Cited by 366Birth, Development, and HealthEpigenetics and DNA MethylationNutrition, Genetics, and Disease

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Early Life Nutrition, Epigenetics and Programming of Later Life Disease

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Vickers, Mark·2014·Nutrients

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Abstract

The global pandemic of obesity and type 2 diabetes is often causally linked to marked changes in diet and lifestyle; namely marked increases in dietary intakes of high energy diets and concomitant reductions in physical activity levels. However, less attention has been paid to the role of developmental plasticity and alterations in phenotypic outcomes resulting from altered environmental conditions during the early life period. Human and experimental animal studies have highlighted the link between alterations in the early life environment and increased risk of obesity and metabolic disorders in later life. This link is conceptualised as the developmental programming hypothesis whereby environmental influences during critical periods of developmental plasticity can elicit lifelong effects on the health and well-being of the offspring. In particular, the nutritional environment in which the fetus or infant develops influences the risk of metabolic disorders in offspring. The late onset of such diseases in response to earlier transient experiences has led to the suggestion that developmental programming may have an epigenetic component, as epigenetic marks such as DNA methylation or histone tail modifications could provide a persistent memory of earlier nutritional states. Moreover, evidence exists, at least from animal models, that such epigenetic programming should be viewed as a transgenerational phenomenon. However, the mechanisms by which early environmental insults can have long-term effects on offspring are relatively unclear. Thus far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification, and microRNA) and permanent changes in cellular ageing. A better understanding of the epigenetic basis of developmental programming and how these effects may be transmitted across generations is essential for the implementation of initiatives aimed at curbing the current obesity and diabetes crisis.

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“Also, it has been reported that early life developmental issues strongly associate with the prevalence of obesity and related metabolic disorders later in life [5,6].”
Background
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Authors: Vickers, M.
Affiliations: University of Auckland (NZ)
Corresponding author: Vickers, Mark
ORCID: Vickers, Mark
Venue: Nutrients
Publisher: MDPI AG
Published: 2014-06-02
Volume: 6
Issue: 6
Pages: 2165-2178
ISSN: 2072-6643 (ISSN-L)
DOI: 10.3390/nu6062165
PMC: PMC4073141
OpenAlex: W2061809258
Cited by: 366
References: 79
Citations by year: 2026: 17 · 2025: 15 · 2024: 18 · 2023: 13 · 2022: 28 · 2021: 23 · 2020: 39 · 2019: 46 · 2018: 41 · 2017: 41 · 2016: 43 · 2015: 29 · 2014: 13
FWCI: 6.24
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (vor)
Locations: Nutrients (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: Royal Society
Royal Society Te Apārangi
Health Research Council of New Zealand
Marsden Fund
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: developmental programming, early life nutrition, epigenetics, obesity, type 2 diabetes, metabolic disorders, developmental plasticity, transgenerational epigenetic inheritance, DNA methylation, histone modifications, microRNA, cellular aging, critical developmental periods
MeSH terms: Aging, Female, Humans, Infant, Infant Nutritional Physiological Phenomena, Metabolic Diseases, Pregnancy, Maternal Nutritional Physiological Phenomena, Epigenomics

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