Psychiatric Annals


Alcoholism as a Family Dysfunction

Brian L Cook, DO; George Winokur, MD


In the family unit, dysfunctional characteristics may be involved in the etiology of alcoholism.


In the family unit, dysfunctional characteristics may be involved in the etiology of alcoholism.

Alcoholism as a disease can be viewed from a variety of perspectives as regards its interaction with the family unit. The alcoholic member of the family can be dysfunctional from the standpoint of alcohol-related symptoms. Thus, one may observe the effects of family violence, abuse, and neglect. The family may experience legal ramifications from alcoholism in areas such as divorce and child custody proceedings. Alcoholism may clearly cause failure to maintain expected social roles, leading to job loss and financial strain. Acute and chronic health effects of alcohol frequently lead to disability and early death. Alcoholics involved in accidents, particularly automobile-related phenomena, account for profound disruptions to their own families, and to innocent victims they randomly collide with.

A second way of viewing alcoholism as a family dysfunction is to start with the family unit, and to look for dysfunctional characteristics that may be involved in the etiology of the disorder. This review will consider a very potent aspect of familial influence on the etiology of alcoholism, i.e., genetic vulnerability. Familial relationships to other psychiatric disorders and their consequent influences will also be discussed.


Alcohol problems have long been observed to be more frequent in family members of alcoholic probands. Literature regarding the familial aspects of alcoholism were summarized by Cotton in 1979.1 In this review, data from families of 6251 alcoholics and 4083 nonalcoholics were presented. This review demonstrated convincingly that rates of alcoholism are substantially higher in relatives of alcoholics than in relatives of nonalcoholics. Cotton's review of the English-language literature supported Goodwin's summary of the world literature, which reported the same finding in 197 1.2

Evidence such as these studies alone do not implicate a genetic factor in the transmission of alcoholism. Clearly, methods to separate out cultural, environmental, and social factors are important if one wants to make a case for genetic factors being etiologically related to this disorder. As in other areas of medicine, twin studies, adoption studies, and family study techniques have been utilized to look for a genetic contribution.

Ttoin Studies

Kaij et al3 studied twins registered by the Swedish Temperance Board in 1960. This study looked at antisocial/ criminal alcoholics due to the method of case ascertainment. When such twins were studied, it was noted that identical twins were concordant for alcoholism more often than were fraternal twins (71% vs. 32%). They also noted that the more severe the alcoholism, the more discrepant the difference became between twin types.

Partanen et al4 looked at heritability of drinking behavior in "normal" twins. They studied 902 twin pairs using a factor analysis to look for components of drinking behavior that could be heritable. They found that drinking behaviors (e.g., quantity and frequency) were more concordant in identical twins, but adverse social consequences were not.

A third twin study using the Veterans Administration Twin Registry5 found concordance in monozygotic twins for organ-specific complications (e.g., alcoholic hallucinosis). Study limitations include the lack of personal interviews with the twins because only registry data were available, probable problems with determination of zygosity, and environmental similarity among the twins. The study does, however, support a genetic role in certain medical complications of alcoholism, as well as the etiology of alcoholism itself.

These twin studies support a genetic role in the etiology of alcoholism, but some of the findings are inconsistent and the influence of an environmental role is not controlled. Adoption studies are useful in separating the role of genetics versus "nurture."

Adoption Studies

An early adoption study by Roe6 in the 1940s is the only negative adoption study concerning alcoholism. This study evaluated 49 foster children, 20 to 40 years of age. Twenty-two of these children were from "normal" parentage and 27 had biologic parents who were "heavy drinkers." Neither group as adults had an excess of drinking problems. This study led to an early lack of interest in genetic factors in alcoholism, and shaped how the illness was viewed at least through the 1960s. The major methodological flaw in the study was their use of "heavy drinkers" rather than what would now be considered a more appropriate group of alcoholics (e.g., those requiring treatment, arrests, etc.). Using the term "heavy drinkers" may be too nonspecific, thus missing many with the illness.

Goodwin7 studied a Danish sample of adoptees who were separated from their biological parents in the first few weeks of life. He had four groups of subjects, all children of alcoholics. His groups consisted of sons and daughters raised either by nonalcoholic foster parents or their alcoholic biological parents. Paired with each group was a control group matched for age and sex, as well as circumstances of adoption in the adopted groups. The subjects were then studied when they were in their early to late 30s by interviewers "blind" to the purpose of the study or family history.

