Childhood Psychopathology in Families with Multigenerational Alcoholism SHIRLEY Y. HILL, PH.D.,

AND

DIANE R. HRUSKA, M.A.

Abstract. The present study examined psychopathology in high-risk children (ages 8 to 18) from families with a multigenerational history of alcoholism and contrasted them with low-risk children from community control families. Similar rates of childhood disorders were found for the high- and low-risk groups whether or not the children lived with an alcoholic parent. These findings suggest that the increased psychopathology commonly reported for children of alcoholics arises from comorbidity within the extended family as a result of assortative mating. When comorbidity is reduced through the selection of families with only alcoholism, a different symptom picture emerges. J. Am. Acad. Child Adolesc. Psychiatry, 1992,31,6:1024-1030. Key Words: psychopathology, alcoholism risk, and K-SADS. Offspring of alcoholic parents have a significantly higher risk for developing alcoholism than do offspring of nonalcoholic parents (Cloninger et aI., 1981; Goodwin et at, 1973; Hill et at, 1977; Schuckit, 1982). Additionally, children of alcoholics experience significant emotional problems. Among the childhood disturbances noted for these offspring are low self-esteem, manipulative or rebellious behavior, school problems, and hyperactivity (El-Guebaly and Offord, 1977; Jacob et at, 1978; Kammeier, 1971; Moos and Billings, 1982; Paolino and McCrady, 1977). A number of reports have noted that emotional difficulties continue to affect the lives of some adult children of alcoholics (Tweed and Ryff, 1991). These observations suggest the need to systematically investigate psychopathology in childhood among individuals who are at higher risk for developing alcoholism in adulthood. If particular disorders in childhood could be found to be associated with later development of alcoholism, then these disorders could be considered as behavioral markers for risk. For example, some reports have shown an association between hyperactivity (attention deficit disorder) in childhood and hysteria (somatization disorder), sociopathy, and alcoholism in adulthood (Morrison and Stewart, 1971). Examining the family histories of hyperactive children, these

Accepted February 24, 1992. From the Alcoholism and Genetics Research Program, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh, PA. The authors are grateful to Nan Boren, M.D. and Linda Humphreys, M.D., the clinicians who assisted in evaluating the children, Timothy Smith, M.A., who evaluated the parents, and Jeannette Locke, B.S., and Shawn Gronlund, B.S., who provided statistical support. We also thank Bonnie Kelly, B.S., for excellent editorial assistance. The help of families who consented to let us evaluate their children and patiently waited during these interviews is greatly appreciated. Finally, special thanks to the staff of the treatment facilities utilized in the present study. We especially thank Gateway Rehabilitation Center and particularly Ms. Sharon Eakes and Dr. Abraham Twerski for their invaluable support. Reprint requests to Dr. Hill, Alcoholism and Genetics Research Program, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, 3811 O'Hara Street, Pittsburgh, PA 15213. 0890-8567/92/3106-1024$03.00/0©1992 by the American Acad-

emy of Child and Adolescent Psychiatry.

1024

authors noted an increased rate of alcoholism among their biological relatives. Similarly, Goodwin et al. (1975) found elevated rates of hyperactivity among alcoholics by retrospective report. However, recent prospective studies of highrisk children have not found a clear association between childhood attention deficit disorder and later development of alcoholism (Gittelman et at, 1985; Mannuzzaet at, 1991; Satterfield et aI., 1982). However, using a retrospective longitudinal design, Robins and Price (1991) report that adult alcoholism, among other externalizing disorders (antisocial personality, drug abuse), is predicted by childhood conduct disorders, a diagnosis often seen among children with attention deficit disorder (Mannuzza et at, 1991). Because the question of psychopathology among highrisk individuals remains controversial, it is important to identify children who are at very high risk for developing alcoholism and to evaluate them using the most comprehensive psychiatric diagnostic instruments available. Moreover, to determine the population prevalence of problems among high-risk children, it is necessary that the children be chosen because of their membership in high-risk families regardless of whether or not they have been referred to a treatment center for problem behaviors. Therefore, the purpose of this study was to examine the prevalence of psychopathology in children who were at very high risk for developing alcoholism. Because these children came from pedigrees characterized by a high density of multigenerational alcoholism, their genetic risk is exceptionally high (Aston and Hill,-1990). Additionally, the family environment of children who come from alcoholic homes is frequently less than ideal. An increased incidence of poverty, divorce, unemployment, and chaos (Fine et at, 1976; Wilson and Orford, 1978) has been noted. All these factors might be expected to impact on the likelihood that a given child might succumb to whatever genetic propensity for developing alcoholism he or she may have (Hill et aI., 1987). In fact, identification of protective environmental factors has been of some interest to a number of research groups (Bennett, 1987; Moos and Billings, 1982; Rutter, 1985; Wolin et aI., 1980). Among the factors that appear to ameliorate the genetic propensity for developing alcoholism are higher socioeconomic status (Jacob and Leonard, 1986; Wolin et al., 1980), J. Am. Acad. Child Adolesc. Psychiatry, 31:6, November 1992

