Prenatal maternal stress prospectively relates to shorter child buccal cell telomere length

Judith E Carroll1, Nicole E Mahrer2, Madeleine Shalowitz3

  • 1University of California, Los Angeles, Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, Los Angeles, CA, United States.

Psychoneuroendocrinology
|September 14, 2020
PubMed

Insights

Maternal stress during the third trimester of pregnancy is linked to shorter child telomere length, a marker of cellular aging. This suggests prenatal stress may impact long-term health through biological aging pathways.

Area of Science:

  • Developmental Psychology
  • Genetics
  • Maternal Health

Background:

  • Prenatal stress exposure is linked to adverse child and adult health outcomes.
  • A proposed mechanism is fetal exposure to maternal stress hormones, altering development.
  • Cellular aging, specifically telomere attrition, is a potential pathway for this effect.

Purpose of the Study:

  • To investigate the hypothesis that prenatal stress accelerates cellular aging in offspring.
  • To examine the association between maternal perceived stress at different life stages and child telomere length.

Main Methods:

  • A cohort study of 111 mother-child dyads was conducted.
  • Maternal stress was assessed over 6+ years, including preconception, third trimester, and postpartum.
  • Child buccal telomere length (bTL) was measured at 3-5 years old.

Main Results:

  • Higher maternal perceived stress in the third trimester predicted shorter child bTL (β = -0.24, p < .05).
  • Maternal stress before conception and postpartum was not associated with child bTL (p > .42).
  • Results were adjusted for child age and concurrent maternal stress.

Conclusions:

  • A specific vulnerable period exists during pregnancy where maternal stress impacts offspring telomere length.
  • Prenatal stress may contribute to adult disease risk by accelerating biological aging pathways.
  • Early life stress can have lasting biological consequences on cellular aging.

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