Maternal Nutrition and Fetal Development
Open accessAbstract
Nutrition is the major intrauterine environmental factor that alters expression of the fetal genome and may have lifelong consequences. This phenomenon, termed "fetal programming," has led to the recent theory of "fetal origins of adult disease." Namely, alterations in fetal nutrition and endocrine status may result in developmental adaptations that permanently change the structure, physiology, and metabolism of the offspring, thereby predisposing individuals to metabolic, endocrine, and cardiovascular diseases in adult life. Animal studies show that both maternal undernutrition and overnutrition reduce placental-fetal blood flows and stunt fetal growth. Impaired placental syntheses of nitric oxide (a major vasodilator and angiogenesis factor) and polyamines (key regulators of DNA and protein synthesis) may provide a unified explanation for intrauterine growth retardation in response to the 2 extremes of nutritional problems with the same pregnancy outcome. There is growing evidence that maternal nutritional status can alter the epigenetic state (stable alterations of gene expression through DNA methylation and histone modifications) of the fetal genome. This may provide a molecular mechanism for the impact of maternal nutrition on both fetal programming and genomic imprinting. Promoting optimal nutrition will not only ensure optimal fetal development, but will also reduce the risk of chronic diseases in adults.
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Multiple biological functions depend on vitamin D, including calcium homeostasis and metabolism, and hypovitaminosis D is associated with higher incidence of fetal miscarriage, preeclampsia, gestational diabetes, bacterial vaginosis, and impaired fetal and childhood growth and development.
“Multiple biological functions in the human body depend on vitamin D, including calcium homeostasis and metabolism, with mounting evidence that hypovitaminosis D is associated with a higher incidence of fetal miscarriage, preeclampsia, gestational diabetes, bacterial vaginosis, and impaired fetal and childhood growth and development [159].”
From The contribution of environmental exposure to the etiology of autism spectrum disorder (2019) · cites this paper as [159]
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- Authors
- Bazer, F. W., Spencer, T. E., Wu, G., Cudd, T. A., & Meininger, C. J.
- Affiliations
- Texas A&M Health Science Center (US)
- Texas A&M University (US)
- Corresponding author
- Wu, Guoyao
- Venue
- The Journal of Nutrition
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 134
- Issue
- 9
- Pages
- 2169-2172
- ISSN
- 0022-3166 (ISSN-L)
- OpenAlex
- W2264616483
- Cited by
- 1,019
- References
- 36
- Citations by year
- 2026: 36 · 2025: 46 · 2024: 59 · 2023: 47 · 2022: 58 · 2021: 59 · 2020: 64 · 2019: 66 · 2018: 52 · 2017: 61 · 2016: 54 · 2015: 43 · 2014: 53 · 2013: 49 · 2012: 43
- FWCI
- 20.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Agriculture
- National Institute of Environmental Health Sciences (ES0-9106, P30ES009106, P30‐ES09106)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- maternal nutrition, fetal programming, fetal origins of adult disease, fetal growth restriction, placental blood flow, nitric oxide, polyamines, epigenetics, DNA methylation, histone modifications, genomic imprinting, maternal undernutrition, maternal overnutrition, fetal development, chronic disease risk
- MeSH terms
- Amino Acids, Animals, Arginine, Female, Embryonic and Fetal Development, Fetal Growth Retardation, Fetus, Humans, Nitric Oxide, Nutrition Disorders, Polyamines, Pregnancy, Pregnancy Complications, Maternal Nutritional Physiological Phenomena
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