CHILDHOOD PSYCHOPATHOLOGY AND ALCOHOLISM RISK

Other variables such as positive relationship with a nonalcoholic parent have been identified by these same authors as possibly protective in nature. Research from our laboratory suggests that adult siblings from high-risk families may be "protected" by achievement orientation (Hill et aI., 1990a) and may have particular cognitive processing characteristics (Hill et aI., 1988; 1990b). The particular characteristics vary by both risk status and the age of the individual (child or adult), suggesting that "markers" at one developmental stage may be inappropriate or replaced by others as the individual matures. Applying this argument to "clinical markers," it may be seen that identification of clinical syndromes in children at high risk for developing alcoholism could be extremely useful. Methods

Subjects The subjects of this report are children between the ages of 8 and 18 years old who are members of pedigrees ascertained for a large family study initiated in 1984 (Cognitive and Personality Factors in Relatives of Alcoholics). The pedigrees acquired were either high- or low-risk for the development of alcoholism. The high-risk pedigrees were ascertained through a proband pair of male adult alcoholics. High-risk families were selected to have a minimum family constellation available: at least one living parent of the proband and additional adult siblings. These adult nuclear families were the subject of a number of previous reports (Hill et aI., 1987; 1988; 1990a). Complete pedigrees for each proband pair were systematically obtained and diagnostic assessments made for every living or deceased first-degree relative of the probands and their spouse by direct interview or through family history obtained from multiple informants. In the majority of cases, both family history and direct interview data were available for determining validity of the family history data. Diagnostic assessment of adult relatives was performed by trained interviewers using structured interviews with a consensus required between the interviewer and another clinician. This methodology is similar to that used by Leckman et al. (1982) who termed it the best-estimate diagnostic procedure. Recently, the opportunity for assessing the children of this sibling generation of individuals from high-risk pedigrees was possible, enabling us to determine the psychopathological characteristics of children for whom a large amount of clinical and laboratory data was available for their parents, grandparents, aunts, and uncles. Thus, the present sample of high-risk children either had multiple seconddegree relatives with alcoholism (grandparents, aunts, and uncles) and a father or mother who was alcoholic or did not have a parent alcoholic but had multiple second-degree relatives affected. Similarly, children from low-risk pedigrees were also available for study. The low-risk pedigrees had been ascertained by requiring that there be two male siblings (over the age of 30) who had parents and siblings available for inclusion in the larger study. Additionally, these male siblings and their first-degree relatives were required to have an J. Am. Acad. Child Ado/esc. Psychiatry, 31:6, November 1992

