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Background:   A critical issue in devising effective interventions for the treatment of children's behavioral and emotional problems identifying genuine family environmental factors that place children at risk. In most twin and family studies, environmental factors are confounded with both direct genetic risk from parents and the indirect effect of genes influencing parents' ability to provide an optimal rearing environment. The present study was undertaken to determine whether parental psychopathology, specifically parental antisocial behavior (ASP), is a genuine environmental risk factor for juvenile conduct disturbance, depression and hyperactivity, or whether the association between parental ASP and children's behavioral and emotional problems can be explained as a secondary consequence of the intergenerational transmission of genetic factors., Methods:   An extended children of twins design comprised of data collected on 2,674 adult female and male twins, their spouses, and 2,454 of their children was used to test whether genetic and/or family environmental factors best accounted for the association between parental antisocial behavior and children's behavioral problems. An age-matched sample of 2,826 juvenile twin pairs from the Virginia Twin Study of Adolescent Behavioral Development was also included to examine developmental differences in gene expression by partitioning child-specific transmissible effects from those effects that persist into adulthood. The fit of alternative models was evaluated using the statistical program Mx., Results:   We found distinct patterns of transmission between parental antisocial behavior and juvenile conduct, depression and hyperactivity. Genetic and family environmental factors accounted for the resemblance between parents' ASP and children's conduct disturbance. Family environmental factors alone explained the association between child depression and parental ASP, and the impact of parental ASP on hyperactivity was entirely genetic., Conclusions:   These findings underscore differences in the contribution of genetic and environmental factors on the patterns of association between parental antisocial behavior and juvenile psychopathology, having important clinical implications for the prevention and amelioration of child behavioral and emotional problems., (© 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health.)

The causes of correlation between parental treatment and offspring behavior are ambiguous since genetic and social factors are correlated in typical family studies. The problem is complicated by the need to characterize the effects of genes and environment on both juvenile and adult behavioral outcomes. A model is developed for the resemblance between juvenile and adult twins and their parents that allows some of these effects to be resolved. Data on childhood adversity, parental anti-social behavior, and longitudinal adult and juvenile anti-social behavior were obtained from 1,412 families of adolescent and young adult twins. A structural model is fitted that allows for the effects of genetic and social transmission of information from parents to children. Environmental effects of parents may be mediated through measured features of the home environment. Parameters were estimated by diagonal weighted least squares applied to the 33 distinct polychoric correlations between relatives and between variables within and between ages. Sub-hypotheses were tested. Results confirmed that effects of genes and environment were both highly significant. Genetic effects were large in juveniles and largely age and sex-specific. Approximately 30% of the variation due to the shared environment was due to the effect of childhood adversity. The remaining shared environmental effects are unexplained. Adversity is affected significantly by maternal anti-social behavior. The correlation between paternal ASP and adversity may be explained by antisocial fathers selecting (or creating) antisocial mothers. All significant environmental effects of parental ASP are mediated through the measure of adversity. Though transmission of ASP is both genetic and social, passive genotype-environment correlation is very small. Assortative mating for ASP has barely detectable consequence for the genetic correlation between siblings. The longitudinal study of twins and their parents makes it possible to demonstrate there is a direct causal effect of childhood adversity on child conduct disorder over and above any indirect genetic correlation.

Background: Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring., Methods: Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program Mx., Results: The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance., Conclusions: These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development.

Considerable evidence from twin and adoption studies indicates that both genetic and shared environmental factors play a substantial role in the liability to antisocial behavior. Although twin and adoption designs can resolve genetic and environmental influences, they do not provide information about assortative mating, parent-offspring transmission, or the contribution of these factors to trait variation. We examined the role of genetic and environmental factors for conduct disorder (CD) using a twin-parent design. This design allows the simultaneous estimation of additive genetic, shared and individual-specific environmental effects, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A retrospective measure of CD was obtained from twins and their parents or guardians in the Virginia Twin Study of Adolescent Behavior Development and its Young Adult Follow up sample. Both genetic and environmental factors play a significant role in the liability to CD. Major influences on individual differences appeared to be additive genetic (38%-40%) and unique environmental (39%-42%) effects, with smaller contributions from the shared environment (18%-23%), assortative mating (-2%), cultural transmission (approximately 2%) and resulting genotype-environment covariance. This study showed significant heritability, which is slightly increased by assortative mating, and significant effects of primarily nonparental shared environment on CD.

