Attenuated DHEA and DHEA-S response to acute psychosocial stress in individuals with depressive disorders

In recent years, a relationship between depression and basal dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) levels has frequently been suggested, but responses of these adrenal steroids to psychosocial stress have not been examined in individuals with depressive disorders. In this study, we examined salivary DHEA, DHEA-S, and cortisol/DHEA response to the Trier Social Stress Test (TSST) in individuals with depressive disorders and in healthy controls to discover whether the responses of DHEA and DHEA-S to acute psychosocial stress could be a more sensitive marker of HPA dysfunction in depressive disorders.

We compared salivary cortisol, DHEA, DHEA-S, and cortisol/DHEA levels to the TSST tests between 38 individuals with depression and 43 healthy controls aged 18.4-25.9 years. Depression severity was assessed by the self-reported Beck Depression Inventory-II (BDI-II). Salivary samples were evaluated at four time points: the baseline (-10 time point), before the TSST started (0 time point), the end of the TSST (+20 time point), and the recovery (+50 time points).

No significant differences existed in the basal adrenal hormonal levels between subjects with depressive disorders and controls; however, at the end of TSST, attenuated DHEA and DHEA-S response was identified in subjects with depressive disorders compared to that found in healthy subjects. The differences in the DHEA and DHEA-S levels at the +20 time point, as well as the differences in the cortisol/DHEA at the +50 time point, exhibited negative correlations with depression severity.

Attenuated DHEA and DHEA-S response to acute psychosocial stress was identified in subjects with depressive disorders. These findings help us to discover the bi-directional relationship between depression and the hypothalamic-pituitary-adrenal (HPA) axis function, hence furthering our understanding of whether altered DHEA and DHEA-S response to psychosocial stress may be a more sensitive method than basal adrenal steroid analysis for detecting HPA axis dysfunction in depressive disorders.

As this is a case control study, we could only draw the conclusion of the bi-directional relationship between the depression and the altered DHEA (S) response to stress, and could not identify whether depression was due to the HPA dysfunction, or vice versa. Prospective studies such as such as cohort studies or epidemiology experiments are needed to further test the cause of depression or HPA dysfunction; and the mechanisms responsible for altered DHEA and DHEA-S in response to acute psychosocial stress in individuals with depressive disorders are also needed to be clarified.