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Maternal adversities during pregnancy and cord blood oxytocin receptor (OXTR) DNA methylation
Author(s) -
Eva Unternäehrer,
Margarete Bolten,
Irist,
Simon Staehli,
Andrea H. Meyer,
Emma Dempster,
Dirk H. Hellhammer,
Roselind Lieb,
Gunther Meinlschmidt
Publication year - 2016
Publication title -
social cognitive and affective neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.229
H-Index - 103
eISSN - 1749-5024
pISSN - 1749-5016
DOI - 10.1093/scan/nsw051
Subject(s) - oxytocin receptor , dna methylation , pregnancy , psychology , epigenetics , medicine , endocrinology , oxytocin , edinburgh postnatal depression scale , offspring , methylation , postpartum depression , biology , genetics , gene , gene expression
The aim of this study was to investigate whether maternal adversities and cortisol levels during pregnancy predict cord blood DNA methylation of the oxytocin receptor (OXTR). We collected cord blood of 39 babies born to mothers participating in a cross-sectional study (N = 100) conducted in Basel, Switzerland (2007-10). Mothers completed the Inventory of Life Events (second trimester: T2), the Edinburgh Postnatal Depression Scale (EPDS, third trimester: T3), the Trier Inventory of Chronic Stress (TICS-K, 1-3 weeks postpartum) and provided saliva samples (T2, T3) for maternal cortisol profiles, as computed by the area under the curve with respect to ground (AUCg) or increase (AUCi) for the cortisol awakening response (CAR) and for diurnal cortisol profiles (DAY). OXTR DNA methylation was quantified using Sequenom EpiTYPER. The number of stressful life events (P = 0.032), EPDS score (P = 0.007) and cortisol AUCgs at T2 (CAR: P = 0.020; DAY: P = 0.024) were negatively associated with OXTR DNA methylation. Our findings suggest that distinct prenatal adversities predict decreased DNA methylation in a gene that is relevant for childbirth, maternal behavior and wellbeing of mother and offspring. If a reduced OXTR methylation increases OXTR expression, our findings could suggest an epigenetic adaptation to an adverse early environment.

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