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Effects of pre- and postnatal maternal stress on infant temperament and autonomic nervous system reactivity and regulation in a diverse, low-income population

  • Nicole R. Bush (a1), Karen Jones-Mason (a1), Michael Coccia (a1), Zoe Caron (a1), Abbey Alkon (a1), Melanie Thomas (a2), Kim Coleman-Phox (a1), Pathik D. Wadhwa (a3), Barbara A. Laraia (a4), Nancy E. Adler (a1) and Elissa S. Epel (a1)...
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We examined the prospective associations of objective and subjective measures of stress during pregnancy with infant stress reactivity and regulation, an early-life predictor of psychopathology. In a racially and ethnically diverse low-income sample of 151 mother–infant dyads, maternal reports of stressful life events (SLE) and perceived stress (PS) were collected serially over gestation and the early postpartum period. Infant reactivity and regulation at 6 months of age was assessed via maternal report of temperament (negativity, surgency, and regulation) and infant parasympathetic nervous system physiology (respiratory sinus arrhythmia [RSA]) during the Still Face Paradigm. Regression models predicting infant temperament showed higher maternal prenatal PS predicted lower surgency and self-regulation but not negativity. Regression models predicting infant physiology showed higher numbers of SLE during gestation predicted greater RSA reactivity and weaker recovery. Tests of interactions revealed SLE predicted RSA reactivity only at moderate to high levels of PS. Thus, findings suggest objective and subjective measures of maternal prenatal stress uniquely predict infant behavior and physiology, adjusting for key pre- and postnatal covariates, and advance the limited evidence for such prenatal programming within high-risk populations. Assessing multiple levels of maternal stress and offspring stress reactivity and regulation provides a richer picture of intergenerational transmission of adversity.

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Corresponding author

Address correspondence and reprint requests to: Nicole R. Bush, Psychiatry and Pediatrics, University of California, San Francisco, 3333 California Street, Suite 465, San Francisco, CA 94118; E-mail:


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This research was supported by NIH Grants 1 U01 HL097973 and NHLBI 5 R01 HL116511, the Robert Wood Johnson Health and Society Scholars Program, and the Lisa and John Pritzker Family Foundation. The authors also acknowledge Michelle Stephens for her assistance with scoring the autonomic nervous system data; Vanessa Tearnan, Marialma Gonzales-Cruz, Yurivia Cervantes, and Amy Engler for their assistance in collecting the autonomic nervous system data; and Holly Wing, Gwen Valencia-Moscoso, Amber Benson, Samantha Schilf, and Danielle Emmet for their assistance with the MAMAS data collection. We are also thankful to the families for their generous participation in this research.



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