Implications of Genetic Models for the Prevention and Treatment of Alcoholism and Drug Dependence

Popular writing and thinking about alcoholism have not assimilated the trend in genetic research and theory away from the search for an inherited mechanism that makes the alcoholic innately incapable of controlling his or her drinking. Rather, popular conceptions are marked by the assumption that any discovery of a genetic contribution to the development of alcoholism inevitably supports classic disease-type notions about the malady. For example, Milan and Ketcham (1983) and Pearson and Shaw (1983) both argue vehemently in favor of a total biological model of alcoholism, one that eliminates any contribution from individual volition, values or social setting (any more than takes place, according to Pearson and Shaw, with a disease like gout). As Milam and Ketcham repeatedly drive home, "the alcoholic's drinking is controlled by physiological factors which cannot be altered through psychological methods such as counseling threats, punishment, or reward. In other words, the alcoholic is powerless to control his reaction to alcohol" (p. 42).

Both of these popular works assume the fundamental biology of alcoholism to be the abnormal accumulation of acetaldehyde by alcoholics, based primarily on Schuckit and Rayses' (1979) finding of elevated acetaldehyde levels after drinking in offspring of alcoholics. Lost entirely among the definitive claims about the causative nature of this process is the excruciating difficulty Schuckit (1984a) described in assessing acetaldehyde levels at particular points after drinking. Such measurement difficulties have prevented the replication of this result by either of the Danish prospective studies and have prompted one team to question the meaning of findings of excessive acetaldehyde (Knop et al., 1981). Schuckit (1984a) has also recommended caution in interpreting the small absolute levels of acetaldehyde accumulations measured, levels which conceivably could have long-term effects but which do not point to an immediate determination of behavior. The indeterminacy inherent in this and other genetic formulations is lost in Milam and Ketcham's (1983) translation of them: "Yet, while additional predisposing factors to alcoholism will undoubtedly be discovered, abundant knowledge already exists to confirm that alcoholism is a hereditary, physiological disease and to account fully for its onset and progression" (p. 46).

Although Cloninger et al. (1985) attempt to delineate a specific subset of alcoholics who represent perhaps one-fourth of those diagnosed for alcoholism, popular versions of the inherited, biological nature of the disease inexorably tend to expand the application of this limited typing. Milam and Ketcham (1983) quote from Betty Ford's autobiography (Ford and Chase, 1979), for example, to make readers aware that alcoholism does not necessarily conform to presumed stereotypes:

Although it may have been beneficial for Mrs. Ford to seek treatment under the rubric of alcoholism, this self-description does not qualify for the inherited subtype put forward by the most ambitious of research-based genetic theories.

Milam and Ketcham (1983) are adamant about the absolute prohibition of drinking by alcoholics. This, too, is an extension of standard practices in the alcoholism field that have traditionally been associated with the disease viewpoint in the United States (Peele, 1984). Yet, genetic models do not necessarily lead to such an ironclad and irreversible prohibition. If, for example, alcoholism could be demonstrated to result from the failure of the body to break down acetaldehyde, then a chemical means for assisting this process--a suggestion less farfetched than others raised in the light of biological research--could presumably permit a resumption of normal drinking. Pearson and Shaw (1983), whose roots are not in the alcoholism movement but rather stem from an equally strong American tradition of biochemical engineering and food faddism, suggest that vitamin therapy can offset acetaldehyde damage and thus mitigate drinking problems in alcoholics. Tarter et al. (1985) discuss Ritalin therapy and other methods that have been utilized with hyperactive children as therapeutic modalities for moderating alcoholic behavior.

It is even possible that behavioral models which emphasize the resilience of habits, built up over years of repeated patterns and reinforced by familiar cues, present a more formidable basis for disallowing controlled drinking than do existing genetic models! It may be only the historical association of genetic ideas about alcoholism with abstinence through A.A. dogma that has created an environment in which controlled drinking has been the exclusive domain of the behavioral sciences. Similarly, genetic discoveries have been built into recommendations that high-risk children--based on pedigree or futuristic biological measurement--should not drink. The indeterminate and gradualistic view of the development of alcoholism that arises from most genetic models does not advance such a position. Tarter et al. (1985) recommend that children with temperaments rendering them susceptible to alcoholism be taught impulse-control techniques, while Vaillant (1983) advises "individuals with many alcoholic relatives should be alerted to recognize the early signs and symptoms of alcoholism and to be doubly careful to learn safe drinking habits" (p. 106).

The conclusions we draw from research on genetic contributions to alcoholism are crucial because of the acceleration of research in this area and the clinical decisions which are being based on this work. Moreover, other behaviors--especially drug misuse--are being grouped with alcoholism in the same framework. Thus, the National Foundation for Prevention of Chemical Dependency Disease announced its mission statement:

To sponsor scientific research and development of a simple biochemical test that can be administered to our young children to determine any predisposition for chemical dependency disease; [and] to promote greater awareness, understanding and acceptance of the disease by the general public so prevention or treatment can be commenced at the age youngsters are most vulnerable. (Unpublished document, Omaha, Nebraska, 1 March 1984.)

This perspective contrasts with that from epidemiological studies showing young problem drinkers typically outgrow signs of alcohol dependence (Cahalan and Room, 1974), often in only a few years (Roizen et al., 1978). College students who display marked signs of alcohol dependence only rarely show the same problems 20 years later (Fillmore, 1975).