The Genetic Model of Alcoholism and Other Addictions
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 of addiction 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 of addiction 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.
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. 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 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, 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).
Laboratory studies of the drinking behavior of alcoholics did far more than disprove the simplistic notion of a biologically based loss of control. The work of Mello and Mendelson (1972), Nathan and O’Brien (1971), and the Baltimore City Hospital group (Bigelow et al., 1974; Cohen et al., 1971) showed that alcoholic behavior could not be described in terms of an internal compulsion to drink, but rather that even alcoholics–while drinking–remained sensitive to environmental and cognitive inputs, realized the impact of reward and punishment, were aware of the presence of others around them and of their behavior, and drank to achieve a specific level of intoxication. For example, Mello and Mendelson (1972) found that alcoholics worked to accumulate enough experimental credits to be able to drink 2 or 3 days straight, even when they were already undergoing withdrawal from previous intoxication. Alcoholics observed by Bigelow et al. (1974) drank less when the experimenters forced them to leave a social area to consume their drinks in a isolated compartment. Many aspects of this laboratory portrait of the social, environmental and intentional elements in alcoholic imbibing correspond to the picture of problem drinking that was provided by the national surveys conducted by Cahalan and his co-workers (Cahalan, 1970; Cahalan and Room, 1974; Clark and Cahalan, 1976).
Contemporary Genetic Research: Inherited Differences in Familial Alcoholism Rates, Reactions to Alcohol and Other Biological Traits
Recent research on genetic mechanisms in alcoholism presupposes that the genetic transmission of alcoholism has been firmly established. Support for this idea has been provided by research which found greater concordance rates in alcoholism for identical versus fraternal twins and on the greater influence of the biologic versus the adoptive family in the development of alcoholism among adoptees (Goodwin, 1979). For example, Goodwin et al. (1973) found that male adoptees with alcoholic parents were four times more likely to become alcoholics than those without, although there was no such relationship with alcohol misuse in adoptive parents. Bohman (1978) and Cadoret and Gath (1978) also found this significantly enhanced liability for alcoholism among adopted male offspring of alcoholics. Similarly, Schuckit et al. (1972) discovered that half-siblings with at least one alcoholic-biologic parent were far more likely to develop alcoholism than those without such a parent, no matter by whom they were raised.
In the absence of an indication that the inability to control drinking is inherited, researchers have begun exploring other biochemical differences that may account for alcoholism. Speculations about metabolic differences have a long history, and the metabolic process that has attracted perhaps the greatest interest recently has been the accumulation of acetaldehyde following drinking (Lieber, 1976; Milam and Ketcham, 1983). Schuckit and Rayses (1979) found that young men with familial histories of alcoholism showed levels of acetaldehyde after drinking that were double the levels of those without such histories. Other metabolic processes that have traditionally been of interest have been the more rapid onset and peak experience of physiological reactions to alcohol, as in the visible flush typical of the drinking in Oriental populations. Working from the opposite direction, Schuckit (1980, 1984b) has found the offspring of alcoholics to be less sensitive to their blood alcohol levels (BALs). This type of finding may indicate that those with a pedigree for alcoholism are not as aware of the onset of intoxication when they drink or that they have a greater tolerance for alcohol.
Since cognitive and neurological impairment have frequently been found in alcoholics, several research teams have investigated the possibility that such abnormalities precede problem drinking and can be inherited. Adolescent sons of alcoholics performed more poorly than those without alcoholic parents in perceptual-motor, memory and language-processing tasks (Tarter et al., 1984), whereas adults with alcoholic relatives did worse than those with no family alcoholism history in abstract problem solving, perceptual-motor tasks and, to a lesser extent, verbal and learning-memory tests (Schaeffer et al., 1984). The discrepancies in the latter study held for those with familial alcoholism whether or not they themselves were alcoholics. Begleiter and his co-workers (1984) found that brain-wave abnormalities that were similar to those measured in alcoholics appeared in young boys with alcoholic fathers who themselves had never been exposed to alcohol. Gabrielli et al. (1982) had found that a similar group of children showed greater fast (beta) wave activity than a group of controls.
