Andres D Roque1, Michelle G Craske2, Michael Treanor2, David Rosenfield3, Thomas Ritz3, Alicia E Meuret4. 1. Department of Psychology, Southern Methodist University, United States. Electronic address: andresr@smu.edu. 2. Department of Psychology, University of California Los Angeles, United States. 3. Department of Psychology, Southern Methodist University, United States. 4. Department of Psychology, Southern Methodist University, United States. Electronic address: ameuret@smu.edu.
Abstract
BACKGROUND: Response rates to first-line treatments for depression and anxiety remain unsatisfactory. Identification of predictors or moderators that can optimize treatment matching is of scientific and clinical interest. This study examined the role of prolonged laboratory-induced stress cortisol reactivity as a predictor of outcome for a treatment of affective dimensions (TAD). Patients received 15-sessions of a treatment targeting reductions in negative affect or increases in positive affect (Craske et al., 2019). A second aim was to examine whether treatment type would moderate the association between cortisol reactivity and treatment outcome. METHODS: Thirty-five participants underwent a 36-minute intermittent stress induction task composed of a mental arithmetic task and a fear-potentiated startle task one week before treatment initiation. Cortisol was collected at five-time points with reactivity being quantified as peak during the task minus basal level of cortisol the evening before the assessment. Using multilevel modeling, we examined the associations between cortisol reactivity and slopes of symptom improvement. RESULTS: Cortisol reactivity was related to treatment outcome, with average and higher levels of stress-induced cortisol response predicting greater decreases in symptoms throughout treatment and 6-month follow-up. Treatment condition differences (moderation) were not observed in the effect of cortisol reactivity on symptoms. CONCLUSION: Our findings demonstrate the impact of greater cortisol stress reactivity on treatment outcome. Future studies should investigate how to enhance this therapeutic benefit through capitalizing on endogenous diurnal fluctuations or exogenous cortisol manipulation.
BACKGROUND: Response rates to first-line treatments for depression and anxiety remain unsatisfactory. Identification of predictors or moderators that can optimize treatment matching is of scientific and clinical interest. This study examined the role of prolonged laboratory-induced stress cortisol reactivity as a predictor of outcome for a treatment of affective dimensions (TAD). Patients received 15-sessions of a treatment targeting reductions in negative affect or increases in positive affect (Craske et al., 2019). A second aim was to examine whether treatment type would moderate the association between cortisol reactivity and treatment outcome. METHODS: Thirty-five participants underwent a 36-minute intermittent stress induction task composed of a mental arithmetic task and a fear-potentiated startle task one week before treatment initiation. Cortisol was collected at five-time points with reactivity being quantified as peak during the task minus basal level of cortisol the evening before the assessment. Using multilevel modeling, we examined the associations between cortisol reactivity and slopes of symptom improvement. RESULTS: Cortisol reactivity was related to treatment outcome, with average and higher levels of stress-induced cortisol response predicting greater decreases in symptoms throughout treatment and 6-month follow-up. Treatment condition differences (moderation) were not observed in the effect of cortisol reactivity on symptoms. CONCLUSION: Our findings demonstrate the impact of greater cortisol stress reactivity on treatment outcome. Future studies should investigate how to enhance this therapeutic benefit through capitalizing on endogenous diurnal fluctuations or exogenous cortisol manipulation.
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