The stress-vulnerability model of psychosis (1) is still a widely used model in the research of psychotic disorders. The stress-vulnerability model suggests that the combination of genetics and previous life stressors determine the vulnerability of psychosis. Cortisol levels are believed to cause alteration of the dopamine regulation resulting in psychotic symptoms. Patients at ultra high-risk (UHR) (9) of developing psychosis and adolescents with schizotypal personality disorder have elevated levels of perceived chronic stress compared to healthy controls and report greater distress in response to life events and daily hassles (10-13). It seems that these high-risk subjects don't experience a higher number of stressful events than healthy controls, but they perceive events more stressful. According to our hypothesis, stress response could be one of the biological systems involved in the development of psychosis. We therefore find it relevant to investigate the biological system involved in the stress response and to examine how the implemented treatment affects the level of stress.