Prenatal and childhood stress exposure and the sex specific response to psychosocial stress in adulthood.

Background: Early life stress exposures may cause dysregulation of the Hypothalamic Pituitary Adrenal (HPA)-axis and cortisol production, with timing and sex-specific effects. Studies examining the impact of early life stress on cortisol responses to stress have focused on severe trauma and have produced inconsistent results. The aim of this study was to investigate whether common early life stressors, experienced prenatally or throughout childhood and adolescence, play a role in the dysregulation of the HPA-axis in early adulthood.

Methods: Exposures to common life stress events were examined prenatally and as longitudinal trajectories of stress exposure from birth to age 17 in males and females from Gen2 of the Raine Study. At age 18 years, 986 participants were assessed for their salivary cortisol response to a psychosocial stressor - the Trier Social Stress Test (TSST).

Results: In males there was an association between high prenatal stress exposure at 18 weeks gestation and a heightened TSST response. We found evidence for sex-specific associations with increasing stress exposure during adolescence (the ascending trajectory) whereby males were more likely to be non-responders to the TSST and females were more likely to be responders.

Conclusion: Our results point to sex differences in how stress exposure in-utero and exposure increasing during adolescence may affect regulation of the HPA-axis later in life. However, overall common life stress events experienced in-utero, during childhood and adolescence show limited impact on the HPA-axis stress response in early adulthood.