Alcohol and Alcoholism Advance Access published online on August 1, 2007
Alcohol and Alcoholism, doi:10.1093/alcalc/agm051
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The Influence of Parental Drinking Behaviour and Antisocial Personality Disorder on Adolescent Behavioural Problems: Results of the Greifswalder Family Study
Department of Psychiatry and Psychotherapy of the Ernst-Moritz-Arndt University, Greifswald, Germany
* Author to whom correspondence should be addressed at: Department of Psychiatry, Ernst Moritz Arndt University of Greifswald, Ellernholzstr. 1-2, 17487 Greifswald, Germany; E-mail: barnow{at}uni-greifswald.de
Received 1 March 2007; first review notified 21 May 2007; accepted 28 May 2007
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ABSTRACT |
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Aim: Contradictory results have been produced by previous research on the question to what extent do children of alcoholics (COAs) differ in measures of externalizing symptoms from children of non-alcoholic parents. The goal of this study was to determine whether COAs are characterized by more behavioural problems than non-COAs, and also to determine the influence of a paternal antisocial personality disorder (ASPD) in this context. Methods: In this study, 340 children and adolescents between the ages of 11 and 18 years and their parents were included. Of this sample, 76 adolescents showed a positive family history of alcoholism (FHalc) and 47 adolescents a positive history of a paternal ASPD (FHaspd). Externalizing symptoms, which where measured on the basis of maternal ratings and self-assessments, were analysed with a two-factorial MANCOVA with FHalc and FHaspd as independent factors. Results: The results of the MANCOVA revealed that only children with paternal ASPD showed significant higher scores in attentional problems, self-rated aggression/delinquency and disruptive behaviour, while there were no differences for FHalc and the interaction effect. Conclusions: Our findings show that the higher of behavioural problems relates primarily to a higher prevalence in both cases of ASPD among fathers. These results were discussed regarding the mediating role of a paternal ASPD for the differences in behavioural problems in COAs and non-COAs. Furthermore, children with FHalc and/or FHaspd represent high-risk groups and should be the focus of prevention and intervention measures.
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Introduction |
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A number of studies report that children of alcoholics (COAs) exhibit a higher prevalence of attention disorders, as well as aggressive and delinquent behaviour (disruptive behaviour) (Alterman et al., 1998
; DeMilio, 1989; Giancola et al., 1996; Jacob et al., 1999; Steinhausen, 1995), whereby these behavioural problems are associated with later alcohol misuse (Barnow et al., 2002a; Barnow et al., 2002c; Caspi et al., 1996). However, not all studies agree that disruptive behaviour is related to the presence of a family history of alcoholism (FHalc) (Barnow and Freyberger, 2003; Barnow et al., 2004a; Barnow et al., 2002b; Pandina and Johnson, 1989; Schuckit et al., 2000).
These contradictory findings can be attributed, at least in part, to methodological difficulties. For example, few studies controlled their results for the family histories of antisocial personality disorder (FHaspd) in parents, even though parental ASPD contributes to the development of behavioural problems in children (Puttler et al., 1998; Rutter et al., 1998). At the same time, antisocial personality disorder (ASPD) is the disorder that is most closely related to substance abuse and dependence—particularly among men (Grant et al., 2004). In the general population, the risk of alcoholism in individuals with ASPD is 21 times higher than that of those without ASPD (Regier et al., 1990). Additionally, some 15–21% of individuals with alcohol problems also exhibit ASPD (Helzer and Pryzbeck, 1988; Kessler et al., 1997). Thus, it is reasonable to suggest that a significant share of the relationship between parental drinking and childhood behavioural problems is mediated by an additional diagnosis of ASPD (Hesselbrock et al., 1992).
