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Zucker RA, Gomberg ESL. Etiology of alcoholism reconsidered: the case for
a biopsychosocial process. Am Psychol 41: 783-793

Article  in  American Psychologist · August 1986

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 Etiology of Alcoholism Reconsidered
The Case for a Biopsychosocial Process
Robert A. Zucker
Edith S. Lisansky Gomberg
ABSTRACT.. The etiology of alcoholism is best understood
within the context of a longitudinal-developmental
framework that includes physiological behavioral and
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
sociocultural variables. The recently reported Vaillant fol-
This document is copyrighted by the American Psychological Association or one of its allied publishers.
low-up study, although ostensibly set within such a frame-
work, in fact understates the role of personality influences
and dismisses childhood effects out of hand. We review
these data and offer a different set of conclusions about
the roles of childhood influences, personality, and cultural
factors in the etiologic process. An alternative integrative
review of the existing longitudinal literature is presented
that sets these findings in the context of a biopsychosocial
process.
Alcoholism is a profoundly damaging disorder whose im-
pact spreads far beyond the one who suffers from it. The
problem of understanding its causes is also an especially
interesting one. Recent evidence suggests that the char-
acteristics that lead an individual to begin drinking may
only be tied loosely to influences on later stage drinking
and problem drinking phenomena. The factors connected
with beginning a pattern of problem use are not neces-
sarily the same as those pharmacological and behavioral
characteristics that contribute to the maintenance of the
alcohol use pattern or to the later build-up of a habitual
problem involving alcohol abuse or dependency. Given
this state of affairs, it is also likely that different orderings
of the importance of etiologic factors will be needed to
adequately describe cause and effect at different stages in
the process. Thus, Korsakoff's syndrome, one end-state
phenomenon of chronic alcohol abuse, is a pathology best
described in neuropathological terms; the direction of ef-
fect is best understood as going from brain dysfunction
to behavior (Wilkinson & Carlen, 1981). In contrast, the
onset of alcohol use is best understood as a phenomenon
predicted by individual difference variables and social in-
fluences (Jessor & Jessor, 1975; Margulies, Kessler, &
Kandel, 1977). The theoretical models and data language
used to describe these multiple phenomena of onset,
maintenance, and dependency involve radically different
levels of explanation and different orderings of physio-
logical, behavioral, and socioenvironmental variables at
different points in the life cycle. It is not surprising, there-
fore, that such a complex multidisciplinary problem has
in earlier times generated simplistic and reductionistic
explanations in an effort to describe its process.
July 1986 9 American Psychologist
Copyright 1986 by the American PsychologicalAssociation, Inc. 0003-066X/86/$00.75
Vol. 41, No. 7, 783-793
Michigan State University
University of Michigan
In the past decade, several etiologically focused lon-
gitudinal studies have been carried out with a broad
enough data set and a multivariate analytic strategy that
begins to allow for the partitioning of variance contri-
butions. However, all of those that have moved far enough
along to warrant publication have been concerned with
the early stages of drinking and problem drinking ac-
quisition (Huba & Bentler, 1984; Jessor & Jessor, 1977;
Kandel & Logan, 1984), or have dealt with a group of
subjects who have had largely normal or at worst episod-
ically disturbed drinking patterns (Fillmore, 1975; Fill-
more, Bacon, & Hyman, 1979). None have dealt with
frankly alcoholic respondents, and none have been suf-
ficiently comprehensive to allow for the evaluation of the
extent of effect contributed by biological (including ge-
netic), psychological, social, and cultural factors. It is,
therefore, a significant event for the field when a data set
is presented that promises to address the etiological ques-
tion of how alcoholism evolves, with a prospective method
and a sufficiently broad array of variables such that the
potential biopsychosocial nature of the disorder can be
examined. This is the importance of a recent report by
Vaillant and Milofsky (1982).
Since its publication, this study has received sub-
stantial attention in the literature. Given the significant
disagreement we have with the authors' interpretation of
their own data as well as their interpretation of earlier
longitudinal work in the area, we felt that an alternative
interpretation of their findings and of the earlier studies
was in order. In the present article, we examine very
closely the details of Vaillant and Milofsky's study with
particular attention to the role of personality and of
childhood influences on alcoholic behavior, reach a dif-
ferent set of conclusions, and find significant support for
an alternative position based on our own integrative re-
view of the prospective literature on alcoholic etiology
that substantially differs from Vaillant and Milofsky's ac-
count.
Vaillant's Follow-up Study
Using a sample of inner-city youth originally studied by
Glueck and Glueck (1950, 1968), Vaillant and his co-
workers relocated these subjects and performed another
follow-up when the sample subjects were 47 years of age.
To the Gluecks' original variable set the authors added a
number of measures that allowed examination of poten-
tial influences from heredity, ethnicity, psychological in-
783
 stability, childhood and adult personality variables, and
family background. The data analytic strategy utilized
was also potentially powerful because it permitted quan-
tification of the amount of variance contributed by dif-
ferent etiologic factors.
Following the analysis of this data set, Vaillant and
Milofsky drew a number of conclusions:
1. Where association exists between alcoholism and
any behavioral traits or symptoms, alcoholism is the cause
of the behaviors or symptoms rather than the result. Al-
coholism is not seen as a disorder whose etiologic ante-
cedents include personality and early environmental fac-
tors.
Alcoholism... appears to be the cause rather than the result
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of passive-dependent traits (Vaillant, 1980), of elevations on the
This document is copyrighted by the American Psychological Association or one of its allied publishers.