Several teams of investigators have now also proposed that there is an important subclass of inherited alcoholism that has at its roots an antisocial personality type (ASP) (Hesselbrock et al., 1984). There is a history of findings of ASP and related traits of aggression and unsocialized power needs in alcoholics (Cox et al., 1983; Peele, 1985a). Hesselbrock and his co-workers (1984) have found that ASP may be more important to the development and progression of alcoholism than is a “positive pedigree for alcoholism.” Cloninger et al. (1981, 1985) have identified a male-limited type of alcoholism with a strong hereditary component linked with impulsiveness and sensation-seeking. Adopted-out children with this variety of alcoholism had biological fathers with records of criminality as well as of alcoholism. Tarter et al. (1985) have presented the broadest argument for a severe type of alcoholism based on an inherited temperament–one characterized by extreme emotional volatility.
Difficulties Confronting Genetic Models of Alcoholism
Although hopes are high for genetic models of alcoholism, recent discoveries have not provided uniform support for any genetic proposition. Results, in particular, of two major Danish prospective studies (Knop at al., 1984; Pollock et al., 1984) and Schuckit’s (1984a) ongoing comparisons of matched pairs of subjects with and without alcoholic relatives–along with results from other independent investigations-have generally not been consistent. Differences in BALs and in rate of elimination of alcohol from the blood following drinking have now been determined by all the research teams almost certainly not to characterize the offspring of alcoholics. Moreover, Schuckit and Rayses’ (1979) finding of elevated acetaldehyde in these subjects has not been replicated by other groups, leading to speculation that this finding is an artifact of a difficult measurement process (Knop et al., 1981). Pollock et al. (1984) have presented only partial support for a lessened sensitivity to the effects of alcohol on alcoholic offspring, whereas Lipscomb and Nathan (1980) found that a family history of alcoholism did not affect subjects’ ability to estimate blood alcohol accurately. Furthermore, brain wave abnormalities discovered by Pollock et al. (1984) in children of alcoholics do not conform to those identified by either Begleiter et al. (1984) or Gabrielli et al. (1982). It is typical of research in this area that distinctive electroencephalogram patterns have been found in each investigation of descendants of alcoholics but that no two sets of results have coincided. Lastly, Schuckit (1984a) has not discovered a special subtype of alcoholism and has not found that men from alcoholic families have antisocial personalities, while Tarter et al. (1984) found such children to be less impulsive than a group of controls.
Genetic theories make little sense out of the enormous differences in alcoholism rates between social groups–like the Irish and the Jews–at opposite ends of the continuum in incidence of alcoholism (Glassner and Berg, 1980; Greeley et al., 1980). Vaillant (1983) found such ethnic distinctions to be more important than inherited tendencies toward alcoholism for determining clinical outcomes like a return to controlled drinking. In addition, the incidence of alcoholism is influenced by social class (Vaillant, 1983) and by gender–so much so in the latter case that theories of inherited alcoholism have been limited solely to men (Öjesjö, 1984; Pollock et al., 1984).
These sociocultural-gender differences have provoked a good deal of theorizing, some of it quite imaginative. Milam and Ketcham (1983) suggest that it is the duration of exposure to alcohol that determines a cultural group’s alcoholism rate, since evolutionary selection will eliminate those susceptible to alcoholism. However. while metabolic differences and variations in sensitivity to alcohol have been found among ethnic and cultural groups (Ewing et al ., 1974; Reed et al ., 1976), these group differences have not been found to predict alcohol misuse (Mendelson and Mello, 1979). The most striking case of divergent cultural patterns of drinking in the face of prominent racial reactions to alcohol is the pattern established by the Chinese and Japanese Americans on the one hand, and the Eskimo and American Indian groups on the other. Drinking in these groups is marked by a distinctive facial reddening and accelerated heart beat, blood pressure and other circulatory system measures, as well as by acetaldehyde and other alcohol metabolism abnormalities. However, the Chinese and Japanese Americans have the lowest alcoholism rates of all American cultural groups and the Eskimos and American Indians have the highest such rates (Stewart, 1964).
