Evidence that the association of childhood trauma with psychosis and related psychopathology is not explained by gene-environment correlation: A monozygotic twin differences approach.


Journal

Schizophrenia research
ISSN: 1573-2509
Titre abrégé: Schizophr Res
Pays: Netherlands
ID NLM: 8804207

Informations de publication

Date de publication:
03 2019
Historique:
received: 13 01 2018
revised: 10 05 2018
accepted: 13 05 2018
pubmed: 26 5 2018
medline: 30 4 2020
entrez: 26 5 2018
Statut: ppublish

Résumé

Converging evidence supports childhood trauma as possible causal risk for psychosis and related psychopathology. However, studies have shown that baseline psychotic symptoms may actually increase risk for subsequent victimization, suggesting that exposure to CT is not random but may result from pre-existing vulnerability. Therefore, studies testing whether the association between CT and psychopathology persists when accounting for gene-environment correlation are much needed. A monozygotic (MZ) twin differences approach was used to examine whether differences in CT exposure among MZ twin pairs would be associated with MZ differences in symptoms. As MZ twins are genetically identical, within-pair correlations between CT exposure and psychopathology rule out the possibility that the association is solely attributable to gene-environment correlation. 266 monozygotic twins (133 pairs) from a larger general population study were available for analysis. CT was associated with symptoms of psychosis (B = 0.62; SE = 0.08, p < .001) and overall psychopathology (B = 43.13; SE = 6.27; p < .001). There were measurable differences within pairs in CT exposure and symptoms, allowing for meaningful within-pair differences. Within-pair differences in CT exposure were associated with within-pair differences in symptoms of psychosis (B = 0.35; SE = 0.16; p = .024), as well as with overall psychopathology (B = 29.22; SE = 12.24; p = .018), anxiety (B = 0.65; SE = 0.21; p = .002) and depression (B = 0.37; SE = 0.18; p = .043). While it is not unlikely that pre-existing vulnerability may increase the risk for traumatic exposures, such gene-environment correlation does not explain away the association between CT and psychopathology. The present findings thus suggest that at least part of the association between CT and psychopathology may be causal.

Sections du résumé

BACKGROUND
Converging evidence supports childhood trauma as possible causal risk for psychosis and related psychopathology. However, studies have shown that baseline psychotic symptoms may actually increase risk for subsequent victimization, suggesting that exposure to CT is not random but may result from pre-existing vulnerability. Therefore, studies testing whether the association between CT and psychopathology persists when accounting for gene-environment correlation are much needed.
METHODS
A monozygotic (MZ) twin differences approach was used to examine whether differences in CT exposure among MZ twin pairs would be associated with MZ differences in symptoms. As MZ twins are genetically identical, within-pair correlations between CT exposure and psychopathology rule out the possibility that the association is solely attributable to gene-environment correlation. 266 monozygotic twins (133 pairs) from a larger general population study were available for analysis.
RESULTS
CT was associated with symptoms of psychosis (B = 0.62; SE = 0.08, p < .001) and overall psychopathology (B = 43.13; SE = 6.27; p < .001). There were measurable differences within pairs in CT exposure and symptoms, allowing for meaningful within-pair differences. Within-pair differences in CT exposure were associated with within-pair differences in symptoms of psychosis (B = 0.35; SE = 0.16; p = .024), as well as with overall psychopathology (B = 29.22; SE = 12.24; p = .018), anxiety (B = 0.65; SE = 0.21; p = .002) and depression (B = 0.37; SE = 0.18; p = .043).
CONCLUSION
While it is not unlikely that pre-existing vulnerability may increase the risk for traumatic exposures, such gene-environment correlation does not explain away the association between CT and psychopathology. The present findings thus suggest that at least part of the association between CT and psychopathology may be causal.

Identifiants

pubmed: 29793818
pii: S0920-9964(18)30282-2
doi: 10.1016/j.schres.2018.05.025
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't Twin Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

58-62

Informations de copyright

Copyright © 2018 Elsevier B.V. All rights reserved.

Auteurs

Aleksandra Lecei (A)

KU Leuven, Dept. of Neurosciences, Research Group Psychiatry, Center for Clinical Psychiatry, Leuven, Belgium.

Jeroen Decoster (J)

UPC KU Leuven, Leuven, Belgium.

Marc De Hert (M)

KU Leuven, Dept. of Neurosciences, Research Group Psychiatry, Center for Clinical Psychiatry, Leuven, Belgium; UPC KU Leuven, Leuven, Belgium.

Catherine Derom (C)

Center of Human Genetics, University Hospital Leuven, KU Leuven, Leuven, Belgium; Department of Obstetrics and Gynecology, Ghent University Hospitals, Ghent University, Ghent, Belgium.

Nele Jacobs (N)

Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, Maastricht, Netherlands; Faculty of Psychology and Educational Sciences, Open University of the Netherlands, Heerlen, Netherlands.

Claudia Menne-Lothmann (C)

Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, Maastricht, Netherlands.

Jim van Os (J)

Department of Psychosis Studies, Institute of Psychiatry, King's Health Partners, King's College London, London, United Kingdom; Department of Psychiatry, Brain Centre Rudolf Magnus, University Medical Centre Utrecht, Utrecht, Netherlands.

Evert Thiery (E)

Department of Neurology, Ghent University Hospital, Ghent University, Ghent, Belgium.

Bart P F Rutten (BPF)

Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, Maastricht, Netherlands.

Marieke Wichers (M)

University of Groningen, University Medical Center Groningen, Department of Psychiatry, Interdisciplinary Center Psychopathology and Emotion Regulation, Groningen, Netherlands.

Ruud van Winkel (R)

KU Leuven, Dept. of Neurosciences, Research Group Psychiatry, Center for Clinical Psychiatry, Leuven, Belgium; UPC KU Leuven, Leuven, Belgium. Electronic address: ruud.vanwinkel@upckuleuven.be.

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