D and Pd scales of the Minnesota Multiphasic Personality In-
ventory (MMPI; Kammeier, Hoffman, & Loper, 1973), and of
passivity, low self-esteem and introversion (McCord & McCord,
1960). Could alcoholism also be the cause, not the result of
unhappy childhood, broken families, and personality disorder?
(p. 494)
[Thus,] although as adults our alcohol-dependent subjects ap-
peared to have personality disorders and to be socially inade-
quate, as children they were no less underprivileged than their
peers who were to drink socially as adults. (p. 497)
2. The investigators noted that premorbid antisocial
behavior contributes significantly to the etiology of al-
coholism. Nonetheless, they did not view the antisocial
behaviors that are manifest before the development of
alcohol problems as "specific personality facets" (p. 501),
and they argued that "specific personality facets are not
major factors in alcoholism" (p. 501).
In addition, the relationship of antisocial behavior
and personality is seen as more equivocal than other sig-
nificant etiologic factors. Thus, "the relationship between
alcoholism and antisocial personality is a two-way street.
Anti-social symptoms are often a result rather than a
cause of alcohol abuse" (p. 501, emphasis added).
3. The significance of the genetic contribution is
such that it probably contributes far more to the risk for
alcoholism in children than does the actual presence and
interaction contributed by growing up in an alcoholic
family. Arguing from their own data and from earlier
cross-fostering studies they stated that "alcoholic biolog-
ical relatives (even if physically absent) apparently con-
tribute far more to the observed increased risk for alco-
holism in children than alcoholics in the environment"
(p. 500).
In the next section we deal with the above issues in
detail. We indicate that evidence exists for continuity of
Preparation of this article was supported in part by grants to E~lithS.
LisanskyGombergfrom the National Instituteon AlcoholAbuse and
Alcoholism(NIAAAProject 5 R01 AA04143)and fromthe Rackham
School of Graduate Studies,Universityof Michigan.The authors also
wish to thank Neal Schmitt, Joel Aronoff,Susan Frank, and Robert
Brook for their commentson an earlierversionof this manuscript.
Correspondence concerningthis article should be addressed to
Robert A. Zuckcr, Department of Psychology,PsychologyResearch
Building,MichiganState University,East Lansing,M148824.
784
process between childhood factors and adult alcoholism,
that the role of personality factors and of antisocial be-
havior in particular has been underestimated in Vaillant
and Milofsky's data analyses, and that the interactive
contributions of genetic factors, cultural influences, and
childhood personality factors has not been adequately
tested by their study.
Interpretive and Methodological P r o b l e m s
With the Vaillant Follow-Up Study
Childhood Functioning and Adult Alcoholism
Reexamination of Vaillant and Milofiky's data shows that
the nature of the prealcoholic childhood environment is
far less benign than they indicated. There is a lack of
relationship between childhood (or adolescent) behavior
and adult, alcohol-related functioning for some, although
not all of the variables they examined. Other data show
continuity between early personality disorder and adult
alcoholism, as well as continuity between early environ-
mental di~culty and later alcoholism.
In examining the possible premorbid predictors of
alcoholism, the authors noted that
in our sample the differencesfrequently observed between al-
coholicand nonalcoholicsubjectsto which retrospectivestudies
often attribute etiological significance---differences in social
class, unemployment, eventual educational achievement, and
mental illness--in fact appear after the development of alco-
holism. (Vaillant & Milofsky, 1982, p. 497)
Recasting some Of the data presented in their Table 2 (p.
497), along with other analyses reported in Vaillant's more
extensive 1983 book on the same data set, shows that
there is a substantial relationship between troubled func-
tioning in adolescence and alcohol-related adult func-
tioning. These data, restructured to show the child-adult
correspondences, are presented here in Table 1. They in-
dicate that, despite a lack of initial differences in intel-
lectual ability, the children who were later to become al-
coholic had more school behavior problems and truancy
and were less likely to go as far in high school. The evi-
dence shows this pattern of earlier social failure is a pattern
that continues into later life. Thus, in adulthood, after
alcoholism has become overt, the alcohol-dependent sub-
jects spent more time unemployed and achieved a lower
adult social status, but such an outcome is predictable
from the earlier social failure, not just from the al-
coholism.
These data also show that a poorer environmental
support system and the greater likelihood of a distant
relationship with the father were present among later-to-
be alcohol-dependent persons. In adulthood we see poorer
mental health and greater evidence of antisocial activity,
strongly indicating continuity of process. Thus, the evi-
dence indicates that some early environmental difficulties
are more common among the alcoholic subjects, that
these characteristics predated the alcoholic adaptation,
and that they are consistent with a perspective of conti-
nuity between childhood functioning and adult alcoholic
outcome.
July 1986 9 American Psychologist
 value (Magnusson, 1967). Thus, the correlations reported
Table 1 here represent a lower boundary for the relationship of
Childhood and Adulthood Correspondences in antisocial behavior to alcohol-related problems, in con-
Functioning That Indicate Behavioral Continuities in trast to other variables that are assessed by way of non-
Male Alcoholic Etiology (in Percentages) dichotomous or of approximately equally dichotomized
Alcohol- measures.
Social dependent The relationship of childhood antisocial behavior to
Variable ddnkers subjects adult alcoholism is more readily dismissed than is true
of other imperfect indicators of etiologic contribution.
