Abstract
We examined whether placental DNA methylation of the glucocorticoid receptor gene, NR3C1 was associated with self-regulation and neuroendocrine responses to a social stressor in infancy. Placenta samples were obtained at birth and mothers and their infants (n = 128) participated in the still-face paradigm when infants were 5 months old. Infant self-regulation following the still-face episode was coded and pre-stress cortisol and cortisol reactivity was assessed in response to the still-face paradigm. A factor analysis of NR3C1 CpG sites revealed two factors: one for CpG sites 1–4 and the other for sites 5–13. DNA methylation of the factor comprising NR3C1 CpG sites 5–13 was related to greater cortisol reactivity and infant self-regulation, but cortisol reactivity was not associated with infant self-regulation. The results reveal that prenatal epigenetic processes may explain part of the development of infant self-regulation.
Highlights
E, Guerin D, Gorman D, Marsit CJ and Lester BM (2015) Prenatal predictors of infant self-regulation: the contributions of placental DNA methylation of NR3C1 and neuroendocrine activity
We examined whether placental DNA methylation of the glucocorticoid receptor gene, NR3C1 was associated with self-regulation and neuroendocrine responses to a social stressor in infancy
We found that greater DNA methylation of CpG sites 5–13 on NR3C1, involved in the neuroendocrine response to stress, was predictive of more cortisol reactivity and infant self-regulation in response to social stress
Summary
A growing literature suggests that the origins of self-regulation in infancy may be identified prenatally (Van den Bergh et al, 2005; Glover et al, 2010; O’Donnell et al, 2013) Most of these studies focus on how prenatal stress, or exposure to prenatal psychopathology is predictive of infant temperament or problem behavior in childhood. Greater stress exposure during pregnancy was related to poorer attention regulation at 8 months and more infant difficult behavior at 3 months (Huizink et al, 2003), as well as lower levels of disruptive temperament and more problem and externalizing behavior at age two DNA methylation and infant self-regulation (Gutteling et al, 2005). One study that we know of includes prenatal epigenetic processes related to temperament in infancy. Alisch et al (2014) using a rhesus macaque model, found that greater DNA methylation of BCL11A and JAG1, genes implicated in neurogenesis, were related to higher levels of anxious temperament in rhesus macaques
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