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Developmental programming of health and disease

Published online by Cambridge University Press:  07 March 2007

Simon C. Langley-Evans*
Affiliation:
School of Biosciences, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, UK
*
*Corresponding author: S Dr Simon Langley-Evans, fax +44 115 951 6122, email Simon.Langley-Evans@Nottingham.ac.uk
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Abstract

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The environment encountered in fetal and neonatal life exerts a profound influence on physiological function and risk of disease in adult life. Epidemiological evidence suggests that impaired fetal growth followed by rapid catch-up in infancy is a strong predictor of obesity, hypertension, non-insulin-dependent diabetes and CHD. Whilst these associations have been widely accepted to be the product of nutritional factors operating in pregnancy, evidence from human populations to support this assertion is scarce. Animal studies clearly demonstrate that there is a direct association between nutrient imbalance in fetal life and later disease states, including hypertension, diabetes, obesity and renal disease. These associations are independent of changes in fetal growth rates. Experimental studies examining the impact of micro- or macronutrient restriction and excess in rodent pregnancy provide clues to the mechanisms that link fetal nutrition to permanent physiological changes that promote disease. Exposure to glucocorticoids in early life appears to be an important consequence of nutrient imbalance and may lead to alterations in gene expression that have major effects on tissue development and function. Epigenetic mechanisms, including DNA methylation, may also be important processes in early-life programming.

Type
Nutrition Society Medal Lecture
Copyright
Copyright © The Nutrition Society 2006

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