Very Significant = p<.001; Significant = p<. 01; NS = Not Significant.
* Thirty men with IQs less than 80 were excluded.
The effect of cultural diversity was tested in the following manner. Sixty-one percent of the Inner City men had parents who had been born in a foreign country, but the men themselves had all grown up in Boston, were fluent in English, and had been sampled and studied in the same way. Thus it was possible to vary ethnicity and culture of rearing while holding other demographic variables constant. In some facets of adult life, parental ethnic differences among the Inner City men were seen to exert a profound effect. For example, as I’ll discuss in Chapter 9, men of white Anglo-Saxon Protestant (WASP) and Irish extractions had rates of alcohol abuse five times those of men of Italian extraction. But there was little cultural difference in defensive style. Dissociation was the only defensive style that appeared to be used significantly more by the WASPs than by Italians.13 (Dissociation was also the defense with the lowest rater reliability.)
But if culture appears to have little effect on defensive style, this is not true of biology. The central nervous systems of some of the Inner City men had been impaired by chronic alcoholism. (By this I do not mean acute intoxication; most men were quite sober when interviewed.) In addition, some men had possible early cognitive impairment, as suggested by IQs less than 80. Both these groups exhibited significantly less mature defensive styles than the rest of the Inner City men. All immature defenses were two to four times as common in these two compromised groups as in the unimpaired sample.
CONCLUSION
Empirical investigation provided clear answers to the Study’s three major questions about involuntary coping mechanisms. First, maturity of defenses can be rated reliably. Second, maturity of defenses demonstrated predictive validity toward future mental health. Third, maturity of defenses is independent of social class and gender, but is affected by biology.
Defense mechanisms are not just one more dogma of the psychoanalytic religion. On the contrary, the brain’s mechanisms of involuntary adaptation are a fit subject for serious study by social and neurological scientists. But, as with all matters of lifetime development, long and deep access is needed to study them. It was the unusual longitudinal and naturalistic nature of the Grant Study that permitted the conclusions in this chapter. Fledgling efforts are now under way to image what the brain does while deploying defenses, but scientists will likely have to wait upon advances in brain imaging technology for further confirmation.14
9
ALCOHOLISM
Remember that we deal with alcohol—cunning, baffling, powerful!
—ALCOHOLICS ANONYMOUS
ALCOHOLISM IS A DISORDER of great destructive power. Depending on how we define it, it afflicts between 6 and 20 percent of all Americans at some time in their lives. In the United States, alcoholism is involved in a quarter of all admissions to general hospitals, and it plays a major role in the four most common causes of death in twenty-to forty-year-old men: suicide, accidents, homicide, and cirrhosis of the liver.1 The damage it causes falls not only on alcoholics themselves but on their families and friends as well—and this damage touches one American family in three. Life is not a cog railway that we step onto at birth and off at death, secure in the knowledge that we are safe from accidental derailments and the tug of gravity. No matter how blessed by good fortune we start out or how blighted by its lack, our circumstances can always change, and so can the conditions under which we meet them. This is the Study’s sixth lesson, and much of what we learned about it came from our prospective longitudinal investigation of alcohol use and abuse.
The Grant Study’s involvement in alcohol research was one of the silver linings of our perpetual anxiety about funding, and true sterling. Without it, I would not have been forced into this last ten years’ reexamination of marriage, divorce, and the development of intimacy. Yet that reexamination called into question not only some cherished assumptions of my own, but also assumptions that predated my tenure at the Study, and the received wisdom of several generations. Lifetime studies are bread cast upon the waters. You can’t know in advance everything you should be finding out. But on the other hand, some of what you find out and have no idea what to do with may turn out to be invaluable unforeseen years later. The work with alcohol was like that.
It isn’t easy to identify who is and is not an alcoholic. Until now, most major longitudinal studies of health (for example, the Framing-ham Study in Massachusetts and the Alameda County Study in California) have taken into account only alcohol consumption, not alcohol abuse.2 Unfortunately, as I’ve said before, reported alcohol consumption identifies alcohol abuse almost as poorly as reported food consumption reflects obesity. In contrast, the Grant Study has always focused on alcohol-related problems. Where alcohol is concerned, it is what people do, not what they say, that is important.
Our study of the College and Inner City cohorts is the longest and most thorough study of alcohol abuse in the world. It has established answers to seven major questions:
1. Is alcoholism a symptom or a disease?
2. Is alcoholism environmental or genetic?
3. Are alcoholics premorbidly different from nonalcoholics?
4. Should the goal of alcohol treatment be abstinence?
5. Can “real” alcoholics ever drink safely again?
6. How can relapse be prevented?
7. Is recovery through AA the exception or the rule?
In several instances, the Study’s longitudinal findings differ from those of well-respected cross-sectional studies.
