Marital adjustment as a moderator for genetic and environmental influences on parenting.

Family systems theory proposes that the parent-child relationship is embedded within the broader system of the family, and that other family subsystems can influence the dynamics and quality of the parent-child relationship. The current paper examines marital adjustment as a context for the parent-child relationship during adolescence. Specifically, the extent to which marital adjustment moderates child-based genetic and environmental effects on the parent-child relationship was assessed. Data for this study were from the initial wave of the Nonshared Environment in Adolescent Development (NEAD) study, and included 720 families with same-sex sibling pairs, ages 10-18 years. A range of sibling and family types was sampled, with 93 monozygotic twin pairs, 99 dizygotic twin pairs, and 95 sibling pairs from nondivorced families, and 182 sibling, 109 half-sibling, and 130 unrelated sibling pairs from stepfamilies. Composite measures of marriage (based on parent reports) and parenting (based child and parent reports and observation ratings) were examined. Results indicate that as marital adjustment declines, evocative child effects on parenting increase, while the role of shared family experiences declines. However, the specific impact of marital adjustment on child-based genetic and child-specific nonshared environmental contributions to parenting differed for mothers and fathers. This study identifies a previously unexplored mechanism through which family subsystems influence each other.

The etiology of stability and change in religious values and religious attendance.

Studies have demonstrated little to no heritability for adolescent religiosity but moderate genetic, shared environmental, and nonshared environmental influences on adult religiosity. Only one longitudinal study of religiosity in female twins has been conducted (Koenig et al., Dev Psychol 44:532-543, 2008), and reported that persistence from mid to late adolescence is due to shared environmental factors, but persistence from late adolescence to early adulthood was due to genetic and shared environmental factors. We examined the etiology of stability and change in religious values and religious attendance in males and females during adolescence and early adulthood. The heritability of both religious values and religious attendance increased from adolescence to early adulthood, although the increase was greater for religious attendance. Both genetic and shared environmental influences contributed to the stability of religious values and religious attendance across adolescence and young adulthood. Change in religious values was due to both genetic and nonshared environmental influences specific to early adulthood, whereas change in religious attendance was due in similar proportions to genetic, shared environmental, and non-shared environmental influences.

The moderating effect of religiosity on the genetic variance of problem alcohol use.

BACKGROUND: Previous studies have demonstrated that the heritability of alcohol-related phenotypes depends upon the social background in which it is measured (e.g., urbanicity, marital status, and religiosity). The aim of the current study was to identify whether religiosity moderated the genetic variance of problem alcohol use in men and women at two time points: adolescence and early adulthood. METHOD: Participants were 312 male MZ pairs, 379 female MZ pairs, 231 male DZ pairs, 235 female DZ pairs, and 275 opposite sex DZ pairs participating in the University of Colorado Center on Antisocial Drug Dependence. Religiosity was measured using the Value on Religion Scale (Jessor and Jessor, 1977), and problem alcohol use was measured using the Composite International Diagnostic Interview-Substance Abuse Module (Cottler et al., 1989). Data were analyzed using a model-fitting approach to the twin data. RESULTS: In adolescence, genetic variance of problem alcohol use decreased significantly with increasing levels of religiosity in both men and women, whereas in early adulthood, religiosity did not moderate the genetic variance of problem alcohol use in either men or women. CONCLUSION: Religiosity appears to moderate the genetic effects on problem alcohol use during adolescence, but not during early adulthood. The reduced genetic variance for problem alcohol use in adolescence may be the consequence of greater social control in adolescence than in young adulthood.

Perceived peer delinquency and the genetic predisposition for substance dependence vulnerability.

