The role of environmental disadvantage in the etiologic moderation of children's antisocial behavior - Project Summary/Abstract Disadvantaged contexts come in myriad forms and robustly predict both aggressive and rule-breaking antisocial behavior1,2. These predictions go beyond simple phenotypic associations, with multiple studies now indicating that the respective magnitudes of genetic and environmental influences on antisocial behavior also vary as a function of neighborhood disadvantage, such that genetic influences are most strongly expressed in ‘average, expectable environments’ and stymied in the context of poverty3-5. Although important, prior genotype-environment interaction (GxE) research has been limited by its sole focus on neighborhood indicators, which is only one of several forms of disadvantage that children can experience. It is thus unclear whether other, correlated forms of disadvantage, including familial (e.g., income), school (e.g., subsidized lunch rate), and chemical (e.g., neurotoxicant exposure) disadvantage, also serve as etiologic moderators of antisocial behavior. Additionally, because no GxE study to date has jointly examined multiple indicators of disadvantage, it is unknown whether they increment one another’s effects or whether one form of disadvantage serves as a primary ‘active ingredient’ in extant GxE. The goal of the proposed study is to fill these gaps in the literature by examining multiple forms of disadvantage as etiologic moderators of aggressive and non- aggressive antisocial behavior, respectively. I will use data from a sample of more than 1,000 twin pairs enriched for disadvantage to carry out the following aims: (1) evaluate whether prior findings for neighborhood disadvantage also extend to three other key forms of disadvantage: familial, school, and chemical, and (2) evaluate whether the various forms of disadvantage synergistically moderate the etiology of antisocial behavior. The proposed analyses will include both the classical twin biometric GxE model and a GxE version of the nuclear twin family design, the latter of which allows for far stronger causal inferences by controlling for additional confounds6. In this way, I will be able to illuminate the ‘active ingredients’ of disadvantage for GxE in antisocial behavior for the very first time. By addressing these aims, I will continue to develop a line of research dedicated to understanding how chronic disadvantage alters developmental outcomes. To further prepare for an academic career conducting GxE research, I am seeking additional training to: (1) gain expertise in the measurement and conceptualization of disadvantage as a multifaceted construct, (2) advance my understanding of genetically informative statistical methods, and (3) develop my manuscript and grant-writing skills. This training will meaningfully contribute to my development as an independent researcher focused on understanding the effects of disadvantage on mental health outcomes, both independently and in conjunction with individuals’ genetic predispositions.
