Childhood maltreatment is extremely common in patients diagnosed with psychotic disorders. Moreover, it has been linked with impaired functioning of the Hypothalamic-Pituitary-Adrenal axis. Furthermore, abnormality of the HPA has been found in psychotic patients. Presence of childhood maltreatment could then explain why the HPA axis is dysfunctional in these subjects. Our objective was to clarify the role of childhood trauma in the cortisol profiles of psychotic patients. Thirty-one patients underwent assessments of childhood maltreatment. Diurnal cortisol and cortisol after a controlled psychosocial stress were also collected. Our results show that childhood trauma is associated with lower cortisol levels during the morning and during 24 hours. In men diagnosed with psychosis, childhood trauma is also associated with a higher cortisol response during psychosocial stress. This suggests an alteration of the HPA axis in psychotic patients, resulting from early trauma. Moreover, our results suggest that looking at specific types of childhood abuse may also be important.

This Master's dissertation explored whether a rapid orienting of attention toward or away from social stress information during a restful state, relates to the magnitude of glucocorticoids (GC) released in response to a stressor, the Trier Social Stress Test (TSST). It also assessed whether childhood rearing in a low socioeconomic status (SES) context mediates this relationship. Subjects rested for 45 minutes during which time they completed a modified version of Posner's attention paradigm, comprising social stress words. Immediately following, participants were exposed to the stressor. Results indicated that a rapid attentional engagement toward social stress words associated with pronounced GC responses to the TSST. Fast engagers displayed lower self-esteem and did not differ in terms of their past SES. These findings demonstrate that attentional biases for social stress information at rest combine with diminished self-esteem to predict the magnitude of GC released during psychological stress irrespective of early SES conditions.

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