DHEA Reactivity to Acute Stress: Examining the Effect of Coping Styles

Background: The culmination of economic and social disadvantages such as chronic exposure to systemic racism, discrimination, access to quality education, substandard housing, affordable health care, and food insecurity experienced by African Americans may result in greater susceptibility to stressors associated with the social determinants of health. Enduring exposure to these risk factors has been linked to a variety of adverse health conditions such as coronary vascular disease, obesity, diabetes, cancers, depression, cognitive impairment, age-related diseases, as well as the inflammatory and immunomodulation system in the body. Based on the adverse effects that chronic stress has on the mental and physical health of African Americans, investigations into the mechanisms associated with adaptive coping strategies may provide novel targets for prevention and intervention. Unfortunately, research on potential mechanisms of exposure to chronic stress that underlie health disparities affecting the African American community has received limited focus in the scientific literature. Purpose: This study aims to provide biomarker support for the potential effects that coping styles have on stress reactivity to acute stress during a controlled laboratory experiment. Identifying mechanisms that work toward an explanation of within-group differences in African American health disparities is both needed and informative for culturally informed prevention and intervention efforts. Methods: A metropolitan sample of African American emerging adults (N = 277) completed a battery of assessments, the Trier Social Stress Test (TSST), and provided six samples of salivary DHEA: before TSST instructions, before speech task, following the TSST, 15 min after TSST, 30 min after TSST, and 45 min after TSST. It was predicted that DHEA levels would increase in response to a controlled laboratory inducement of acute stress and individual coping strategy parameters: engagement in active coping (John Henryism), coping styles (Coping with Stressful Situations), and coping self-efficacy (Coping Self Efficacy) will affect DHEA reactivity to acute stress. Partial correlations between coping strategy parameters, Area under the Curve (AUC), and peak DHEA response (PDR) were run while controlling for age and sex. A two-level HLM was run with predictors of DHEA in acute stress included at the within-subjects level (i.e., level 1). Results: Marginally significant correlations between PDR and CISS avoidance subscale scores were found (r=-0.135, p=0.051). Avoidance coping styles (CISS_A=-1.645, t (200) =-1.89, p=0.061) was a marginally significant predictor of DHEA response during acute stress with a significant interaction also present between PDRCISS_A (PDRCISS_A=0.008, t (200) = 2.07, p=0.040). Conclusion: The results of this study suggest that the use of avoidance-focused coping styles may be a prime target for further investigation as a modifiable risk factor for the deleterious effects of chronic stress on the stress regulatory system. Additional research on identifying mechanisms for different indicators of HPA axis functioning in acute stress (e.g., reactivity vs. overall hormonal levels) may assist in further understanding of within-group differences in African American health disparities as well as being informative for culturally sensitive prevention and intervention efforts.