absence of Axis I DSM-III psychopathology. Thus, the 8to 18-year-old children assessed had parents, aunts, uncles, and grandparents who had had comprehensive clinical and laboratory assessments performed. (By way of note, the sibling generation in low-risk pedigrees was required to be more than 30 years old to reduce the chance that those without a diagnosis would not convert at a later time to an affected status. Although this is not guaranteed, the chance of alcoholism developing in men after the age of 30 is greatly reduced.) These pedigrees described form the "target" pedigrees. In the case of the minor children who form the basis of the present report, one parent' 'married-in" to these target families. Every effort was made to determine by family history the psychopathological characteristics of the family of the spouse (parent of the children in question). Psychiatric Evaluation of Parents Presence or absence of alcoholism and other Axis I DSMIII psychopathology was determined through the use of a structured interview that included portions of the Diagnostic Interview Schedule (DIS), a lifetime drinking history, and questions needed to determine whether or not the individual met DSM-III or Feighner Criteria (Feighner et aI., 1972) for alcoholism where the proband parent was interviewed directly. The majority of the proband parents (97%) were interviewed in person. The parent who married the proband parent also was interviewed in person in the majority of cases (60%), with the remainder assessed through family history information obtained from the spouse. High-risk children: The children comprising the study group were all from high-risk pedigrees characterized by multigenerational alcoholism. Each child had one parent who was a member of the high-risk target pedigree and had been identified as part of the larger family study described above. The other parent who had married into the high-risk pedigree was solicited for participation so that each of the nuclear families of each child could be properly characterized by clinical evaluation. The spouses who married into the high-risk pedigrees were similarly diagnosed according to the Research Diagnostic Criteria (RDC) and DSM-III criteria outlined. As a result of the selection strategy used in the larger study, children available for evaluation were the offspring of the male alcoholic proband pair or their siblings (male and female) whose diagnosis was free to vary (alcoholism present or absent). Because more than one child was available from these nuclear families, 53 children of 27 fathers and 11 mothers from our target families were studied. Some children had one or both parents alcoholic; others had none. Although some children might not have lived with an alcoholic parent, all of the children had an exceptionally highrisk for developing alcoholism (4.1 first- and second-degree relatives were so affected). The spouses who married into the high-risk (target) families were similarly diagnosed according to the RDC and DSM-III criteria outlined. Low-risk children: The normal control children were deemed to be at low-risk for developing alcoholism because they were from pedigrees selected for an absence of psychopathology. These pedigrees were identified through a volun1025

HILL AND HRUSKA

teer who responded to an advertisement in the local newspapers. The volunteer was interviewed to determine whether a pair of brothers over the age of 30 years, and at least one parent, were available for possible participation in the study. When such a constellation was identified through the volunteer respondent, permission to contact relatives was requested. If this were granted, all living first-degree relatives were contacted for possible participation in the study. Whereas one might assume that the initial respondent could have a volunteer bias, the remaining members of the pedigree had not specifically volunteered but had been solicited. Potential control pedigrees were screened through psychiatric interviews performed by phone. If the family qualified by having an absence of psychopathology, members were invited to participate and psychiatric status was determined by direct interview. In these families, no firstor second-degree relative met criteria for Axis I DSM-III and RDC psychopathology including alcoholism (Spitzer et aI., 1975). Therefore, the 27 biological proband parents were free of Axis I DSM-III psychopathology. Persons who married into these low-risk families were similarly diagnosed by direct interview or through use of family history information. Psychiatric Evaluation of Children

All available children between the ages of 8 and 18 participated in a diagnostic assessment that included administration of the Schedule for Affective Disorders and Schizophrenia for School-Aged Children (K-SADS), Epidemiologic version (E) and the K-SADS, Present version (P) (Chambers et aI., 1985; Orvaschel et aI., 1982) by trained (B.A. or M.S.W.) interviewers. These interviewers had achieved diagnostic reliability with one of the authors (J P-A) of the K-SADS instrument (Chambers et aI., 1985) and were blind to the risk status of the child. Interrater reliability required for certification as a trained interviewer by this research group is 90% agreement or better (Susan Dachielle, personal communication, for Dr. Puig-Antich [deceased)). A modified best-estimate diagnostic procedure was employed in which each child was evaluated by a resident child psychiatrist blind to the risk status of the child's family. The child psychiatrist independently conducted an unstructured interview, reviewed all material obtained from the parent and the child, and assigned his or her own diagnosis. When discrepancies arose, the two independent interviewers discussed the cases and resolved them in the presence of a third source clinician. The initial level of agreement between the two interviewers was 82%. So that a determination of both current and past clinical status of each child could be made, both forms of the K-SADS were administered to the parent who reported on the child's behavior and mood and to each child who reported on his or her own symptoms. The E version covers the child's entire life span; the P form assesses psychopathology within a year of the time of the interview. Certain diagnoses are not systematically assessed by the P form (dysthymia, cyclothymia, overanxious disorder, attention deficit disorder, oppositional disorder, alcohol or drug abuse). However, these diagnoses are covered in the K-SADS-E. Using the 1026

TABLE

1. Age and Gender of Children by Proband Parent Group Family Type" Gender

M F

Age Range

High Risk

Low Risk

Total

8-12 13-18 8-12 13-18

20 8 18 7 53 38

17 5 12 8 42 27

37 13 30 15 95 65

Total number of children Total number of parents "Number of subjects

K-SADS-E, when a child reports a history of one of these disorders, present episodes also are covered, thus, supplementing the P form of the instrument. Therefore, both instruments were employed to obtain a complete symptom picture for each child.

