Analyzing the Causative Chain in Modern Genetic Models of Alcoholism

The fundamental issue of brain-behavior relationships persists even within the most optimistic of the current models of genetic transmission of alcoholism. As Tarter et al. (1985) acknowledge, theirs is an indeterminate model in which the same inherited predisposition may be expressed in a variety of behaviors. Although Tarter et al. emphasize the pathology of these various expressions, they also note Thomas and Chess's (1984) valuable dictum: "No temperament confers an immunity to behavior disorder development, nor is it fated to create psychopathology" (p. 4). Given an extreme emotional lability, different people may still behave quite differently--including harnessing their emotional energies in entirely constructive ways. For example, would not some with this trait become artists and athletes? Or, in highly socialized families or groups, would some not simply learn to effectively suppress their impulses altogether?

Introducing mediating factors such as temperament and ASP into genetic models adds another degree of indeterminacy--that which comes from variations in the definition of phenomena on which fundamental agreement is often lacking. In addition, temperament and ASP call into play strong environmental influences; for example, Cadoret and Cain (1980), exploring the same gene-environment interaction used to investigate causality in alcoholism, discovered environmental factors to be as powerful as inherited ones in identifying ASP in adolescents. The antisocial acting-out Cahalan and Room (1974) found to coincide with alcohol problems in young men was a function of social class and of blue-collar cultures. Thus, not only is it difficult to pinpoint an inherited disposition that causes ASP, but also family and social input can create those behaviors central to the very definition of ASP. To separate this layer of environmental interaction from the additional layer presented by drinking behavior is a dauntingly complex task that can make us cautious about tracing an ultimate path to alcoholism.

Tarter et al. (1984) were faced with the duty of explaining why children of alcoholics were less impulsive than a control group from within their framework that alcoholism is an expression of an inherited temperament: 'There may be different outcomes in individuals possessing these disturbances, of which alcoholism and antisocial personality are two such conditions" (pp. 220-221). These adolescent subjects, however, did not display the hypothesized disturbance (i.e., heightened impulsiveness), so that the variety of forms this given temperament may take does not seem relevant to the results here. Since the subjects had parents who were alcoholics--which the authors maintain is one demonstration of this heritable temperament--it is not clear why this trait would not be apparent in these offspring. Cadoret et al, (1985) have now found that adult ASP and alcoholism are inherited independent of each other.

The Tarter et al. (1985) model may be more indeterminate than the authors recognize. The model offers an experiential description of the relationship between drug and alcohol use and the high-risk temperament it identifies. That is, while stressing the basis of their model in genetics and neurophysiology, Tarter et al. explain addictive substance use based on the mood-altering functions these substances have for those persons with hyperreactive temperaments. Apparently, those with this heightened sensitivity seek psychotropic effects to lower their reactivity to stimulation. Whatever the relationship of this hyperemotional nature to inheritance or environment, there is still a great deal of room in the model for the intercession of alternate values, behavioral options and past conditioning in how people respond to hyperemotionality. What do people from different backgrounds consider to be relaxing experiences? How do their different values affect their choice of one means over another for blocking external stimuli? Why do they accept mood modification of any sort instead of preferring to remain sober or to tolerate excitement, anguish or other emotional states?

What is, after all, the relationship between any of the genetic mechanisms thus far proposed for alcoholism and a person's compulsive imbibing of alcohol? Do those with cognitive deficiencies or abnormal brain waves find alcohol's effects especially rewarding? If this were the case, we would still need to know why this individual accepts such rewards in place of others (like family and job) with which alcoholism interferes. In other words, while genetic predisposition may influence the alcoholism equation, it does not obviate the need for a differential analysis of all the factors that are present in the individual's choice of behavior. This complexity may be best illustrated by exploring the implications of Schuckit's (1984a, 1984b) proposal that those at high risk to develop alcoholism may experience less of an effect from the alcohol they consume.

As Schuckit (1984b) makes clear, an inherited, diminished sensitivity to alcohol only constitutes a contributory step toward the development of alcoholism. For those less aware of how much they have drunk need still to seek specific intoxication effects or else to drink unknowingly at sufficient levels to lead to addictive symptomatology. Even if it takes a greater amount of alcohol to create the state of intoxication they seek what explains their desire for this state? Alternately such high-risk prospects for alcoholism may be unaware that they chronically achieve high BALs on which they eventually become dependent. This then is a second step--that of the development of alcohol dependence--in a putative model of alcoholism. However, a chronic exposure-chemical dependence version of alcoholism is by itself inadequate to explain addictive behavior (Peele, 1985a); this was revealed in the laboratory finding with rats by Tang et al. (1982) "that a history of ethanol overindulgence was not a sufficient condition for the maintenance of overdrinking" (p. 155).

Whatever the nature of the process of alcohol addiction, given that it cannot be explained solely by repeated high levels of alcohol consumption, the slow, gradual nature of the process adumbrated by the Schuckit proposal is borne out by the natural history of alcoholism. Vaillant's (1983) study, which covered 40 years of subjects' lives, offered "no credence to the common belief that some individuals become alcoholics after the first drink. The progression from alcohol use to misuse takes years" (p. 106). In the absence of a genetic compulsion to overimbibe, what maintains the persistence of motivation required to attain the alcoholic condition? The almost unconscious nature of the process implied by high-risk drinkers' lower awareness of the effects of alcohol could not withstand the years of negative consequences of alcohol misuse that Vaillant details.