Triumphs of Experience: The Men of the Harvard Grant Study (40 page)

Figure 9.1 Final alcohol outcome status.

Figure 9.1
reflects the men’s alcohol status at age sixty.
7
In the case of death or institutionalization, outcome status was based on the last three years of community residence prior to death or chronic institutional care.

By age seventy (approximately 1990 for the College men and
2000
for the Inner City men), 65 (46 percent) of the 140 Inner City alcoholics and 19 (35 percent) of the 54 College alcoholics were dead. (Recall that under “alcoholics” I am subsuming both alcohol-abusing and alcohol-dependent men.) In 2003, we found that all but 3 of the 18 alcohol-dependent College alcoholics had died by age eighty, and that their lifespans on average had been seventeen years shorter than those of their social-drinking Study peers.

Figure 9.1
illustrates vividly why the prevalence of alcoholics goes down with time. The problem isn’t “burnout” (as AA members put it, getting “sick and tired of being sick and tired”); this is rare among alcoholics. Nor is it poor case-finding among the elderly. It’s that over time, alcoholics become abstinent or die.

Active alcoholics die twice as fast as abstinent alcoholics, but even the latter die significantly sooner than social drinkers—often because cigarette abuse continues after alcohol consumption stops. As we will see, it is only for the first ten years of abusive drinking that the diagnosis of alcoholism is ambiguous. Over decades, alcoholism becomes a black-or-white disease.

THE SEVEN QUESTIONS

1. Is alcoholism an evanescent symptom or a chronic disease?
Social scientists generally consider matters such as intelligence, drinking behavior, and even eyesight as continua; physicians in the trenches have little patience for such nuances. Who is right? Both. The definition of retardation, alcoholism, or blindness may depend upon a host of independent contextual, interpersonal, and motivational factors. But when an alcoholic actually goes to the expense and inconvenience of seeking help for a self-acknowledged disease, there tends to be a certain crispness of definition as to what the problem is.

The medical model of alcoholism is one of inexorable progres
sion.
It was made famous by William Hogarth in the series of paintings known as
The Rake’s Progress.
8
It has been retrospectively documented by E. M. Jellinek.
9
It is taken as an article of faith by Alcoholics Anonymous.
10
Yet how can this model be reconciled with the unpredictable oscillations observed in fine-grained prospective studies of alcoholics?
11
Short-term prospective investigations indicate that during any given month a majority of alcoholics are either abstinent or drinking asymptomatically. This cannot be said of either cigarette or heroin addicts. Is alcoholic progression therefore a myth? When does the state of drunkenness (which is often voluntary) become the trait of chronic problem drinking (which is largely involuntary)? The Study helped to clarify.

Virtually every alcohol abuser in the Study, no matter how chronic, had periods of abstinence lasting a month or longer. In fact, a history of going “on the wagon” is a commonly accepted criterion for the diagnosis of alcoholism. The more physiologically dependent and symptomatic the alcoholic, the more likely he or she is to have attempted abstinence, usually more than once. As I’ve said elsewhere, Mark Twain found it so easy to stop smoking that he did it twenty times.

That is why it is only the number and frequency of alcohol-related
problems
that can truly define the clinical phenomenon known as alcoholism. Alcoholism is a construct of a higher order of complexity than mumps or retardation. It does not reflect a specific pathogen, like mumps. It is like retardation in being another diagnosis that depends on where a clinician draws the line. But more than anything else, like Type II diabetes, hypertension, and coronary artery disease, the disease of alcoholism is the endstage effect of bad habits on facilitating genes.

Although its symptoms may come and go, alcoholism acts like a chronic disease, and chronic diseases are forever. Without specific
treatment,
diabetes will plague you until you die—young. The Harvard Study of Adult Development’s seventy-five years have enabled us to document that without sustained abstinence, the vast majority of problem drinkers continue to have alcohol-related problems until they, too, die young. Seventy-two percent of the College social drinkers lived to be eighty, but only 47 percent of the College alcohol abusers and a minuscule 14 percent of the alcohol-dependent College men—a very significant decline.