Findings from the Danish adoption studies were most striking in males. Sons of alcoholics were found to be four times more likely to be alcoholic than sons of nonalcoholics. This finding was not dependent upon whether the sons were raised in alcoholic or nonalcoholic homes. In this study, unlike that of Roe,6 alcoholics and not "heavy drinkers" were used, and thus the potential problem noted above was avoided. Results from the daughters were inconclusive regarding alcoholism, but those daughters raised by alcoholics had a sixfold increase in the rate of treatment for depression as compared to control daughters (30% vs. 5%).

The findings from the Danish studies have been supported by independent work in Sweden by Bohman8 and again by Cloninger.9 In the Cloninger study, a cross-fostering analysis was used, and efforts were further made to look at genetic as well as environmental interactions both before and after adoptive placement. From this work, two types of alcoholism were proposed. Type I (milieulimited) was associated with recurrent alcohol abuse in the biological parents without criminality, with postnatal environment strongly deterniining both the frequency and severity of alcoholism in susceptible sons. The Type II (malelimited) form was noted to be highly heritable in sons. This type is associated with extensive treatment for both alcohol abuse and criminaHty in the biological fathers, and the postnatal environment plays no role in the frequency of alcohol problems in affected sons.

A final type of adoption study supportive of a genetic role in alcoholism was done by Shuckit et al.10 In this study of half-siblings, it was noted that subjects were more likely to be alcoholic if their biological parents were considered alcoholic than if their surrogate parent was alcoholic.

These findings suggest that alcoholism in biological parents strongly predicts alcoholism in male offspring, regardless of adoptive placement. Finally, family studies support a genetic etiology in at least subgroups of alcoholics.

Family Studies

Jellinek11 first proposed the diagnostic category "familial alcoholism," but Goodwin has more recently actively supported this concept. Features of the "familial positive alcoholic" include a family history of alcoholism, early onset of alcoholism, severe symptoms of alcoholism requiring treatment early on, and absence of other conspicuous psychopathology. Various groups have investigated such relationships, and many findings have supported this concept.

Studies done by our group12 found early onset of alcoholism in the familial positive group, and more severe symptoms. We found, however, that familial positive alcoholics were more likely to have family histories of antisocial personality disorder, and we postulated that this might have significant effects on the type of alcoholism manifested by the proband.


Alcoholics have a personal history of increased rates of a number of psychiatric disorders, including anxiety disorders, affective disorders, and personality disorders, to name a few. Starting with alcoholic probands and then looking for familial psychiatric dysfunction that exists among their relatives reveals a number of interesting findings. These relationships offer another way to view the issue of alcoholism as a family dysfunction.

Alcoholism and Antisocial Personality Disorder (ASPD)

Familial interactions between alcoholism and antisocial personality disorder have been extensively studied by Cadoret.13 He used an adoption study paradigm to explore biological (genetic) and environmental relationships between alcoholism and ASPD primarily in male adoptees. Adoption records were carefully reviewed to facilitate diagnoses of alcoholism and/or ASPD in biological first-degree relatives of the adoptees. The adoptive home environment was then assessed, blind to proband status or biological background.

Results from these data reveal that biological background of alcoholism or ASPD increase adopted-away rates of these disorders respectively. Adoptee placement into an alcoholic family was noted to result in a 3.7-fold increase in alcoholism in the adoptees, controlling for antisocial background and alcoholism background. Being placed in an antisocial family resulted in a 16.6-fold increase in ASPD in the adoptee controlling for alcoholism and ASPD in the biological relatives. Regardless of "how" the adoptee became alcoholic (e.g., through placement in adoptive alcoholic family or having a biological first-degree relative with alcoholism), ASPD was additionally seen in the adoptee at a rate of 11.8 times the control rate, controlling for biological relatives with ASPD.

These findings demonstrate, at least in adoptees who were removed from their biological families very early on, that family alcohol problems significantly increase adoptee alcohol problems. Further, it is clear that such alcoholic adoptees are much more likely to have antisocial behavioral problems than adoptees without such environmental or biological backgrounds. Behavior problems manifested by the antisocial families and probands included things such as writing bad checks, felony convictions, failure to comply with social norms, promiscuity, and other DSM-III symptoms of ASPD. Obviously, such individuals and families would fit most definitions of dysfunctional. The Cadoret13 adoption studies thus demonstrate that even when one controls for biological background for alcohol problems and antisocial behavior in first-degree relatives, alcohol problems in the adoptive family are a strong predictor of other family and individual dysfunction.

Alcoholism and Depression

Depression is a second form of psychopathology in which familial alcoholism appears to impart significant influence. Winokur proposed in 197814 a method of subdividing patients with unipolar depression into those with a family history of depression only (familial pure depressive disorder), those with a family history of alcoholism or sociopathy (depression spectrum disorder), and those with no ill family members (sporadic depressive disorder). Based on this classification, the depression spectrum disorder background confers a more chronic form of depression, which is symptomatically more mild but less amenable to treatment.