Early school trouble and later occupational difficulties
Correlations reported in Vaillant and Milofsky's Table 3
IQ < 90 ='b 28 30 (p. 498) show that adult alcoholism (variously measured)
Less than 10 grades of is associated with familial presence of alcoholism (var-
education a 28 42 iously measured, and interpreted to be evidence of the
School behavior problems extent of genetic loading for alcoholism) to virtually an
and truancy a 2 13 identical degree as is true of the relationship between al-
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10+ years unemployed c 4 24

coholism and premorbid antisocial behavior. The first as-
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Lowest adult social class ~ 4 21

Early personality disorder/social deprivation and later
behavioral and psychological disturbance
School behavior problems
and truancy a 2 13
Childhood environmental
strengths ("warm")a 26 13
Close relationship with
father a 30 13
Health Sickness Rating
Scale (lower score =
poorer global mental
health)~ 24 51
2 + times in jailc 4 16
Note. Portions of the data are from "The Etiology of Alcoholism: A Prospective
Viewpoint" by G. E. Vaillant and E. S. Milofsky, 1982, American Psychologist,
37, p. 497. Copyright 1982 by the American Psychological Association. Used
by the permission of the authors. The remainder of the data are from The
Natural History of Alcoholism (p. 57) by G. E. Vaillant, 1983, Cambfldge, MA:
Harvard University Press. Copyright 1983 by Harvard University Press. Used
by permission. The N for social dflnkars was 254 + 6; the N for alcohol-de-
pendent subjects was 69 + 2. All ps < .05.
9Childhood. e No differences are present (nor would be expected) for this
measure.
o Adulthood,
Other Interpretive and Methodological Issues
The relationship of premorbid antisocial behavior to al-
coholism has been underestimated in this data set. The
antisocial behavior variable is frequently considered to
be a continuous one (e.g., Loeber, 1985; Rutter & Giller,
1984), but in this data set it is assessed by way of the
measure "school behavior problems and truancy," coded
dichotomously.~ It is well known that dichotomous coding
attenuates the estimate of the relationship. In addition,
the use of an arbitrary and unequal coding split (96% of
subjects coded 0; 4% coded 1) leads to further restriction
of the relationship and further underestimation of its true
Code 1 indicatesthe presenceof four or more items relating to
presence of repeated truancy, disciplinary complaints from teachers,
fights with students, expulsion,suspension, and so on, and 0 indicates
anything less thanfour of these items (see Vaillant, 1983, p. 328).
sociation ranges between .10 and .28 (M = .192) de-
pending upon which measure of alcoholism and which
measure of familial presence of alcoholism is used; the
second underestimated association ranges between .10
and .20 (M = . 197).
The first association is admittedly only a very crude
index of the connection between alcoholism and genetic
endowment. As the authors clearly indicated, alcohol
abuse in one's aunts, uncles, grandparents, parents, and
siblings bears some connection to particular genetic load,
but it is also likely to be an indicator of the social density
of alcoholism in the immediate environment of the in-
dividual as he or she grows up. Nonetheless, this associ-
ation was viewed as "perhaps due more to heredity than
environment" (p. 494) and was taken at face value.
On the other hand, the correlation between pre-
morbid antisocial activity and alcoholism was explained
away as insufficient to play a major etiologic role. The
fact that these authors viewed adult antisocial behavior
among alcoholics as a result of alcoholism is irrelevent
to their etiologic correlation showing a relationship be-
tween prealcoholic (childhood) antisocial activity and
later alcoholic outcomes. They also described this variable
as a comparatively unimportant factor that "cannot be
invoked as playing a major etiologic role for most of the
alcohol-dependent men in the study" (p. 498). The study's
use of a heavily skewed measure that only classified 4%
of the subjects as antisocial facilitates this inappropriate
conclusion. To set coding criteria so that they apply to
hardly anyone, and then to describe the factor as unim-
portant, is an inappropriate way to test the issue.
The Role o f Personality in Alcoholic Etiology
Antisocial behavior is part of personality and it plays a
significant etiological role. In VaiUant and Milofsky's
account, "personality" factors are primarily equated with
a psychoanalytic conceptualization of personality disorder
largely involving passive dependency; because no caus-
ative link to alcoholism has been established, it is con-
cluded that personality plays no role in alcoholic etiology.
They concluded that
if one controls for antisocial childhood [emphasis added], cul-
tural attitudes toward alcohol use and abuse, for alcoholic

July 1986 9 American Psychologist 785

 heredity, and most especially for the effects of alcohol abuse,
then many of the childhood and adult personality variables to
which adult alcoholism has traditionally been attributed will
appear as carts, not horses. Indeed, our findings suggest that
. . previous investigators may have sometimes erroneously in-
.
terpreted their data to support the retrospective illusion that
alcoholism must be a symptom of personality disorders.
(p. 502)
What is strange about this conclusion is that the one
personality variable that the authors have themselves
demonstrated as playing a significant etiological role,
namely antisocial childhood, is dismissed as not having
causal relevance. Yet, this variable appears continually
as a significant antecedent in a variety of cross-sectional
and longitudinal studies of the development of drinking
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This document is copyrighted by the American Psychological Association or one of its allied publishers.
problems (Gomberg, 1982; Jessor & Jessor, 1977; Zucker
& Fillmore, 1968).
There are several possible explanations for this dis-
missal. For one, there is a failure to realize that, although
older notions of alcoholism as relating to "oral depen-
dency" have not survived hypothesis testing, other per-
sonality variables have consistently been demonstrated
to have etiological significance. A second explanation is
that the term personality disorder is confused and equated
with the term personality variable. The former refers to
specific psychiatric nosological categories. The latter refers
to individual differences in psychological characteristics
that reflect consistencies and coherencies in a person's
behavior over time and across situations. There is strong
and consistent evidence that some personality variables---
including antisocial behavior--are premorbidly present
in persons who later become alcoholic. A third expla-
nation is that there is a bias against psychosocial variables
as etiologic factors.