Like many behavioral phenotypes, generalized vulnerability to substance dependence in adolescence has a complex etiology; it is influenced by both genetic and environmental risks, with a heritability of approximately 0.40 [Button, T.M., Hewitt, J.K., Rhee, S.H., Young, S.E., Corley, R.P., Stallings, M.C., 2006. Examination of the causes of covariation between conduct disorder symptoms and vulnerability to drug dependence. Twin Res. Hum. Genet. 9, 38-45]. However, the extent to which the magnitudes of genetic and environmental risk for substance dependence are contextually moderated is unclear. The aim of the current study was to determine whether the etiology of substance dependence vulnerability (DV; total lifetime symptom count of dependence criteria endorsed across numerous substances divided by the number of substances used) varies depending on the extent of affiliation with delinquent peers as perceived by the adolescent. Results show that affiliation with delinquent peers moderates both the unstandardized (absolute) and the relative contribution of genetic, shared, and non-shared environmental risks to the variance of DV. The genetic variance was estimated to be higher among subjects who perceived their peers to be least delinquent and among those who considered their peers to be the most delinquent. The magnitudes of both shared and non-shared environmental influences were negligible among those who perceived their peers to be least delinquent and were greater among those with higher levels of perceived peers' delinquency.

Sex differences in the heritability of resilience.

We examine the heritability of psychological resilience among US adults aged 25 to 74 years. Using monozygotic and same sex dizygotic twin pairs from the National Survey of Mid-Life Development in the United States (MIDUS) we show that positive affect is equally heritable among men (h2 = .60) and women (h2 = .59). We then estimate the heritability of positive affect after controlling for an exhaustive list of social and inter-personal stressors, and we operationalize the residual for positive affect as resilience. According to this specification, the heritability of resilience is higher among men (h2 = .52) compared to women (h2 = .38). We show that self-acceptance is one of the most important aspects of psychological functioning that accounts for the heritability of resilience among both men and women. However, compared to women, men appear to derive additional benefits from environmental mastery that may enable otherwise sex-neutral resilient tendencies to manifest.

Delinquent peer affiliation and conduct problems: A twin study.

Many putative environmental risks correlate with individuals' genotypes. The association between delinquent peer affiliation and conduct problems may occur because of shared genetic liability. Five hundred fifty three monozygotic and 558 dizygotic twin pairs, aged 11 to 18 years, were assessed for delinquent peer affiliation and conduct problems. The authors investigated whether genes contribute to both delinquent peer affiliation and the correlation between delinquent peer affiliations and conduct problems. Delinquent peer affiliation was influenced by genetic, shared environmental, and nonshared environmental factors; genetic factors also contributed to the correlation between delinquent peer affiliations and conduct problems, providing evidence for genotype-environment correlation. The magnitude of the genetic variance of conduct problems was contextually dependent on levels of delinquent peer affiliation and was greater at higher levels of delinquent peer affiliation.

Parenting and adolescent antisocial behavior and depression: evidence of genotype x parenting environment interaction.

BACKGROUND: Little is known about the interplay of genotypes and malleable risk factors in influencing adolescent psychiatric symptoms and disorders. Information on these processes is crucial in designing programs for the prevention of psychiatric disorders. OBJECTIVE: To assess whether latent genetic factors and measured parent-child relationships interact (G x E) in predicting adolescent antisocial behavior and depression. DESIGN: We characterized risk of antisocial behavior and depression in adolescents by means of a genetically informed design. We used in-home questionnaire and observational measures of adolescent outcomes and environmental moderators (parenting), and a latent variable behavior genetic analytic model. SETTING: A nationally distributed sample recruited from random-digit dialing and national market panels. PARTICIPANTS: A total of 720 families with at least 2 children, 9 through 18 years old, stratified by genetic relatedness (monozygotic and dizygotic twins, full biological siblings in nondivorced and stepfamilies, and half-siblings and biologically unrelated siblings in stepfamilies). MAIN OUTCOME MEASURES: Antisocial behavior and depressive symptoms. RESULTS: There was an interaction of genotype and both parental negativity and low warmth predicting overall antisocial behavior, as well as aggressive and nonaggressive forms of antisocial behavior, but not depression. Genetic influence was greater for adolescent antisocial behavior when parenting was more negative or less warm. Genotype-environment correlation was partialled out in the analysis and thus did not account for the results. CONCLUSION: This study demonstrates, on the basis of careful measurement and appropriate analytic methods, that a continuous measure of parenting in the normative range moderates the influence of genotype on antisocial behavior.

