The fetal and early life origins of adult disease
The fetal and early life origins of adult disease
The fetal origins of adult disease (FOAD) hypothesis is based on the observation that men and women who were small at birth (low birthweight) have an increased risk of atherosclerotic cardiovascular disease (CVD) and the related diseases hypertension, type 2 diabetes and the Insulin Resistance Syndrome. Risk is increased further if they showed rapid weight gain in childhood or become obese. The hypothesis proposes that CVD is ‘programmed’ by under nutrition during critical periods of early development and that ‘poverty’ during early life creates a permanent vulnerability to ‘diseases of affluence’. This concept is arguably of greatest relevance to developing countries, where fetal growth restriction still affects large numbers of people, where economic progress is leading to the emergence of childhood and adult obesity, and where CVD and type 2 diabetes are rising rapidly. Its implication is that the prevention of adult disease should include strategies to improve maternal health and fetal growth. This paper reviews work leading to the FOAD hypothesis and the results of FOAD research in India. It also discusses some of the controversies surrounding the hypothesis, notably the debate as to whether the link between fetal growth restriction and adult CVD is mediated by environmental factors (such as maternal nutrition) or by genes.
adult disease, fetal, low birthweight, obesity
480-502
Fall, Caroline H. D.
7171a105-34f5-4131-89d7-1aa639893b18
2003
Fall, Caroline H. D.
7171a105-34f5-4131-89d7-1aa639893b18
Fall, Caroline H. D.
(2003)
The fetal and early life origins of adult disease.
Indian pediatrics, 40 (5), .
Abstract
The fetal origins of adult disease (FOAD) hypothesis is based on the observation that men and women who were small at birth (low birthweight) have an increased risk of atherosclerotic cardiovascular disease (CVD) and the related diseases hypertension, type 2 diabetes and the Insulin Resistance Syndrome. Risk is increased further if they showed rapid weight gain in childhood or become obese. The hypothesis proposes that CVD is ‘programmed’ by under nutrition during critical periods of early development and that ‘poverty’ during early life creates a permanent vulnerability to ‘diseases of affluence’. This concept is arguably of greatest relevance to developing countries, where fetal growth restriction still affects large numbers of people, where economic progress is leading to the emergence of childhood and adult obesity, and where CVD and type 2 diabetes are rising rapidly. Its implication is that the prevention of adult disease should include strategies to improve maternal health and fetal growth. This paper reviews work leading to the FOAD hypothesis and the results of FOAD research in India. It also discusses some of the controversies surrounding the hypothesis, notably the debate as to whether the link between fetal growth restriction and adult CVD is mediated by environmental factors (such as maternal nutrition) or by genes.
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Published date: 2003
Keywords:
adult disease, fetal, low birthweight, obesity
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Local EPrints ID: 25482
URI: http://eprints.soton.ac.uk/id/eprint/25482
ISSN: 0019-6061
PURE UUID: 5663cbe4-2a71-4396-9c16-c42c41c5ba5b
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Date deposited: 07 Apr 2006
Last modified: 23 Jul 2022 01:33
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