The summary regression analysis of potential etio-
logical variables (Vaillant & Miiofiky, Table 7, p. 500)
underestimates the contribution of cultural and personality
factors to the variance explaining alcohol-related prob-
lems. This analysis also potentially underemphasizes the
role of early environmental characteristics as etiologic
factors.
When no previously specified order is given, multiple
regression programs will typically enter first into the
analysis the variable with the largest individual correlation
to the criterion. Judging by the data presented in Vaillant
and Milofsky's Table 3 (p. 498), in two out of three in-
stances relating to the prediction of alcoholism this would
have involved selecting the ethnicity variable to be entered
first into the regression equation. Yet in the analysis re-
ported in their article, this variable was one of the last
two entered into the regression, thus minimizing its vari-
ance contribution. Similarly, the marker variable used to
assess antisocial behavior--the truancy/school behavior
problems measure--on a univariate basis shows itself in
Table 3 to be one of the most potent (even when atten-
uated) individual predictors of alcoholism; this measure
also was entered into the regression following the other
four variables. In short, the estimates of amount of vari-
ance contributed by these cultural and personality vari-
786
ables are minimum values, because the contribution of
the previously entered variables has already been par-
tialed out.
There is, of course, no statistical solution to the
problem of relative importance of indexes in multiple
regression equations where the variables are intercorre-
lated (Darlington, 1968). A hierarchical regression pro-
cedure is appropriate when an investigator has a particular
theoretical notion that needs to be tested in a prescribed
fashion. Such was the case with Vaillant and Milofsky's
analysis. However, their analysis and the conclusions they
reached comprise only one approach among a number
of alternatives, and the one they have selected effectively
minimizes the role of social and personality factors. Other
analyses, which enter these variables into the predictive
equation earlier, would show a greater contribution of
psychosocial factors.
A parallel analysis in VaiUant's 1983 volume (Table
2.16, p. 88) confirms this. Using one of the alternate ver-
sions of alcohol-related problems (the Problem Drinking
Scale) as the dependent variable, "Absence of Mediter-
ranean Ethnicity" is entered first into the regression
equation and explains 8.1% of the variance. This is in
contrast to the 3.5% of variance accounted for in the 1982
report (Table 7, p. 500) when this measure is entered late
(fifth or sixth) into the equation. In other words, the vari-
ance attributable to ethnicity is more than doubled by
this alternate entry procedure. The authors stated that
as an independent cheek on the conclusions of Table 7, the
contributions of the six variables to alcohol abuse as defined by
the DSM-III, by the PDS, and by the Cahalan scale were sep-
arately examined. The multiple regression results did not differ
appreciably from those in Table 7 either in percentage of ex-
plained variance or in beta weights. (Vaillant & Milofsky, 1982,
p. 501)
Given the more than twofold increase in explained vari-
ance and in order of importance of the cultural influence
variable, this statement is not substantiated. 2
Last, other analyses reported in Vaillant and Mi-
lofsky's article and in Vaillant's 1983 report also indicate
that order of entry of variables into the predictive equation
radically changes the conclusions about priority of etio-
logic factors. Thus, when a composite of early environ-
mental factors--including father's alcoholism, marital
conflict, lax maternal supervision, many moves, no at-
tachment to father, and no family cohesiveness---is used
to predict subsequent alcohol abuse and is entered first
into the predictive equation, it explains 7% of the variance;
when entered last, it explains only 1% (see Vaillant &
Milofsky, 1982, p. 501). In short, these data are as sup-
portive of the contribution of culture, personality, and
2A requestwasmadefor a copyofthe completecorrelationmatrix
of Table 3 variables,alongwith the AlcoholRelatedProblemsmeasure
of Table 7, if possible. It was our intent to rerun the regression,exper-
imentingwith a numberof other orders of entry of the variables.As of
the time of acceptanceof this manuscript, this request had not been
fulfilled.
July 1986 9 American Psychologist
 early experience as they are for the role of heredity in
determining eventual alcoholic outcome. Thus, a biopsy-
chosocial characterization of the etiologic process that
takes careful account of each of these variance compo-
nents seems most appropriate.
Developmental Issues in Interpreting Data
The effect of childhood influences on later alcoholic be-
havior has not been tested by this study; the "'childhood"
measures were obtained when target respondents were al-
ready adolescents. VaiUant and Milofsky's study was
based on follow-up investigation of Glueck and Glueck's
(1950, 1968) long-term delinquency study in which ad-
olescents were age 14 (plus or minus two years) when the
work began. All of the ostensible childhood variables were,
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in fact, coded from retrospective interview data from the
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teenagers, their parents (some of whom were themselves
alcoholic and possibly subject to distortion in their mem-
ory of earlier events because of their current distress),
and from collateral source material collected at this time
(i.e., when the subject's were between ages 12 and 16)
from teachers, social agency reports, and some field work
investigation) Careful inspection of the Gluecks' de-
scription of their information-gathering procedures leads
to the conclusion that the Vaillant study data base is most
accurate in reflecting respondents' functioning during
adolescence and is subject to varying degrees of distortion
for periods earlier than that. This is especially true of the
data collected via parental interview (see Livson & Peskin,
1980; Robbins, 1963; Yarrow, Campbell, & Burton,
1970). What are reported to be prospective measures of
ostensible childhood variables are best interpreted as ret-
rospective, recollective data that cannot answer questions
relating to the influence of childhood factors on adult
behavior.
