Life history theory posits father absence and associated stressors are key for regulating the development of reproductive phenotypes. The causal status of father absence has been questioned, however, because genetic confounding can account for this association. The purpose of the current study was to replicate and extend prior work that evaluated the androgen receptor gene’s (AR) contribution to the interrelations between father absence and daughters’ age at menarche (AAM) and sexual behaviors by evaluating the GGC, as well as the better characterized CAG polymorphisms. Using structural models on a sample of 269 Caucasian women, we found no evidence to support the genetic confounding hypothesis, though a main effect of CAG variation on earlier AAM was detected independent of father absence. In addition, we tested the hypothesis that associations between father absence and daughter’s sexual behaviors would be mediated by AAM and that indirect effects of father absence would be conditioned by AR variation. Results showed AR variation moderated the association between father absence and AAM and the indirect effects of father absence on daughter’s sexual behaviors, most strongly by the CAG repeat. Implications of these results are discussed in terms of genetic contributions to life history phenotypes and importance of examining gene–environment transactions.

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The most extensively studied influence on adolescent conduct problem behaviors is peers, and the literature points to genetics as one source of individual differences in peer influence. The purpose of this study was to test the hypothesis that an environmental sensitivity genetic index comprised of DRD4, 5‐HTTLPR, and GABRA2 variation would moderate the association between peer and adolescent conduct problems. Latent growth modeling was applied to PROSPER project longitudinal data from adolescents and their peers. Results showed the hypothesis was supported; adolescents with more copies of putative sensitivity alleles were more strongly influenced by their peers. The interaction form was consistent with differential susceptibility in follow‐up analyses. Strengths and weaknesses of genetic aggregates for sensitivity research are discussed.

Background: Meperidine is an opioid analgesic which undergoes N-demethylation by hepatic cytochrome P450 (CYP)