A second methodological problem is that several authors have identified a FHalc solely on the basis of children's assessments or parents' self-assessments (Pandina and Johnson, 1989), which means that no reliable diagnosis of parental drinking behaviour was performed. Thirdly, information about disruptive behaviour should be obtained from multiple sources, as there may be only a moderate correlation between the assessments of these problems by mothers and children (Achenbach, 1994; Barnow, 2001). Finally, it is essential to precisely define behavioural problems. The Child Behaviour Checklist (CBCL) (Achenbach, 1991a), and the corresponding self-report version titled the Youth Self Report (YSR) (Achenbach, 1991b) divide, for example, external symptoms into attention problems and broadband behaviour problems, which are on a scale made up of aggressive conduct problems and delinquent or non-aggressive conduct problems (Achenbach et al., 1989; Earls, 1994; Frick et al., 1993; Verhulst and Achenbach, 1995). In this study, we used the term ‘behavioural problems’ with respect to aggressive and delinquent behaviour according to Achenbach's classification (Achenbach, 1991a). Furthermore, we computed a composite score, which included the YSR and CBCL broadband behavioural problem scales, as well as the subscales of attention problems. We refer to this construct by its more generic descriptor: disruptive behaviour problems.
With the aid of the data on 340 adolescents and their parents, we have addressed the methodological problems cited above. The question of whether COAs differed from non-COAs in terms of the extent of disruptive behaviour such as aggression, delinquency and attention problems described by themselves and their mothers is evaluated, as well as the extent to which the added presence of paternal ASDP had a significant impact on the results of these group comparisons. In this context, we hypothesized that COAs would differ from non-COAs, with respect to the extent of disruptive behaviour problems, only where a FH of ASPD was also present.
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Methods |
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Sample
Participants were recruited from the population-based sample Study of Health in Pomerania, Germany (SHIP), (John et al., 2001
). In SHIP, 3748 probands aged 20 to 79 years were chosen at random between March 1997 and May 2000, proportional to the population size of each community, and stratified by age and gender. A sub-sample of SHIP was recruited for the ‘Greifswalder Family Study’ mainly investigating pathways to addiction and personality disorders in adults and children. For this purpose, 527 individuals were selected from among those who lived in a household with a minimum of one child between the ages of 11 and 18 years. Among these, 141 persons could not be located or did not respond to at least four phone calls and two letters. At least one member from 71 families refused to participate, resulting in 315 family groups (381 adolescents) who gave written informed consent (for more information see: Barnow et al., 2002a; Barnow et al., 2004a; Barnow et al., 2004b; Barnow et al., 2004c; Barnow et al., 2007). In this study, forty-one of the 381 children were excluded from analysis because of missing data in relevant scales. Selection analyses showed that the 340 adolescents studied differed from the forty-one excluded adolescents in terms of whether they lived at home with one or both parents, and in terms of parental education level. The children excluded from the study were more likely to be living with one parent only (41.5% vs 21.2%; df = 1, 
2 = 8.41; P < 0.01) and their parents' education levels were lower (2 = 6.74; df =2, P < 0.05), i.e. there were relatively more parents with 9th-grade leaving certificates (10.8% vs 2.9%; P < 0.05). The mean age of the remaining 340 adolescents was 15.0 years (SD = 2.17); girls and boys were roughly equally distributed (46.5% boys).
Instruments
The status of a FHalc was determined using the Structured Interview for the Genetics of Alcoholism (SSAGA) (Bucholz et al., 1994; Hesselbrock et al., 1999). Cross-centre studies of the SSAGA indicate good reliability regarding alcohol use disorders (AUDs), with test-retest agreement (Kappas) for the DSM-III-R diagnoses of between 0.87—and 0.89 for dependence, and 0.57–0.74 for abuse (the range reflects the results of different studies) (Bucholz et al., 1994).
Seventy-six adolescents with a parent with an AUD according to DSM-IV (American Psychiatric Association, 1995) were identified from the total of 259 families. While most of the children had a father with an AUD (N = 68), six offspring came from families with an alcoholic mother, and two adolescents lived in a family with both parents having an AUD.
ASPD in parents were identified with the German version of the Structured Clinical Interview for DSM-III-R Axis II (SCID-II, Wittchen et al., 1993). The questionnaire is usually used in combination with an interview process, which was eliminated in this study due to time economy. First et al. (1995) provided data on the stability of SKID-II, citing a value of 
= 0.71 for a clinical sample on the scale for ASPD. In cases in which more than three questions regarding ASPD were answered positively for the biological father, the corresponding child was assigned the status FHaspd+.