An Alternative Etiological Perspective
Convergences in Prior Work
Even though much is left unsettled about etiology on the
basis of Vaillant and Milofsky's data analyses, careful
scrutiny of the existing longitudinal studies shows a sub-
stantial amount of convergence that has been overlooked
in their literature review. Before considering these findings
in detail, one point needs to be stressed; neither the follow-
up data obtained from the Gluecks" study nor most of
the other longitudinal studies are adequately designed to
test the question of a possible heritable basis for alcoholic
etiology. Family studies that document a greater loading
of alcoholic relatives among alcoholic patients now num-
ber well over 50 (Cotton, 1979; Goodwin, 1984). Such
evidence is suggestive rather than definitive for a genetic
hypothesis; it remained for a series of adoption studies of
the last decade to establish that such a genetic basis exists,
(Cadoret, Cain, & Grove, 1980; Goodwin, Schulsinger,
Hermansen, Guze, & Winokur, 1973; Goodwin et al.,
1974). We emphasize this point because our earlier cri-
tique might be misconstrued as partisan to a socioenvi-
ronmental theory of alcoholic etiology, simply because
July 1986 9 American Psychologist
the criticisms focus on the extent to which cultural, per-
sonality, and environmental factors have been underes-
timated in the etiologic equation.
Turning to the longitudinal etiologic evidence, our
review covers all of the studies originating in childhood
and adolescence that followed respondents into adulthood
and established an adult diagnosis of either alcoholism
or problem drinking. 4 Table 2 describes the sample char-
acteristics for all of these investigations. The detailed
findings from many of these investigations have already
been charted in an earlier publication (Zucker & Noll,
1982). Here we summarize across study results and focus
on commonalities; all of the findings are based on com-
parisons with suitable control groups (see Table 2; studies
are numbered 1 through 6).
Childhood antisocial behavior is consistently related
to later alcoholic outcome. All five of the studies (1-5)
that coded for this variable found greater amounts of an-
tisocial and aggressive activity among those who later be-
came alcoholics. The behaviors reported include more
aggressive and sadistic behavior (1, 4), more antisocial
activity (1, 2, 3, 5), and more rebelliousness (4). What is
especially significant about this attribute is that it is be-
ginning to show up in high-risk samples that were tracked
when considerably younger (e.g., kindergarten age; Kel-
lain, Simon, & Ensminger, 1981; Rydelius, 1981). The
evidence for the importance of this factor is 'thus increas-
ingly compelling.
More childhood difficulty in achievement-related ac-
tivity is consistently found in later-to-be alcoholics (2, 4,
5, 6). These failures include poorer school performance
(5), less productivity in high school (4), completion of
fewer years of schooling (5, 6), and more school truancy
(2). These findings also are appearing in recent studies
of not-yet-alcoholic but high-risk populations (Hegedus,
Alterman, & Tartar, 1984; Knopf, Teasdale, Schulsinger,
& Goodwin, 1985). It would be premature to attribute
all of these difficulties to lack of achievement strivings in
the prealcoholic group. Learning factors, including pos-
sible neurological deficits, have also been posited as likely
underlying mechanisms for the behavioral differences. But
whatever the underlying mechanisms, the evidence is in-
creasingly mounting that such achievement-related dif-
ficulties are more likely to appear as a risk factor.
A greater activity level is identified as a possible eti-
3In fact,the one completecasehistoryprotocolavailable(reported
in Glueck & Glueck, 1968) describesan interviewdone with the 16-
year-oldrespondent'smother, with no notes taken during the interview
(exceptfor recordingthe boy'shealthhistory).Earlierschoolinformation
data, asidefroman interviewwiththe subject'smostrecentteacher,was
obtainedby a questionnairesent to the superintendentof schoolsin the
boy's town.Thus, there are otherdistortionsas wellthat mayalso have
intruded on this data base.
4Studiesthat began in the collegeyears(i.e., postchildhood,such
as Fillmoreet al., 1979;Kammeieret al.,1973;VaiUant,1980)havebeen
omitted.Alsonot includedare prospectivestudiesthat wouldmeetthese
criteria but are not yet far enoughalong for the respondentsto have
becomealcoholic(e.g.,Kcllamet al., 1983;Pandina,Labouvie,& White,
1984; Rydelius,1981;Zucker,Baxter,Noll, Theado, & Weft, 1982).
787
 Table 2
Prospective Studies of Influences During Childhood and Adolescence Related
to Alcoholism in Adulthood: Descriptive Characteristics
Childhood
r and Age at first Time to Cfltaflon for a d u l t Characteristice
of control
Study source of subjects contact follow-up diagnosis (comparison)samples

1. McCord & McCord Predalinquent 9 20+ years Public records Predellnquents from
(1960, 1962) males, identified (hospital, same study with no
for a youth welfare, court) public record of
project alcohol problems
preventive
program; blue
collar
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2. Robins, Bates, & Males and females, Mdn = 13 30 years Personal interview (e) Other clinic patients
This document is copyrighted by the American Psychological Association or one of its allied publishers.