On the one hand, the Study demonstrated that alcohol abuse is inexorably progressive only in its initial stages. Once a drinker’s alcohol consumption has gotten “out of control” and become a source of problems, it can remain so for a lifetime without necessarily progressing to morning drinking, job loss, or even severe withdrawal symptoms. Seven of the eighty-year-old College alcohol abusers had misused alcohol for decades (about thirty years, on average), but without evidence of worsening symptomatology. Similar courses can be seen in cigarette dependency.

On the other hand, alcoholism does not get better. Those same seven men over those same thirty years continued to report alcohol-related problems affecting their self-esteem, their health, and their families. In this, alcoholism does conform to the conventional disease model, and here too there is a resemblance to cigarette dependency. Two-pack-a-day smokers rarely revert to half-a-pack-a-day social smoking, and once an alcoholic has developed the problems typical of dependence, he or she is unlikely to revert to social drinking or even abuse. More on this in a moment.

Thus I think it is both appropriate and useful to consider alcoholism a disease. The diagnosis is not made so lightly that social drinkers are likely to suffer from incorrect labeling. Nor are the manifestations of alcohol abuse so varied as to render a unifying diagnosis meaningless. There is a benefit in calling severe problem drinking a disease; alcoholics
who label themselves “ill”—as opposed to “bad”—will feel less helpless; they will have higher self-esteem; and they will likely try harder to change and to let others help change them.

A final reason to consider alcoholism a disease is that it kills people—tens of thousands of people a year. By age eighty, a College alcoholic was twice as likely to be dead as a nonalcoholic. By age seventy, almost half (46 percent) of the alcohol-abusing Inner City men were dead, as opposed to 29 percent of the nonabusers. Admittedly, much of this increased mortality does not reflect direct physical effects of alcohol itself, but it does point up graphically that cigarette consumption among problem drinkers was vastly greater than that of social drinkers. The average nonalcoholic smoked for fourteen-pack years (half a pack a day for twenty-eight years or two packs a day for seven years would both equal fourteen-pack years). But the average alcohol abuser smoked for twenty-seven-pack years, and the average alcohol-dependent individual for
fifty
—more than three times the cigarette consumption of social smokers. There is no evidence that heavy smoking increases drinking. However, as of 2010, one College alcoholic in four had died of heart disease. Of the social smokers, only one in eight had. Three percent of the College social drinkers died of lung cancer; 15 percent, five times as many, of the alcoholics did. Similarly, Inner City alcoholics were twice as likely to die from lung cancer as social drinkers.

The overlap between drinking and smoking does not indicate the presence of an “addictive” or “oral” personality or any other such abstraction, only the concrete reality that conscience and judgment are soluble in ethanol. Alcoholics are fearless in barrooms and automobiles. They’re not careful about safe sex, and they don’t worry about cigarettes, either. Deaths from cirrhosis, accident, suicide, and pharyngeal cancer were also far more common among alcohol abusers. Study findings in this regard are very similar to those from eight
other
longitudinal studies of premature mortality in alcoholics reviewed elsewhere.
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2. Is alcoholism environmental or genetic?
In 1938, the year the Grant Study began, Karl Menninger, America’s most famous psychiatrist, made a bold statement: “The older psychiatrists . . . considered alcoholism to be a hereditary trait. Of course, scarcely any scientist believes so today. Although it’s still a popular theory, alcoholism cannot possibly be a hereditary trait, but for a father to be an alcoholic is an easy way for a son to learn how to effect the retaliation he later feels compelled to inflict.”
13

Menninger was wrong. When it comes to alcoholism, genes trump environment. Our data revealed that a family history of alcoholism more than doubled the chance that a Study member would become alcoholic, even when all other suspected etiologies (such as ethnicity, social class, and multiple family problems) were statistically controlled. But children with alcoholic stepparents were
not
more likely to become alcoholic. Here the data from the Inner City men was even more convincing than that from the Grant men.

