Prenatal exposure to maternal stress hormones and the risk of autism: a neuroendocrine–epigenetic scoping review
- 1Department of Applied Psychology, Faculty of Social Sciences, Midlands State University
- 2Department of Clinical Psychology, School of Medicine, Sefako Makgatho Health Sciences University
- 3Department of Psychology, University of Witwatersrand
Abstract
Maternal psychosocial stress during pregnancy is increasingly recognized as a factor capable of shaping fetal neurodevelopment through alterations in the hypothalamic–pituitary–adrenal (HPA) axis and placental regulatory systems. When maternal stress hormones, particularly cortisol, rise persistently during gestation, they may exceed the buffering capacity of the placenta, influencing fetal brain pathways implicated in social communication, sensory processing, and emotional regulation. Empirical evidence from prospective cohorts has shown that elevated maternal cortisol, altered diurnal HPA rhythms, and increased placental corticotropin-releasing hormone (CRH) trajectories are associated with neurodevelopmental outcomes relevant to autism spectrum disorder (ASD), although results remain heterogeneous across populations and methods [1–3]. This scoping review examines confirmed studies on prenatal stress hormones, placental enzymatic processes, epigenetic changes and their relation to stress, and the diagnosis of ASD and ASD-related traits on a continuum. Per the guidance of the Joanna Briggs Institute and the Scoping Reviews and Mapping Approaches (PRISMA-ScR) framework, we cataloged the eligible studies on their research design, biomarkers, gestational periods, and outcomes by neurobiological processes, and of the children in question. Across studies with multiple methodologies, there is a consensus that disruptions in maternal HPA axis functioning and placental signaling contribute to early changes in the trajectory of ASD development, with the moderating variables of fetal sex, maternal mental health and environmental adversity. While there is no compelling evidence of a causal relationship, the strength and consistency of the proposed mechanisms support the idea that prenatal HPA and epigenetic processes play an important role in shaping the development of ASD. The review highlights the importance of cross study harmonization of biomarkers, expanded longitudinal study designs with varied and several gestational samplings, and the need to pinpoint the timing, magnitude, and detail of the relationships between the stress biology of pregnancy and ASD with outcomes. Collectively, the findings present a framework and strengthened the linkage of the maternal stress physiology to the neurodevelopment of the fetus. This provides a pathway for future mechanistic research and further applied research [10].
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BibTeX
@article{munsaka2026prenatal,
title = {{Prenatal exposure to maternal stress hormones and the risk of autism: a neuroendocrine–epigenetic scoping review}},
author = {Temba Munsaka and Mqemane Tshababa and Phumuzani Mpofu and Mokoena Patronella Maepa},
journal = {BMC Psychiatry},
year = {2026},
month = jul,
doi = {10.1186/s12888-026-08399-x},
url = {https://doi.org/10.1186/s12888-026-08399-x},
note = {CC BY},
}
RIS
TY - JOUR
TI - Prenatal exposure to maternal stress hormones and the risk of autism: a neuroendocrine–epigenetic scoping review
AU - Temba Munsaka
AU - Mqemane Tshababa
AU - Phumuzani Mpofu
AU - Mokoena Patronella Maepa
PY - 2026
DA - 2026/07/01
JO - BMC Psychiatry
DO - 10.1186/s12888-026-08399-x
UR - https://doi.org/10.1186/s12888-026-08399-x
AB - Maternal psychosocial stress during pregnancy is increasingly recognized as a factor capable of shaping fetal neurodevelopment through alterations in the hypothalamic–pituitary–adrenal (HPA) axis and placental regulatory systems. When maternal stress hormones, particularly cortisol, rise persistently during gestation, they may exceed the buffering capacity of the placenta, influencing fetal brain pathways implicated in social communication, sensory processing, and emotional regulation. Empirical evidence from prospective cohorts has shown that elevated maternal cortisol, altered diurnal HPA rhythms, and increased placental corticotropin-releasing hormone (CRH) trajectories are associated with neurodevelopmental outcomes relevant to autism spectrum disorder (ASD), although results remain heterogeneous across populations and methods [1–3]. This scoping review examines confirmed studies on prenatal stress hormones, placental enzymatic processes, epigenetic changes and their relation to stress, and the diagnosis of ASD and ASD-related traits on a continuum. Per the guidance of the Joanna Briggs Institute and the Scoping Reviews and Mapping Approaches (PRISMA-ScR) framework, we cataloged the eligible studies on their research design, biomarkers, gestational periods, and outcomes by neurobiological processes, and of the children in question. Across studies with multiple methodologies, there is a consensus that disruptions in maternal HPA axis functioning and placental signaling contribute to early changes in the trajectory of ASD development, with the moderating variables of fetal sex, maternal mental health and environmental adversity. While there is no compelling evidence of a causal relationship, the strength and consistency of the proposed mechanisms support the idea that prenatal HPA and epigenetic processes play an important role in shaping the development of ASD. The review highlights the importance of cross study harmonization of biomarkers, expanded longitudinal study designs with varied and several gestational samplings, and the need to pinpoint the timing, magnitude, and detail of the relationships between the stress biology of pregnancy and ASD with outcomes. Collectively, the findings present a framework and strengthened the linkage of the maternal stress physiology to the neurodevelopment of the fetus. This provides a pathway for future mechanistic research and further applied research [10].
SN - 1471-244X
ER -