Vaillant (1983) finally rejected the idea of a special form of familial alcoholism because his data did not show that those with alcoholic relatives began to have drinking problems earlier than did those without such relatives. Both of the Danish prospective studies (Knop et al., 1984; Pollock et al., 1984) have agreed that such progeny do not display differences in early drinking patterns from those of other young men who do not have alcoholic relatives. Vaillant did discover earlier problem drinking among one group--subjects who had personal and family histories of antisocial behavior. Rather than viewing this concurrence as a genetic heritage, however, Vaillant attributed it to family disturbances. Tarter et al. (1984), who likewise found such disturbances to characterize the backgrounds of children of alcoholics, noted:

The underlying mechanisms responsible for the impairments in the alcoholics' children, however, cannot be ascertained. whether the deficits are sequelae of the physical abuse received from the father, perinatal complications ... or expressions of a genetic vulnerability remains to be elucidated. The findings presented herein suggest the matter is not at all clear cut.... Since the historical variables are ... correlated with each other, it is prudent to conclude that the relatively poor test performance in the children of alcoholics is the result of a complex interaction of genetic, developmental, and familial factors (p. 220).

The subjects Vaillant (1983) studied who misused alcohol and who came from alcoholic families did not in his judgment express a different or more virulent form of alcoholism. They were as likely as those without such family histories to return to controlled drinking, a development not consistent with the suppositions that those who suffer from an inbred alcoholism show not only an earlier onset of problem drinking, but greater severity of alcohol misuse and a worse prognosis for controlling their alcoholism (Goodwin, 1984; Hesselbrock et al., 1984). Hesselbrock et al. noted that Cahalan and Room (1974) found antisocial acting out to coexist with early drinking problems; however, the young problem drinkers (1974) in Cahalan and Room's epidemiological surveys regularly modulated their use of alcohol as they matured. Similarly, the imprisoned alcoholics that Goodwin et al. (1971) studied showed an unusually high degree of controlled-drinking out-comes. Indeed, Sanchez-Craig et al. (1987) found that young socially integrated problem drinkers were more likely to achieve controlled-drinking goals in therapy when they had a history of family alcoholism.

Inheritance of Addictions Other than Alcoholism

Speculation about a genetic basis for addictions other than alcoholism, and particularly narcotic addiction, has been retarded by the popular belief that "heroin is addictive for almost 100 percent of its users" (Milam and Ketcham, 1983, p. 27). According to this view, there would be no point to ferreting out individual variations in susceptibility to addiction. Recently, however, there has been a growing clinical awareness that approximately the same percentage of people become addicted to a range of psychoactive substances, including alcohol, Valium, the narcotics and cocaine (McConnell, 1984; Peele, 1983). Moreover, there is a high carryover among addictions to different substances both for the same individuals and cross-generationally within families. As a result, somewhat belatedly, clinical and biomedical investigators have begun to explore genetic mechanisms for all addictions (Peele, 1985a).

The first prominent example of a genetic theory of addiction other than in the case of alcoholism arose from Dole and Nyswander's (1967) hypothesis that heroin addiction was a metabolic disease. For these researchers, incredibly high relapse rates for treated heroin addicts indicated a possible physiological basis for addiction which transcended the active presence of the drug in the user's system. What this permanent or semipermanent residue from chronic use might comprise was not clearly specified in the Dole-Nyswander formulation. Meanwhile, this disease theory was confused by evidence not only that addiction occurred for a minority of those exposed to narcotics, but that addicts--especially those not in treatment--often did outgrow their drug habits (Maddux and Desmond, 1981; Waldorf, 1983) and that quite a few were subsequently able to use narcotics in a nonaddictive fashion (Harding et al., 1980; Robins et al., 1974).

The idea that addiction was not an inevitable consequence of narcotics use--even for some who had been previously dependent on the drug--prompted theorizing about inbred biological differences that produced differential susceptibility to narcotic addiction. Several pharmacologists posited that some drug users suffered a deficiency in endogenous opioid peptides, or endorphins, which made them particularly responsive to external infusions of narcotics (Goldstein, 1976, Snyder 1977). Endorphin shortages as a potential causative factor in addiction also offered the possibility of accounting for other addictions and excessive behavior like alcoholism and overeating, that might affect endorphin levels (Weisz and Thompson, 1983). Indeed other pathological behaviors such as compulsive running were thought by some to be mediated by this same neurochemical system (Pargman and Baker, 1980).

However, strong reservations have been expressed about this line of reasoning. Weisz and Thompson (1983) noted no solid evidence 'to conclude that endogenous opioids mediate the addictive process of even one substance of abuse' (p. 314). Moreover, Harold Kalant, a leading psychopharmacological researcher, pointed out the unlikelihood of accounting pharmacologically for cross-tolerance between narcotics, which have specific receptor sites, and alcohol, which affects the nervous system via a more diffuse biological route (cited in 'Drug research is muddied . . . ,' 1982). Yet, as evidenced by their cross-tolerance effects, alcohol and narcotics are relatively similar pharmacologically compared with the range of activities and substances sometimes claimed to act through a common neurological mechanism (Peele, 1985b). Thus, Peele asserted: "The fact of multiple addictions to myriad substances and nonsubstance-related involvements is primary evidence against genetic and biological interpretations of addiction" (1985a, p.55).