Genetic and environmental influences on pubertal hormones in human hair across development.

Puberty is a complex biopsychosocial process that can affect an array of psychiatric and medical disorders emerging in adolescence. Although the pubertal process is driven by neuroendocrine changes, few quantitative genetic studies have directly measured puberty-relevant hormones. Hair samples can now be assayed for accumulation of hormones over several months. In contrast to more conventional salivary measures, hair measures are not confounded by diurnal variation or hormonal reactivity. In an ethnically and socioeconomically diverse sample of 1286 child and adolescent twins and multiples from 672 unique families, we estimated genetic and environmental influences on hair concentrations of testosterone, DHEA, and progesterone across the period of 8-18 years of age. On average, male DHEA and testosterone were highly heritable, whereas female DHEA, progesterone, and puberty were largely influenced by environmental components. We identified sex-specific developmental windows of maximal heritability in each hormone. Peak heritability for DHEA occurred at approximately 10 years of age for males and females. Peak heritability for testosterone occurred at age 12.5 and 15.2 years for males and females, respectively. Peak heritability for male progesterone occurred at 11.2 years, while the heritability of female progesterone remained uniformly low. The identification of specific developmental windows when genetic signals for hormones are maximized has critical implications for well-informed models of hormone-behavior associations in childhood and adolescence.

Developmental differences in reward sensitivity and sensation seeking in adolescence: Testing sex-specific associations with gonadal hormones and pubertal development.

Sensation seeking has been found to increase, on average, from childhood to adolescence. Developmental scientists have hypothesized that this change could be driven by the rise of gonadal hormones at puberty, which affect reward-related processing in the brain. In a large, age-heterogeneous, population-based sample of adolescents and young adults (N = 810; ages 13-20 years), we tested for sex-specific associations between age, self-reported pubertal development, gonadal hormones (estradiol and testosterone) as measured in saliva, reward sensitivity as measured by a multivariate battery of in-laboratory tasks (including the Iowa gambling task, balloon analogue risk task, and stoplight task), and self-reported sensation seeking. Reward sensitivity was more strongly associated with sensation seeking in males than females. For both males and females, reward sensitivity was unrelated to age but was higher among those who reported more advanced pubertal development. There were significant sex differences in the effects of self-reported pubertal development on sensation seeking, with a positive association evident in males but a negative association in females. Moreover, gonadal hormones also showed diverging associations with sensation seeking-positive with testosterone but negative with estradiol. Overall, the results indicate that sensation seeking among adolescents and young adults depends on a complex constellation of developmental influences that operate via sex-specific mechanisms. (PsycINFO Database Record

Twin models of environmental and genetic influences on pubertal development, salivary testosterone, and estradiol in adolescence.

OBJECTIVE: Research on sources of variation in adolescent's gonadal hormone levels is limited. We sought to decompose individual differences in adolescent testosterone, estradiol, and pubertal status, into genetic and environmental components. DESIGN: A sample of male and female adolescent twins from the greater Austin and Houston areas provided salivary samples, with a subset of participants providing longitudinal data at 2 waves. PARTICIPANTS: The sample included 902 adolescent twins, 49% female, aged 13-20 years (M = 15.91) from the Texas Twin Project. Thirty-seven per cent of twin pairs were monozygotic; 30% were same-sex dizygotic (DZ) pairs; and 33% were opposite-sex DZ pairs. MEASUREMENTS: Saliva samples were assayed for testosterone and estradiol using chemiluminescence immunoassays. Pubertal status was assessed using self-report. Biometric decompositions were performed using multivariate quantitative genetic models. RESULTS: Genetic factors contributed substantially to variation in testosterone in males and females in the follicular phase of their menstrual cycle (h2  = 60% and 51%, respectively). Estradiol was also genetically influenced in both sexes, but was predominately influenced by nonshared environmental factors. The correlation between testosterone and estradiol was mediated by a combination of genetic and environmental influences for males and females. Genetic and environmental influences on hormonal concentrations were only weakly correlated with self-reported pubertal status, particularly for females. CONCLUSIONS: Between-person variability in adolescent gonadal hormones and their interrelationship reflects both genetic and environmental processes, with both testosterone and estradiol containing sizeable heritable components.