Pathways from racial discrimination to cortisol/DHEA imbalance: protective role of religious involvement

ABSTRACT

Objective: Racial discrimination (RD) is hypothesized to dysregulate the production of stress reactive hormones among African Americans. Psychological processes that may mediate the association between RD and such dysregulation (e.g. cortisol/DHEA ratio) are not well articulated. Organizational religious involvement (ORI) has been discussed as a psychological protective factor within the context of RD, but our understanding of ORI as a physiological protective factor remains limited. We evaluated whether RD was directly and indirectly (through depressive symptoms) associated with an imbalance of cortisol and DHEA hormones, and whether ORI buffered these direct and/or indirect pathways.

Design: Data were drawn from the Flint Adolescent Study, an ongoing interview study of youth that began in 1994. Participants were 188 African American emerging adults (47.3% Female, ages 20–22). We used mediation and moderated-mediation analyses, as outlined by Hayes [2012. PROCESS SPSS Macro. [Computer Software and Manual]. http://www.afhayes.com/public/process.pdf], to evaluate the study aims.

Results: We found that depressive symptoms mediated the association between RD and the cortisol/DHEA ratio. We also found that depressive symptoms mediated the association between RD and the cortisol/DHEA ratio for individuals reporting low and moderate levels of ORI, but not at high levels.

Conclusions: Our findings support the socio-psychobiological model of racism and health [Chae et al. 2011. “Conceptualizing Racial Disparities in Health: Advancement of a Socio-Psychobiological Approach.” Du Bois Review: Social Science Research on Race 8 (1): 63–77. doi:10.1017/S1742058X11000166] and suggest that the psychological toll of RD can confer physiological consequences. Moreover, ORI may disrupt pathways from RD to cortisol/DHEA ratio by buffering the psychological toll of RD.

KEYWORDS:

• Racial discrimination
• neuroendocrine response
• religion
• resilience

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This research was supported by a grant from National Institute on Drug Abuse (NIDA) [grant number R01-DA-07484-09]. The first author (D.B.L.) was supported by a grant from the National Institute of Child Health and Human Development (NICHD) (T32 HD 79350-3). The second author (M.K.P.) was supported by a grant from the NICHD (T32 HD007109-36).