The Tipping Point

by Malcolm Gladwell

  This is a critical point, and one that is often lost in the heated rhetoric of the war on smoking. The tobacco industry, for instance, has been pilloried for years for denying that nicotine is addictive. That position, of course, is ridiculous. But the opposite notion often put forth by anti smoking advocates—that nicotine is a deadly taskmaster that enslaves all who come in contact with it—is equally ridiculous. Of all the teenagers who experiment with cigarettes, only about a third ever go on to smoke regularly. Nicotine may be highly addictive, but it is only addictive in some people, some of the time. More important, it turns out that even among those who smoke regularly, there are enormous differences in the stickiness of their habit. Smoking experts used to think that 90 to 95 percent of all those who smoked were regular smokers. But several years ago, the smoking questions on the federal government’s national health survey were made more specific, and researchers discovered, to their astonishment, that a fifth of all smokers don’t smoke every day. There are millions of Americans, in other words, who manage to smoke regularly and not be hooked—people for whom smoking is contagious but not sticky. In the past few years, these “chippers”—as they have been dubbed—have been exhaustively studied, with the bulk of the work being done by University of Pittsburgh psychologist Saul Shiffman. Shiffman’s definition of a chipper is someone who smokes no more than five cigarettes a day but who smokes at least four days a week. As Shiffman writes:

  Chippers’ smoking varies considerably from day to day, and their smoking patterns often include days of complete abstinence. Chippers reported little difficulty maintaining such casual abstinence and reportedly experienced almost no withdrawal symptoms when abstaining from smoking.... Unlike regular smokers who smoke soon on waking to replenish the nicotine that has cleared overnight, chippers go several hours before smoking their first cigarette of the day. In short, every indicator examined suggests that chippers are not addicted to nicotine and that their smoking is not driven by withdrawal relief or withdrawal avoidance.

  Shiffman calls chippers the equivalent of social drinkers. They are people in control of their habit. He says:

  Most of these people had never been heavy smokers. I think of them as developmentally retarded. Every smoker starts out as a chipper, in the early period, but then graduates more heavily into more dependent smoking. When we collected data about the early period of smoking, the chippers look like everyone else when they start out. The difference is that over time, the heavy smokers escalated whereas the chippers stayed where they were.

  What distinguishes chippers from hard core smokers? Probably genetic factors. Allan Collins of the University of Colorado, for example, recently took several groups of different strains of mice and injected each with steadily increasing amounts of nicotine. When nicotine reaches toxic levels in a mouse (nicotine is, after all, a poison) it has a seizure—its tail goes rigid; it begins running wildly around its cage; its head starts to jerk and snap; and eventually it flips over on its back. Collins wanted to see whether different strains of mice could handle different amounts of nicotine. Sure enough, they could. The strain of mice most tolerant of nicotine could handle about two to three times as much of the drug as the strain that had seizures at the lowest dose. “That’s about in the same range as alcohol,” Collins says. Then he put all the mice into cages and gave them two bottles to drink from: one filled with a simple saccharin solution, one filled with a saccharin solution laced with nicotine. This time he wanted to see whether there was any relationship between each strain’s genetic tolerance to nicotine and the amount of nicotine they would voluntarily consume. Once again, there was. In fact, the correlation was almost perfect. The greater a mouse’s genetic tolerance for nicotine, the more of the nicotine bottle it would drink. Collins thinks that there are genes in the brains of mice that govern how nicotine is processed—how quickly it causes toxicity, how much pleasure it gives, what kind of buzz it leaves—and that some strains of mice have genes that handle nicotine really well and extract the most pleasure from it and some have genes that treat nicotine like a poison.

