Morristown, New Jersey

Abstract

The kind of clear-cut model of the genetic sources of alcoholism perceived by the public and presented in popular tracts does not accurately reflect the state of knowledge in this area. No persuasive genetic mechanism has been proposed to account for accumulated data about alcoholic behavior, social differences in alcoholism rates or the unfolding of the disease. Biological findings about the offspring of alcoholics have been inconsistent and grounds exist to challenge the notion of an enhanced genetic liability for alcoholism that has been accepted wisdom for the last decade. Genuine attempts to forge data and theory into genetic models have been limited to men alcoholics and to a minority of severely afflicted alcoholics with other special characteristics. However, several investigators dispute the idea of a special type of inherited alcoholism affecting only such groups. Even for these populations, balanced genetic models leave room for the substantial impact of environmental, social and individual factors (including personal values and intentions) so that drinking to excess can only be predicted within a complex, multivariate framework. The denial of this complexity in some quarters obscures what has been discovered through genetically oriented research and has dangerous consequences for prevention and treatment policies. (J. Stud. Alcohol 47: 63-73, 1986)

Introduction

A tremendous amount of attention and research has recently been concentrated on the inheritance of alcoholism and on the possibility of accounting genetically for drunken behavior. The major impetus for this research was the adoption studies conducted in Scandinavia in the 1970s which found reliable genetic (but not adoptive) transmission of alcoholism. This contemporary research focuses on the offspring of alcoholics and on the biochemical or neurological abnormalities they inherit that may lead to pathological drinking. Or, alternatively, investigations may focus on a gestalt of personality traits (centering on impulsiveness and antisocial activity) that can culminate in alcoholism or other psychopathology. In the words of one popular article on the topic, "A decade ago such a theory [of inherited antisocial personality and alcoholism] would have been dismissed out of hand" (Holden, 1985, p. 38). Today such a viewpoint has gained broad acceptance. Other popular works have created more ambitious deterministic models of alcoholism based on biological concepts models which have had a major impact on the thinking of both the public and clinical workers in the field. This article surveys the state of our--knowledge in this area, including-- along with biological investigations of alcoholics and their descendants-- social-scientific investigations which bear on biological determination of alcoholic behavior. The article also examines the epistemological underpinnings of genetic models and draws conclusions about their actual and potential ability to describe alcoholism. Particular attention is given to the hypothesis that alcoholism is a disease completely determined by biological predisposition (Milam and Ketcham, 1983) and to the implications of this assumption for prevention and treatment.

Early Genetic Theories of Alcoholism and the Behavioral Challenge to Naive Geneticism

The modern conception of the alcoholic's inbred, biological susceptibility to alcoholism arose in the aftermath of the repeal of Prohibition in 1933 and was a central tenet of the contemporary alcoholism movement's version of alcoholism from the inception of Alcoholics Anonymous (A.A.) in 1935. Beauchamp (1980) has made clear that this was a very different version of alcoholism from that presented by the 19th-century temperance movement. In that earlier era, alcoholism was viewed as a danger inherent in the consumption of alcohol--one that could befall any habitual imbiber. This view--which in itself was a matter of hot dispute among different ethnic, religious and social groups and carried a good deal of moral baggage (Gusfield, 1963)--was finally discarded when national Prohibition failed and with it the idea that the United States could reasonably hope to prevent all its citizens from drinking.

The modern definition of alcoholism, as embodied by A.A. (1939), instead claimed that the alcoholic was a person who from birth was destined to be unable to control his or her drinking. The mechanism posited for this perpetual inability was an inbred 'allergy' to alcohol, one which dictated that from a first single drink the alcoholic was set on an inexorable path to intoxication and to an eventual diseased state. It is important to note that the cultural and epidemiological milieu of alcohol consumption in the United States made possible--in fact demanded--such a view of alcoholism in the 20th century. That is, the evident truth that many people could drink regularly without becoming drunkards pointed toward an individually based source for alcoholism. However, what is "evident truth" in one time and place is incomprehensible to those of another era. Alcohol was believed by many in the 19th century to be inexorably addictive (an idea which has had a resurgence recently), just as narcotics are generally viewed to be today (Peele, 1985a). Yet, in the 19th century, opiate use was commonplace and widespread and habitual narcotics users were deemed to have something akin to a bad habit (Berridge and Edwards, 1981; Isbell, 1958).

The central mechanism proposed to account for alcoholism since the beginning of the 19th century was the drinker's "loss of control," an idea which itself marked a departure from colonial American conceptions of drinking and drunkenness (Levine, 1978). With the transfer of the crucial mechanism from the substance to the consumer, A.A. presented the view-- however unsystematically--that the compulsion to drink was biologically preprogrammed and thus inevitably characterized drinking by alcoholics. This null hypothesis (although hardly presented by A.A. as such) was readily investigated empirically and prompted a number of laboratory studies of the "priming effect," i.e., the result of giving an alcoholic a dose of the drug. These studies found no basis for believing that alcoholics lost control of their drinking whenever they tasted alcohol (Marlatt et al., 1973; Merry, 1966; Paredes et al., 1973).