Sara Jaffee

Longitudinal, epidemiological studies have identified robust risk factors for youth antisocial behavior, including harsh and coercive discipline, maltreatment, smoking during pregnancy, divorce, teen parenthood, peer deviance, parental psychopathology, and social disadvantage. Nevertheless, because this literature is largely based on observational studies, it remains unclear whether these risk factors have truly causal effects. Identifying causal risk factors for antisocial behavior would be informative for intervention efforts and for studies that test whether individuals are differentially susceptible to risk exposures. In this article, we identify the challenges to causal inference posed by observational studies and describe quasi-experimental methods and statistical innovations that may move researchers beyond discussions of risk factors to allow for stronger causal inference. We then review studies that used these methods, and we evaluate whether robust risk factors identified from observational studies are likely to play a causal role in the emergence and development of youth antisocial behavior. There is evidence of causal effects for most of the risk factors we review. However, these effects are typically smaller than those reported in observational studies, suggesting that familial confounding, social selection, and misidentification might also explain some of the association between risk exposures and antisocial behavior. For some risk factors (e.g., smoking during pregnancy, parent alcohol problems), the evidence is weak that they have environmentally mediated effects on youth antisocial behavior. We discuss the implications of these findings for intervention efforts to reduce antisocial behavior and for basic research on the etiology and course of antisocial behavior.

Early childhood antisocial behaviour is a strong prognostic indicator for poor adult mental health. Thus, information about its etiology is needed. Genetic etiology is unknown because most research with young children focuses on environmental risk factors, and the few existing studies of young twins used only mothers' reports of behaviour, which may be biased. We investigated genetic influences on antisocial behaviour in a representative-plus-high-risk sample of 1116 pairs of 5-year-old twins using data from four independent sources: mothers, teachers, examiner-observers previously unacquainted with the children, and the children themselves. Children's antisocial behaviour was reliably measured by all four informants; no bias was detected in mothers', teachers', examiners', or children's reports. Variation in antisocial behaviour that was agreed upon by all informants, and thus was pervasive across settings, was influenced by genetic factors (82%) and experiences specific to each child (18%). Variation in antisocial behaviour that was specific to each informant was meaningful variation, as it was also influenced by genetic factors (from 33% for the children's report to 71% for the teachers' report). This study and four others of very young twins show that genetic risks contribute strongly to population variation in antisocial behaviour that emerges in early childhood. In contrast, genetic risk is known to be relatively modest for adolescent antisocial behaviour, suggesting that the early-childhood form has a distinct etiology, particularly if it is pervasive across situations.

The disciplines of developmental psychopathology and behavior genetics are concerned with many of the same questions about the etiology and course of normal and abnormal behavior and about the factors that promote typical development despite the presence of risk. The goal of this paper is to summarize how research in behavior genetics has shed light on questions that are central to developmental psychopathology. We briefly review the origins of behavior genetics, summarize the findings that have been gleaned from several decades of quantitative and molecular genetics research, and describe future directions for research that will delineate gene function as well as pathways from genes to brain to behavior. The importance of environmental contributions, at both genetic and epigenetic levels, will be discussed. We conclude that behavior genetics has made significant contributions to developmental psychopathology by documenting the interplay among risk and protective factors at multiple levels of the organism, by clarifying the causal status of risk exposures, and by identifying factors that account for change and stability in psychopathology. As the tools to identify gene function become increasingly sophisticated, and as behavioral geneticists become increasingly interdisciplinary in their scope, the field is poised to make ever greater contributions to our understanding of typical and atypical development.

BackgroundObservational studies consistently have identified that social support is negatively associated with depression among adolescents. The causal connections between these two factors, however, are not well understood. Does the relationship between social support and depression indicate that social support protects against depression, or that characteristics of these less depressed adolescents make it easier for them to obtain social support? To