  Humans, obviously, aren’t mice, and drinking nicotine from a bottle in a cage isn’t the same as lighting up a Marlboro. But even if there is only a modest correlation between what goes on in mice brains and ours, these findings do seem to square with Pomerleau’s study. The people who didn’t get a buzz from their first cigarette and who found the whole experience so awful that they never smoked again are probably people whose bodies are acutely sensitive to nicotine, incapable of handling it in even the smallest doses. Chippers may be people who have the genes to derive pleasure from nicotine, but not the genes to handle it in large doses. Heavy smokers, meanwhile, may be people with the genes to do both. This is not to say that genes provide a total explanation for how much people smoke. Since nicotine is known to relieve boredom and stress, for example, people who are in boring or stressful situations are always going to smoke more than people who are not. It is simply to say that what makes smoking sticky is completely different from the kinds of things that make it contagious. If we are looking for Tipping Points in the war on smoking, then, we need to decide which of those sides of the epidemic we will have the most success attacking. Should we try to make smoking less contagious, to stop the Salesmen who spread the smoking virus? Or are we better off trying to make it less sticky, to look for ways to turn all smokers into chippers?

  5.

  Let’s deal with the issue of contagion first. There are two possible strategies for stopping the spread of smoking. The first is to prevent the permission givers—the Maggies and Billy G.’s—from smoking in the first place. This is clearly the most difficult path of all: the most independent, precocious, rebellious teens are hardly likely to be the most susceptible to rational health advice. The second possibility is to convince all those who look to people like Maggie and Billy G. for permission that they should look elsewhere, to get their cues as to what is cool, in this instance, from adults.

  But this too is not easy. In fact, it may well be an even more difficult strategy than the first, for the simple reason that parents simply don’t wield that kind of influence over children.

  This is a hard fact to believe, of course. Parents are powerfully invested in the idea that they can shape their children’s personalities and behavior. But, as Judith Harris brilliantly argued in her 1998 book The Nurture Assumption, the evidence for this belief is sorely lacking. Consider, for example, the results of efforts undertaken by psychologists over the years to try and measure this very question—the effect parents have on their children. Obviously, they pass on genes to their offspring, and genes play a big role in who we are. Parents provide love and affection in the early years of childhood; deprived of early emotional sustenance, children will be irreparably harmed. Parents provide food and a home and protection and the basics of everyday life that children need to be safe and healthy and happy. This much is easy. But does it make a lasting difference to the personality of your child if you are an anxious and inexperienced parent, as opposed to being authoritative and competent? Are you more likely to create intellectually curious children by filling your house with books? Does it affect your child’s personality if you see him or her two hours a day, as opposed to eight hours a day? In other words, does the specific social environment that we create in our homes make a real difference in the way our children end up as adults? In a series of large and well designed studies of twins—particularly twins separated at birth and reared apart—geneticists have shown that most of the character traits that make us who we are—friendliness, extroversion, nervousness, openness, and so on—are about half determined by our genes and half determined by our environment, and the assumption has always been that this environment that makes such a big difference in our lives is the environment of the home. The problem is, however, that whenever psychologists have set out to look for this nurture effect, they can’t find it.

  One of the largest and most rigorous studies of this kind,
for example, is known as the Colorado Adoption Project. In the mid 1970s, a group of researchers at the University of Colorado led by Robert Plomin, one of the world’s leading behavioral geneticists, recruited 245 pregnant women from the Denver area who were about to give up their children for adoption. They then followed the children into their new homes, giving them a battery of personality and intelligence tests at regular intervals throughout their childhood and giving the same sets of tests to their adoptive parents. For the sake of comparison, the group also ran the same set of tests on a similar group of 245 parents and their biological children. For this comparison group, the results came out pretty much as one might expect. On things like measures of intellectual ability and certain aspects of personality, the biological children are fairly similar to their parents. For the adopted kids, however, the results are downright strange. Their scores have nothing whatsoever in common with their adoptive parents: these children are no more similar in their personality or intellectual skills to the people who raised them, fed them, clothed them, read to them, taught them, and loved them for sixteen years than they are to any two adults taken at random off the street.

  This is, if you think about it, a rather extraordinary finding. Most of us believe that we are like our parents because of some combination of genes and, more important, of nurture—that parents, to a large extent, raise us in their own image. But if that is the case, if nurture matters so much, then why did the adopted kids not resemble their adoptive parents at all? The Colorado study isn’t saying that genes explain everything and that environment doesn’t matter. On the contrary, all of the results strongly suggest that our environment plays as big—if not bigger—a role as heredity in shaping personality and intelligence. What it is saying is that whatever that environmental influence is, it doesn’t have a lot to do with parents. It’s something else, and what Judith Harris argues is that that something else is the influence of peers.

