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Prenatal Major Depressive Disorder, Placenta Glucocorticoid and Serotonergic Signaling, and Infant Cortisol Response

Laura R Stroud1, George D Papandonatos, Stephanie H Parade

  • 1From the Department of Psychiatry and Human Behavior (Stroud, Parade, Salisbury, Lester), Warren Alpert Medical School, Brown University; Providence, Rhode Island; Centers for Behavioral and Preventive Medicine (Stroud), The Miriam Hospital, Providence, Rhode Island; Department of Biostatistics, School of Public Health (Papandonatos), Brown University, Providence, Rhode Island; Bradley/Hasbro Children's Research Center (Parade), Providence, Rhode Island; Department of Pediatrics (Salisbury, Lester, Padbury), Warren Alpert Medical School, Brown University, Providence, Rhode Island; Women & Infants' Hospital of Rhode Island (Salisbury, Phipps, Lester, Padbury), Providence, Rhode Island; Department of Obstetrics and Gynecology (Phipps), Warren Alpert Medical School, Brown University, Providence, Rhode Island; and Department of Environmental Health (Marsit), Rollins School of Public Health, Emory University, Atlanta, Georgia.

Psychosomatic Medicine
|November 5, 2016
PubMed

Insights

Maternal prenatal major depressive disorder (MDD) is linked to altered infant cortisol regulation, particularly in daughters. Placental gene expression and methylation pathways influence this intergenerational risk transmission.

Area of Science:

  • Developmental Psychology
  • Neuroendocrinology
  • Genetics

Background:

  • Prenatal adversity, including maternal major depressive disorder (MDD), is associated with altered infant development.
  • Infant cortisol regulation is a key indicator of stress response and can be influenced by prenatal environment.
  • Placental signaling pathways, such as glucocorticoid and serotonin, may mediate the effects of maternal MDD on infant outcomes.

Purpose of the Study:

  • To investigate the association between maternal prenatal MDD and infant cortisol regulation.
  • To examine the moderating roles of placental HSD11B2 methylation and SLC6A4 gene expression in this association.
  • To differentiate the effects of prenatal MDD from preconception-only MDD on infant cortisol.

Main Methods:

  • 153 mother-infant pairs from a low-income, diverse sample were recruited.
  • Mothers were diagnosed with prenatal MDD, preconception-only MDD, or were controls using structured interviews.
  • Placental samples were analyzed for HSD11B2 methylation and SLC6A4 gene expression; infant cortisol was measured at 1 month.

Main Results:

  • Infants of mothers with prenatal MDD exhibited significantly higher baseline and stress-responsive cortisol levels compared to controls and infants of mothers with preconception-only MDD.
  • Placental HSD11B2 methylation moderated the relationship between prenatal MDD and infant baseline cortisol.
  • Placental SLC6A4 gene expression moderated the relationship between prenatal MDD and cortisol response in male infants.

Conclusions:

  • The findings underscore the specific impact of prenatal MDD, distinct from preconception MDD, on infant cortisol regulation.
  • Placental glucocorticoid and serotonergic pathways are crucial and complex mediators in the intergenerational transmission of risk from maternal prenatal adversity.
  • This research highlights potential biological mechanisms linking maternal mental health during pregnancy to infant stress system development.
Abstract

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