The 119-item YSR (German version: Arbeitsgruppe Deutsche Child Behaviour Checklist, 1993b) was used to determine disruptive behaviour problems of the adolescents. Second-order principal factor analyses have revealed two broadband groupings of the syndromes, labelled as emotional problems and behavioural problems. In this study, we used the attention problem scale (
= 0.77 and = 0.70 for boys and girls) and the behavioural broadband scale, which contains the subscales of aggression ( = 0.84 and = 0.82) and delinquency ( = 0.70 and = 0.77). Additionally, the similar CBCL (German version: Arbeitsgruppe Deutsche Child Behaviour Checklist, 1993a) was answered by the mother. The reliability and validity of this scale is assessed as to be comparable to those of the YSR, and the allocation of items to the syndrome scales has also been verified through factor analysis (Achenbach, 1994). The correlations between mothers' (CBCL) and children's (YSR) ratings in the attention problem scales and broadband scales of behavioural problems were only moderate, with a correlation coefficient (Pearson) of r = 0.30 (P < 0.001) for attention problems and r = 0.36 (P < 0.001) for the broadband scales of behavioural problems (includes aggression and delinquency). Symptoms of disruptive behaviour including the scales of attention problems, and aggression/delinquency were measured by the combination of z-score transformed values from the YSR and CBCL raw externalizing scores ( = 0.78).
Statistical procedures
In the first step, subjects of the study were divided into four groups, taking into account the respective status of a parental AUD and a paternal ASPD. The first group (Group 1: no FHalc and no FHaspd; N = 238) comprised children of parents without AUD, in which neither the father nor the step-father had an ASPD. Group 2 (no FHalc but FHaspd; N = 26) comprised children whose parents did not have an AUD but whose fathers had an ASPD. Assigned to Group 3 (Fhalc but no FHaspd; N = 55) were children and adolescents with at least one parent diagnosed as having an AUD but neither of whose parents were diagnosed with an additional ASPD. Group 4 (Fhalc and FHaspd; N = 21) was composed of adolescents whose fathers showed both AUD and ASPD.
Analyses entails calculation of group comparisons (a univariate analysis of variance (ANOVA) for continuous variables and Chi square (2) for categorical items) between the four groups. In cases of failure to meet the conditions for the 2 test (e.g. where cell frequency was lower than five), Fisher's exact test was computed.
In the second step, we calculated a two-factorial MANCOVA using FHalc and FHaspd as independent factors and number of children living in the household as a covariate. This allows us to test our hypothesis that COAs differ from non COAs with respect to disruptive behaviour problems only where a FH of ASPD is also present. Group interaction (FHaspd x FHalc) was included in the model. The requirements for a Multivariate Analysis of Variance (MANOVA), multivariate normal distribution of dependent variables and homogeneity of variance and of the covariance matrices, were verified using the Levene test (Levene, 1960) and were found to be unfulfilled only for the broadband aggression/delinquency scale in the CBCL. In order to determine the extent to which this influenced the results of the MANOVA, results were re-evaluated using the ‘Kruskal–Wallis H’ non-parametric comparison test for multiple independent samples.
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Results |
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As shown in Table 1, the number of children per household differed significantly across the four groups with significantly more children in Group 4 (FHalc and FHaspd) who came from the same household, compared to adolescents of groups 1 (no FHalc and no FHaspd) and 3 (Fhalc but no FHaspd).
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In Table 2, we show the univariate means and standard deviations for each variable (YSR and CBCL: attention problem scales, behavioural problems broadband scales and composite measure of disruptive behaviour problems), allowing the reader to inspect our results. Results reveal a tendency to more attention problems as rated by mothers of adolescents of Group 4 compared to adolescents of Group 3. Group comparisons of self-rating scores indicate significant differences for attention problems and a tendency for aggression/delinquency, with highest values for Group 4. In addition, the sum composite score for disruptive behaviour problems tended to be higher for adolescents of Group 4 compared to offspring of groups 1 and 3 (see Table 2).