Background: Very little is known about how different sets of risk factors interact to influence risk for psychiatric disorder., Objective: To replicate a recent report of a genotype-environment interaction that predicts risk for antisocial behavior in boys., Design: Characterizing risk for conduct disorder in boys in association with monoamine oxidase A genotype and exposure to familial adversity, defined by interparental violence, parental neglect, and inconsistent discipline., Setting: A community-based sample of twin boys., Participants: Five hundred fourteen male twins aged 8 to 17 years., Main Outcome Measure: Conduct disorder., Results: There was a main effect of adversity but not of monoamine oxidase A on risk for conduct disorder. Low monoamine oxidase A activity increased risk for conduct disorder only in the presence of an adverse childhood environment. Neither a passive nor an evocative genotype-environment correlation accounted for the interaction., Conclusion: This study replicates a recent report of a genotype-environment interaction that predicts individual variation in risk for antisocial behavior in boys.

Background: It is not known if the prevalence of parental psychiatric disorders is higher in stepfather than intact families, or if parental alcoholism is differentially associated with risk for conduct disorder (CD) symptoms in stepfather families versus intact families., Method: The sample comprised 839 girls and 741 boys from 792 intact families and 99 girls and 67 boys from 83 stepfather families from a population-based registry of twins aged between 8 and 17 years. Children's current psychiatric symptoms were assessed at personal interview with the child, mother and father. Parental histories of psychiatric disorder were assessed at personal interview with each residential parent. Associations between CD symptoms and parental alcoholism were characterized using both linear and Poisson regression, and results are presented with and without adjustment for maternal drug use during pregnancy, parental conflict, and estimated socioeconomic status (SES) based on census tract data., Results: Mothers from stepfather families had a higher lifetime prevalence of alcoholism, antisocial personality disorder, depression and social phobia than mothers from intact families. Stepfathers had a higher lifetime prevalence of alcoholism and depression than biological fathers from intact families. Children from stepfather families had more externalizing (CD/ODD) symptoms than children from intact families. Girls who lived with an alcoholic stepfather had significantly more CD symptoms than girls who lived with an alcoholic biological father. Boys who lived with an alcoholic stepfather had significantly fewer CD symptoms than boys who lived with an alcoholic biological father. This sex difference was statistically significant. Adjustment for maternal drug use during pregnancy, parental conflict, and estimated SES based on census tract data did not change these findings., Conclusions: Children living in stepfather families are exposed to more parental psychiatric risk factors than children from intact families. The increased risk for CD symptoms in girls (but not boys) from stepfather families is partly mediated by or associated with the stepfather's history of alcoholism.

Background: We undertook this study to determine whether the widely replicated link between maternal smoking and conduct disturbance (Cd) is better explained by a model of direct causation or of mother-offspring transmission of a latent Cd variable., Methods: Family data collected on 538 adolescent twin boys from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) was used to compare two alternative models: 1) a model composed of a latent transmissible factor that influences mother's juvenile conduct symptoms, smoking during pregnancy, and subsequent Cd and smoking in her adolescent boys; and 2) a model specifying a direct causal path from mother's smoking to child Cd., Results: The maternal-offspring transmission model fit the data as well as a model specifying a direct causal path from maternal smoking to child Cd., Conclusions: Our results suggest that the association between maternal smoking during pregnancy and boys' Cd symptoms may be attributed to the transmission of a latent Cd factor and not to a direct effect of the smoking. Our results challenge previous findings of a direct effect of prenatal smoke exposure on risk to Cd once other etiologic factors are considered.

