Maternal mood disorder and newborn neurobehavior

A great number of women experience depression or anxiety while pregnant, and exposure of the fetus to these maternal mood disorders may lead to long-term emotional and behavioral problems in the offspring. Many studies have shown that the fetal environment has a strong influence on offspring neurobehavioral outcomes by altering the developing brain, although the exact mechanisms by which this occurs are not completely understood.

Researchers from the Brown Center for the Study of Children at Risk, Women and Infants Hospital of Rhode Island, Brown University, in Providence, RI, have now tested the influence of maternal depression and/or anxiety during pregnancy on newborn neurobehavior by specifically looking at epigenetic changes (modifications on the DNA that are different from changes in DNA sequence) in two genes expressed in the placenta that have been previously implicated in perturbations of the HPA axis (a system that controls reactions to stress and regulates many body processes).

In a study published in the December 2013 issue of Epigenetics, the authors report that specific adjustments that occur in the fetus (more specifically in the regulation of gene expression) in response to cues from the intrauterine environment, in this case an increased exposure to maternal cortisol, may lead to poor neurodevelopmental outcomes.

The researchers found support for the idea that transmission of risk for poor neurodevelopmental outcomes may actually occur prenatally. This research highlights the importance of treating maternal prenatal depression and anxiety so that risk for poor newborn behavioral outcomes is mitigated.

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Exposure to maternal mood disorder in utero may program infant neurobehavior via DNA methylation of the glucocorticoid receptor (NR3C1) and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD-2), two placental genes that have been implicated in perturbations of the hypothalamic pituitary adrenocortical (HPA) axis. We tested the relations among prenatal exposure to maternal depression or anxiety, methylation of exon 1F of NR3C1 and 11β-HSD-2, and newborn neurobehavior. Controlling for relevant covariates, infants whose mothers reported depression during pregnancy and showed greater methylation of placental NR3C1 CpG2 had poorer self-regulation, more hypotonia, and more lethargy than infants whose mothers did not report depression. On the other hand, infants whose mothers reported anxiety during pregnancy and showed greater methylation of placental 11β-HSD-2 CpG4 were more hypotonic compared with infants of mothers who did not report anxiety during pregnancy. Our results support the fetal programming hypothesis and suggest that fetal adjustments to cues from the intrauterine environment, in this case an environment that could be characterized by increased exposure to maternal cortisol, may lead to poor neurodevelopmental outcomes.

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Andrew Thompson
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Landes Bioscience

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