[Foetal programming of nutrition-related chronic diseases]

Hélène Delisle
Santé: Cahiers D'étude et de Recherches Francophones 2002, 12 (1): 56-63
Intrauterine growth retardation, which reflects in large part maternal malnutrition in poorer communities, contributes to chronic disease risk through foetal programming, according to the early origins hypothesis of Barker. Foetal programming implies that during critical periods of prenatal growth, permanent changes in metabolism or structures result from adverse intrauterine conditions. Observational studies first showed an association between lower birth weights and higher rates of coronary disease in the 80s, in England and Scandinavia. The link between low birth weights, or other indicators of small birth size, and cardiovascular disease was later confirmed in many epidemiological studies, including in the USA and in India. Similarly, a reverse relationship of birth weight and systolic blood pressure was shown in men and women, in developed as well as developing countries, and in all age groups, although it was less consistent in adolescents. Insulin resistance and type-2 diabetes have also been found to be independently related to small size at birth in several studies around the world. Insulin resistance associated with small size at birth was frequently shown to be present at a young age. The association of small birth size with chronic disease tends to increase with catch-up growth and obesity, and usually persists after adjusting for confounding factors such as age, family history, and socio-economic status. Several, but not all, twin studies lend support to the hypothesis. There is a tendency for lighter members of twin pairs to have a higher blood pressure, and more diabetes. Observations in people exposed to the Dutch famine while in utero also tend to corroborate the hypothesis. Those who were exposed early in their intrauterine life did not have lower birth weights, but they were prone to becoming obese later on. In contrast, those exposed towards the end of gestation had lower birth weights, and showed a higher rate of impaired glucose tolerance, while having a lower risk of obesity. Dietary manipulations in animal models provide further support and mechanistic explanations, in particular protein deficiency in pregnant rats, which elevates blood pressure, impairs glucose tolerance, and increases the likelihood of obesity in the progeny. Although there are still controversial areas, there is at present sufficient scientific evidence for foetal programming to be regarded as an additional risk factor for chronic disease, in interaction with genetic and lifestyle risk factors. The fact that intrauterine growth retardation may predispose to nutrition-related chronic disease has serious implications for developing countries, particularly those undergoing rapid nutritional transition, as it may further increase the rates of obesity, cardiovascular disease and diabetes when diets and lifestyles are in themselves "atherogenic". The challenge is for programmes to simultaneously combat apparently opposite nutrition problems, malnutrition and "over-nutrition". Improving the nutrition of women is even more imperative when considering that it may contribute to preventing chronic diseases in the next generation, in addition to enhancing health and survival of mothers and children.

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