Trauma, Stress Mechanisms, And Risk For Psychosis

Background: Increasing evidence suggests that childhood trauma confers risk for psychosis, perhaps through later dysregulated stress responsivity. However, few studies have examined this model in “clinical-high-risk” (CHR) individuals, prior to psychosis onset. Methods: We assessed salivary cortisol during the Trier Social Stress Test and across the day, along with trauma history, in CHRs and age-matched healthy controls (HCs). CHRs were characterized clinically every 6 months for 2 years. Results: Consistent with other studies, CHRs (N = 102) more often reported a history of traumatic experiences than HCs (N = 64; Fisher’s z = 4.0, P < .0001), particularly interpersonal trauma (Fisher’s z = 4.0, P < .0001), and traumatic events experienced before age 12 (Fisher’s z = 4.7, P = .0001). Transition to full psychosis by 12 months (N = 10 Converted, N = 38 Not Converted) was predicted by the total number of traumatic events (β = .38, P = .019), all traumatic events prior to age 12 (β = .57, P = .0012) and interpersonal traumatic events prior to age 12 (β = .62, P = .037). CHRs demonstrated trends towards significantly higher cortisol levels than HCs upon waking (t = 1.89, P = .052) and in anticipation of the Trier (t = 1.55, P = .062). CHRs with a trauma history (N = 31) secreted significantly more cortisol upon waking than CHRs without trauma (N = 15; t = −2.86, P = .006). Conclusion: These results confirm the relationship between trauma history and transition to psychosis, with the first preliminary evidence of a link between trauma and HPA-axis dysregulation in this population. CHRs also demonstrated elevated cortisol responses in multiple ways compared to healthy participants. Future work will follow this sample longitudinally in order to test direct relationships between stress responsivity and transition to psychosis.