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Low rates of growth in early life are now known to be associated with an increase in age related disease in later life.1 This is thought to reflect programming, the process whereby a stimulus or insult acting at a critical period of development in early life, has lasting or lifelong importance.2 In animal experiments that have examined the mechanisms responsible for programming, attention has focused on prenatal undernutrition and its influence on gene expression, cell division and differentiation, and tissue structure.
Fetal growth and adult disease
Epidemiological studies have shown that markers of poor fetal growth, including low early weight, thinness, and shortness at birth, are associated with increased mortality and morbidity from cardiovascular disease in later life.1 3 Correlations have also been shown between poor early growth and the major cardiovascular risk factors—raised blood pressure,4raised plasma fibrinogen5 and serum cholesterol concentrations,6 impaired glucose tolerance7and reduced arterial compliance.8 These associations were first established by studies in Hertfordshire, where from 1911 to 1948, every newborn baby was weighed and followed up to the age of 1 year. The prevalence of non-insulin diabetes and impaired glucose tolerance, for example, falls threefold between men who weighed 5.5 pounds at birth and those who weighed 9.5 pounds.7 These associations have been replicated in several different countries including the United States9 and India10 as well as in Britain. The associations are independent of adult lifestyle, and are not limited to cardiovascular disease. Chronic obstructive pulmonary disease11 and reduced bone mineral content12 13 are both associated with reduced growth in utero and during infancy. The major determinant of fetal growth is nutrition14-16 and the fetal origins hypothesis proposes that fetal undernutrition programmes the long term adverse sequelae of small size at birth. Cardiovascular disease, impaired …
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