Abstract

This paper will review a series of studies using the Experience Sampling Method that suggest that altered sensitivity to stress is an endophenotype for psychosis. The Experience Sampling Method is a structured diary technique allowing the assessment of emotional reactivity to stressors occurring in normal daily life. Elevated emotional reactivity to stress was found in subjects vulnerable to psychosis, suggesting that affective responses to stressors in the flow of daily life are an indicator of genetic and/or environmental liability to psychosis. Indeed, the small stressors in daily life associated with affective responses also predict more intense moment-to-moment variation of subtle positive psychotic experiences.

Increased emotional reactivity was found to be independent from cognitive impairments, and argued to constitute evidence of an affective pathway to psychosis that may underlie a more episodic, reactive, good-outcome type of psychosis. Evidence for this hypothesis was found in data suggesting that the experience of stressful life events and early trauma were associated with increased stress-sensitivity, and that women were more likely to display elevated stress-reactivity. These findings are discussed in the light of recent biological and psychological mechanisms.

Article Outline

1. Introduction

2. Stress and psychosis

3. Emotional reactivity to stress in daily life

3.1. The Experience Sampling Method

3.2. Emotional reactivity to stress in psychosis

4. How does emotional stress-reactivity relate to cognition?

5. Are the different pathways associated with different psychopathological expressions?

6. Additional evidence for the affective pathway to psychosis

6.1. Role of enduring environmental liabilities: association with life events

6.2. Role of enduring environmental liabilities: association with early trauma

6.3. Gender differences?

7. Vulnerability for psychosis or vulnerability for psychopathology in general?

8. Is there a direct effect on psychosis?

9. Possible mechanisms

9.1. Biological mechanisms

9.2. Psychological mechanisms

10. Clinical implications

11. Limitations

12. Conclusion

Acknowledgements

References