Social aggression (e.g., gossiping, ostracism, and threatening to end a friendship) is a form of antisocial behavior that puts both the victim and perpetrator at increased risk for mental illness and socio-emotional suffering. Social aggression is perpetrated across the lifespan, but our understanding of its developmental origins remain limited, in part because the biological factors involved remain understudied. Furthermore, sex differences in its perpetration, which has remained a primary area of investigation since the field’s inception, remain inconclusive, in part due to key moderating factors not being considered. Therefore, the purpose of this dissertation was to identify and integrate distinct biological risk factors (e.g., sex, genes, pubertal development, and neurological processes) to explore whether their interactions can help resolve extant inconsistencies in the literature regarding the development and presentation of social aggression. We capitalized on a unique longitudinal twin study of emotional and behavioral development that consists of both childhood and adolescent waves of data collection. First, we took a behavioral genetic approach to examining the roles of sex, genes, and puberty on the etiology of social aggression. One of the most striking findings from this investigation was that although univariate results were consistent with prior research suggesting that there were no sex differences in the etiology of social aggression, a two-moderator GxE model indicated that there were indeed sex differences in the etiology of social aggression once we adjusted for the effects of puberty. Not only were genetic influences on social aggression were stronger for boys than for girls and non-shared environmental influences were stronger for girls than for boys once we adjusted for puberty, but they were also jointly moderated by sex and puberty together such that genetic influences more than doubled from pre-puberty to puberty in girls but not boys. Second, we took a neuroscience approach to examining the roles of sex and pubertal development on the association between social aggression and neural functioning. Specifically, we examined the association between social aggression and amygdala reactivity during a socio-emotional face processing task. Although we anticipated finding that social aggression was associated with increased amygdala reactivity, we observed that social aggression was not associated with amygdala reactivity during this task, even after controlling for sex, age, puberty, and their interactions. Although we did not observe associations between neural activation and social aggression, neuroscience studies remain a promising area of future investigation.Taken together, the analyses conducted in this dissertation emphasize the importance of taking a developmental psychopathology approach to studying social aggression. The defining features of developmental psychopathology include investigating psychopathology developmentally, across all relevant levels of analysis, and consideration of the interactions between puberty and sex did indeed led to new insights into the etiology of social aggression. Future research should continue to employ longitudinal and person-centered approaches to investigate social and biological risk factors and processes implicated in social aggression across time.
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