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Nutrients 2014, 6(6), 2165-2178; doi:10.3390/nu6062165

Early Life Nutrition, Epigenetics and Programming of Later Life Disease

Liggins Institute and Gravida, National Centre for Growth and Development, University of Auckland, 85 Park Road, Grafton, Auckland 1142, New Zealand
Received: 17 March 2014 / Revised: 21 April 2014 / Accepted: 19 May 2014 / Published: 2 June 2014
(This article belongs to the Special Issue Nutritional Epigenetics)
View Full-Text   |   Download PDF [203 KB, uploaded 2 June 2014]

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. View Full-Text
Keywords: developmental programming; maternal nutrition; epigenetics; DNA methylation; transgenerational developmental programming; maternal nutrition; epigenetics; DNA methylation; transgenerational
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Vickers, M.H. Early Life Nutrition, Epigenetics and Programming of Later Life Disease. Nutrients 2014, 6, 2165-2178.

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