Vaillant (1983) suggested a modified cross-generational selection process to explain the large difference in the appearance of alcohol dependence between his college and his core-city sample: the lower incidence of dependence in the college group could be due to the economic and social failures of fathers of alcoholics that made it less likely their children would enter college. However, in explaining his extremely strong finding of ethnic differences in alcoholism, Vaillant relied on standard interpretations of how different cultures view alcohol and socialize its use. What makes Vaillant’s reference to genetic determinism for his social-class results more surprising is his overall recommendation that: “At the present time, a conservative view of the role of genetic factors in alcoholism seems appropriate” (p. 70)
Vaillant (1983) was led to such conservatism by a number of his data. Although he did find that subjects with alcoholic relatives had three to four times the alcoholism rates of those without traces of familial alcoholism, this result appeared in the absence of the statistical controls needed to separate genetic and environmental causality. When Vaillant examined differences between those with alcoholic relatives who did not live with them and those with no alcoholic relatives as a kind of environmental control, the ratio of the incidence of alcoholism was reduced to 2 : 1. There could also be additional environmental factors besides this one of immediate modeling effects of drinking that could reduce this ratio even further. Indeed, the Vaillant study disputes the alcoholism concordance rates that have been found in genetically similar and environmentally dissimilar populations which recent genetic models presuppose.
Other data fail to support biological inheritance of alcoholism. Gurling et al. (1981), when comparing MZ and DZ twins, found that the nonidentical pairs showed a higher pairwise concordance rate for alcohol dependence. This British group has also presented a comprehensive critique of the twin and adoption studies (Murray et al., 1983). Regarding Goodwin and his colleagues’ (1973) seminal discovery of an alcoholism inheritance among adoptees, Murray et al. noted that the investigators’ definition of alcoholism was unique, including a low cutoff in the amount of consumption (daily drinking, with six or more drinks consumed 2 or 3 times a month) combined with reported loss of control. The definitions in Goodwin et al.’s study are crucial since control adoptees (those without biological-alcoholic relatives) were more often problem drinkers than were index adoptees (those with biological-alcoholic relatives)–a finding which was reversed for subjects identified as alcoholics. Murray et al. commented: “Could it be that Goodwin’s findings are simply an artifact produced by the threshold for alcoholism accidentally dividing heavy drinkers in the index and control groups unevenly?” (p. 42).
Murray et al. (1983) point out that such definitional issues frequently raise questions in the genetic studies. For example, Schuckit et al.’s (l972) finding–that half-siblings with an alcoholic-biological parent who were reared by nonalcoholic parents showed a heightened risk of alcoholism–defined alcoholism as “drinking in a manner that interferes with one’s life.” This seems a better description of alcohol misuse than of alcoholism. In other words, this study identified genetic transmission of alcoholism in a category for which Goodwin et al. (1973) had rejected it. Consider also that Cadoret and Gath’s (1978) finding of genetic determination in adoptees held only for a primary diagnosis of alcoholism, and that a larger group of subjects with a secondary diagnosis of alcoholism came entirely from among those without alcoholic-biological parents. These shifting definitional boundaries actually enhance the statistical likelihood of uncovering alcoholic inheritance in each study.
Vaillant addressed himself particularly to the notion, first put forward by Goodwin (1979), that inherited alcoholism marks a distinct and separate variety of the disease. This is, of course, a reworking of the A.A. (1939) version of alcoholism. Working against this view of alcoholism–and its updated models of inherited sex-linked differences in alcoholism etiology and of a special variety of alcoholism characterized by inherited ASP–are findings that the same socially based differences in alcoholism rates pertain as well for less severe gradations of alcohol misuse. That is, those same ethnic, social class and gender groups that have a high incidence of problem drinking (Cahalan and Room, 1974; Greeley et al., 1980) also display a high incidence of alcoholism (Armor et al., 1978; Vaillant, 1983). It simply strains scientific credulity to imagine that the same factors which act in a socially mediated way to determine alcohol misuse also operate through separate genetic paths to influence alcoholism. Moreover, epidemiological studies such as Vaillant’s and the Cahalan group’s have always found more severe forms of alcohol dependence to merge imperceptibly and gradually with lesser degrees of problem drinking, so that a distinct, pathological variety of alcoholism does not stand out along a population curve of those who have drinking problems (Clark, 1976; Clark and Cahalan, 1976). Collations of measures of neurophysiological impairment likewise describe a smooth distribution of data points (Miller and Saucedo, 1983).
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).
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.
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:
The reason that I rejected the idea that I was an alcoholic was that my addiction wasn’t dramatic…. I never drank for a hangover…. I hadn’t been a solitary drinker … and at Washington luncheons I’d never touched anything but an occasional glass of sherry. There had been no broken promises … and no drunken driving…. I never wound up in jail (p. 307).
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).
