irth weight of people is related to their risk of noninsulin dependent diabetes mellitus (NIDDM), which may reflect intra-uterine programming of disease risk, or common genetic factors related both to birth weight and to NIDDM risk. The latter has been called the ''fetal insulin hypothesis''. 1 Currently there is little direct evidence for this hypothesis, although two studies have shown an inverse association between fathers' risk of diabetes and the birth weight of their offspring. 2 3 Findings with respect to paternal diabetes are of particular interest because they cannot directly reflect an influence of the intra-uterine environment. Conversely, impaired glucose tolerance in pregnant women is associated with greater offspring birth weight, 4 and as women with impaired glucose tolerance during pregnancy are at an increased risk of developing diabetes 5 the expecta- tion is of a positive association between offspring birth weight and maternal diabetes risk. This evidence suggests that as time increases after the birth of offspring an inverse association emerges between offspring birth weight and maternal insulin resistance 6 and diabetes.
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George Davey Smith (2004) studied this question.
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