Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birth weight.
Early life experiences, including those in utero, have been linked to increased risk for adult-onset chronic disease. The underlying assumption is that there is a critical period of developmental plasticity in utero when selection of the fetal phenotype that is best adapted to the intrauterine environment occurs. The current study is the first to test the idea that extreme maternal psychosocial stressors, as observed in the Democratic Republic of Congo, may modify locus-specific epigenetic marks in the newborn resulting in altered health outcomes. Here we show a significant correlation between culturally relevant measures of maternal prenatal stress, newborn birth weight and newborn methylation in the promoter of the glucocorticoid receptor NR3C1. Increased methylation may constrain plasticity in subsequent gene expression and restrict the range of stress adaptation responses possible in affected individuals, thus increasing their risk for adult-onset diseases.
Department of Anthropology, University of Florida, Gainesville, FL, USA. cmulligan@ufl.edu
Connie J
CJ
Mulligan
Nicole C
NC
D'Errico
Jared
J
Stees
David A
DA
Hughes
D001724:Birth Weight / Q000235:genetics*; D019175:DNA Methylation / Q000235:genetics* / Q000502:physiology; D015023:Democratic Republic of the Congo / Q000453:epidemiology; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics* / Q000503:physiopathology; D011401:Promoter Regions, Genetic; D011965:Receptors, Glucocorticoid / Q000235:genetics*; D013315:Stress, Psychological / Q000453:epidemiology / Q000235:genetics* / Q000503:physiopathology
C497713:NR3C1 protein, human; D011965:Receptors, Glucocorticoid