Maternal self-reported prenatal depressive symptoms predict infant NR3C1 1F and BDNF IV DNA methylation.

Prenatal maternal psychological distress increases risk for adverse infant outcomes.
However, the biological mechanisms underlying this association remain unclear.
Prenatal stress can impact fetal epigenetic regulation that could underlie changes in
infant stress responses. It has been suggested that maternal glucocorticoids may
mediate this epigenetic effect. We examined this hypothesis by determining the
impact of maternal cortisol and depressive symptoms during pregnancy on infant
NR3C1 and BDNF DNA methylation. Fifty-seven pregnant women were recruited
during the second or third trimester.

Participants self-reported depressive symptoms
and salivary cortisol samples were collected diurnally and in response to a stressor.
Buccal swabs for DNA extraction and DNA methylation analysis were collected from
each infant at two months of age, and mothers were assessed for postnatal depressive
symptoms. Prenatal depressive symptoms significantly predicted increased NR3C1 1F
DNA methylation in male infants ( 2.147 = س , P = 0.044). Prenatal depressive
symptoms also significantly predicted decreased BDNF IV DNA methylation in both
male and female infants ( -3.244 = س , P = 0.013). No measure of maternal cortisol
during pregnancy predicted infant NR3C1 1F or BDNF promoter IV DNA
methylation. Our findings highlight the susceptibility of males to changes in NR3C1
DNA methylation and present novel evidence for altered BDNF IV DNA methylation
in response to maternal depression during pregnancy. The lack of association between
maternal cortisol and infant DNA methylation suggests that effects of maternal
depression may not be mediated directly by glucocorticoids. Future studies should
consider other potential mediating mechanisms in the link between maternal mood
and infant outcomes