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Prenatal stress exposure, oxytocin receptor gene ( OXTR ) methylation, and child autistic traits: The moderating role of OXTR rs53576 genotype
Author(s) -
Rijlaarsdam Jolien,
van IJzendoorn Marinus H.,
Verhulst Frank C.,
Jaddoe Vincent W. V.,
Felix Janine F.,
Tiemeier Henning,
BakermansKranenburg Marian J.
Publication year - 2017
Publication title -
autism research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 66
eISSN - 1939-3806
pISSN - 1939-3792
DOI - 10.1002/aur.1681
Subject(s) - oxytocin receptor , autism , allele , methylation , dna methylation , psychology , genotype , oxytocin , genetics , developmental psychology , biology , gene , neuroscience , gene expression
Findings of studies investigating OXTR SNP rs53576 (G‐A) variation in social behavior have been inconsistent, possibly because DNA methylation after stress exposure was eliminated from consideration. Our goal was to examine OXTR rs53576 allele‐specific sensitivity for neonatal OXTR DNA methylation in relation to (1) a prenatal maternal stress composite, and (2) child autistic traits. Prospective data from fetal life to age 6 years were collected in a total of 743 children participating in the Generation R Study. Prenatal maternal stress exposure was uniquely associated with child autistic traits but was unrelated to OXTR methylation across both OXTR rs53576 G‐allele homozygous children and A‐allele carriers. For child autistic traits in general and social communication problems in particular, we observed a significant OXTR rs53576 genotype by OXTR methylation interaction in the absence of main effects, suggesting that opposing effects cancelled each other out. Indeed, OXTR methylation levels were positively associated with social problems for OXTR rs53576 G‐allele homozygous children but not for A‐allele carriers. These results highlight the importance of incorporating epi‐allelic information and support the role of OXTR methylation in child autistic traits. Autism Res 2017, 10: 430–438 . © 2016 International Society for Autism Research, Wiley Periodicals, Inc.