Meanwhile, in another development, Timmen Cermak, one of the founders of the newly formed National Association for Children of Alcoholics, stated in an interview that “children of alcoholics require and deserve treatment in and of themselves, not as mere adjuncts of alcoholics,” and that they can be just as legitimately diagnosed as can alcoholics, even in the absence of actual drinking problems (Korcok, 1983, p. 19). This broad diagnostic net is being utilized in combination with a far more aggressive thrust in treatment services (Weisner and Room, 1984). For example Milam and Ketcham (1983), while in other places reinforcing traditional contentions about the disease of alcoholism with contemporary biological research, take issue with A.A.’s reliance on the alcoholic to “come to grips with his problem and then get himself into treatment” in favor of “forc(ing) the alcoholic into treatment by threatening an even less attractive alternative” (p. 133). Such an approach entails confronting the individual’s resistance to seeing the true nature of his or her drinking problem.
How all of this may be interpreted by treatment personnel is illustrated in two articles (Mason, 1985; Petropolous, 1985) in a recent issue of Update, published by the Alcoholism Council of Greater New York. One article takes the vulgarization of genetic discoveries, as outlined in Milam and Ketcham’s (1983) book, somewhat further:
Someone like the derelict . . ., intent only on getting sufficient booze from the bottle poised upside-down on his lips to obliterate … all of his realities … [is] the victim of metabolism, a metabolism the derelict was born with, a metabolic disorder that causes excessive drinking…. The derelict, unfortunately, has superb tolerance. He cannot help but get hooked as the enzyme back-up in his liver, along with other biochemical disturbances, make his discomfort without more ‘hair of the dog’ so intense. He will got to any length to drink… which turns into more acetaldehyde production … more withdrawal… no amount is ever enough. Tolerance to alcohol is not learned. It is built into the system (Mason, 1985, p. 4).
The other article describes how the son of an alcoholic had to be forced into treatment based on a rather vague symptomatology and his need to face up to his clinical condition:
Jason, a sixteen-year old boy with serious motivational problems, was brought in by his parents because of failing grades. His alcoholic father was sober one year, the approximate length of time his son had begun experiencing school problems, including cutting classes and failing grades. The boy was aloof and closed off to his feelings. The counselor suspected some drug involvement because of his behavior. It was clear that the boy needed immediate help. He was referred to an alcoholism clinic offering specific help for young children of alcoholics, as well as to Alateen. He balked at the idea, but with pressure from his parents he accepted an intake appointment at the clinic. He will need a lot of help to recognize and accept his feelings…. (Petropolous, 1985, p. 8).
Is there anyone listening to this boy’s plea that the standard diagnostic categories for which he has been fitted are not appropriate? Is the denial of his self-perception and personal choice justified by what we know about the etiology of alcoholism and chemical dependence and by firm conclusions about the genetic and other legacies that offspring of alcoholics carry?
Those who investigate the genetic transmission of alcoholism offer a different cast to their models of the predisposition to become alcoholics than do the models quoted in the previous section. Schuckit (1984b), for example, announces “that it is unlikely that there is a single cause for alcoholism that is both necessary and sufficient to produce the disorder. At best, biologic factors explain only a part of the variance….” (p. 883). Vaillant, in an interview published in Time (“New insights into alcoholism,” 1983) following publication of his book, The Natural History of Alcoholism (1983), put the matter even more succinctly. He indicated that finding a biological marker for alcoholism “would be as unlikely as finding one for basketball playing” and likened the role of heredity in alcoholism to that in “coronary heart disease, which is not due to twisted genes or to a specific disease. There is a genetic contribution, and the rest of it is due to maladaptive life-style” (p. 64).
Vaillant’s quote is entirely consistent with his and other data in the field, all of which support an incremental or complex, interactive view of the influence of inheritance on alcoholism. No findings from genetically-oriented research have disputed the significance of behavioral, psychodynamic, existential and social-group factors in all kinds of drinking problems, and results of laboratory and field research have repeatedly demonstrated the essential role of these factors in explaining the drinking of the alcoholic individual. To overextend genetic thinking so as to deny these personal and social meanings in drinking does a disservice to the social sciences, to our society and to alcoholics and others with drinking problems. Such an exclusionary approach to genetic formulations defies ample evidence already available to us and will not be sustained by future discoveries.
I thank Jack Horn, Arthur Alterman, Ralph Tarter and Robin Murray for invaluable information they provided and Archie Brodsky for his help in preparing the manuscript.
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