  Why, Harris asks, do the children of recent immigrants almost never retain the accent of their parents? How is it the children of deaf parents manage to learn how to speak as well and as quickly as children whose parents speak to them from the day they were born? The answer has always been that language is a skill acquired laterally—that what children pick up from other children is as, or more, important in the acquisition of language as what they pick up at home. What Harris argues is that this is also true more generally, that the environmental influence that helps children become who they are—that shapes their character and personality—is their peer group.

  This argument has, understandably, sparked a great deal of controversy in the popular press. There are legitimate arguments about where—and how far—it can be applied. But there’s no question that it has a great deal of relevance to the teenage smoking issue. The children of smokers are more than twice as likely to smoke as the children of nonsmokers. That’s a well known fact. But—to follow Harris’s logic—that does not mean that parents who smoke around their children set an example that their kids follow. It simply means that smokers’ children have inherited genes from their parents that predispose them toward nicotine addiction. Indeed studies of adopted children have shown that those raised by smokers are no more likely to end up as smokers themselves than those raised by nonsmokers. “In other words, effects of rearing variation (e.g. parents’ lighting up or not, or having cigarettes in the home or not) were essentially nil by the time the children reached adulthood,” the psychologist David Rowe writes in his 1994 book summarizing research on the question, The Limits of Family Influence. “The role of parents is a passive one—providing a set of genes at loci relevant to smoking risk, but not socially influencing their offspring.”

  To Rowe and Harris, the process by which teens get infected with the smoking habit is entirely bound up in the peer group. It’s not about mimicking adult behavior, which is why teenage smoking is rising at a time when adult smoking is falling. Teenage smoking is about being a teenager, about sharing in the emotional experience and expressive language and rituals of adolescence, which are as impenetrable and irrational to outsiders as the rituals of adolescent suicide in Micronesia. How, under the circumstances, can we expect any adult intervention to make an impact?

  “Telling teenagers about the health risks of smoking—It will make you wrinkled! It will make you impotent! It will make you dead!—is useless,” Harris concludes. “This is adult propaganda; these are adult arguments. It is because adults don’t approve of smoking—because there is something dangerous and disreputable about it—that teenagers want to do it.”

  6.

  If trying to thwart the efforts of Salesmen—if trying to intervene in the internal world of adolescents—doesn’t seem like a particularly effective strategy against smoking, then what of stickiness? Here the search for Tipping Points is very different. We suspect, as I wrote previously, that one of the reasons some experimenters never smoke again and some turn into lifelong addicts is that human beings may have very different innate tolerances for nicotine. In a perfect world we would give heavy smokers a pill that lowered their tolerance to the level of, say, a chipper. That would be a wonderful way of stripping smoking of its stickiness. Unfortunately we don’t know how to do that. What we do have is the nicotine patch, which delivers a slow and steady dose of nicotine so that smokers don’t have to turn to the dangers of cigarettes to get their fix. That’s an anti sticky strategy that has helped millions of smokers. But it is fairly clear that the patch is far from perfect. The most exhilarating way for an addict to get his fix is in the form of a “hit”—a high dose delivered quickly, that overwhelms the senses. Heroin users don’t put themselves on a heroin intravenous drip: they shoot up two or three or four times a day, injecting a huge dose all at once. Smokers, on a lesser scale, do the same. They get a jolt from a cigarette, then pause, then get another jolt. The patch, though, gives you a steady dose of the drug over the course of the day, which is a pretty boring way to ingest nicotine. The patch seems no more a Tipping Point in the fight against the smoking epidemic than SlimFast milkshakes are a Tipping Point in the fight against obesity. Is there a better candidate?