Results Demographic Characteristics of Families

The children from high- and low-risk families were comparable with respect to age and gender (Table I). All the families were white, and almost all were native born (one mother was born in Japan). The socioeconomic status (SES) for each nuclear family within each of the risk groups was determined by employing Hollingshead's Four Factor Index of Social Status (Hollingshead, 1975). The number of cases in each of five SES levels (unskilled, semi-skilled, skilled, semi-professional, and technical and professional) was determined. Both groups had a relatively high SES. Approximately 40% of the highrisk children and 65% of the low-risk children were reared

in families having an SES reflecting either semiprofessional or professional occupations among their parents. Although exactly the same percentage of parents in both groups held skilled occupations (26%), the greater proportion of controls at the higher end of the SES range contributed to the overall SES results being statistically significant (X2 = 6.86, df = I, p < 0.009). Psychiatric Disorders in Children

Differences between high- and low-risk children within major diagnostic categories are shown in Table 2. Compared with the nonrtal control children from low-risk pedigrees, high-risk children did not have statistically significant higher lifetime prevalence rates of major depression, anxiety disorders, attention deficit disorders, conduct disorders, or substance abuse. Additionally, the overall rate of psychopathology was comparable in the two groups, with 37.8% of high-risk children having one or more diagnoses and 33.3% of low-risk children so affected. Parental Mating Types

Although the children in the high-risk group may be presumed to have a higher genetic risk for developing alcoholism (multiple affected relatives, early onset in parents, J. Am. Acad. Child Ado/esc. Psychiatry, 31:6, November 1992

CHILDHOOD PSYCHOPATHOLOGY AND ALCOHOLISM RISK TABLE

2. Rates/JOO Children of DSM-Ill Diagnoses by Family Type (Lifetime Prevalence) Proband Parent Group

Diagnosis in Offspring

High Risk

Low Risk

Number of Offspring (N = 53)

Number of Offspring (N = 42)

11.3

9.5 21.4 2.4 2.4

Major depression/dysthymia Anxiety disorders Attention deficit disorder Conduct disorder Alcohol abuse Any diagnosis Multiple diagnoses (2 or » Mean number of diagnoses/child

22.6 3.8 5.7 3.8 37.8 20.8 0.59

presence of a major gene [Aston and Hill, 1990]), the environmental risk factors did vary from child to child. Within the high-risk group, some children lived with an alcoholic parent and others did not (Table 3). Specifically, 32 of 51 children (two children of one parent was unknown) had at least one alcoholic parent. The present study attempted to exclude families with any major Axis I diagnosis other than alcoholism, but some parents experienced at least one depressive episode. However, none met strict criteria for recurrent depression. Table 3 also addresses the issue of whether there is increased psychopathology among children with a familial diathesis for alcoholism who additionally live with an alcoholic parent. Whether or not a child was raised in a home with an alcoholic parent appears to have a minimal effect on the likelihood of receiving a K-SADS diagnosis. Children having an alcoholic father displayed the same rate of psychopathology as did children from the control families. Comparison of the rates of illness by whether the child resided with an alcoholic was statistically nonsignificant (X 2 = 3.95, df = 3, p < 0.27).

Discussion Although there is general agreement that parental alcohol abuse has negative effects on children, there is a paucity of empirical data describing the salient environmental, genetic, and teratogenic factors that increase the risk for psychopathology. One study (Moos and Billings, 1982), which looked at predictors of childhood psychopathology, suggested that the extent of the child's exposure to an alcoholic parent was predictive but additionally found that the degree .of emotional, physical, and occupational functioning of both parents was equally predictive. Thus, not surprisingly, Moos and Billings found that the emotional well-being of children with alcoholic parents who were in remission was no differTABLE