O'Neal (1962); childhood data and public not diagnosed as

Robins (1966) psychiatric clinic records . alcoholic;
patients, (b) elementary school
primarily blue pupils without
collar, heavily behavior
court and social problems--
agency referred matched for
residence, sex,
and age
3. Berry (1967); Ricks Males, child 11-16 Adulthood Hospital diagnostic Cilnic patients with later
& Berry (1970) guidance clinic record socially adequate
patients, mixed outcomes
social class
4. Jones (1968, 1971) Males (M) and 10 3 contacts: 23, 28, Extensive interview Growth Study subjects
females (F); and 33 years data and medical who were not
Oakland Growth after TI exam diagnosed as problem
Study, primarily drinkers
middle class
5. Vaillant & Milofsky Adolescent males 12-16 3 contacts: 11, 17, Extensive Same cohort; subjects
(1982); ValUant living in Boston and 33 years semlstructured who had been rated
et al. (1982); area, lower after TI interview at age as'social ddnkers
Valllant (1983) socioeconomic 47, plus medical thorughout the
status, originally and police course of adulthood
chosen as records
normal controls
for a delinquency
study; over half
were first
generation U.S.
citizens
6. Monnelly, Hartl, & Males in Boston 15-21 5 contacts: 5, 17, Interview, social Program participants
Elderkin (1983); area enrolled in a 23, 32, and 37 agency, jail and whose adult lives
Sheldon (1949) residential years after TI hospital records, were free of medical
treatment and death and psychiatric
program for certificates; difficulty
behavior interviews with
problems relatives

ological factor in two studies. One study (1) reported
more hyperactivity and another (4) reported a greater
likelihood of rapid tempo in children who later become
alcoholic. These prospective associations parallel the
findings of greater activity level found in other high-risk
but nonlongitudinal investigations (Cantwell, 1972; Mor-
risen & Stewart, 1973; Rimmer, 1982; Tarter, Hegedus,
Goldstein, Shelly, & Alterman, 1984).
Insofar as activity has sometimes been identified as
a biologically based temperamental difference, it is rele-

788 July 1986 9 American Psychologist

 vant to note reports of other potential diatheses in the
longitudinal group of studies. A history of more neural
disorders was found among the prealcoholic group in one
investigation (l); another (5) found a greater incidence of
infant nervousness and fretfulness, suggesting the possi-
bility of some early neural integrative deficit; a third (6)
reported greater evidence of poorer physical coordination.
There is also substantial agreement across studies
that males who later become alcoholics are more loosely
tied to others interpersonally. These studies indicate that
such children are less dependent, less considerate, and
less accepting of dependency (4), show a greater incidence
of leaving home earlier (2, 6), are more indifferent to their
mothers, and are also more cool and indifferent to siblings
than are those who do not become alcoholic in adulthood
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
(l). The interpersonal deficits one might infer from such
This document is copyrighted by the American Psychological Association or one of its allied publishers.
data cannot be separated from the more generalized ef-
fects of antisocial character and parent-child conflict.
Clearly, some relationship among these three aspects of
behavior would be expected, but the degree of indepen-
dence of the variables and the extent of their separate
etiologic contribution remains to be tested.
Heightened marital conflict is reported with consis-
tently greater frequency in the prealcoholic homes (1, 2,
4, 5). The mechanism by which the conflict contributes
to later childhood alcoholism still requires elaboration.
Two of the most plausible explanations for this relation-
ship are that (a) parental conflict leads to the child's
greater estrangement from the family, which moves the
child more quickly into the heavier drinking peer culture,
or alternately, (b) conflict leads to other sequelae (e.g.,
antisocial behavior) that in turn become the direct path-
way to alcoholism.
Interestingly, one factor associated with adult alco-
holism can also be accounted for by this finding. On the
basis of modeling principles, we can propose a linkage
between the childhood experience of observing parental
conflict and the consistently high divorce rates found
among alcoholic individuals. Parental conflict in child-
hood exposes the child to a greater repertoire of conflict-
maintaining responses that are activated in adulthood.
Of course, another explanation has traditionally been used
to account for marital difficultyin alcoholic families; that
is, current marital discord results from excessive drinking.
The longitudinal studies raise the possibility that this out-
come is overdetermined by both earlier and current ex-
perience.
Parent-child interaction in prealcoholic families is
characterized by inadequate parenting and the child's lack
of contact with the parent(s) (1-6). These interactions
are variously described in the studies as involving inad-
equate or lax supervision, the absence of parental de-
mands, parental disinterest, or lack of affection for the
child; however, the most overarching characterization is
one of inadequate contact. Other ingredients relating to
poor disciplinary practices may eventually be implicated,
but they are not clearly substantiated by these data.
Parents Ofprealcoholics are also more often inade-
quate role models for later normalcy (1, 2, 4, 5, 6). They
July 1986 9 American Psychologist
are more likely to be alcoholic, antisocial or sexually
deviant. These studies consistently connect parental
drinking to the child's later alcoholism. Antisocial or sex-
ually deviant behavior by parents has not been as fre-
quently reported, but in half of the studies these variables
were simply not assessed. When they have been measured,
such linkages consistently have been found (1, 2).
There are still some consistent omissions in these
studies that make integration difficult at this time. It
would not be surprising to discover that these parental
effects are interrelated, with some contributing more to
etiology than others. The nature of the data reported
makes partialing and regression techniques impossible to
apply in dealing with this question.
Another problem with the available data is that the
precise nature of maternal versus paternal effects cannot
be established. These studies were done at a time when
investigators were not as sensitized as they are now to the
possibilities of differential effects of mothers' versus fa-
thers' parenting and so did not obtain parallel data from
both parents. It is not currently possible to sort out the
precise nature of each parent's contribution to this pro-
cess, although the bulk of the existing data, at least with
later-to-be male alcoholics, indicates that mothers are
more often characterized by their lack of restrictiveness
and lack of contact, and fathers are notable for their role
deviancy (l, 4). Again we offer the caution that this is the
picture reported in later childhood and adolescence; we
know little about what happens earlier.
