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Page 1 of 11 Stanton Peele
Bruce K. Alexander
In many cases, addiction theorists have now progressed beyond stereotyped disease conceptions of alcoholism or the idea that narcotics are inherently addictive to anyone who uses them. The two major areas of addiction theory—those concerning alcohol and narcotics—have had a chance to merge, along with theorizing about overeating, smoking, and even running and interpersonal addictions. Yet this new theoretical synthesis is less than meets the eye: It mainly recycles discredited notions while including piecemeal modifications that make the theories marginally more realistic in their descriptions of addictive behavior. These theories are described and evaluated in this chapter as they apply to all kinds of addictions. They are organized into sections on genetic theories (inherited mechanisms that cause or predispose people to be addicted), metabolic theories (biological, cellular adaptation to chronic exposure to drugs), conditioning theories (built on the idea of the cumulative reinforcement from drugs or other activities), and adaptation theories (those exploring the social and psychological functions performed by drug effects).
While most addiction theorizing has been too unidimensional and mechanistic to begin to account for addictive behavior, adaptation theories have typically had a different limitation. They do often correctly focus on the way in which the addict's experience of a drug's effects fits into the person's psychological and environmental ecology. In this way drugs are seen as a way to cope, however dysfunctionally, with personal and social needs and changing situational demands. Yet these adaptation models, while pointing in the right direction, fail because they do not directly explain the pharmacological role the substance plays in addiction. They are often considered—even by those who formulate them—as adjuncts to biological models, as in the suggestion that the addict uses a substance to gain a specific effect until, inexorably and irrevocably, physiological processes take hold of the individual. At the same time their purview is not ambitious enough (not nearly so ambitious as that of some biological and conditioning models) to incorporate nonnarcotic or nondrug involvements. They also miss the opportunity, readily available at the social-psychological level of analysis, to integrate individual and cultural experiences.
Genetic Theories
How Is Alcoholism Inherited?
Cigarette smoking, alcoholism, and overweight—like divorce, child abuse and religion—run in families. This addictive inheritance has been most studied in the case of alcoholism. Studies endeavoring to separate genetic from environmental factors, such as those in which adopted-away offspring of alcoholics were compared to adopted children with nonalcoholic biological parents, have claimed a three to four times greater alcoholism rate for those whose biologic parents were alcoholic (Goodwin et al. 1973). Vaillant (l983) approvingly cited the Goodwin et al. and other research indicating genetic causality in alcoholism (see especially Vaillant and Milofsky 1982), but his own research did not support this conclusion (cf. Peele 1983a). In the inner-city sample that formed the basis for Vaillant's primary analysis, those with alcoholic relatives were between three and four times as likely to be alcoholic as those without alcoholic relatives. Since these subjects were reared by their natural families, however, this finding does not distinguish effects of alcoholic environment from inherited dispositions. Vaillant did find that subjects with alcoholic relatives they did not live with were twice as likely to become alcoholic as subjects who had no alcoholic relatives at all.
Yet further nongenetic influences remain to be partialed out of Vaillant's results. The chief of these is ethnicity: Irish Americans in this Boston sample were seven times as likely to be alcohol dependent as were those of Mediterranean descent. Controlling for such large ethnicity effects would surely reduce the 2 to 1 ratio (for subjects with alcoholic relatives compared to those without) in alcoholism substantially even as other potential environmental factors that lead to alcoholism (besides ethnicity) would still remain to be controlled for. Vaillant reported two other tests of genetic causality in his sample. He disconfirmed Goodwin's (1979) hypothesis that alcoholics with alcoholic relatives—and hence a presumed inherited predisposition to alcoholism—inevitably develop problems with drinking earlier than do others. Finally, Vaillant found no tendency for the choice of moderate drinking versus abstinence as a resolution for drinking problems to be related to number of alcoholic relatives, although it was associated with the drinker's ethnic group.
Proposing genetic mechanisms in alcoholism on the basis of concordance rates does not provide a model of addiction. What are these mechanisms through which alcoholism is inherited and translated into alcoholic behavior? Not only has no biological mechanism been found to date to underlie alcoholism, but research on alcoholics' behavior indicates that one cannot be found in the case of the loss of control of drinking that defines alcoholism. Even the most severely alcoholic individuals "clearly demonstrate positive sources of control over drinking behavior" so that "extreme drunkenness cannot be accounted for on the basis of some internally located inability to stop" (Heather and Robertson 1981: 122). Intriguingly, controlled-drinking theorists like Heather and Robertson (1983) propose exceptions to their own analyses: Perhaps "some problem drinkers are born with a physiological abnormality, either genetically transmitted or as a result of intrauterine factors, which makes them react abnormally to alcohol from their first experience of it" (Heather and Robertson 1983: 141).
While it is certainly a fascinating possibility, no research of any type supports this suggestion. Vaillant (1983) found that self-reports by AA members that they immediately succumbed to alcoholism the first time they drank were false and that severe drinking problems developed over periods of years and decades. The exceptions to this generalization were psychopaths whose drinking problems were components of overall abnormal lifestyles and behavior patterns from an early age. However, these kinds of alcoholics showed a greater tendency to outgrow alcoholism by moderating their drinking (Goodwin et al. 1971), indicating they also do not conform to a putative biological model. Prospective studies of those from alcoholic families also have failed to reveal early alcoholic drinking (Knop et al.1984).
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