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Briley, D. A.

Publications and source records attributed to Briley, D. A..

2 recordsLinked to original sources

Weak and uneven associations of home, neighborhood and school environments with stress hormone output across multiple time scales.

The progression of lifelong trajectories of socioeconomic inequalities in health and mortality begins in childhood. Dysregulation in cortisol, a stress hormone that is the primary output of the hypothalamus-pituitary-adrenal (HPA) axis, has been hypothesized to be a mechanism for how early environmental adversity compromises health. However, despite the popularity of cortisol as a biomarker for stress and adversity, little is known about whether cortisol output differs in children being raised in socioeconomically disadvantaged environments. Here, we show that there are few differences between advantaged and disadvantaged children in their cortisol output. In 8- to 14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different time-scales: (1) diurnal fluctuation in salivary cortisol (n = 400), (2) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (3) and cortisol concentration in hair (n = 1,210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We then tested differences in cortisol output across nine aspects of social disadvantage at the home (e.g., family socioeconomic status), school (e.g., average levels of academic achievement), and neighborhood (e.g., concentrated poverty). Children living in neighborhoods with higher concentrated poverty had higher diurnal cortisol output, as measured in saliva; otherwise, child cortisol output was unrelated to any other aspect of social disadvantage. Overall, we find limited support for alteration in HPA axis functioning as a general mechanism for the health consequences of socioeconomic inequality in childhood.

physiology↗

Genetic and Environmental Influences on Pubertal Hormones in Human Hair across Development

Background: Puberty is a complex biopsychosocial process that is linked to an array of psychiatric and medical disorders that emerge in adolescence and persist across the lifespan. 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.\n\nMethods: In an ethnically and socioeconomically diverse sample of 1,286 child and adolescent twins and multiples from 672 unique families, we estimated genetic and environmental influences on concentrations of testosterone, DHEA, and progesterone in hair across the period of 8 to 18 years of age.\n\nResults: We identified sex-specific developmental windows of maximal heritability in each hormone. Peak heritability for DHEA occurred at age 9.8 years for males and 10.0 years for 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.\n\nConclusion: This is the first study of genetic influences on pubertal hormone concentrations in human hair and is the largest of the heritability of pubertal hormones in any form. 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.

genetics↗