Associations between childhood family stress and systemic inflammation in adulthood: Contributions of pubertal timing and waist circumference in adolescence.
TL;DR
Associations between childhood family stress and inflammation in early adulthood among women are examined, considering pubertal timing and adolescent adiposity as potential biobehavioral mediators as well as differences by race.
Abstract
Objective
Evidence from retrospective studies suggests that childhood experiences relate to levels of systemic inflammation across the lifespan, particularly for women. This prospective study examined associations between childhood family stress and inflammation in early adulthood among women, considering pubertal timing and adolescent adiposity as potential biobehavioral mediators as well as differences by race.
Method
The sample included 1,362 participants of the Pittsburgh Girls Study followed from middle childhood to adulthood. Childhood family stress was estimated as a second-order latent variable from measures of harsh punishment, caregiver-partner conflict, and caregiver depression assessed annually between ages 5 and 9. Inflammation was measured as plasma levels of interleukin-6 (IL-6) (Mage = 23.57 years). Household receipt of public assistance between ages 5 and 9 was included as a binary covariate. Age at menarche and waist circumference at age 12 served as mediators in structural equation models.
Results
Greater childhood family stress was associated with higher levels of IL-6 in early adulthood, independently of household public assistance (β = .10, p = .011). Childhood family stress was also indirectly related to adult IL-6 via pubertal timing (β = .01, confidence interval [0.000, 0.004]) and waist circumference (β = .05, confidence interval [0.002, 0.021]). When modeling both mediators together, only waist circumference contributed independent variance to the association between childhood family stress and adult IL-6, and results varied by race.
Conclusions
Stress within the childhood family environment may relate to long-term systemic inflammation, both directly and indirectly through pubertal timing and adolescent adiposity, independently of household public assistance. The identification of life course cascades underlying cardiometabolic risk could inform early health promotion efforts. (PsycInfo Database Record (c) 2026 APA, all rights reserved).