting drug.… One does not have to be a trained behavioral scientist to come to this conclusion. Simply ask, and honestly answer, the question as to how many people would board a plane piloted by someone who had just consumed an addicting drug (alcohol, cocaine, barbiturates) versus a plane piloted by someone who had just had a cup of coffee and smoked a cigarette.” (Johnston would use the same words in his congressional testimony.)

Other behavioral psychologists, however, agreed with the new definition of nicotine as a dependence-producing, or addictive, drug. Intoxication was not central to dependence, they argued. In the end, it was a matter of the industry's out-of-date, scientifically frivolous, “common sense” public position against basic biology. The companies knew the difference, of course.

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T
HE
M
ERRELL
W
ILLIAMS PAPERS
told plaintiffs' lawyers like Gauthier that in private, three decades ago, the company scientists had never bothered with the semantic distinction between habituation and addiction. Sir Charles Ellis, the chief scientist at BAT, the Brown & Williamson parent company, had said in a 1962 in-house conference that smoking “is a habit of addiction…” A 1963 BAT research paper entitled “The Fate of Nicotine in the Body” begins, “[Nicotine] appears to be intimately involved with the phenomena of tobacco habituation (tolerance) and/or addiction.” Brown & Williamson's own chief counsel, Addison Yeaman, wrote in a 1963 memo, “We are, then, in the business of selling nicotine, an addictive product.”

But toward the end of the '60s there were hints that company legal departments were at work. In a draft report of a 1967 BAT research conference, company scientists listed some “main” assumptions—among them, “There is a minimum level of nicotine. Smoking is an addictive habit attributable to nicotine.…” The draft notes that these assumptions were made “without any attempt to justify them [or] to agree on their correctness at this time,” and then a handwritten edit on the document changes the phrase “an addictive habit” to “a habit.”

While the companies in public used the words “taste,” “satisfaction,” and “impact” to describe the effects of nicotine, in their private research papers they talked about the pharmacology of nicotine, its effects on the brain, and the “need” of the smoker for those effects. People smoked primarily for their dose of nicotine. “The cigarette should be conceived not as a product but as a package. The product is nicotine.… Think of the cigarette as a storage container for one day's supply of nicotine,” wrote William Dunn, Philip Morris's research scientist, in 1972. “As with eating and copulating, so it is with smoking,” Dunn wrote. “The physiological effect serves as the primary incentive; all other incentives are secondary.” Another BAT study in 1976 referred to “Low Need” and “High Need” nicotine smokers. “The indications are that cigarettes delivering around 1.0 to 1.5 mg [of nicotine] are better suited to Low Need clusters, while cigarettes delivering 1.5 to 2.0 are better suited to High Need clusters.”

In the early '70s, the tobacco companies explored the possibility of finding a replacement for nicotine that would not cause health problems. For example, the companies were aware of the harmful effects of nicotine on the cardiovascular system—it increases pulse rate and contracts blood vessels—and they would try to find a chemical substitute, a so-called analogue, that would mimic the effects of the drug on the brain without affecting the blood supply.