The role of conduct disorder in explaining the comorbidity between alcohol and illicit drug dependence in adolescence.

BACKGROUND: Conduct disorder (CD), alcohol dependence (AD), and illicit drug dependence (IDD) frequently co-occur. This paper describes the result of an investigation of the extent to which comorbid alcohol and illicit drug dependence in adolescents are explained by etiological factors in common with conduct disorder. METHODS: Participants were 645 MZ twin pairs, 702 DZ twin pairs, 429 biological sibling pairs, and 96 adoptive sibling pairs, aged 12-18 years, from a community based sample. Conduct disorder was measured using the Diagnostic Interview Schedule for Children-IV. Alcohol and illicit drug dependence were assessed using the Composite International Diagnostic Interview-Substance Abuse Module (CIDI-SAM). For each outcome, subjects were categorized into those with no symptoms, those with one or more symptoms but no diagnosis, and those with a diagnosis. RESULTS: The heritability estimates for CD, AD, and IDD were 58, 66, and 36%, respectively. The genetic correlation between AD and IDD was partially explained by the genetic risk they both share with conduct disorder. CONCLUSIONS: We conclude that conduct disorder in adolescents explains, in part, the co-occurrence of alcohol and illicit drug dependence. Specifically, the genetic contribution to their covariation is explained partially by the genetic contribution in common with conduct disorder.

Examination of the causes of covariation between conduct disorder symptoms and vulnerability to drug dependence.

Conduct disorder (CD) symptoms and substance dependence commonly co-occur. Both phenotypes are highly heritable and a common genetic influence on the covariation has been suggested. The aim of this study was to determine the extent to which genes and environment contribute to the covariance between CD and drug dependence using twins from the Colorado Longitudinal Twin Sample and the Colorado Twin Registry. A total of 880 twin pairs (237 monozygotic [MZ] female, 195 MZ male, 116 dizygotic [DZ] female, 118 DZ male and 214 DZ opposite-sex) aged 13 to 18 (mean = 15.65) were included in the analysis. CD was assessed by lifetime Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) symptom count and a polysubstance dependence vulnerability index was developed from responses to the Composite International Diagnostic Interview--Substance Abuse Module. A bivariate Cholesky Decomposition model was used to partition the cause of variation and covariation of the two phenotypes. No sex-limitation was observed in our data, and male and female parameter estimates were constrained to be equal. Both CD symptoms and dependence vulnerability were significantly heritable, and genes, shared environment and nonshared environment all contributed to the covariation between them. Genes contributed 35% of the phenotypic covariance, shared environment contributed 46%, and nonshared environmental influences contributed the remaining 19% to the phenotypic covariance. Therefore, there appears to be pleiotropic genetic influence on CD symptoms and dependence vulnerability.

Do aggressive and non-aggressive antisocial behaviors in adolescents result from the same genetic and environmental effects?

Antisocial behavior (ASB) in adolescents can broadly be separated into two forms; aggressive and non-aggressive. Both are heritable and it has been suggested that aggressive ASB is more heritable. The extent to which genes contribute to the correlation between the two is unknown. Structural equation modeling was applied to a population-based twin sample of 258 twins pairs aged 11-18 to estimate the heritability of each form of ASB and to estimate the extent to which the phenotypic correlation was the consequence of shared genes and environmental factors. Non-shared environment and genetic factors substantially influenced both forms of ASB. The heritability of aggressive (but not non-aggressive) ASB was significantly higher in girls than in boys. Combining both sexes, a model in which the genetic effects on aggressive and non-aggressive ASB were identical could be rejected. Our results suggest a partial genetic overlap with a specific genetic effect contributing to the variance of aggressive ASB and a stronger genetic effect on aggression in females than in males.