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Prior work has suggested that inter-parental conflict likely plays an etiological role in child behavior problems. However, family-level measurement of inter-parental conflict in most traditional child twin studies has made it difficult to tease apart the specific causal mechanisms underlying this association. The Children's Perception of Inter-parental Conflict scale (CPIC) provides a child-specific measurement tool for examining these questions, as its subscales tap multiple dimensions of conflict assessed from the child's (rather than the parent's) perspective. The current study examined (1) the degree of genetic and environmental influence on each of the CPIC subscales, and (2) etiological contributions to the covariation between the CPIC scales and parental reports of child behavioral problems. The CPIC was completed by 1,200 child twins (aged 6-11 years) from the Michigan State University Twin Registry (MSUTR). Parents completed the Child Behavior Checklist (CBCL) to assess child internalizing and externalizing behavior problems. Multivariate models were examined to evaluate the relative contributions of genetic and environmental factors to both the CPIC scales and to their overlap with child behavioral outcomes. Modeling results indicated no significant moderation of sex or age. Significant environmental overlap emerged between the CPIC conflict properties scale and child internalizing and externalizing problems. By contrast, significant genetic correlations emerged between the CPIC self-blame scale and externalizing problems as well as between the CPIC threat scale and internalizing problems. Overall, findings suggest that the subscales of the CPIC are somewhat etiologically diverse and may provide a useful tool for future investigations of possible gene-environment interplay.

A recent meta-analysis of 103 studies Burt ("Clinical Psychology Review," 29:163-178, 2009a) highlighted the presence of etiological distinctions between aggressive (AGG) and non-aggressive rule-breaking (RB) dimensions of antisocial behavior, such that AGG was more heritable than was RB, whereas RB was more influenced by the shared environment. Unfortunately, behavioral genetic research on antisocial behavior to date (and thus, the research upon which the meta-analysis was based) has relied almost exclusively on the classical twin model. This reliance is problematic, as the strict assumptions that undergird this model (e.g., shared environmental and dominant genetic influences are not present simultaneously; there is no assortative mating) can have significant consequences on heritability estimates when they are violated. The nuclear twin family model, by contrast, allows researchers to relax and statistically evaluate many of the assumptions of the classical twin design by incorporating parental self-report data along with the more standard twin data. The goal of the current study was thus to evaluate whether prior findings of etiological distinctions between AGG and RB persisted when using the nuclear twin family model. We examined a sample of 312 child twin families from the Michigan State University Twin Registry. Results strongly supported prior findings of etiological distinctions between AGG and RB, such that broad genetic influences were observed to be particularly important to AGG whereas shared environmental influences contributed only to RB. Nevertheless, the current findings also implied that additive genetic influences on antisocial behavior may be overestimated when using the classical twin design.

Identification of gene x environment interactions (GxE) for attention-deficit hyperactivity disorder (ADHD) is a crucial component to understanding the mechanisms underpinning the disorder, as prior work indicates large genetic influences and numerous environmental risk factors. Building on prior research, children's appraisals of self-blame were examined as a psychosocial moderator of latent etiological influences on ADHD via biometric twin models, which provide an omnibus test of GxE while managing the potential confound of gene-environment correlation. Participants were 246 twin pairs (total n = 492) ages 6-16 years. ADHD behaviors were assessed via mother report on the Child Behavior Checklist. To assess level of self-blame, each twin completed the Children's Perception of Inter-parental Conflict scale. Two biometric GxE models were fit to the data. The first model revealed a significant decrease in genetic effects and a significant increase in unique environmental influences on ADHD with increasing levels of self-blame. These results generally persisted even after controlling for confounding effects due to gene-environment correlation in the second model. Results suggest that appraisals of self-blame in relation to inter-parental conflict may act as a key moderator of etiological contributions to ADHD.

There are two common approaches to sub-typing the well-documented heterogeneity within antisocial behavior: age-of-onset (i.e., childhood-onset versus adolescence-onset; see "Moffitt" 1993) and behavioral (i.e., physical aggression versus non-aggressive rule-breaking). These approaches appear to be associated, such that aggression is more characteristic of childhood-onset antisocial behavior whereas rule-breaking is linked to both child- and adolescence-onset antisocial behavior. However, it remains unclear which approach, if either, better explains the heterogeneity within antisocial behavior. We examined this question in a prospective sample of male twins, assessed at the ages of 11, 14, 17, and 24 years. Although the age-of-onset subtypes predicted adult antisocial behavior in the expected direction when analyzed alone, this association dissipated once we controlled for aggression and rule-breaking. Such findings suggest that the behavioral sub-types of antisocial behavior may be a stronger predictor of later antisocial outcomes than is its age-of-onset.

It has recently been argued that shared environmental influences are moderate, identifiable, and persistent sources of individual differences in most forms of child and adolescent psychopathology, including antisocial behavior. Unfortunately, prior studies examining the stability of shared environmental influences over time were limited by possible passive gene-environment correlations, shared informants effects, and/or common experiences of trauma. The current study sought to address each of these limitations. We examined adolescent self-reported antisocial behavior in a 3.5 year longitudinal sample of 610 biological and adoptive sibling pairs from the Sibling Interaction and Behavior Study (SIBS). Results revealed that 74-81% of shared environmental influences present at time 1 were also present at time 2, whereas most non-shared environmental influences (88-89%) were specific to a particular assessment period. Such results provide an important constructive replication of prior research, strongly suggesting that shared environmental contributions to antisocial behavior are systematic in nature.

