Co-development of Internalizing Symptoms, Obesity Risk and Relative Pubertal Timing in Adolescence: A Pair of Genetically Informed Investigations

This dissertation sought to contribute a pair of genetically informed studies strategically designed to make potentially causal inferences about potential co-developing processes of internalizing symptoms, body mass index (BMI) and relative pubertal timing during adolescence. Paper 1 used the Early Growth and Development Study (EGDS; N=561), a prospective adopted-at-birth design which primarily accounts for passive gene environment correlation by virtue of youth having been adopted at birth and placed in non-relative adoptive families. Paper 2 used the discordant sibling design from a subsample of siblings from the Adolescent Brain Cognitive Development (ABCD) Study (N=3792), which by design accounts for all confounding of the effects of a risk factor with all shared familial influences that siblings share and all environmental differences that exist between families. The hypothesized associations were further examined in subsamples of twins and MZ twins to make increasingly strict, potentially causal inferences. Across the two studies, I hypothesized that higher internalizing symptoms and higher BMI would positively co-develop at the within person and within family level, respectively for each paper. I hypothesized that there would be unidirectional within person effects of relatively earlier pubertal development on higher internalizing symptoms, across both studies. Finally, I hypothesized that there would be positive co-development of higher BMI and earlier relative pubertal timing early on in both studies, but that only higher BMI would continue to unidirectionally predict earlier relative pubertal timing across the two studies’ ends. In paper 1, specific hypotheses were completely unsupported. In Paper 2, hypotheses were partially supported for two of out three pairs of phenotypes. Specifically, there was evidence of one within family cross-lagged effect between higher discordance in internalizing symptoms at age 10 and higher discordance in BMI at age 11. There was also evidence of one within family cross-lagged effect between higher discordance in relative pubertal timing at age 12 and higher discordance in internalizing symptoms at 13. Findings from both papers indicated that the association between BMI and relative pubertal timing is likely largely confounded by common stable between person, stable discordance, and stable family average factors. Implications and limitations are discussed.