Abstract

Abstract It is hypothesized that the risk of cardiovascular disease and diabetes in adult life is programmed in utero by specific patterns of abnormal fetal growth associated with maternal undernutrition. This hypothesis raises fundamental questions about patterns of fetal growth in utero and about the role of factors other than nutrition in fetal growth and development. An unambiguous concept of nutrition that relates to the mother’s diet, growth, and development in childhood, and her diet during pregnancy, facilitates the testing of precisely formulated hypotheses in work on nutrition, fetal growth and adult disease. Different patterns of fetal growth retardation in pregnancy form a continuum that depends mainly on the severity and timing of thenutritional or other insult. Growth failure in the third trimester tends to be asymmetrical, with weight loss but a relative sparing of fetal length. The hypothesis that nutritional insults in early pregnancy set the fetus on a low growth trajectory leading to symmetrical growth retardation is less securely based. The concept of nutritional programming is undoubtedly plausible in biological terms. However, a less discrete and deterministic model of programming is proposed, involving interactions between the maternal and fetal genotype, the mother’s environment and life style (including diet), her prepregnancy nutritional status, metabolism and physiology, the hormonal, metabolic and circulatory milieu which sustains fetal growth and the infant’s postnatal environment. The effects of prenatal nutrition on fetal growth in man depend on the timing of nutritional exposures in relation to critical periods of development and on interactions with the mother’s prepregnancy nutritional status and aspects of the mother’s metabolism and physiology such as glucose tolerance and blood pressure.

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