Maternal stress and social support prospectively predict infant inflammation

Benjamin W. Nelson, Dorianne B. Wright, Nicholas B. Allen, Heidemarie K. Laurent

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Maternal stress has been suggested to be a risk factor for offspring health, while social support has been shown to be a protective factor for offspring functioning. Currently, research has yet to investigate how both of these factors may relate to infant inflammatory processes and associated biological aging in the first years of life. In 48 mother-infant dyads, we investigated whether maternal parenting stress and social support when infants were 12 and 18 months of age were cross-sectionally associated with infant salivary C-reactive protein (sCRP) during these times. In addition, we investigated whether parenting stress and social support were prospectively associated with later sCRP and changes in sCRP from 12 to 18 months of age, as well as whether those changes in sCRP were associated with subsequent infant salivary telomere length (sTL), a marker of biological aging. Analyses revealed that while there were no cross-sectional associations between maternal factors and infant sCRP, maternal parenting stress and social support when infants were 12 months of age predicted infant sCRP at 18 months of age. Further, maternal social support predicted changes in infant sCRP from 12 to 18 months of age. We observed a null association between infant sCRP and sTL. Implications for the ways that maternal mental health and social support may impact biological mechanisms related to disease processes in infants are discussed.

Original languageEnglish (US)
Pages (from-to)14-21
Number of pages8
JournalBrain, Behavior, and Immunity
Volume86
DOIs
StatePublished - May 2020
Externally publishedYes

Keywords

  • C-reactive protein
  • Infant
  • Inflammation
  • Maternal parenting stress
  • Maternal social support
  • Telomere length

ASJC Scopus subject areas

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience

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