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Cited by 14Birth, Development, and HealthEpigenetics and DNA MethylationNutrition, Genetics, and Disease

Maternal Nutrition, Toxicants, and Epigenetic Programming of Obesity Across Generations

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Alum, Esther, Aloh, Henry, Obasi, David, Okoroh, Prince, Aniokete, Ugonna, Emeruwa, Akunna·2025·Diabetes, Metabolic Syndrome and Obesity
DOI 10.2147/dmso.s579409PMC PMC12765939
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Abstract

Background: The developmental origins of health and disease (DOHaD) framework highlights the importance of the intrauterine environment in shaping lifelong health outcomes. Maternal nutrition, toxic exposures, and epigenetic reprogramming are key factors influencing offspring susceptibility to obesity and cardiometabolic disorders. However, prior reviews have typically addressed nutrition and toxicants separately, limiting insights into their combined effects on the fetal epigenome. This review integrates current evidence on how maternal nutrition and toxicant exposures converge through epigenetic mechanisms to influence obesity risk, while outlining translational opportunities for mitigating intergenerational metabolic disease. Methods: A narrative review was conducted of studies published from 2000 to 2025, sourced from PubMed, Scopus, and Web of Science, supplemented by manual screening. Search terms included maternal nutrition, environmental toxicants, epigenetic mechanisms, and offspring obesity outcomes. Studies on animal models, human cohorts, and intervention trials were included, focusing on links between maternal exposures, epigenetic changes, and metabolic disease. Results: Maternal dietary imbalances, such as deficiencies in one-carbon donors or excess caloric intake, cause persistent epigenetic changes on genes regulating adipogenesis and energy homeostasis, increasing offspring obesity risk. Prenatal exposure to environmental toxicants, including endocrine disruptors and heavy metals, amplifies these vulnerabilities by altering DNA methylation, histone modifications, and noncoding RNA networks. Combined nutritional deficits and toxicant exposures, particularly in low- and middle-income countries (LMICs), create a “dual burden” that intensifies epigenetic instability. Nutrients like methyl donors and antioxidants may mitigate toxicant-induced epimutations, offering potential for precision maternal nutrition interventions. Conclusion: Maternal nutrition and toxicant exposures interact through epigenetic mechanisms to program obesity and related diseases. Addressing these factors through precision nutrition, stricter environmental regulations, and early-life epigenetic biomarkers offers promising prevention strategies. Large, diverse, multi-generational cohorts and multi-omics approaches are needed to strengthen causal inference and inform equitable policies to break the intergenerational cycle of metabolic disease. Plain Language Summary: This study explores how a mother’s diet and exposure to environmental pollutants during pregnancy can shape her child’s future risk of obesity and related diseases such as diabetes and heart disease. It explains that what happens in the womb can “program” a baby’s metabolism for life through changes in gene activity known as epigenetic modifications which are chemical tags that switch genes on or off without changing DNA. Poor maternal nutrition, whether from eating too much fat and sugar or lacking key vitamins like folate and B 12 can alter these epigenetic marks, increasing the child’s tendency to gain weight. At the same time, exposure to environmental toxicants like plastics (which contains BPA), heavy metals, or pesticides can make these effects worse. When both poor nutrition and toxic exposure occur together, especially in low-income settings, the risk becomes even greater. The review also highlights that healthy diets rich in folate, antioxidants, and omega-3 fats may help protect against these harmful effects. New technologies that study genes, metabolites, and gut bacteria together (multi-omics) are helping scientists identify early biomarkers of risk. Ultimately, the study calls for integrated maternal health policies that combine good nutrition with stronger environmental protections to prevent obesity from being passed down across generations. Keywords: toxic exposures, epigenetics, histone modifications, endocrine disruptors, fetal programming, maternal precision nutrition

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  • Such changes may also modify placental nutrient transport, promote compensatory nutrient delivery, and predispose offspring to metabolic disorders later in life.

    “Such changes may also modify placental nutrient transport, promote compensatory nutrient delivery and predispose offspring to metabolic disorders later in life [18,173,174].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [174]

    The Epigenetic Biomarkers of Maternal Exposures section (page unavailable) links maternal exposures to altered methylation at placental nutrient-transport genes and associates placental epigenomic signatures with later childhood adiposity. The Key Insights section (page unavailable) likewise says fetal epigenetic changes can predispose offspring to obesity and related disorders. Neither passage establishes compensatory nutrient delivery, so that part of the claim is unsupported. (LLM, conf=0.83)

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Cited by

Sorted by citations

Authors
Alum, E., Aloh, H., Obasi, D., Okoroh, P., Aniokete, U., & Emeruwa, A.
Affiliations
  • Kampala International University (UG)
  • Alex Ekwueme Federal University, Ndufu-Alike (NG)
  • David Umahi Federal University of Health Sciences Uburu (NG)
Corresponding author
Alum, Esther
ORCID
Venue
Diabetes, Metabolic Syndrome and Obesity
Publisher
Informa UK Limited
Published
2025-12
Volume
Volume 18
Pages
4873-4911
ISSN
1178-7007 (ISSN-L)
DOI
10.2147/dmso.s579409
PMC
PMC12765939
OpenAlex
W7117762602
Cited by
14
References
9
Citations by year
2026: 14
FWCI
3.47
Type
journal article
Language
en
Open access
Licence
Locations
  • Diabetes Metabolic Syndrome and Obesity (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc)
  • Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Nutrition, Genetics, and Disease
Keywords
maternal nutrition, environmental toxins, epigenetic programming, intergenerational obesity, developmental origins of health and disease, prenatal exposure, endocrine disruptors, heavy metals, DNA methylation, histone modifications, non-coding RNA, folic acid, methyl donors, antioxidants, cardiometabolic disease, low- and middle-income countries, epigenetic biomarkers

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