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Prenatal cortisol exposure predicts infant cortisol response to acute stress

Thomas G O'Connor1, Kristin Bergman, Pampa Sarkar

  • 1Department of Psychiatry, Wynne Center for Family Research, University of Rochester Medical Center, 300 Crittenden Blvd, Rochester, New York 14642, USA. tom_oconnor@urmc.rochester.edu

Developmental Psychobiology
|February 9, 2012
PubMed

Insights

Prenatal cortisol exposure in amniotic fluid predicts infant stress response. Higher in-utero cortisol levels are linked to altered hypothalamic-pituitary-adrenal (HPA) axis function in infants.

Area of Science:

  • Developmental Psychology
  • Neuroendocrinology
  • Human Development

Background:

  • Animal studies suggest early stress and glucocorticoids program the hypothalamic-pituitary-adrenal (HPA) axis.
  • The applicability of these findings to human development remains unclear.
  • Understanding prenatal influences on HPA axis programming is crucial for child development.

Purpose of the Study:

  • To investigate the association between prenatal cortisol exposure and infant HPA axis function in humans.
  • To determine if amniotic fluid cortisol levels predict infant cortisol response to stress.
  • To examine the predictive value of prenatal cortisol on HPA axis functioning in early development.

Main Methods:

  • Prospective longitudinal study involving 125 mothers and their children.
  • Amniotic fluid collection at approximately 17.2 weeks gestation.
  • Assessment of infant behavior and cortisol response to separation-reunion stress at 17 months.

Main Results:

  • Prenatal cortisol levels in amniotic fluid significantly predicted infant cortisol response to stress.
  • Infants with higher in-utero cortisol exposure exhibited higher baseline cortisol and a blunted stress response.
  • This association remained significant, independent of prenatal, obstetric, socioeconomic factors, and child-parent attachment.

Conclusions:

  • Prenatal cortisol exposure is a significant predictor of HPA axis functioning in human infants.
  • These findings provide strong evidence for the programming of the HPA axis by the prenatal environment.
  • Early life stress programming via glucocorticoids may begin in utero, impacting infant stress reactivity.

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