Questioning the role of genes and maternal nutrition

Papers pp 1325, 1330

The weight of evidence linking reduced size at birth to raised blood pressure is now substantial1 and that for an increased risk of non-insulin dependent diabetes and coronary heart disease is increasingly convincing. Despite continuing scepticism,2 initial concerns that these statistical associations were due to chance, artefact, or confounding by factors in later life have been largely resolved. Attention is now turning towards elucidating underlying mechanisms and the public health importance of the “fetal origins” hypothesis.

Over the past five years the biological plausibility that circumstances in utero can “program” the fetus, such that postnatal physiology and disease risk are altered, has been bolstered by evidence from animal models. Experimental manipulation of the environment of the fetus in utero, through modifying the maternal diet and other means, can undoubtedly have profound long term effects on structure and function.3

The direct relevance of these animal models to humans has not been adequately assessed, particularly with regard to maternal nutrition Nevertheless, they provide an important counterpoint to the suggestion that genetic rather than environmental factors drive the association between impaired growth and later disease in humans.4 More direct human evidence about the possibility …