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As shown in Table 3, there was no significant FHalc x FHaspd interaction in the multivariate model (using the number of children in the household as covariate). The MANCOVA main effects indicated that there were significant differences between the extent of behaviour problems of FHaspd groups (but not between the FHalc groups) on the CBCL scale of attention problems and for the YSR scales of attention problems and aggression/delinquency. Furthermore, the composite measure of disruptive behaviour problems was also significant. For simplification, Table 3 only displays group differences for the FHaspd groups (absence vs presence of paternal ASPD). The means, standard deviations, univariate F-tests and significance levels for main and interaction effects are presented in Table 3.
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Because the requirements for a MANOVA (multivariate normal distribution of dependent variables and homogeneity of variance and of the covariance matrices) were not fulfilled for the broadband aggression/delinquency scale in the CBCL, the results were re-evaluated using non-parametric tests (not shown). This did not influence, however, the results as reported in Table 3.
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Discussion |
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The study addressed the question to what extent COAs differ from non-COAs with respect to disruptive behaviours such as delinquency, aggression, and attention problems. It was hypothesized that COAs differ from non-COAs in terms of the extent of these problems only in the presence of an additional FHaspd. Our results support this hypothesis and are in keeping with findings indicating that higher values of disruptive behaviour among COAs are mediated primarily by a higher incidence of co-morbidity of parents involving, in particular, an ASPD in the father (Hesselbrock et al., 1992
; Helzer and Pryzbeck, 1988). Specifically, the results of the two-factorial MANCOVA reveal that only an ASPD in the father was significantly related to disruptive behaviour problems. The values for children with a positive FH of paternal ASPD on the CBCL scale of attention problems and for the YSR scales of attention and behavioural problems, as well as in the composite measure of disruptive behaviour problems were significantly higher than those of children from homes without a FH of paternal ASPD. In summary, we conclude that children with a FHalc and paternal FHaspd represent a high-risk group in terms of the development of behavioural and attention problems. It seems that the pivotal factor here is paternal antisocial behaviour. However, our data do not allow conclusions about the extent to which the relationship between a paternal ASPD and an increased prevalence of externalizing problems in children is determined more or less by environmental factors (e.g. negative parenting practices, more life stress) as compared to genetic factors (e.g. temperament). Further examinations of this sample will include analyses of genetic material of these families, and might be helpful in examining this issue in more detail.
There are some additional methodological problems attending our study. First, cause-effect relationships could not be determined from this cross-sectional data. Prospective examinations of this sample are underway and might be more helpful in establishing causality. Second, because of the small sample size, only moderate effects are likely to be shown with sufficient power (ß = 0.8, = 0.05). Third, because there were multiple children in some families, observations were not fully independent. Fourth, selection analyses show that the sample must be seen as a positive selection from the total sample of children recruited for the study where the majority of children came from homes with well-educated parents. Fifth, only the SKID-II self-rating questionnaire was used to determine the presence or absence of paternal ASPD. Thus, the prevalence of paternal ASPD is quite high and does not reflect general prevalence rates in the community. Finally, because we did not separate our analysis for boys and girls in our study, we are not able to make any statements about the role of gender of the offspring in association with paternal antisocial behaviour and adolescent disruptive behaviour. Furthermore, considering the fact that our sample was, at least to some degree, positively selected and that our definition of ASPD only considers occurrence of antisocial behaviour since 15 years of age, therefore not corresponding to the diagnostic criteria of DSM-IV, results of our study cannot be generalized beyond this sample. We, therefore, emphasize the necessity to investigate this issue in more detail by using longitudinal data on larger samples.
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ACKNOWLEDGEMENTS |
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This work is part of the Community Medicine Research net (CMR) of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research (grant no. ZZ9603), the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania. The CMR gathers several research projects which are sharing data of the population-based Study of Health in Pomerania (SHIP; http://www.medizin.uni-greifswald.de/cm).
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