title: Maternal prenatal cortisol and infant cognitive development: moderation by infant-mother attachment.
abstract: BACKGROUND
  Experimental animal studies suggest that early glucocorticoid exposure may have lasting effects on the neurodevelopment of the offspring; animal studies also suggest that this effect may be eliminated by positive postnatal rearing. The relevance of these findings to humans is not known.
  
  
  METHODS
  We prospectively followed 125 mothers and their normally developing children from pregnancy through 17 months postnatal. Amniotic fluid was obtained at, on average, 17.2 weeks gestation; infants were assessed at an average age of 17 months with the Bayley Scales of Infant Development, and ratings of infant-mother attachment classification were made from the standard Ainsworth Strange Situation assessment.
  
  
  RESULTS
  Prenatal cortisol exposure, indexed by amniotic fluid levels, negatively predicted cognitive ability in the infant, independent of prenatal, obstetric, and socioeconomic factors. This association was moderated by child-mother attachment: in children with an insecure attachment, the correlation was [r(54) = -.47, p < .001]; in contrast, the association was nonexistent in children who had a secure attachment [r(70) = -.05, ns].
  
  
  CONCLUSIONS
  These findings mimic experimental animal findings and provide the first direct human evidence that increased cortisol in utero is associated with impaired cognitive development, and that its impact is dependent on the quality of the mother-infant relationship.
authors.affiliation: Institute of Reproductive and Developmental Biology, Imperial College London, London, United Kingdom.
authors.forename: Kristin
authors.initials: K
authors.lastname: Bergman
authors.forename: Pampa
authors.initials: P
authors.lastname: Sarkar
authors.forename: Vivette
authors.initials: V
authors.lastname: Glover
authors.forename: Thomas G
authors.initials: TG
authors.lastname: O'Connor
mesh_terms: D000328:Adult; D000653:Amniotic Fluid / Q000737:chemistry; D002657:Child Development / Q000502:physiology*; D003071:Cognition / Q000502:physiology*; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000032:analysis / Q000097:blood*; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008431:Maternal-Fetal Exchange / Q000502:physiology; D008875:Middle Aged; D009034:Mother-Child Relations; D009769:Object Attachment; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D011446:Prospective Studies; D011863:Radioimmunoassay; D012044:Regression Analysis; D013312:Stress, Physiological / Q000502:physiology
chemical_list: D006854:Hydrocortisone