Three studies report data on ethnic differences (I,
2, 5). All replicate earlier cross-sectional work that links
cultural differences to alcoholic consumption patterns.
As confirmed again by Vaillant and Milofsky's follow-up
study, alcoholics are more likely to come from Irish than
from Italian ethnic backgrounds. This result, of course,
is another instance of a substantial and enduring finding
from the alcohol literature that relates ethnicity to pat-
terns of alcohol use and abuse. Data reported about the
Chinese, the Italians, the Jews, and the Irish (Bales, 1962;
Barnett, 1955; Lolli, Serianni, Golder, & Luzzatto-Fegia,
1958; Snyder, 1962) have been generally accepted, and
more current information about linkages between na-
tionality and cultural differences and differences in pat-
terns of drinking is also available (Everett, Waddell, &
Heath, 1976; Marshall, 1979). Although knowledge of
ethnicity may be useful in developing a predictive etiologic
equation, it is essential to remember that ethnic differ-
ences relate not only to norms about child and adult al-
cohol use and intoxication, but they also mark a wide
range of individual and interpersonal differences in ed-
ucational and occupational aspiration, cohesiveness of
kinship networks, and 'cultural values about sexuality,
marriage, and other elements of socialized behavior
(Greeley & McCready, 1975; McGoldrick, Pearce, &
Giordano, 1982; Sowell, 1981). These latter character-
istics also have been linked to patterns of temperate and
intemperate alcohol use. Additional work is needed to
disentangle the precise sources of contribution to alco-
holism that are lumped under the ethnic umbrella.
789
 Unsolved Etiologic Issues and New Directions
The across-study correspondences we have noted are sig-
nificant; they are bolstered by their close correspondence
with the recent longitudinal work that traces the earlier
process of drinking behavior acquisition, including be-
ginning drinking and the development of problem drink-
ing in adolescence (see footnote 4). The studies in Table
2 also dovetail with cross-sectional work on individual
differences in problem drinking in adolescence. (The in-
terested reader is referred to several extensive literature
reviews in these areas, namely Kandel, 1978, 1980;
Zucker & Noll, 1982). Although the convergences are im-
pressive and are of considerable practical significance for
the clinician, from the perspective of etiological under-
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
standing the work done so far is incomplete.
This document is copyrighted by the American Psychological Association or one of its allied publishers.
Causal pathways rather than simple time-lagged as-
sociations, need to be established for all the characteristics
so far identified by way of longitudinal studies. To some
exteht this has been a problem with the designs, because
the large majority only cover two time points and offer
no path an~ytic tests of competing pathways of influence.
The one study that assessed at least three time points
(Vaillant & Milofsky, 1982), and thus offered the potential
for tracing genuine order of precedence and the estab-
lishment of direction of effect, did not make use of the
advantages of the repeated measures design in the analysis.
Such fine-grained design and analysis is essential to es-
tablish the true antecedents and consequent sequelae of
alcohol abuse. The statistical technology for this is already
available (Bentler, 1980).
Related to the above point, any theorizing about the
etiology of psychopathology in general, and about the
causes of alcoholism in particular, needs to take account
of symptom formation as a developmental process that
may be differently influenced at different developmental
epochs. Studies of young people's drinking (e.g., Margui-
lies, Kessler, & Kandel, 1977) and of transitions from
nonproblem drinking to problem-drinking status at older
ages (e.g., Cahalan, !970) underscore the point that dif-
ferent influences (such as parent inputs) play a role at
different developmental stages, and that the entry into or
out of problem-drinking status, at any point in the life
cycle, needs to be understood not only as a move toward
or away from alcoholism but also as a response to influ-
ences that are developmentally relevant at that life stage
(Fillmore, Bacon, & Hyman, 1979; Gomberg & Lisansky,
1984; Kissin & Begleiter, 1983; Yamaguchi & Kandel,
1984).
The other side of this coin needs to be underscored
as well. Despite significant evidence for developmental
discontinuities, another body of data suggests that there
are substantial continuities over fairly large segments of
the life course, and what is most relevant to the present
discussion, that these continuities can at the least be es-
tablished between early childhood and late adolescence.
These continuities are of two kinds, the first between early
conduct problems and later heightened substance use
(Kellam, Simon, & Ensminger, 1983; Rydelius, 1981),
790
and the second between early conduct problems and
adult antisocial behavior for a subset of conduct-disor-
dered children (Loeber, 1982, 1985). On both of these
grounds one would anticipate that some continuity will
eventually be demonstrated between quite early person-
ality (behavioral) characteristics and later alcohol abuse
or alcoholism.
The role of current peer influences on etiology has
been insufficiently examined. A number of recent studies
of early drinking and drinking problems have established
the powerful contribution of peer influences in initiating
and maintaining this behavior (Huba, Wingard, & Bentler,
1979; Jessor & Jessor, 1977; Kandel, Kessler, & Margnlies,
1978). Other cross-sectional and theoretical analyses have
intimated that the spouse, family, and social networks of
adulthood may play an equally important and parallel
role (Cahalan & Room, 1974; Gomberg, 1981; Moos,
Finney, & Gamble, 1982; Zucker, 1979). These factors
have largely been ignored in psychiatrically conceived re-
cent work (Knopf, Goodwin, Teasdale, Mikkelsen, &
Schulsinger, 1984; Schuckit, 1984). Given the exception-
ally large amounts of variance that peer influence has
contributed in the studies that have measured it, its in-
fluence in triggering and maintaining abusive drinking
patterns needs to be more thoroughly investigated.
