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No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

dc.contributor.authorMartin, Lindi
dc.contributor.authorHemmings, Sian Megan Joanna
dc.contributor.authorKidd, Martin
dc.contributor.authorSeedat, Soraya
dc.date.accessioned2018-08-06T07:00:25Z
dc.date.available2018-08-06T07:00:25Z
dc.date.issued2018
dc.identifier.citationMartin, L., et al. 2018. No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample. European Journal of Psychotraumatology, 9(1):1472987, doi:10.1080/20008198.2018.1472987
dc.identifier.issn2000-8066 (online)
dc.identifier.otherdoi:10.1080/20008198.2018.1472987
dc.identifier.urihttp://hdl.handle.net/10019.1/104223
dc.descriptionCITATION: Martin, L., et al. 2018. No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample. European Journal of Psychotraumatology, 9(1):1472987, doi:10.1080/20008198.2018.1472987.
dc.descriptionThe original publication is available at https://www.tandfonline.com
dc.descriptionPublication of this article was funded by the Stellenbosch University Open Access Fund.
dc.description.abstractBackground: Anxiety disorders in youth are attributable to multiple causal mechanisms, comprising biological vulnerabilities, such as genetics and temperament, and unfavourable environmental influences, such as childhood maltreatment (CM). Objective: A gene-environment (G x E) interaction study was conducted to determine the interactive effect of the BDNF Val66Met polymorphism and CM to increase susceptibility to anxiety sensitivity (AS) in a sample of mixed race adolescents. Method: Participants (n = 308, mean age = 15.8 years) who were all secondary school students and who completed measures for AS and CM were genotyped for the BDNF Val66Met polymorphism. Hierarchical multiple regression analysis was conducted to assess G x E influences on AS. Age and gender were included in the models as covariates as age was significantly associated with AS total score (p < .05), and females had significantly higher AS scores than males (p < .05). Results: A main effect of CM on AS was evident (p < .05), however, no main effect of BDNF genotype on AS was observed (p> .05). A non-significant G x E effect on AS was revealed (p <.05). Conclusions: Our results suggest that CM does not have a moderating role in the relationship between the BDNF Val66Met genotype and the increased risk of anxiety-related phenotypes, such as AS. Given the exploratory nature of this study, findings require replication in larger samples and adjustment for population stratification to further explore the role of BDNF Val66Met and CM on AS in mixed race adolescents.en_ZA
dc.description.urihttps://www.tandfonline.com/doi/full/10.1080/20008198.2018.1472987
dc.format.extent12 pages
dc.language.isoen_ZAen_ZA
dc.publisherTaylor & Francis Open
dc.subjectChild abuseen_ZA
dc.subjectAnxiety disordersen_ZA
dc.subjectPsychic trauma in children
dc.titleNo gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sampleen_ZA
dc.typeArticleen_ZA
dc.description.versionPublisher's version
dc.rights.holderAuthors retain copyright


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