Alcohol and the Addictive Brain, by Kenneth Blum, with James E. Payne, New York: Free Press, 320 pages, $24.95
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 the 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 non-alcoholics. 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 that the gene variation occurred in people with several disorders—including Tourette's syndrome, hyperactivity, and autism—at least as often as in alcoholics.
This finding runs counter to the "addictive brain" theory since people with autism or 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 Plomin, 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 an individual's bliological 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 those 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.
Furthermore, the medical and research communities are split over the wisdom of classifying excessive behavior other than alcoholism and drug abuse—such as overeating, gambling, and sex and love addiction (or codependence)—as diseases. Many biological scientists find it difficult to imagine that a single mechanism could encompass such a wide range of human behavior. In their view, to call gambling, sexual excess, overeating, and alcoholism versions of a single addictive process is to eliminate the possibility of a biological cause.
Blum and Payne obscure differences among competing genetic and biological theories of alcoholism, giving the false impression that biological researchers are working toward identifying a single source of excessive drinking. While they cite favorably the work of Henri Begleiter of Downstate Medical Center in identifying anomalous brain waves in alcoholics and their offspring, for example, such work really has no bearing on dopamine theory. Begleiter is one of many genetic investigators who has not endorsed dopamine as an important factor in alcoholism.
Blum is notable among those exploring the role of genes in alcoholism for his enthusiastic support of Alcoholics Anonymous. A large part of Alcohol and the Addictive Brain reviews the 12 steps of A.A. and such faddish movements as adult children of alcoholics (ACoA). A.A. is in many ways the progenitor of the 20th-century disease view of alcoholism, but it seems strange that a spiritual fellowship and medical research should fit together like hand and glove, as Blum and Payne repeatedly insist they do. Yet wedding these two odd bedfellows allows Blum to market his products more effectively to treatment centers and to gain support among A.A. members.
But if, as Blum claims, genetic discoveries will bring tremendous progress in fighting alcoholism, prayer will no longer be the primary treatment for the disease. Alcoholics might even be able to drink normally once their flawed, addictive genes are modified (a futuristic procedure Blum describes) or when the chemical imbalances the genes cause are remedied by drug therapy. This inherent conflict between A.A. and medical approaches leads Blum and Payne, on the one hand, to attack those who question the disease theory and think "alcoholism can be arrested, and often cured," and, on the other, to predict that "the next forty years will bring cures…for compulsive diseases such as alcoholism, drug addiction, and food disorders."
In reality, we are so far from even imagining a biological cure for alcoholism that purported genetic discoveries serve only to reinforce the idea that excessive drinking is a disease. When genetic screening techniques become precise and cheap enough, we may be able to tell adolescents they have genes that investigators like Blum think predispose them to alcoholism. But what should they do with this information? Even by Blum's account of the genetic contribution to alcoholism, most of these teens will not become alcoholics. And psychological research finds that the expectation of losing control over alcohol consumption is often a self-fulfilling prophecy. So such a genetic early warning system is likely to produce more problem drinking than it prevents. This is surely a cure that is worse than the disease.
Contributing Editor Stanton Peele is a psychologist specializing in addiction research.