A decade ago when the first modern adoption study
data on the heritability of alcoholism were reported, much
of the controversy centered around that old but futile
question, Is alcoholism inherited? (Goodwin, Schulsinger,
Hermansen, Guze, & Winokur, 1973; Goodwin, Schul-
singer, Moiler, Hermansen, Winokur, & Guze, 1974;
Goodwin, Schulsinger, Knop, Mednick, & Guze, 1977;
Toler & Tamerin, 1973). The framework of such a ques-
tion, particularly in the context of the measures and sta-
tistical analyses used~ required this simple either-or an-
swer. More recent work, utilizing more sophisticated an-
alytic strategies, a larger sample, and a more varied
environmental data base, has pursued the problem dif-
ferently andhas established at least two types of suscep-
tibility to alcohol abuse involving differing levels of her-
itability, differing modes of transmission (patrilineal vs.
inherited from both parents), and differing environmental
presses (sometimes associated with lower as compared to
relatively higher socioeconomic status) in both men and
women (Bohman, Sigvardsson, & Cloninger, 1981; Clon-
inger, Bohman, & Sigvardsson, 1981). Premorbid parental
criminality is also implicated in the process. These more
recent studies mark an advance in understanding the
contributions of nature and nurture. Concern is with
mapping the pathways of the diatheses, establishing their
particular impact in environmental milieus that facilitate
or inhibit the appearance of the alcoholic disorders, and
understanding the physiological and psychological path-
ways and mechanisms of special susceptibility (McClearn
& Erwin, 1982; Tarter, Alterman, & Edwards, 1985). This
is more straightforwardly a quantitative genetic perspec-
tive that is cognizant of the manifold environmental in-
fluences (e.g., cultural variations) that are involved in
learning about drinking and in socializing nonalcohol-
July 1986 9 American Psychologist
 related but environmentally relevant individual differ-
ences so that they create a more risk-prone and alcohol-
involved career. Such formulations will eventually need
to take careful account of the varieties of physiological
diathesis that may be present, including both nonspecific-
to-alcohol central nervous system differences and meta-
bolic differences in response to alcohol consumption (Be-
gleiter, Projesz, & Kissin, 1982; Schukit & Rayses, 1979).
In the meantime, a crude but useful way of differentiating
types of susceptibility has been to classify subjects in terms
of positive versus negative history of alcoholism in first
degree relatives (Goodwin, 1984; Schukit & Rayses, 1979;
Tartar, Hegedus, Goldstein, Shelly, & Alterman, 1984).
H o w m a n y different kinds o f alcoholism are there?
In the study of schizophrenia significant research advances
This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.
were made when investigators moved away from a de-
This document is copyrighted by the American Psychological Association or one of its allied publishers.
scriptive base that classified individuals primarily on the
basis of existing symptoms and moved into the extensive
use of history and course variables in understanding the
multiple etiologies of schizophreniform problems. The
alcohol field is only in the early stages of making this
distinction. DSM-III (American Psychiatric Association,
1980) makes a simple severity-chronicity distinction be-
tween abuse and dependence. Others in the field have
suggested that a premorbid history of sociopathic (or in
the language of the current review, antisocial) behavior
in either parents or self is another distinguishing char-
acteristic in men and possibly also in women (Gomberg,
1982; Schuckit, 1973). Presence of affective disorder in
the history is another (Schuckit, Pitts, Reich, King, &
Winokur, 1969). Differentiations related to good versus
poor premorbid history (Knight, 1937; Levine & Zigler,
1973) and to course (early vs. late onset; Blane, 1979)
also appear to be powerful factors that the field has been
slow to embrace. It is essential that these distinctions
among potentially different etiologic pathways and dif-
ferent courses be sorted out (Zucker, in press). This will
happen only when investigators draw their samples from
a sufficiently broad population array so that the varieties
of the alcoholisms are adequately displayed. Otherwise,
the selectiveness of clinical samples will tend to color and
bias the findings.
To truly understand etiology is to understand also
how alcoholism does not develop and what produces in-
sulation against it, as well as what contributes to it. It has
been frequently noted that even high-risk studies involv-
ing a heavy loading of family vulnerability typically find
that less than half the at-risk offspring themselves become
symptomatic (Cotton, 1979). It is as important to un-
derstand the multiple pathways to adaptations that avoid
the development of problems as it is to understand how
those problems are produced. Given the evidence for the
involvement of genetic, personality, and cultural factors
in the etiologic equation, one plausible possibility is that
antisocial characteristics may potentiate genetic endow-
ment in producing adult alcohol dependence, whereas
the absence o f such characteristics might moderate the
endowment. This is only one of several pathways that
must be traced out.
July 1986 9 American Psychologist
Conclusions
Scientific knowledge about cause at any one time is bound
to be incomplete. Nonetheless, the evidence reviewed here
continues to document that physiological factors as me-
diated by genetic endowment are important, but that the
process of becoming alcoholic also occurs in a social world
and is influenced by a biopsychosocial process. The work
of effectively charting such a phenomenon must therefore
take place both across developmental time and across
levels of data. The critical issue for the field is its ability
to specify and integrate these different levels of causative
influence without falling into one or another attractive
but reductionistic traps.
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