Epigenetic Changes in Early Life and Future Risk of Obesity
Abstract
The rapid increase in incidence of obesity over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environments also strongly influence the risk of developing obesity in later life. Initially, human studies showed that low birth weight was associated with an increased risk of obesity but increasingly there is evidence that overnutrition in the early life can also increase susceptibility to future obesity. These findings have now been replicated in animal models, which have shown that both maternal under- and overnutrition can induce persistent changes in gene expression and metabolism. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. In this review, we discuss the recent evidence that shows that early-life environment can induce altered epigenetic regulation leading to the induction of an altered phenotype. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of obesity opens the possibility that interventions, either through nutrition or specific drugs, may modify long-term obesity risk and combat this rapid rise in obesity.
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Epigenetic changes induced by maternal overnutrition may be transmitted across generations.
“Emerging evidence suggests that epigenetic changes induced by maternal overnutrition may be transmitted across generations”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [7]
Developmental effects of suboptimal intrauterine environments are mediated by epigenetic mechanisms that influence gene expression without altering the DNA sequence.
“A growing body of evidence suggests that these developmental effects are mediated by epigenetic mechanisms, which collectively influence gene expression patterns without altering the DNA sequence [6,7].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [7]
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References 119 · Cited by 222
- Authors
- Lillycrop, K. A., & Burdge, G. C.
- Affiliations
- University of Southampton (GB)
- Corresponding author
- Lillycrop, K A
- Venue
- International Journal of Obesity
- Published
- 2010-06-15
- Volume
- 35
- Issue
- 1
- Pages
- 72-83
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- OpenAlex
- W2079926361
- Cited by
- 222
- References
- 119
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 9 · 2023: 3 · 2022: 10 · 2021: 7 · 2020: 13 · 2019: 13 · 2018: 15 · 2017: 17 · 2016: 9 · 2015: 16 · 2014: 20 · 2013: 32 · 2012: 30
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- International Journal of Obesity (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- 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 › Genetic Syndromes and Imprinting
- Keywords
- epigenetic regulation, early life environment, obesity risk, low birth weight, maternal undernutrition, maternal overnutrition, fetal programming, postnatal nutrition, gene expression, metabolism, obesity prevention
- MeSH terms
- Animals, Female, Humans, Infant, Infant, Newborn, Male, Obesity, Pregnancy, Risk Factors, DNA Methylation, Prenatal Nutritional Physiological Phenomena, Epigenesis, Genetic, Fetal Development, Rats
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