Impact of vulnerability to stress in the development and course of first psychotic episode

Abstract

Introduction

The stress diathesis hypothesis is one of the leading models of etiology of psychotic disorders. Cortisol is one of the most researched stress hormone; yet its role in first psychotic episode is currently subject of many researches. Psychotic disorder occurs when “enough” stress attacks vulnerable personality. Stress response activates HPA axis that results in cascade effects on several body systems (immune, neuroendocrine and inflammatory). Dysregulation of the HPA axis and increased cortisol levels have been implicated in psychotic as well as in other psychiatric disorders.

Objective

To follow treatment response through changes in clinical status and stress biomarkers evaluation in longitudinal 18 months research in drug naive FEP.

Aim

To assess endocrine and autonomic responses to acute psychosocial stress, their associations with onset of the first psychotic episode and their subsequent remission.

Methods

We studied 17 subjects with FEP and age and gender matched controls who were exposed to the Trier Social Stress Test. Other materials have explored clinical status through standardized clinical psychiatric interview and validated psychiatry scales as well as measured laboratory biomarkers (cortisol, prolactin, insulin).

Results

Our preliminary findings on a sample of 40 participants indicate a differences between patients and controls in terms of response to stress measured by TSST.

Conclusion

In our continued longitudinal research, we plan to further explore the role of hypothalamic-pituitary-adrenal activity in onset and course of psychotic disorder and its relation with other biomarkers.

Disclosure of interest

The authors have not supplied their declaration of competing interest.