Childhood trauma, BDNF Val66Met and subclinical psychotic experiences. Attempt at replication in two independent samples

dc.contributor.authorCastro Catala, Marta de
dc.contributor.authorvan Nierop, Martine
dc.contributor.authorBarrantes Vidal, Neus
dc.contributor.authorCristóbal Narváez, Paula
dc.contributor.authorSheinbaum, Tamara
dc.contributor.authorKwapil, Thomas R.
dc.contributor.authorPeña Lozano, Elionora
dc.contributor.authorJacobs, Nele
dc.contributor.authorDerom, Catherine
dc.contributor.authorThiery, Evert
dc.contributor.authorvan Os, Jim
dc.contributor.authorvan Winkel, Ruud
dc.contributor.authorRosa de la Cruz, Araceli
dc.date.accessioned2018-10-01T17:40:11Z
dc.date.available2018-10-01T17:40:11Z
dc.date.issued2016-12
dc.date.updated2018-10-01T17:40:12Z
dc.description.abstractChildhood trauma exposure is a robust environmental risk factor for psychosis. However, not all exposed individuals develop psychotic symptoms later in life. The Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) has been suggested to moderate the psychosis-inducing effects of childhood trauma in clinical and nonclinical samples. Our study aimed to explore the interaction effect between childhood trauma and the BDNF Val66Met polymorphism on subclinical psychotic experiences (PEs). This was explored in two nonclinical independent samples: an undergraduate and technical-training school student sample (n = 808, sample 1) and a female twin sample (n = 621, sample 2). Results showed that childhood trauma was strongly associated with positive and negative PEs in nonclinical individuals. A BDNF Val66Met x childhood trauma effect on positive PEs was observed in both samples. These results were discordant in terms of risk allele: while in sample 1 Val allele carriers, especially males, were more vulnerable to the effects of childhood trauma regarding PEs, in sample 2 Met carriers presented higher PEs scores when exposed to childhood trauma, compared with Val carriers. Moreover, in sample 2, a significant interaction was also found in relation to negative PEs. Our study partially replicates previous findings and suggests that some individuals are more prone to develop PEs following childhood trauma because of a complex combination of multiple factors. Further studies including genetic, environmental and epigenetic factors may provide insights in this field.
dc.format.extent9 p.
dc.format.mimetypeapplication/pdf
dc.identifier.idgrec663788
dc.identifier.issn0022-3956
dc.identifier.pmid27596955
dc.identifier.urihttps://hdl.handle.net/2445/124981
dc.language.isoeng
dc.publisherElsevier Ltd
dc.relation.isformatofVersió postprint del document publicat a: https://doi.org/10.1016/j.jpsychires.2016.08.014
dc.relation.ispartofJournal of Psychiatric Research, 2016, vol. 83, p. 121-129
dc.relation.urihttps://doi.org/10.1016/j.jpsychires.2016.08.014
dc.rightscc-by-nc-nd (c) Elsevier Ltd, 2016
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es
dc.sourceArticles publicats en revistes (Biologia Evolutiva, Ecologia i Ciències Ambientals)
dc.subject.classificationPsicosi
dc.subject.classificationInfància
dc.subject.classificationTraumes psíquics
dc.subject.otherPsychoses
dc.subject.otherChildhood
dc.subject.otherPsychic trauma
dc.titleChildhood trauma, BDNF Val66Met and subclinical psychotic experiences. Attempt at replication in two independent samples
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/acceptedVersion

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