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Markers of fetal onset adult diseases.

The fetal origins hypothesis, proposes that non-communicable diseases including coronary heart disease, type 2 diabetes and hypertension originate through the responses of a fetus to undernutrition, that permanently change the structure and function of the body. Associations between low birthweight and disease in later life have been widely studied in Europe and the USA. Studies in southern India have shown that babies who are short and fat tend to become insulin deficient and have high rates of non-insulin dependent diabetes. These findings have important public health implications as it suggests that associations with body size at birth underestimate the contribution of intrauterine development to later disease, and also, that while the primary prevention of coronary heart disease and non-insulin dependent diabetes may ultimately depend on changing the body composition and diets of young women. Therefore, more immediate benefit may come from preventing imbalances between prenatal and postnatal growth among children. The basic premise of the thrifty gene hypothesis is that certain populations may have genes that determine increased fat storage, which in times of famine represent a survival advantage, but in a modern environment result in obesity and type 2 diabetes. The fetal origins theory is of greatest relevance to the developing world and the implications of this work for global health are enormous. To reduce chronic diseases, we need to understand how the human fetus is nourished and how malnutrition changes its physiology and metabolism, so that interventions be implemented to limit the damage. The challenge for the next decade must be to discover the cellular and molecular mechanisms giving rise to these associations. If this aim is accomplished, it might be possible to devise strategies to reduce the impact of these disabling chronic and expensive diseases.