Lack of Association between Oxytocin Receptor (OXTR) Gene Polymorphisms and Alexithymia: Evidence from Patients with Obsessive-Compulsive Disorder

PLoS One. 2015 Nov 23;10(11):e0143168. doi: 10.1371/journal.pone.0143168. eCollection 2015.

Abstract

Oxytocin receptor gene single nucleotide polymorphisms have been associated with structural and functional alterations in brain regions, which involve social-emotional processing. Therefore, oxytocin receptor gene polymorphisms may contribute to individual differences in alexithymia, which is considered to be a dysfunction of emotional processing. The aim of this study was to evaluate the association between oxytocin receptor gene single nucleotide polymorphisms or haplotypes and alexithymia in patients with obsessive-compulsive disorder. We recruited 355 patients with obsessive-compulsive disorder (234 men, 121 women). Alexithymia was measured by using the Toronto Alexithymia Scale. We performed single-marker and haplotype association analyses with eight single nucleotide polymorphisms (rs237885, rs237887, rs2268490, rs4686301, rs2254298, rs13316193, rs53576, and rs2268498) in the oxytocin receptor gene. There were no significant associations between any of the eight single nucleotide polymorphism of the oxytocin receptor gene and alexithymia. In addition, a six-locus haplotype block (rs237885-rs237887-rs2268490-rs4686301-rs2254298-rs13316193) was not significantly associated with alexithymia. These findings suggest that genetic variations in the oxytocin receptor gene may not explain a significant part of alexithymia in patients with obsessive-compulsive disorder.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Affective Symptoms / complications*
  • Affective Symptoms / genetics*
  • Demography
  • Female
  • Genetic Association Studies*
  • Genetic Predisposition to Disease*
  • Haplotypes / genetics
  • Humans
  • Linkage Disequilibrium / genetics
  • Male
  • Obsessive-Compulsive Disorder / complications
  • Obsessive-Compulsive Disorder / genetics*
  • Polymorphism, Single Nucleotide / genetics*
  • Quantitative Trait Loci / genetics
  • Receptors, Oxytocin / genetics*

Substances

  • Receptors, Oxytocin

Grants and funding

This research was supported by a grant (to S. J. Kim) from the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010-0022363). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.