o

33.3 11.9 0.41

ent than children of controls. In contrast, the children of relapsed alcoholic parents had significantly poorer emotional functioning. In general, we find that the overall functioning of children from extended pedigrees in which multiple cases of alcoholism are occurring is comparable with that found in a community control sample of children. Because of the sample selection procedures used for the larger family study from which both high c and low-risk pedigrees were ascertained, it may be concluded that differences in risk between the two samples were maximized by the procedures used in this study. With respect to the high-risk children, it should be noted that each child had an average of four alcoholic relatives, placing them at exceptionally high lifetime risk for developing alcoholism. The control children were at exceptionally low-risk for developing alcoholism or other psychiatric disorders because of the strategy used to ascertain the pedigrees from which they were drawn. The index case provided information concerning his family constellation. Once a minimum constellation was assured, each first-degree relative was screened for the absence of DSM-III Axis I psychiatric illness. Only families who showed an absence of illness were included in the set of low-risk pedigrees. Thus, the minor children from these pedigrees had an exceptionally low-risk for psychiatric disorders based on their family history of psychopathology. A number of studies have attempted to relate behaviors of childhood to adult psychopathology (Rimmer and Jacobsen, 1980; Robins, 1966; Robins et aI., 1971; Robins and Hill, 1970). The largest sample available for studying these relationships has come out of the National Institute of Mental Health Epidemiological Catchment Area program (Regier et aI., 1984), in which a total of 19,482 respondents participated. This survey provided an opportunity to examine the

3. Children with K-SADS Number of Diagnoses by Alcoholism in Parent Home High Risk (N

Alcoholism in Parental Home Internalizing disorders Externalizing disorders No diagnosis J. Am. Acad. Child Adolesc. Psychiatry, 31:6, November 1992

= 51)

(N = 19) None

(N = 29) Father Only

6 I

4

o

12

20

I

5

(N = 3) Both 2

Low Risk (N

= 42)

None 12 2 28

/027

HILL AND HRUSKA

effects of childhood conduct disorders on the emergence of 10 adult disorders. As noted by Robins and Price (1991), conduct disorder was the only childhood disorder systematically investigated in the Epidemiological Catchment Area material, therefore, they comment, "We cannot investigate whether conduct disorder is unique in increasing the likelihood of appearance of a variety of adult disorders, or whether this is a pattern common to other childhood disorders as well." It would appear that three alternatives are available for studying the relationship between childhood psychopathology and adult disorders. We can await the transition of children to adulthood, observing them prospectively for many years to determine adult outcome, rely on the retrospective report of adults' sometimes imperfect recall of childhood disorders, or focus on the cross-sectional examination of the childhood disorders occurring in children who are at high risk for developing particular adult disorders. In addition, a combined longitudinal and cross-sectional approach can be taken within the same high-risk sample of children. Although the long-term goal of our research effort includes prospective follow-up of these high-risk children, we believe that cross-sectional examination of the childhood disorders might be of interest with respect to prevention efforts. Can we find behavioral risk markers that would identify particular children who might benefit from intervention efforts? The major findings of this cross-sectional analysis of our on-going work with children is as follows: (1) our sampling strategy for high-risk pedigrees resulted in greater familial loading for alcoholism than is normally seen, yet the children from these pedigrees had no higher prevalence of childhood disorders than did children from control pedigrees; (2) children who had an extraordinary high level of familial loading

In attempting to understand why the present findings fail to document the often cited negative effects of parental alcoholism on offspring, a number of alternatives were considered. First, it might be argued that the rate of psychopathology in the control group was sufficiently high to mask any difference between it and the high-risk group. The rate of illness for the control group was 33.3%. Thus, although 37.7% of the high-risk children were affected, the relatively high rate of illness among controls greatly reduces the significance of these problems. Secondly, the socioeconomic status of the high-risk children is probably somewhat higher than is typically seen. This may have led to an amelioration of problems in the high-risk group. With respect to the issue of whether or not our control group may have had somewhat higher rates of psychopathology than might have been expected, we find that the rate of illness exhibited among our control children is similar to that found in other high-risk studies employing community controls (Merikangas et aI., 1988; Weissman et al., 1987). Weissman etaI., studying children of depressed proband parents and community control parents, have reported that 64.8% of children of controls had one or more diagnoses. Merikangas et al., who further characterized the Weissman sample by noting the psychiatric diagnosis in both parents (proband and spouse), classified them by whether or not they had one or two disorders (depression only, anxiety only, or both disorders) and related these variables to the prevalence of disorders in their children. As a result, rates of psychiatric disorders in the children of affected parents could be contrasted with those among children whose parents had no psychiatric illness. Among normal parents (neither parent with a psychiatric disorder), 34.6% of children were found to have one or more disorders. Thus, the rates observed in the present sample are within the range pre-