Until very recently, most social scientists believed unhappy childhoods to be a cause of alcoholism. Our data showed that the association of childhood environmental weaknesses with future risk of alcohol abuse exactly paralleled the extent of parental alcohol abuse: that is, the more severe a parent’s alcoholism, the more it will be reflected in his child’s environment, and in the severity of alcoholism in the child. Contrary to Menninger’s belief, however, alcoholism does not arise in children in response to an unhappy childhood or even to life with an alcoholic stepparent. It is the
fact
of an alcoholic biological parent, whether or not the child lives under the same roof, that increases the child’s risk. Of the fifty-one men who had few childhood environmental weaknesses and an alcoholic parent, 27 percent became
alcohol-dependent.
Of the fifty-six men with many environmental weaknesses and no alcoholic parent, only 5 percent became alcohol-dependent. Alcoholic parents do not have to live with their children to pass on the disease.

The presence of a genetic component does not free us from issues of nature and nurture. While the number of alcoholics in one’s ancestry increases the likelihood of alcohol abuse for genetic reasons, it also increases the likelihood of lifelong teetotalling, presumably for environmental reasons. Almost half of the forty-eight teetotalers of Anglo-Irish-American descent in the Glueck Study had an alcoholic parent.

3. Are alcoholics premorbidly different?
This question essentially explores whether alcoholism is a symptom of mental illness or a cause. It has long and widely been considered the former. In the year the Grant Study was conceived, Robert Knight, a prominent psychoanalyst at the Austen Riggs Center, said it directly: “Alcohol addiction is a symptom rather than a disease. . . . There is always an underlying personality disorder evidenced by obvious maladjustment, neurotic character traits, emotional immaturity or infantilism.”
14
In 1940 Paul Schilder, an Austrian psychiatric researcher who has given his name to four diseases, concurred. “The chronic alcoholic person is one who from his earliest childhood on has lived in a state of insecurity.”
15
Two decades later, E. M. Jellinek, Yale’s great alcoholism scholar, wrote: “In spite of a great diversity in personality structure among alcoholics, there appears in a large proportion of them a low tolerance for tension coupled with an inability to cope with psychological stresses.”
16
And in 1980, psychiatrist Michael Selzer wrote more generally in the leading textbook of psychiatry: “Despite occasional disclaimers, alcoholics do not resemble a randomly chosen population.”
17
None of these world-renowned experts, however, possessed any prospectively
gathered
data as to what alcoholics were like
before
they became alcoholic.

Three premorbid personality types have repeatedly been proposed as causal contributors to alcoholism: the dependent, the depressed, and the sociopathic.
18
The Grant Study confirmed none of these hypotheses.

The College alcohol abusers did not exhibit more premorbid evidence of dependent personality disorder than men who remained social drinkers all their lives, and 58 percent of the College men who became alcohol abusers did not lose control of their alcohol use until after age forty-five.

There were men who displayed many dependent traits as young adults and who showed lifelong difficulties with loving, with perseverance, and with postponement of gratification. Such so-called oral-dependent men were also more anxious and more inhibited about expressing aggression. Yet these traits in young adulthood were not significantly more common in future alcohol abusers than in everyone else. Oral-dependent traits did become very common in the College men, however, once they began to abuse alcohol.

It is also true that alcohol-abusing College men were five times more likely to report severe depression than men who did not abuse alcohol. Furthermore, of the thirty-one men who ever appeared to manifest major depressive disorder, fourteen (44 percent) also manifested alcoholism. Following these men for twenty-five years, I received the impression that many of the fourteen had turned to alcohol to relieve their depression. In 1990, however, the longitudinal data were subjected to blind analysis, and that impression proved to be illusion.
19
One psychiatrist, blind to age of onset of depression, reviewed each man’s entire record and estimated the year that he first manifested evidence of alcohol abuse. A second psychiatrist, blind to age of onset of alcoholism, reviewed each man’s record and determined the
age
of onset of major depressive disorder (or probable major depressive disorder). In four of the fourteen cases, the psychiatrist looking for evidence of primary depression believed that the depressive symptoms could be explained entirely by alcohol abuse. In six more cases, the rater noted that the first episode of major depressive disorder had occurred (on average twelve) years after the patient met the criteria of alcohol abuse. In only four cases had a man’s depression actually preceded his alcoholism. Given the prevalence of alcoholism and affective disorder among the 268 men in the College sample, chance alone could account for primary alcoholism and primary depression occurring independently in four cases or even more.