METHODS
The Study’s unique structure gave it three advantages as we made our usual effort to replace opinion with science. First, the men were followed for their entire lifetimes—a rarity but a necessity, because alcoholism is a relapsing and evolving disease. Second, the Study quantified alcoholism not by reports of quantity or frequency of drinking, but by objective numbers of alcohol-related problems. Third, over its own lifespan the Study has had between thirty and fifty contacts with each of its members, which greatly facilitated the collection of this data.
A few notes on how the men were studied. The questionnaires they received every two years asked if they, their friends, their families, or their physicians had expressed concern about their drinking, and whether and for how long they had ever stopped drinking (evidence not of control, but of loss of control). At interview, alcohol abuse or its absence was always specifically recorded. When the men reached forty-seven, 87 percent of them participated in a two-hour semi-structured interview with a detailed twenty-three-item section on lifetime problem drinking.3 Since forty-seven, they have undergone physical examinations every five years. Any man not previously classified as an alcohol abuser who answered yes twice in a row to two or more of the four concern questions, or who through interview or telephone contact acknowledged alcohol abuse, or whose physical exam revealed evidence of alcohol abuse, was classified an alcohol abuser. The age that each participant first met DSM-III criteria for alcohol abuse was estimated from all available data: questionnaires, any relevant court records, social service data, family interviews, etc.
(In 1962, before the Inner City cohort joined the Harvard Study of Adult Development, arrest records and records of psychiatric hospitalization, if any, had been searched for more than 95 percent of the men, who were at high risk for alcoholism, and for the preceding two generations of their families.4 These are data that are well-nigh irreplaceable, as recent privacy legislation now precludes such searches.)
By mining interviews, clinical data, objective documents, and self-reports obtained from the participants by clinicians experienced in treating alcoholism, we were able to establish both a categorical and a dimensional scale of alcohol use for the men of both cohorts. The categorical scale was derived from DSM-III, the third edition of the Diagnostic and Statistical Manual of the American Psychiatric Association; that was the version current in 1977–1980, when thi
s analysis was taking place.5 It distinguished three types of alcohol use: social drinking (that is, no chronic problems related to alcohol use), alcohol abuse (chronic problems but no physiological dependence), and alcohol dependence (presence of withdrawal symptoms or hospitalization for detoxification). In this chapter, I will use the term alcoholism to refer to both of the latter two categories.
The dimensional scale, the Problem Drinking Scale, or PDS, assessed problem drinking on a continuum of severity by means of sixteen equally weighted questions (similar to those of the Michigan Alcoholism Screening Test).6 The PDS inquired about social, legal, medical, and job problems caused by alcohol abuse. It also asked about blackouts, going on the wagon, seeking treatment, withdrawal symptoms, and problems with control. Scores of 4–7 on the PDS usually met the DSM-III criteria for “alcohol abuse,” and scores of 8–12 usually met the criteria for “alcohol dependence.” Men with fewer than 4 lifetime problem points on the dimensional scale were usually classified as social drinkers.
Observant readers will note that the numbers in this chapter vary sometimes from those in older reports. This is because in those earlier analyses we included all the Study men who had ever met DSM-III criteria for alcohol abuse (153 out of the 456 original Inner City men and 56 of the original 268 College men). In refining the original analysis for this book, however, men whose problem drinking scores were borderline (3 or 4) and who abused alcohol for less than five years and who returned to social drinking for the rest of their lives (13 Inner City and 2 College men) were reclassified as social drinkers.
We have excellent and inclusive death data, including death certificates for all Study members, including those who withdrew, except for two who died abroad. Survival or mortality has been ascertained and documented through the National Death Index or credit agencies, whichever was applicable, and death certificates obtained. Data from death certificates, and recent physical examinations from participating Study members, were used to infer major causes of death.
We assessed the alcohol status of all cooperating Study members, whether or not they had been alcoholic in the past, every year between the ages of twenty and seventy, using the biennial questionnaires and triangulating them with other material. (Since the Glueck men had not been personally followed between thirty-two and forty-five, for those years we had to depend on history and public records, including records of arrests.) We categorized the alcoholics as follows: Abstinent: less than one drink (0.5 ounces of ethanol) a month for a year. Return-to-controlled-drinking: a former alcohol abuser consuming more than one drink a month for at least three years with no reported problems. Continued alcohol abuse: Clear past history of sustained alcohol abuse and one or more acknowledged problems caused by drinking in the past three years. When data was missing for three years, the yearly status was rated as unknown. Data on alcohol abuse for every man was obtained between twenty and forty times over sixty (on average) years of observation. Nonresponders for two consecutive questionnaires were interviewed in person or by telephone. Men were classified as Dropped if they asked to withdraw or ignored questionnaires and follow-up telephone calls for ten years.
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 progression. 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.
&
nbsp; 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.
Triumphs of Experience: The Men of the Harvard Grant Study Page 29
