Within-Person Coupling of Changes in Cortisol and DHEA in Response to Acute Stress

Introduction: Changes in output hormones of the hypothalamic-pituitary-adrenal (HPA) axis (i.e., cortisol, dehydroepiandrosterone [DHEA]) have been identified as early indicators of disease vulnerability. To this end, researchers are beginning to explore the within-person “couplings” of changes in HPA-axis hormones and their effect on other bodily systems (e.g., HPG axis). The ways in which cortisol and DHEA respond to stressors together (i.e., coupled responses) versus separately (i.e., uncoupled) may better index the endogenous hormonal environment and provide a more comprehensive characterization of one’s current physiological state. Currently, our understanding of within-person couplings of stress physiology among rural African Americans remains understudied. However, disproportionate burdens of chronic stress exposure make the African American community particularly vulnerable to HPA-axis dysregulations. Observed disparities in health within this population further underscore the need to characterize coupled stress reactivity curves.  This study thus seeks to (1) characterize within-person couplings of HPA-axis hormones in response to acute stress among rural African American emerging adults, and (2) identify relevant predictors of HPA-axis reactivity to acute stress.

Methods: Participants were 60 (63.3% female) rural African American emerging adults with an average age of 19.93 (SD = 1.13). Participants completed a battery of self-report assessments and underwent an experimentally-induced social stress paradigm - the Trier Social Stress Test (TSST). 6 saliva sample were collected: (1) Baseline/Pre-TSST, (2) Immediately Post-TSST, (3) 15mins Post-TSST, (4) 30mins Post-TSST, (5) 45mins Post-TSST, and (6) 60mins Post-TSST. Tobacco consumption over the past 90 days was measured using the Timeline Follow-Back method (Sobell & Sobell, 1992). Using a main effects bivariate model, salivary measures of cortisol were examined to test if the levels of cortisol production in response to acute stress – via the TSST - were associated with the levels of salivary DHEA production within each person (Cortisol = β₀ + β_1DHEA + r).

Results:  Changes in cortisol and DHEA within individuals was positively coupled in response to the TSST (β_1DHEA = 4.8x10^-4, t(56) = 7.32, p < .001). As it relates to DHEA reactivity to acute stress (DHEA = β₀ + β_1TIME + r), the data suggested that tobacco use was positively associated with DHEA production (β_1CIGS = .171, t(55) = 2.25, p = .029). Additional predictors of HPA reactivity to acute stress will also be reported.

Conclusions: These findings characterize within-person couplings of HPA-axis reactivity to acute stress in a rural African American sample and underscore the impact of tobacco use on stress maintenance mechanisms. These findings have significant implications for public health prevention efforts by characterizing coupled HPA-axis indicators of altered homeostatic activity and slowed recovery in response to acute stress. These findings further highlight relevant predictors of HPA-axis reactivity to acute stress, which can be used to guide future prevention efforts within this population.