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Journal Article

Citation

Zhang M, Liu N, Chen H, Zhang N. BMC Psychiatry 2020; 20(1): e332.

Copyright

(Copyright © 2020, Holtzbrinck Springer Nature Publishing Group - BMC)

DOI

10.1186/s12888-020-02710-0

PMID

32580785

Abstract

BACKGROUND: Borderline personality disorder (BPD) is caused by a variety of biological and environmental factors. Accumulating evidence suggests that childhood maltreatment is a risk environmental factor in the development of BPD, but research on the genetic pathology of BPD is still in its early stages, and very little is known about the oxytocin receptor (OXTR) gene. The purpose of this study is to further explore the interactive effects between OXTR gene polymorphisms and childhood maltreatment on BPD risk.

METHODS: Among the 1804 Chinese Han male inmates, 765 inmates who had BPD or antisocial personality disorder (ASPD) or highly impulsive or violent crime were considered as high-risk inmates and included in this study. Childhood maltreatment, BPD, antisocial personality disorder (ASPD) and impulsivity were measured by self-reported questionnaires. Peripheral venous blood was collected for the genotype test.

RESULTS: Analyses revealed that the BP group (inmates with BPD features) had higher rs53576 AA genotype frequency and rs237987 AA genotype frequency than the non-BP group, while the statistical significances were lost after Bonferroni correction. Total childhood maltreatment score, emotional abuse and neglect could positively predict BPD risk. Among the high-risk samples, rs53576 GG genotype carriers had higher BPD scores at higher levels of physical abuse and sexual abuse and had lower BPD scores at lower levels of physical abuse and sexual abuse.

CONCLUSIONS: The findings suggest that the interaction between OXTR gene variations and childhood maltreatment is an important mechanism for the development of BPD. The moderating role of the OXTR gene provides evidence for gene plasticity.


Language: en

Keywords

Childhood maltreatment; Borderline personality disorder; OXTR; Single-nucleotide polymorphism

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