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Peer-reviewedCC BY 4.0Nutrients

Maternal DHA Supplementation and Fetal Brain Development: Benefits, Risks, and Individual Needs

4 affiliations
  1. 1Department of Biology and Chemistry, School of Health Sciences Liberty University, Lynchburg, VA 24515, USA
  2. 2Department of Biochemistry and Molecular Biology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA
  3. 3Department of Biomedical Sciences, West Virginia School of Osteopathic Medicine, Lewisburg, WV 24901, USA
  4. 4Department of Biology, School of Sciences and Agriculture, Ferrum College, Ferrum, VA 24088, USA

Abstract

Maternal nutrition is a key determinant of fetal development, particularly in the context of neural regulation and maturation. Omega-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), play an essential role in neural differentiation, synaptogenesis, myelination, and neuroprotection. While the neurodevelopmental benefits of DHA are well-documented, the effects of excessive maternal DHA intake and the potential long-term consequences on offspring neurophysiology remain poorly understood. The purpose of this review is to synthesize current findings on the role of DHA in fetal neural development, emphasizing biochemical mechanisms and developmental outcomes. It further explores emerging concerns associated with excessive intake, the varied responses to intake, the varied sources of supplements, and the influence of maternal metabolic conditions, such as diabetes, on DHA bioavailability and fetal brain development. Finally, the review highlights the need for individualized supplementation strategies in maternal nutrition and considers the potential epigenetic implications of prenatal DHA exposure, to ultimately inform future research and therapeutic strategies in maternal–fetal health and neurodevelopmental biology.

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BibTeX
@article{whatley2026maternal,
  title = {{Maternal DHA Supplementation and Fetal Brain Development: Benefits, Risks, and Individual Needs}},
  author = {Emma Whatley and Abigail Frommack and Emily Bayliss and Merritt Smith and Seth Woodfin and Ersilia Mirabelli and Dane Fausnacht and Kayla R. Gilley-Connor and William Moore},
  journal = {Nutrients},
  year = {2026},
  month = oct,
  doi = {10.3390/nu18203438},
  url = {https://www.mdpi.com/2072-6643/18/20/3438},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Maternal DHA Supplementation and Fetal Brain Development: Benefits, Risks, and Individual Needs
AU  - Emma Whatley
AU  - Abigail Frommack
AU  - Emily Bayliss
AU  - Merritt Smith
AU  - Seth Woodfin
AU  - Ersilia Mirabelli
AU  - Dane Fausnacht
AU  - Kayla R. Gilley-Connor
AU  - William Moore
PY  - 2026
DA  - 2026/10/01
JO  - Nutrients
DO  - 10.3390/nu18203438
UR  - https://www.mdpi.com/2072-6643/18/20/3438
AB  - Maternal nutrition is a key determinant of fetal development, particularly in the context of neural regulation and maturation. Omega-3 polyunsaturated fatty acids, especially docosahexaenoic acid (DHA), play an essential role in neural differentiation, synaptogenesis, myelination, and neuroprotection. While the neurodevelopmental benefits of DHA are well-documented, the effects of excessive maternal DHA intake and the potential long-term consequences on offspring neurophysiology remain poorly understood. The purpose of this review is to synthesize current findings on the role of DHA in fetal neural development, emphasizing biochemical mechanisms and developmental outcomes. It further explores emerging concerns associated with excessive intake, the varied responses to intake, the varied sources of supplements, and the influence of maternal metabolic conditions, such as diabetes, on DHA bioavailability and fetal brain development. Finally, the review highlights the need for individualized supplementation strategies in maternal nutrition and considers the potential epigenetic implications of prenatal DHA exposure, to ultimately inform future research and therapeutic strategies in maternal–fetal health and neurodevelopmental biology.
SN  - 2072-6643
ER  -