Life stress and cortisol reactivity: An exploratory analysis of the effects of stress exposure across life on HPA-axis functioning

TLDR

Stressful experiences influence the HPA axis and are linked to poorer health, yet the impact of stressors at different developmental stages on adult cortisol reactivity remains poorly understood. The study examined how cumulative, biological embedding, and sensitization models of life stress predict cortisol reactivity to a modified Trier Social Stress Test in a 37‑year longitudinal high‑risk birth cohort. Using 112 participants from a long‑term birth cohort, the authors assessed cortisol responses to a modified TSST to test the three stress‑reactivity models. Results showed that cumulative and early‑life stress predicted blunted cortisol responses, with early childhood stress having a stronger effect than cumulative stress, and middle‑childhood stress also associated with reduced reactivity.

Abstract

Abstract Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.