Childhood trauma, cortisol secretion and risk for psychosis

Presentation First Author: 
Rachel L. Lowey

Increasing evidence suggests that childhood trauma confers risk for later psychosis, with dysregulated stress responsivity via the hypothalamic-pituitary-adrenal (HPA) axis as a hypothesized mechanism. However, few studies have examined this model prospectively, prior to psychosis onset. We assessed childhood trauma and salivary cortisol levels in adolescents and young adults at clinical high risk (CHR) for psychosis and age-matched healthy controls (HCs). Cortisol samples were taken to assess diurnal rhythms, response to a laboratory stressor task, and response to dexamethasone. CHR participants are assessed 6, 12 and 24 months later. Interim analyses show that, compared to HCs (N= 41), CHR individuals (N= 58) report higher rates of trauma, especially experienced before age 13, produce more cortisol in anticipation of a laboratory stressor task and a trend towards slower return of cortisol to basal levels after the stressor. Both groups suppressed natural cortisol production in response to dexamethasone administration (.05 mg), with a trend towards stronger suppression for the CHR group. Diurnal rhythms were nearly identical across groups. At baseline, CHRs with a trauma history had more anxiety, PTSD symptoms and trends towards more suspiciousness and more motivation than CHRs without a trauma history. CHRs with trauma were more likely to convert to full psychosis by 12-month follow-up, and converters had experienced a greater number of traumatic events. Results of this ongoing study suggest that CHR youth experience more childhood trauma than their healthy peers, which may be related to risk for psychosis, and show a dysregulated cortisol response to psychosocial stressors.

Conference Name: 
Presentation Date: 
January, 2013
Additional Authors: 
Rachel L. Loewy, Rahel Pearson, Danielle Schlosser, Barbara Stuart, Daniel Mathalon, Sophia Vinogradov
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