Associations of Severity of Early Life Stress with Coupling of Cortisol and DHEA Across Puberty

• In Event: 3-069 - Multimodal Investigation of Childhood Adversity, Stress System Regulation, and Adolescent Physical and Mental Health

Integrative Statement

Background: Early life stress (ELS) has been associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis undergoes changes during the transition to puberty; moreover, the effect of ELS on the HPA axis may differ as a function of pubertal status (King et al., 2017; Quevedo et al., 2012). We know less, however, about how hormonal changes associated with pubertal maturation, including increases in adrenal hormones, are related to changes in HPA axis functioning. In the current study, we examined the effect of ELS on the coupling of cortisol and a pubertal androgen, dehydroepiandrosterone (DHEA), across puberty.
Method: Youth ages 9-13 years (55% female; N=146) completed assessments of ELS, cortisol, and DHEA during earlier puberty (Time 1 [T1]; mean Tanner stage for boys = 1.89 [0.61]; mean Tanner stage for girls = 2.12 [.78]). Ninety of these participants returned for a follow-up assessment two years later (Time 2 [T2]). At T1, children completed interviews about their lifetime exposure to stressful events, and trained coders rated the objective severity of each endorsed event on a scale from 0 (no impact) to 4 (extremely severe). Using these ratings, we calculated an index of the severity of threat-related ELS by summing ratings for interpersonally harmful and potentially life-threatening events. Finally, at each time point, children provided saliva samples at waking for the analysis of cortisol and DHEA.
Results: Both waking cortisol (t(89)=2.07, p=.041) and waking DHEA (t(89)=3.19, p=.002) increased significantly from T1 to T2. DHEA was positively associated with cortisol at both time points (T1: r(144)=.34; T2: r(88)=.47), and this association was marginally stronger at T2 than at T1 (Figure 1). Increases in DHEA from T1 to T2 were associated with increases in cortisol across this period (B=0.23, SE=0.08, t(84)=2.79, 95% CI [.07, .38], p=.006). Further, the severity of threatening ELS interacted with change in DHEA from T1 to T2 to explain change in cortisol (B=-0.09, SE=0.04, t(83)=-2.47, 95% CI [-.17, -.02], p=0.016). Simple slopes analyses indicated that whereas children who were exposed to less severe ELS evidence significantly positive coupling of cortisol and DHEA from T1 to T2 (B=0.47, SE=0.13, t(83)=3.67, 95% CI [-.45, -.25], p<.001), children who were exposed to more severe ELS evidenced non-significant and comparatively blunted coupling of cortisol and DHEA across this period (B=0.11, SE=0.09, t(83)=1.24, 95% CI [-.07, .29], p=0.219; Figure 2). Sex did not moderate any of these effects.
Conclusion: These findings indicate that hormonal changes associated with pubertal maturation, specifically increases in DHEA, are associated with changes in cortisol production across this developmental period. Puberty is hypothesized to be a sensitive period during which the neurobiological effects of environmental adversity emerge or change (Piekarski et al., 2016). Exposure to more severe ELS appears to be associated with deviations from a normative pattern of positive coupling of cortisol and DHEA with advancing puberty. Longitudinal data, which are forthcoming, will allow for tests of whether the lack of coordination between these two hormones have implications for mental and physical health across the transition to puberty.

Authors

• Lucy S. King, Stanford University, Department of Psychology
  Presenting Author

• Madelaine Graber, Stanford University, Department of Psychology
  Non-Presenting Author

• Ian H. Gotlib, Stanford University, Department of Psychology
  Non-Presenting Author