BMJ 1999;319:1313-1314 ( 20 November )

Editorials

Twins and fetal programming of blood pressure

Questioning the role of genes and maternal nutrition

Papers pp   1325 , 1330

The first 150 words of the full text of this article appear below.

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 . . . [Full text of this article]

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