Few genetically-informative studies have attempted to explicitly identify the "shared environmental" (i.e., those environmental influences that contribute to sibling similarity) factors now known to contribute to adolescent delinquency. The current study therefore examined whether the parent-child relationship served as one source of these shared environmental influences. Participants were 610 adoptive and biological families from the Sibling Interaction and Behavior Study (SIBS). Parents and adolescents reported on their parent-child conflict and parental involvement with child, and adolescents reported on their own delinquent behaviors. We employed structural equation modeling and supplementary multilevel modeling, finding consistent evidence that the association between delinquency and the parent-child relationship is at least partially shared environmental in origin. Such findings provide an important extension of previous twin studies, as they suggest that passive genotype-environment correlations do not explain earlier findings of shared environmental influences on this association.

Prior research has suggested that disadvantaged neighborhood contexts alter the etiology of youth antisocial behavior (ASB). Unfortunately, these studies have relied exclusively on governmental data collected in administratively-defined neighborhoods (e.g., Census tracts or block groups, zip codes), a less than optimal approach for studying neighborhood effects. It would thus be important to extend prior findings of GxE using neighborhood sampling techniques, in which disadvantage is assessed via resident informant-reports of the neighborhood. The current study sought to do just this, examining two independent twin samples from the Michigan State University Twin Registry. Neighborhood disadvantage was assessed via maternal and neighbor informant-reports, the latter of which were analyzed multiple ways (i.e., all neighbors within 1 km, nearest neighbor, and all neighbors within the County). Analyses revealed clear and consistent evidence of moderation by neighborhood disadvantage, regardless of informant or the specific operationalization of neighborhood. Shared environmental influences on ASB were observed to be several-fold larger in disadvantaged contexts, while genetic influences were proportionally more influential in advantaged neighborhoods. Such findings indicate that neighborhood disadvantage exerts rather profound effects on the origins of youth ASB. Efforts should now be made to identify the active ingredients of neighborhood disadvantage. [ABSTRACT FROM AUTHOR]

There is a strong relationship between sleep and behavioral problems. These findings are often interpreted via environmental explanations, such that poor sleep directly exacerbates or causes symptoms of aggression and behavior problems. However, there are other possible explanations, such that the genes predicting poor sleep also predict aggression or rule-breaking. The current study sought to elucidate the origin of this relationship. The sample was composed of 1030 twin pairs (426 monozygotic and 604 dizygotic). The sample was 51.3% male with a mean age of 8.06 years (range 6-11.96; SD = 1.45). Aggression, rule-breaking and sleep were assessed through the Child Behavior Checklist (CBCL). We fitted bivariate Cholesky genetic models to the data, decomposing the variance within, and the covariance among, aggression, rule-breaking, and sleep functioning into their genetic and environmental components. Genetic correlations between all sleep variables and aggression were significant and moderate to large in magnitude, but mostly small and non-significant between sleep and rule-breaking. We did not find evidence of a causal or environmental relationship between the majority of sleep variables and aggression, but rather clear evidence of genetic pleiotropy. However, the pattern of associations between rule-breaking and sleep measures was less consistent. Aggression and rule-breaking appear to be differentially associated with sleep. [ABSTRACT FROM AUTHOR]

Although the phenomenology of overt or aggressive antisocial behavior during childhood is well-documented, far less is known about covert or non-aggressive, rule-breaking (RB) antisocial behavior. Gaps in knowledge include issues as basic as RB's typical symptom presentation during childhood and which symptoms differ across sex. The current study sought to fill these gaps in the literature by establishing the prevalence and psychometric properties of specific RB behaviors in a sample of 1022 twin boys and 1010 twin girls between the ages of 6 and 10 years. Legal RB behaviors (e.g., breaking rules, swears, lying or cheating) were present to varying degrees in most children, regardless of whether or not they passed the clinical threshold for RB. They were also more common in boys than in girls regardless of their clinical status. In sharp contrast, illegal RB behaviors (e.g., stealing, vandalism, setting fires) were rarely observed in typically-developing children, but were seen at moderate levels in boys and girls with clinically-significant levels of RB. Moreover, sex differences in illegal RB behaviors were observed only for those youth with clinically meaningful levels of RB. Such findings collectively imply that while legal RB behaviors can be found (albeit at different frequencies) in children with and without clinically meaningful levels of RB, illegal RB behaviors may function as relatively 'unambiguous' indicator of clinically-significant levels of RB. [ABSTRACT FROM AUTHOR]

Prior studies have indicated that the relationship between parent-child conflict and adolescent antisocial behavior is at least partially shared environmental in origin. However, all available research on this topic (to our knowledge) relies exclusively on parent and/or adolescent informant-reports, both of which are subject to various forms of rater bias. As the presence of significant shared environmental effects has often been attributed to rater bias in the past (Baker et al. Journal of Abnormal Psychology 16:219-235, ; Bartels et al. Journal of the American Academy of Child and Adolescent Psychiatry 42:1351-1359, , Twin Research 7:162-175, ; Hewitt et al. Behavior Genetics 22:293-317, ), it would be important to confirm that findings of shared environmental mediation persist when even examining (presumably more objective) observer-ratings of these constructs. The current study thus examined the origins of the relationship between parent-child conflict and adolescent acting-out behavior, as measured using both observer-ratings and various informant-reports. Participants included 1,199 adopted and non-adopted adolescents in 610 families from the Sibling Interaction and Behavior Study (SIBS). Results indicated that parent-child conflict consistently predicts acting-out behavior in adopted adolescents, and moreover, that this association is equivalent to that in biologically-related adolescents. Most importantly, these findings did not vary across parent- and adolescent-reported or observer-ratings of parent-child conflict and acting-out behavior. Such findings argue strongly against rater bias as a primary explanation of shared environmental mediation of the association between parent-child conflict and adolescent antisocial behavior. [ABSTRACT FROM AUTHOR]