Background: The aim was to compare the psychometric properties of absolute versus differential ratings of the within-family environments and to examine their associations with conduct problems in 8-16-year-old twins., Methods: The sample comprised 1117 pairs of like-sex male and female twins and their parents, recruited from the school population of Virginia. The within-family environment was assessed from the Twin Inventory of Relationships and Experiences (TIRE), which provided measures of differential parental criticism, parental preference for one twin, and twins' peers' conduct problems, as rated by mothers, fathers and each of the twins. Twins' conduct problems were assessed by a modified version of the Olweus questionnaire., Results: Although differential ratings and absolute ratings had similar psychometric properties, the use of absolute ratings to differentiate the twins resulted in a construct with weak inter-rater agreement and low stability over time. Differential ratings of the twins' environment showed significant associations with differences in conduct problems between the twins, whereas the difference in absolute ratings of each twin did not. The differential parental criticism effect was uninfluenced by the overall level of criticism in the family., Conclusions: A direct contrast between siblings or twins, as part of the rating procedure (as provided by differential ratings), may be a more efficient way to assess aspects of the within-family environment that are reliable and which are associated with psychopathology. Both differential parental criticism and peers' conduct disturbance were associated with conduct problems in the twins.

In this report we characterize associations between parental psychiatric disorders and children's psychiatric symptoms and disorders using a population-based sample of 850 twin families. Juvenile twins are aged 8-17 years and are personally interviewed about their current history of DSM-III-R conduct, depression, oppositional-defiant, overanxious, and separation anxiety disorders using the CAPA-C. Mothers and fathers of twins are personally interviewed about their lifetime history of DSM-III-R alcoholism, antisocial personality disorder, generalized anxiety disorder, major depression, panic disorder/agoraphobia, social phobia, and simple phobia using a modified version of the SCID and the DIS. Generalized least squares and logistic regression are used to identify the juvenile symptoms and disorders that are significantly associated with parental psychiatric histories. The specificity of these associations is subsequently explored in a subset of families with maternal, plus parental psychiatric histories with a prevalence > 1%. Parental depression that is not comorbid or associated with a different spousal disorder is associated with a significantly elevated level of depression and overanxious disorder symptoms and a significantly increased risk for overanxious disorder. Risks are higher for both symptomatic domains in association with maternal than paternal depression, and highest in association with maternal plus paternal depression. Risks for other juvenile symptoms and disorders index the comorbid and spousal histories with which parental depression is commonly associated. Paternal alcoholism that is not comorbid or associated with a maternal disorder is not significantly associated with current psychiatric symptoms or disorders in offspring. Risks for oppositional-defiant or conduct symptoms/disorders in the offspring of alcoholic parents index parental comorbidity and/or other spousal histories. [ABSTRACT FROM AUTHOR]

We introduce an overlapping cohort sequential longitudinal study of behavioral development and psychopathology in a representative sample of 1412 pairs of twins aged 8 through 16 years. Multiple phenotypic assessments involve a full psychiatric interview with each child and each parent, and supplementary parental, teacher, and child interview material and questionnaires. For the first wave of assessments, the numbers of reported DSM-III-R symptoms of Major Depressive Disorder (MDD), Separation Anxiety Disorder (SAD), Overanxious Disorder (OAD), Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), and Attention Deficit Hyperactivity Disorder (ADHD), assessed through interviews, confirm patterns of age and sex trends found in other epidemiological samples, but underscore their dependence on whether the child or the parent is the informant. Correlations across domains for symptoms reported by the same informant are often as large as correlations across informants for the same domain of symptoms. Factor analyses of these symptom counts, taking account of informant view and unreliability of assessment, show the high degree of correlation between SAD and OAD, between MDD and OAD, and between CD and ODD. ADHD symptoms are relatively independent of the other domains, but show moderate correlations with CD, ODD, and MDD. Factorially derived dimensional questionnaire scales, based on child, parental, and teacher reports, show patterns of relationship to symptom counts consistent with both convergent and discriminant validity as indices of liability to clinical symptoms. Across informants, questionnaire scales provide as good a prediction of symptoms as do clinical interviews. Multitrait-multimethod confirmatory factor analysis reveals the patterns of relationship between symptoms of psychiatric disorder in children taking due account of informant and unique sources of variance. Gender differences are consistent within the correlated clusters of ODD/CD and MDD/SAD/OAD, although there are disorder-specific age trends. There are large informant-specific influences on the reporting of symptoms in clinical interviews. Dimensional questionnaire scales provide a useful source of additional information. In subsequent analyses of genetic and environmental etiology of childhood psychopathology we must expect that results may differ by informant and method of assessment. Multivariate and developmental analyses that explore the sources of these differences will shed new light on the relationship between genetic and environmentally influenced vulnerability and the manifestation of psychopathology in specific circumstances. [ABSTRACT FROM AUTHOR]