Cortisol, DHEA and DHEA-S during exposure therapy in patients with 
obsessive-compulsive disorder - secretion patterns and prediction of treatment 
response

Kellner, Michael; Yassouridis, Alexander; Adel, Fred; Muhtz, Christoph; Jelinek, Lena; Wiedemann, Klaus

doi:10.1016/j.psychres.2020.113288

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Cortisol, DHEA and DHEA-S during exposure therapy in patients with obsessive-compulsive disorder - secretion patterns and prediction of treatment response

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Yassouridis, Alexander
Max Planck Institute of Psychiatry, Max Planck Society;

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Citation

Kellner, M., Yassouridis, A., Adel, F., Muhtz, C., Jelinek, L., & Wiedemann, K. (2020). Cortisol, DHEA and DHEA-S during exposure therapy in patients with obsessive-compulsive disorder - secretion patterns and prediction of treatment response. PSYCHIATRY RESEARCH, 291: 113288. doi:10.1016/j.psychres.2020.113288.

Cite as: https://hdl.handle.net/21.11116/0000-0008-C2CC-7

Abstract

The cortisol response in patients with obsessive-compulsive disorder (OCD) during exposure with response prevention (ERP), a stressful but very effective psychotherapeutic treatment, has shown contradictory findings in three prior studies with low sample sizes. In a larger cohort of 51 patients with OCD we repeatedly measured subjective units of distress (SUD) and the adrenocortical stress hormones cortisol, dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) in saliva during the very first session of ERP and on the day before. Expectedly, SUD were increased on the ERP day before the session and further rose during ERP, but salivary cortisol and DHEA were statistically indistinguishable from the comparison condition. Interestingly, DHEA-S was significantly elevated throughout the ERP versus the comparison day, but did not further increase in acute response to ERP. According to an explorative analysis in a subsample, hormone levels on the comparison or the ERP day did not predict anti-OCD treatment response one month later. These results corroborate our prior findings of cortisol non-response despite considerable subjective stress in ERP. The role of DHEA-S in anticipatory anxiety and the effects of augmentative cortisol therapy in ERP need further study.