Title: Longitudinal effects of family psychopathology and stress on pubertal maturation and hormone coupling in adolescent twins
Legend: Structural equation modeling of distal and concurrent family factors examining effects on hormone coupling in females. Note: Unstandardized beta coefficients are included first and standard error of the mean in parentheses. All variables were standardized prior to analysis. Hormone coupling variables were the empirical Bayes estimates extracted from the Hierarchical Linear Model (HLM) equations 1–3. The first listed hormone in each square box is the outcome hormone, and the second listed hormone is the predictor hormone. Only paths that were significant at p < .05 (or trend level) shown. Time 1 = 8 years of age. Time 2 = 13 years of age. Puberty = pubertal stage. B = unstandardized beta coefficient. p < .10+, p < .05*, p < .01**, p < .001***
Citation: Phan, J. M., Van Hulle, C. A., Shirtcliff, E. A., Schmidt, N. L., & Goldsmith, H. H. (2021). Longitudinal effects of family psychopathology and stress on pubertal maturation and hormone coupling in adolescent twins. Developmental psychobiology, 63(3), 512–528. https://doi.org/10.1002/dev.22028
Abstract: Adolescents experience profound neuroendocrine changes, including hormone “coupling” between cortisol, testosterone, and dehydroepiandrosterone. Emerging research has only begun to elucidate the role of hormone coupling, its genetic and environmental etiology, and the extent to which coupling is impacted by gender, puberty, and family context. We included measures on parent and child mental health, parenting stress, and family conflict of 444 twin pairs and their parents across two timepoints, when youth were on average 8 and 13 years old, respectively. Structural equation models examined the impact of family context effects on coupling during adolescence. Biometric twin models were then used to probe additive genetic, shared, and non-shared environmental effects on hormone coupling. Hormones were more tightly coupled for females than males, and coupling was sensitive to parental depression and co-twin psychopathology symptoms and stress exposure in females. The association between family context and coupling varied across specific neuroendocrine measures and was largely distinct from pubertal maturation. Biometric models revealed robust shared and non-shared environmental influences on coupling. We found that family antecedents modify the strength of coupling. Environmental influences account for much of the variation on coupling during puberty. Gender differences were found in genetic influences on coupling.
About the Lab: Goldsmith’s research concerns children’s emotional development, behavioral challenges, and the autism spectrum. The research incorporates perspectives of psychology, genetics, neuroscience, and developmental epidemiology. He is recognized as a leading theorist of human temperament and a key empirical contributor to the fields of developmental behavioral genetics and childhood psychopathology. Goldsmith is principal investigator on six external grants, an investigator in three centers, and a faculty member on three training grants. His highly collaborative research involves many UW faculty and colleagues at other institutions. Visit the Wisconsin Twin Research lab for more information.