S225. STRESS SENSITIZATION IN INDIVIDUALS WITH SUBCLINICAL SYMPTOMS INDICATIVE OF PSYCHOPATHOLOGY

BACKGROUND: Repeated exposure to stressors can sensitize the stress system and in turn propel the development of various psychiatric disorders. Stress sensitization can be identified through stress reactivity patterns. Individuals at risk of developing psychosis for example, already show aberrant patterns of daily stress reactivity prior to clinical diagnosis, with blunted physiological responses to mild stressors that could be indicative of a dysregulation of the hypothalamic pituitary adrenocortical axis. In parallel, while they do not show significant physiological responses to the stressor, they report significant increases in negative affect (NA) ensuing from it. This study aims to test whether sensitization can already be observed in healthy volunteers exhibiting only subclinical symptoms. METHODS: Thirty, first year students took part in two laboratory sessions where stress was induced using a modified version of the Montreal Imaging Stress Task (MIST), one week apart. Baseline measures of psychopathology were collected using the Symptom Checklist 90 (SCL-90). During the laboratory sessions, continuous ECG signals were collected, as well as five subjective stress measures per session. We calculated average heart rate (HR) and heart rate variability (HRV) per condition. Multilevel models testing the three-way interaction between psychopathology, session, and condition with individual data points nested within days were used to assess overall psychopathology and more specifically subclinical symptoms of psychosis in repeated stress reactivity. RESULTS: Mixed models investigating repeated stress in overall psychopathology indicates a significant three way interaction for HR (β = -.15, SE=.01, p< .01), and HRV (β = -.01, SE=.04, p= .02), with individuals scoring lower on the scl-90 exhibiting comparable increases in HR and decreases in HRV on both sessions. In contrast, individuals scoring higher on the scale show a blunted response on the second session compared to the first. Analyses with stress (β = .03, SE= .01, p= .01), and NA (β = .06, SE=.29, p= .03) show that generally the stressor elicited a mild negative subjective response with a decrease in stress and NA that was comparable on both sessions for individuals scoring lower on the scl-90. No subjective reactivity was reported on the second session for participants scoring high on the scale. Likewise, models that focused on subclinical psychotic symptoms found similar significant interactions. In the same way as in the analyses with psychopathology we find significant interactions for stress (β = .36, SE= .11, p< .01), NA (β = .06, SE=.03, p= .03) HR (β = -1.08, SE=.13 p< .01), and HRV (β = 3.72, SE=.39, p< .01). Analyses show the same comparable patterns of reactivity in both sessions for participants low in psychosis, and a blunted response on the second session for participants high in psychosis. DISCUSSION: Symptoms of psychopathology and more specifically psychosis are related to blunted stress reactivity during a second exposure to the same stressor. Psychopathological vulnerability may be reflected in a blunting response to repeated stress in healthy individuals with subclinical symptoms. Findings suggest that dysregulation in the stress system may be present long before individual complaints, further highlighting the need for early intervention.