Intrauterine factors, adiposity, and hyperinsulinaemia

摘要

The first world congress on fetal origins of adult disease was held in Mumbai, India, in 2001. The second congress was recendy held in Brighton, United Kingdom. In spite of their diverse locations both these meetings were dominated by data from developed countries. This is largely a consequence of the extreme rarity of good historical records of birth size from developing countries. The recent insights emerging from prospective studies by Yajnik et al in Pune in India are therefore notable and deserve attention. The core of the theory of fetal origins of disease is that nutritional deprivation of the fetus during critical periods of development forces the baby to resort to adaptive survival strategies, which entail a resetting of the normal course of metabolic, physiological, and anatomical development These adaptations become mala-daptive if the organism encounters contrasting nutritional circumstances in later life. In relation to insulin action and diabetes Hales and Barker have described this phenomenon as the "thrifty phenotype. In the words of J V Neel, the initial proponent of the thrifty genotype hypothesis, the thrifty phenotype is "rendered detrimental by progress" and leads to high rates of metabolic syndrome and type 2 diabetes. Recently it has become apparent that it is the disharmony between fetal growth and later growth rates that seems to be the best predictor of the later pathology.