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Evidence that genes for depression impact on the pathway from trauma to psychotic-like symptoms by occasioning emotional dysregulation

Published online by Cambridge University Press:  11 August 2011

I. M. A. Kramer*
Affiliation:
GGz Eindhoven en de Kempen, Eindhoven, The Netherlands Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands
C. J. P. Simons
Affiliation:
GGz Eindhoven en de Kempen, Eindhoven, The Netherlands Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands
I. Myin-Germeys
Affiliation:
Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands
N. Jacobs
Affiliation:
Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands Faculty of Psychology, Open University of The Netherlands, Heerlen, The Netherlands
C. Derom
Affiliation:
Department of Human Genetics, University Hospital Gasthuisberg, Katholieke Universiteit Leuven, Belgium
E. Thiery
Affiliation:
Association for Scientific Research in Multiple Births, Ghent, Belgium
J. van Os
Affiliation:
Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands Department of Psychosis Studies, Institute of Psychiatry, King's College London, King's Health Partners, UK
M. Wichers
Affiliation:
Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, European Graduate School of Neuroscience, Maastricht, The Netherlands
*
*Address for correspondence: I. M. A. Kramer, GGzE, Department of Research and Development, PO Box 909, 5600 AX Eindhoven, The Netherlands. (Email: i.kramer@maastrichtuniversity.nl)

Abstract

Background

Genes for depression may act by making individuals more sensitive to childhood trauma. Given that childhood adversity is a risk factor for adult psychosis and symptoms of depression and psychosis tend to cluster within individuals and families, the aim was to examine whether the association between childhood adversity and psychotic-like symptoms is moderated by genetic liability for depression. A secondary aim was to determine to what degree a depression-related increase in stress sensitivity or depressive symptoms themselves occasioned the moderating effect.

Method

Female twins (n=508) completed both prospective and retrospective questionnaires regarding childhood adversity [the Symptom Checklist-90 – Revised (SCL-90-R) and SCID-I (psychotic symptoms)] and psychotic trait liability [the Community Assessment of Psychic Experiences (CAPE)]. Stress sensitivity was indexed by appraisals of event-related stress and negative affect (NA) in the flow of daily life, assessed with momentary assessment technology for five consecutive days. Multilevel regression analyses were used to examine moderation of childhood adversity by genetic liability for depression in the prediction of follow-up psychotic experiences.

Results

The effect of childhood adversity was significantly moderated by genetic vulnerability for depression in the model of both follow-up psychotic experiences (SCL-90-R) and follow-up psychotic trait liability (CAPE). The moderation by genetic liability was mediated by depressive experience but not by stress sensitivity.

Conclusions

Genetic liability for depression may potentiate the pathway from childhood adversity to psychotic-like symptoms through dysfunctional emotional processing of anomalous experiences associated with childhood trauma.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2011

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