  I think there are two possibilities. The first can be found in the correlation between smoking and depression, a link discovered only recently. In 1986, a study of psychiatric outpatients in Minnesota found that half of them smoked, a figure well above the national average. Two years later, Columbia University psychologist Alexander Glassman discovered that 60 percent of the heavy smokers he was studying as part of an entirely different research project had a history of major depression. He followed that up with a major study published in the Journal of the American Medical Association in 1990 of 3,200 randomly selected adults. Of those who had at some time in their lives been diagnosed with a major psychiatric disorder, 74 percent had smoked at some point, and 14 percent had quit smoking. Of those who had never been diagnosed with a psychiatric problem, 53 percent had smoked at some point in their life and 31 percent had managed to quit smoking. As psychiatric problems increase, the correlation with smoking grows stronger. About 80 percent of alcoholics smoke. Close to 90 percent of schizophrenics smoke. In one particularly chilling study, a group of British psychiatrists compared the smoking behavior of a group of twelve to fifteen year olds with emotional and behavioral problems with a group of children of the same age in mainstream schools. Half of the troubled kids were already smoking more than 21 cigarettes a week, even at that young age, versus 10 percent of the kids in the mainstream schools. As overall smoking rates decline, in other words, the habit is becoming concentrated among the most troubled and marginal members of society.

  There are a number of theories as to why smoking matches up so strongly with emotional problems. The first is that the same kinds of things that would make someone susceptible to the contagious effects of smoking—low self esteem, say, or an unhealthy and unhappy home life—are also the kinds of things that contribute to depression. More tantalizing, though, is some preliminar
y evidence that the two problems might have the same genetic root. For example, depression is believed to be the result, at least in part, of a problem in the production of certain key brain chemicals, in particular the neurotransmitters known as serotonin, dopamine, and norepinephrine. These are the chemicals that regulate mood, that contribute to feelings of confidence and mastery and pleasure. Drugs like Zoloft and Prozac work because they prompt the brain to produce more serotonin: they compensate, in other words, for the deficit of serotonin that some depressed people suffer from. Nicotine appears to do exactly the same thing with the other two key neurotransmitters—dopamine and norepinephrine. Those smokers who are depressed, in short, are essentially using tobacco as a cheap way of treating their own depression, of boosting the level of brain chemicals they need to function normally. This effect is strong enough that when smokers with a history of psychiatric problems give up cigarettes, they run a sizable risk of relapsing into depression. Here is stickiness with a vengeance: not only do some smokers find it hard to quit because they are addicted to nicotine, but also because without nicotine they run the risk of a debilitating psychiatric illness.

  This is a sobering fact. But it also suggests that tobacco may have a critical vulnerability: if you can treat smokers for depression, you may be able to make their habit an awful lot easier to break. Sure enough, this turns out to be the case. In the mid 1980s, researchers at what is now the Glaxo Wellcome pharmaceutical firm were doing a big national trial of a new antidepressant called bupropion when, much to their surprise, they began getting reports about smoking from the field. “I started hearing that patients were saying things like, ‘I no longer have the desire to smoke,’ or ‘I’ve cut down on the number of cigarettes I’m smoking,’ or ‘Cigarettes don’t taste as good anymore,’” said Andrew Johnston, who heads the psychiatry division for the company. “You can imagine that someone in my position gets reports about everything, so I didn’t put much stock in them. But I kept getting them. It was very unusual.” This was in 1986, before the depression smoking link was well understood, so the company was initially puzzled. But what they soon realized was that bupropion was functioning as a kind of nicotine substitute. “The dopamine that nicotine releases goes to the prefrontal cortex of the brain,” explains Johnston. “That’s the pleasure center of the brain. It’s what people believe is responsible for the pleasure, the sense of well being, associated with smoking, and that’s one of the reasons it’s so hard to quit. Nicotine also increases norepinephrine, and that’s the reason that when you try to quit smoking and you no longer get so much norepinephrine, you get agitation and irritability. Bupropion does two things. It increases your dopamine, so smokers don’t have the desire to smoke, then it replaces some of the norepinephrine, so they don’t have the agitation, the withdrawal symptoms.”