Review of Alcohol and the Addictive Brain, by Kenneth Blum, with James E. Payne, New York: Free Press.

Morristown, NJ

According to a Gallup poll, the overwhelming majority of Americans (about 90 percent) believe that alcoholism is a medical disease. Schools teach children the disease theory as scientific fact, and the news media take it for granted. For Kenneth Blum and James E. Payne, authors of Alcohol and the Addictive Brain, the disease theory of alcoholism is only a starting point. Blum, a University of Texas pharmacologist, and Payne, executive director for the National Foundation of Addictive Diseases, seek to demonstrate not only "that alcoholism is a biogenetic disease characterized by genetic anomalies" but that a wide range of excessive behavior can be traced to a similar defect.

Blum's claims about the amino-acid-and-vitamin mixtures he markets for treatment of alcoholism, cocaine and heroin addiction, and obesity are based on the idea that all addictions stem from the "addictive brain" in the book's title. Blum says his supplements compensate for the depletion of neurotransmitters such as dopamine, an abnormality that he claims marks alcoholics, addicts, and obsessive eaters.

Dopamine figures prominently in Blum and Payne's effort to formulate a "neurogenetic theory of compulsive disease." They argue that a special need for dopamine stimulation is caused by what they call the "pleasure gene," which limits the natural intake of dopamine and, therefore, the ability to achieve pleasure. People thus afflicted must pursue "abnormal pleasure-seeking activity," leading not only to alcoholism and heroin addiction but to "other compulsive diseases such as cocaine abuse, food disorders, gambling, and sexual promiscuity."

This theory seemed to receive a boost in 1990, when Blum and psychiatrist Ernest Noble identified a defect in the dopamine D2 receptor gene as the common thread in alcoholism. Examining brain tissue of 70 dead subjects, half of them alcoholics, Blum and Noble found a variant of this gene in 69 percent of the alcoholics but only 20 percent of the nonalcoholics. This finding, published in The Journal of the American Medical Association, received nationwide publicity and was trumpeted as the discovery of the "alcoholic gene."

Several subsequent studies, however, failed to find such a remarkable occurrence of the gene defect in alcoholics. Two studies published in JAMA after Blum and Noble's paper found little or no relationship between alcoholism and the D2 receptor gene. Other studies have found a relationship weaker than the one measured by Blum and Noble. A study reported in the October 2 issue of JAMA found the gene variation occurred in people with several disorders — including Tourette's syndrome, hyperactivity, and autism — at least as often as alcoholics.

This finding runs counter to the "addictive brain" theory since people with autism and Tourette's syndrome are not thought to be especially pleasure seeking. No study has found that members of a family who become alcoholic are more likely than nonalcoholic family members to have the gene variation, which is the conventional test for establishing a genetic cause of a disease.

So Blum and Noble's dramatic finding turns out to be far less credible than originally believed. Nevertheless, the impression that scientists have identified the genetic basis for alcoholism remains widespread. This misperception is typical of a general attitude that exaggerates the significance of research pointing to genetic or biological factors in alcoholism, ignores caveats and qualifications, and overestimates the consensus within the scientific community. Blum and Payne, for example, imply that opposition to the disease model is limited to "a few psychologists [among whom I am numbered] and a philosopher, who ignore the vast body of research findings over the past four decades."

But the "addictive brain" theory faces opposition from genetic and medical researchers as well. A leading American behavioral geneticist, Robert Plonin, says, "A.A. wants it to be a genetic disease," but "the evidence isn't all that convincing." Canadian physician and pharmacologist Harold Kalant, the researcher most identified with discovering the basic biological properties of excessive drinking, says that "alcoholism is now seen as a disorder of behavior, rather than a metabolic disease caused by something which obligatorily makes a person drink." In this view, genetics may influence the individual's biological reaction to alcohol, but this reaction is not the same thing as alcoholism.

Instead, Kalant says, it is necessary to focus "on the social and individual controls that normally keep drinking within healthy bounds, and on the factors which remove these controls." In other words, since an inexorable craving for alcohol is not inherited, whatever sensations alcohol does produce for the individual must be balanced against his or her values, expectations, and social milieu, which either encourage or discourage repetitive intoxication.

This view jibes with the findings of psychologists and sociologists. A great deal of evidence, more consistent and extensive than anything yet established by biological research, shows that social categories are the best predictors of drinking problems and alcoholism. For example, in one study of Boston ethnics, Irish Americans were seven times as likely to become alcoholic over a 40-year period as Italian Americans living in the same neighborhoods. Research uniformly finds alcoholism to be 3 to 10 times as prevalent among men as among women. Even researchers with a biological orientation acknowledge that group differences of such magnitude cannot be explained by genetic factors; certainly no such genes have been identified.

Psychological studies also find a strong connection between problem drinking and individual beliefs about alcohol. For example, research shows that alcoholics believe alcohol has a greater impact than do nonalcoholics. Longitudinal studies find that expectations about the powerful and beneficial effects of alcohol predict problem drinking even when measured in preteens who have not yet begun to drink.