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


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 8–14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different timescales: (a) diurnal fluctuation in salivary cortisol (n = 400), (b) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (c) cortisol concentration in hair (n = 1210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We 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.

Molecular Psychiatry