More recently, the concept of depression spectrum disorder has evolved into attempts to define a more homogeneous subgroup of depressives (i.e., neuroticreactive depression).15 In this classification system, alcoholism in the family again predicts a form of depression characterized by stormy lifestyles, personality abnormalities, presence of life events before the onset of depression, and poor treatment response. While symptoms differ somewhat between neurotic and nonneurotic depressives, the former characteristics and the family history of alcoholism are better discriminators.

The relationship between familial alcoholism and other forms of psychopathology thus appears quite strong in both depression and antisocial personality disorder. Does this imply a causative role? At present, the etiologies of such relationships are unknown. While the associations noted are strong, clearly many factors are involved with the complexities of such disorders.


This review first presents evidence from a genetic standpoint clearly demonstrating that alcoholism has a large heritability factor. Search for a single gene responsible for alcoholism has been disappointing (e.g., note the A1 allele of the D2 receptor controversy). Despite the lack of such a gene, genetic factors must surely be included as contributing to dysfunction in families burdened with alcoholism.

In addition to this, we have attempted to point to more distal ways in which alcoholism exerts a more subtle force on the family. As noted earlier, direct dysfunction in the family caused by alcoholism is relatively easy to detect. The ramifications of having a biological relative with alcoholism or of being raised in an alcoholic family are just now emerging. The influence of such a background in personal development of alcoholism and antisocial personality disorder indicate a significant gene-environment interaction. The compound effect of one on the other is much greater than the sum of either individually.

In depression, a family history of alcoholism predicts a host of features in the individual that point to a dysfunction (personality abnormalities, lifestyle, etc.) and illness course. In the context of such difficulties, ongoing family problems are common.

This review could not encompass many other forms of psychiatric disorders with associations to alcoholism, nor could it address many of the social and/or legal dysfunctions that arise in alcoholic families. Rather, it is hoped that the examples discussed give rise to an appreciation of the many ways that alcoholism permeates family dysfunction.


1. Cotton NS. The familial incidence of alcoholism: a review. J Stud Alcohol. 1979; 40:89-116.

2. Goodwin DW. Is alcoholism hereditary? A review and critique. Arch Gen Psychiatry. 1971; 10:209-214.

3. Kaij L. Alcoholism in Twins. Stockholm, Sweden: Almquist and Wiksell; 1960.

4. Partanen J, Bruun K, Markkanen T. Inheritance of Drinking Behavior: A Study on Intelligence, Personality, and Use of Alcohol of Adult Twins. Helsinki, Finland: Finnish Foundation for Alcohol Studies; 1966.

5. Hrubec Z, Omenn GS. Evidence of genetic predisposition to alcoholic cirrhosis and psychosis: twin concordances for alcoholism and its biological end points by zygosity among male veterans. Alcoholism. 1981; 5:207-215.

6. Roe A. The adult adjustment of children of alcoholic parents raised in foster homes. Q J Stud Alcohol. 1944; 5:378-393.

7. Goodwin DW, Schulsinger F, Hermansen L, Guze SB, Winokur G. Alcohol problems in adoptees raised apart from alcoholic biological parents. Arch Gen Psychiatry. 1973; 28:238-243.

8. Bohman PA. Genetic aspects of alcoholism and criminality. Arch Gen Psychiatry. 1978; 35:269-276.

9. Cloninger R, Bohman M, Sigvardsson S. Inheritance of alcohol abuse. Arch Gen Psychiatry. 1981; 38:861-868.

10. Schuckit MA, Goodwin DW, Winokur G. A halfsibling study of alcoholism. Am J Psychiatry. 1972; 128:1132-1136.

11. Jellinek EM, Jolliffee N. Effect of alcohol on the individual. QJ Stud Alcohol. 1940; 1:110-181.

12. Cook BL, Winokur GA. Family study of familial positive vs. familial negative alcoholics. J Nerv Ment Dis. 1985; 173:175-178.

13. Cadoret RJ, Troughton E, O'Gorman TW. Genetic and environmental factors in alcohol abuse and antisocial personality. J Stud Alcohol. 1987; 48:1-8.

14. Winokur G, Behar D, van Valkenburg C. Is familial definition of depression both feasible and valid? J Nerv Ment Dis. 1978; 166:764-768.

15. Winokur G. The validity of neurotic-reactive depression. Arch Gen Psychiatry. 1985; 42:1116-1122.


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