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Updated: Jun 10, 2026

Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
Published on: June 13, 2021
Maternal prenatal stress and cortisol reactivity to stressors in human infants
M S Tollenaar1, R Beijers, J Jansen
1Department of Developmental Psychology, Behavioural Science Institute, Radboud University Nijmegen, Montessorilaan 3, PO Box 9104, 6500 HE, Nijmegen, The Netherlands.
Insights
Maternal prenatal anxiety, specifically fear of bearing a handicapped child, influences infant cortisol reactivity. This effect varies with infant age and stressor type, highlighting early life stress impacts on the hypothalamic pituitary adrenal (HPA) axis.
Area of Science:
- Developmental Psychology
- Neuroendocrinology
- Maternal-Child Health
Background:
- Early life experiences significantly impact the developing hypothalamic pituitary adrenal (HPA) axis.
- Maternal prenatal stress is a potential early environmental factor influencing offspring HPA axis development.
- Limited research exists on the direct relationship between maternal prenatal stress and infant cortisol reactivity.
Purpose of the Study:
- To longitudinally investigate the association between maternal prenatal stress and cortisol reactivity in human infants.
- To examine how different types of infant stressors and ages interact with maternal prenatal anxiety.
- To identify specific maternal prenatal factors predicting infant HPA axis responses.
Main Methods:
- A longitudinal study tracked 173 mothers and their infants.
- Maternal stress, anxiety, and cortisol levels were measured during pregnancy.
- Infant cortisol reactivity was assessed at 5 weeks, 8 weeks, 5 months, and 12 months in response to various stressors (bathing, vaccination, still-face, separation).
Main Results:
- Maternal prenatal fear of bearing a handicapped child consistently predicted infant cortisol reactivity.
- Higher maternal fear correlated with increased cortisol reactivity to bathing but decreased reactivity to vaccination and separation.
- Pregnancy-specific anxieties were stronger predictors than general stress or maternal cortisol levels.
Conclusions:
- Pregnancy-specific maternal anxieties predict infant cortisol reactivity in the first year of life.
- The direction of the HPA axis response is modulated by infant age and the nature of the stressor.
- Further research is needed to elucidate the mechanisms underlying these associations and incorporate diverse HPA axis measures.
Abstract:
Early life factors can shape the development of hypothalamic pituitary adrenal (HPA) axis. Maternal prenatal stress might constitute such an early environmental factor. As little is known about the relation between maternal prenatal stress and cortisol reactivity in human offspring, we performed a longitudinal study including four assessments of infant cortisol reactivity to stressful events in a non-clinical population. General and pregnancy-related feelings of stress and anxiety, as well as circadian cortisol levels, were measured in 173 mothers in the last trimester of pregnancy. Infant cortisol reactivity was measured at 5 weeks to a bathing session, at 8 weeks to a vaccination, at 5 months to a stressful mother-infant interaction (still face procedure), and at 12 months to a maternal separation (strange situation procedure). Maternal prenatal fear of bearing a handicapped child was a consistent predictor of infant cortisol reactivity. Although the effects were mild, higher fear was significantly related to higher salivary cortisol reactivity to the bathing session and to decreased cortisol reactivity to vaccination and maternal separation. Thus, pregnancy-specific anxieties predict infant cortisol reactivity in the first year of life, but the direction of the effect depends on infant age and/or the nature of the stressor. While this specific anxiety was a better predictor than stress experience or maternal cortisol concentrations, the underlying mechanisms of these associations remain unclear. Future studies should try to incorporate multiple measures of HPA-axis reactivity during development when studying the long-term consequences of maternal prenatal stress.
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