Maternal psychological distress during pregnancy has been associated with an increased risk of altered neurodevelopmental outcomes in the offspring, yet the mechanisms linking prenatal exposures to later physiological, behavioral, and socio-emotional outcomes remain incompletely understood. This narrative review examines the potential role of postnatal caregiving in mediating or moderating some of these associations. Evidence suggests that prenatal distress often persists into the postpartum period and may impair the quality of early maternal caregiving, thereby providing a potential postnatal pathway through which risk is transmitted. A limited number of human studies support mediation by caregiving quality, although findings are inconsistent. Evidence for moderation is similarly mixed, but several studies indicate that sensitive caregiving can attenuate associations between prenatal distress and poorer cognitive, behavioral, temperamental, and stress-related outcomes, whereas low-quality caregiving may amplify vulnerability. Biological pathways that may underlie these effects are discussed, including caregiver-dependent calibration of the infant stress response systems, oxytocin-related stress regulation, epigenetic modification of stress-related genes, and experience-dependent development of neural circuits involved in emotion regulation. Overall, the available evidence challenges deterministic models of fetal programming and supports a broader developmental perspective in which prenatal and postnatal influences jointly shape neurodevelopment. Future research in humans adopting longitudinal, multi-method, and biologically integrated approaches may clarify when, how, and for whom caregiving is protective. Clinically, integrating antenatal mental health care with postnatal interventions that support caregiver-infant relationships may contribute to reduce risk for psychopathology and promote children's resilience.
From maternal womb to parents’ arms: the influence of postnatal caregiving in the association between prenatal stress exposure and infant development
Nazzari, S.
;
2026-01-01
Abstract
Maternal psychological distress during pregnancy has been associated with an increased risk of altered neurodevelopmental outcomes in the offspring, yet the mechanisms linking prenatal exposures to later physiological, behavioral, and socio-emotional outcomes remain incompletely understood. This narrative review examines the potential role of postnatal caregiving in mediating or moderating some of these associations. Evidence suggests that prenatal distress often persists into the postpartum period and may impair the quality of early maternal caregiving, thereby providing a potential postnatal pathway through which risk is transmitted. A limited number of human studies support mediation by caregiving quality, although findings are inconsistent. Evidence for moderation is similarly mixed, but several studies indicate that sensitive caregiving can attenuate associations between prenatal distress and poorer cognitive, behavioral, temperamental, and stress-related outcomes, whereas low-quality caregiving may amplify vulnerability. Biological pathways that may underlie these effects are discussed, including caregiver-dependent calibration of the infant stress response systems, oxytocin-related stress regulation, epigenetic modification of stress-related genes, and experience-dependent development of neural circuits involved in emotion regulation. Overall, the available evidence challenges deterministic models of fetal programming and supports a broader developmental perspective in which prenatal and postnatal influences jointly shape neurodevelopment. Future research in humans adopting longitudinal, multi-method, and biologically integrated approaches may clarify when, how, and for whom caregiving is protective. Clinically, integrating antenatal mental health care with postnatal interventions that support caregiver-infant relationships may contribute to reduce risk for psychopathology and promote children's resilience.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
