[Fetal programming--the intrauterine origin of adult morbidity]
- PMID: 16128013
[Fetal programming--the intrauterine origin of adult morbidity]
Abstract
Many epidemiological studies have demonstrated an association between low birth weight and the subsequent development of hypertension, insulin resistance, type 2 diabetes and cardiovascular disease. This association appears to be independent of classic lifestyle risk factors such as smoking, overweight, social class, alcohol consumption and lack of exercise, which are additive to the effect. The association holds for the full range of birth weights, including those within the normal range. In addition, it was suggested that faster postnatal catch-up growth may also predict later risk of cardiovascular disease. 'Fetal programming' has been proposed as a mechanism underlying the link related to low birth weight, rapid neonatal growth and adult disease. The fetal programming hypothesis suggests that the intrauterine environment during critical periods of organogenesis and tissue growth may permanently alter organ structure and function in an epigenetic manner. Indeed, evidence from both human and animal studies suggests that diseases of adult life are induced by the fetal environment. This review describes epidemiological and physiological evidence that the programming phenomenon is a major factor in determining later life diseases. Better management of pregnancy in the present will have long term wide-scale effects on the health of our society.
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