Our results suggest that maternal CMV infections may influence ASD symptoms. These findings are being further evaluated in ongoing prospective studies with larger population samples.

Sex differences in the etiology of youth antisocial behavior are an intuitively appealing hypothesis given the consistently higher prevalence of antisocial behavior in boys versus girls. Although a few early studies supported this possibility, reporting stronger genetic influences in females and stronger environmental influences in males, subsequent meta-analyses found that antisocial behavior was equally heritable in males and females. Critically however, none of the meta-analyses evaluated whether sex differences in etiology might be enhanced in particular subpopulations or contexts. The current study sought to do just this. We examined 1,030 child twin pairs from the Michigan State University Twin Registry, half of whom were oversampled for neighborhood disadvantage, thereby allowing us to meaningfully evaluate whether sex differences in etiology were enhanced in disadvantaged contexts. We also directly evaluated the possibility of sex differences in the etiology of teacher- versus maternal-informant reports of antisocial behavior, evaluating each informant-report for possible sex differences. Results were not consistent with differential effects of sex on etiology in disadvantaged versus advantaged contexts, but did suggest moderation by informant-report. Namely, genetic influences were stronger in girls, and environmental influences were stronger in boys, when antisocial behavior was assessed using teacher informant-reports, but not when assessed using maternal informant-reports. Critically, these findings were confirmed when we reanalyzed meta-analytic data from Burt (2009a) separately by informant. Such findings suggest that, at least in school contexts, the etiology of antisocial behavior does indeed vary across sex. Implications are discussed. (PsycINFO Database Record

BackgroundPrior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature.MethodsWe examined maternal and teacher reports of youth physical and social aggression in over 1000 6–10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed.ResultsThe covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50–57% of the genetic factors, 74–100% of the shared environmental factors, and 28–40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex.ConclusionsThese findings argue against the common assumption that social aggression is the ‘female version’ of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology.

Available twin-family data on sex differences in antisocial behavior (ASB) simultaneously suggest that ASB is far more prevalent in males than in females, and that its etiology (i.e. the effects of genes, environments, hormones, culture) does not differ across sex. This duality presents a conundrum: How do we make sense of mean sex differences in ASB if not via differences in genes, environments, hormones, and/or cultures? The current selective review and critique explores possible contributions to these seemingly incompatible sets of findings. We asked whether the presence of sex differences in behavior could be smaller than is typically assumed, or confined to a specific set of behaviors. We also asked whether there might be undetected differences in etiology across sex in twin-family studies. We found little evidence that bias or measurement invariance across sex account for phenotypic sex differences in ASB, but we did identify some key limitations to current twin-family approaches. These included the questionable ability of qualitative sex difference analyses to detect gender norms and prenatal exposure to testosterone, and concerns regarding specific analytic components of quantitative sex difference analyses. We conclude that the male preponderance in ASB is likely to reflect a true sex difference in observed behavior. It was less clear, however, that the genetic and environmental contributions to ASB are indeed identical across sex, as argued by prior twin-family studies. It is our hope that this review will inspire the development of new, genetically-informed methods for studying sex differences in etiology.

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 1,022 twin boys and 1,010 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.

Although the specific NTF parameter estimates varied across informants, social aggression generally emerged as largely additive genetic (A = 0.15-0.77) and sibling environmental (S = 0.42-0.72) in origin. Such findings not only highlight an important role for individual genetic risk in the etiology of social aggression, but also raise important questions regarding the role of the environment.