for alcoholism, who additionally lived with at least one

viously reported for community samples. It is possible that

alcoholic parent, did not appear to be at higher risk for psychiatric disorder, than did children with a high familial loading but without an alcoholic parent present. The present findings are consistent with those of Merikangas et aI. (1988), who reported that paternal alcoholism was not related to differential risk of any psychiatric disorders in offspring. Other studies (Reich et aI., 1988; Steinhausen et aI., 1984) reported increased rates of psychopathology in children of alcoholic parents. However, in one of these (Steinhausen et aI., 1984), the subjects studied were children in attendance at a child psychiatric clinic, a sample that could be expected to have higher rates of psychopathology. A comparison of the present study with that of Reich and colleagues deserves mention because of the divergent findings. Reich and colleagues studied children of alcoholic parents but did not specify whether comorbidity in firstdegree relatives was assessed. If psychiatric comorbidity in parents of these children were free to vary, one would assume that the alcoholic parent had other psychiatric disorders in his or her pedigree. This might have resulted in higher rates of psychopathology among the children of alcoholics than among their control children because of the presence of familial loading for these other disorders (e.g., affective disorders).

all three studies (Merikangas et aI., 1988; Weissman et aI., 1987; and the present one) may have obtained somewhat elevated rates of psychopathology because of the setting in which the children were evaluated. All were assessed in medical centers where it is more likely that a given child might receive a psychiatric diagnosis, particularly if interviewers have previous experience as evaluators in a clinical situation. With respect to the issue of socioeconomic status of the children evaluated, it should be noted that others have commented on the protective effect of higher socioeconomic status on the outcome of the high-risk children (Jacob and Leonard, 1986; Wolin et aI., 1980). Although this may have served to reduce the psychopathology in the high-risk children, one would assume that having a higher socioeconomic status also would tend to reduce the prevalence of psychopathology among the controls. If so, one would assume that the present sample, which was characterized by exceptionally high socioeconomic functioning among controls, would have a minimal level of problems as well. Although the findings of this study are based on a restricted sample of individuals, this should not have altered our conclusions. Controls were selected because of an exceptionally low-risk for alcoholism and other psychiatric

1028

J. Am. Acad. Child Adolesc. Psychiatry, 31:6, November 1992

CHILDHOOD PSYCHOPATHOLOGY AND ALCOHOLISM RISK

disorders. High-risk children were selected because of the exceptionally high-risk for alcoholism due to ascertainment through two alcoholic adults, which resulted in each child having an average of four first- and second-degree relatives so affected. Selecting pedigrees who were at the extremes of risk was necessary to increase the homogeneity of the samples investigated. We cannot argue that all children of alcoholics show no greater risk for psychopathology than do children of nonalcoholics, but we can state that children from family history positive pedigrees with multiple cases of alcoholism, uncontaminated by other psychiatric comorbidity, do not have higher rates of psychopathology. This suggests that attempts to identify possible risk markers for alcoholism in high-risk children using behavioral characteristics may not be as useful as investigating other biological markers such as event-related potentials characteristics (Hill et al., 1990b; Hill and Steinhauer, in press). Reports of increased psychological disturbance among children of alcoholics may have been largely due to environmental factors rather than behavioral-genetic characteristics ofthe children. Factors that so often go along with alcoholism in the home, such as low socioeconomic status, divorce, and lack of family cohesion, may be the determining factors. The present sample was relatively high functioning in these respects although, of course, the familial loading for alcoholism risk was exceptionally high. In summary, the present findings suggest that parental alcoholism alone does not result in increased psychopathology in offspring. Instead, other factors such as low socioeconomic status and comorbid disorders in the parents may be the determining variables. When these factors are controlled, children from alcoholic and control families have remarkably similar psychiatric histories.

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J. Am. Acad. Child Adolesc. Psychiatry, 31:6, November 1992

Childhood psychopathology in families with multigenerational alcoholism.

The present study examined psychopathology in high-risk children (ages 8 to 18) from families with a multigenerational history of alcoholism and contr...
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