The association between prenatal maternal anxiety and infant hypothalamic pituitary adrenal axis function

M. P. Austin, K. A. Grant, C. Mcmahon

    Research output: Contribution to journalMeeting abstractpeer-review


    Background: Animal studies have amply demonstrated the negative
    impact of maternal prenatal stress on offspring behavioural
    adjustment and emotional reactivity. Experimental laboratory evidence
    points to changes in the hypothalamic-pituitary-adrenal
    (HPA) axis as one mechanism mediating this link. Although a
    small number of studies suggest that analogous effects occur
    in humans, the data is presently limited [1,2]. This study will
    investigate the impact of maternal stress and anxiety in pregnancy
    on infant behavioural and neuroendocrine responses to stress.
    Aim: to prospectively examine the association between maternal
    prenatal anxiety and infants’ HPA axis responses to a
    laboratory stressor at 7 months postpartum. A novel contribution
    of the study is the use of an interactive stress paradigm (the
    “still-face” procedure) to measure both maternal sensitivity and
    infant stress reactivity. The findings of this study are expected
    to enhance the understanding of the mechanisms that underlie
    individual differences in infants’ responses to stress.
    Method: Maternal anxiety was assessed during the third
    trimester of pregnancy (mean 32 weeks) using both self-report
    Spielberger State and Trait Anxiety Questionnaire) and clinical
    diagnostic interview (a modified version of the MINI). The
    association between maternal anxiety and infant HPA axis was
    assessed by measuring infant salivary cortisol upon arrival at the
    laboratory, and at 15-, 25-, and 40-minutes following the still-face
    procedure. The still-face procedure consists of two minutes play
    between mother and infant; 2 minutes when mother reenters the
    room but remains completely expressionless (the “still face”); and
    then 2 minutes when she re-engages with the infant. We added an
    extra component of 1 minute when mother was absent from the
    room prior to the still-face segment. This laboratory procedure
    has been demonstrated to be a stressfull activation paradigm for
    the infant.
    Results: 149 women were recruited but data could only be
    analysed for 71 women and their 7 month-old infants, due to
    a signficant attrition rate and missing data. Initial attrition was
    related to maternal psychological risk, but data loss at follow up
    was unrelated to maternal demographic variables or any infant
    birth or clinical characteristics.
    The sample was homogeneous in terms of maternal obstetric
    history and outcomes (infant gestation, weight), socioeconomic
    and marital status, and age. Repeated measures MANOVA yielded
    significant interactions indicating that infants’ patterns of cortisol
    response following the laboratory procedures differed as a function
    of maternal prenatal anxiety, after adjusting for the effects of
    maternal postnatal anxiety and depression symptoms. The results
    were identical for maternal prenatal anxiety assessed using self
    report, and diagnostic interview, Wilks’ Lambda = 0.91, F(2,65),
    p = 0.03. The analyses remained significant after adjusting for the
    effects of maternal postnatal anxiety and depression symptoms.
    Infants of mothers who were less anxious during pregnancy
    generally displayed a post-stress increase in cortisol, followed
    by a decrease to below baseline at 40 minutes post-stress. In
    contrast, the infants of prenatally anxious women typically showed
    little change in their cortisol response from baseline through 40
    minutes post-stress. Thus infants of prenatally anxious women
    demonstrated what appears to be a blunted or diminished pattern
    of HPA axis activity.
    Conclusion: This study provides evidence that exposure to
    prenatal anxiety in humans may be associated with subsequent
    alterations in infants’ HPA axis responses to challenge. We shall
    comment on how maternal sensitivity may also modulate infant
    stress reactivity.
    Original languageEnglish
    Article numberP.7.a.001
    Pages (from-to)S554-S554
    Number of pages1
    JournalEuropean Neuropsychopharmacology
    Issue numberSupplement 4
    Publication statusPublished - Aug 2008
    Event21st Congress of the European-College-of-Neuropsychopharmacology - Barcelona, Spain
    Duration: 30 Aug 20083 Sept 2008


    • STRESS


    Dive into the research topics of 'The association between prenatal maternal anxiety and infant hypothalamic pituitary adrenal axis function'. Together they form a unique fingerprint.

    Cite this