Barker DJP. The fetal origins of coronary heart disease. Acta Paediatr 1997; Suppl42278-82. Stockholm.Animal studies have shown that undernutrition before birth programmes persisting changes in a range of metabolic, physiological and structural parameters. Studies in humans have shown that men and women whose birthweights were at the lower end of the normal range, who were thin or short at birth or small in relation to placental size have increased rates of coronary heart disease. We are beginning to understand something of the mechanisms underlying these associations. R Binhweight, coronary heart disease, fetal undernutrition, placental size, programming DJP Barker,

No abstract

Recent finding suggest that many fetuses have to adapt to a limited supply of nutrients and in doing so they permanently change their physiology and metabolism. These 'programmed' changes may be the origins of a number of diseases in life, including coronary heart disease and the related disorders stroke, diabetes and hypertension.

Objectives-To examine the relation between disproportionate fetal growth and adult blood pressure and to investigate whether arterial compliance in adult life is related to early development. Design-A follow up study of a group of men and women whose birth weights and other measurements of body size had been recorded at birth. Setting-Home and outpatient study. Subjects-337 men and women born in the Jessop Hospital, Sheffield, between 1939 and 1940. Main outcome-Adult systolic and diastolic blood pressures and arterial compliance as measured by pulse wave velocity in two arterial segments. Results-Both systolic and diastolic blood pressures were higher in people whose birth weight was low, who were short or who had small abdominal or head circumferences at birth. Systolic blood pressure decreased by 2f7 mm Hg (95% CI 0f8 to 4.6) for each pound (454 g) gain in birth weight and by 3'4 mm Hg (95% CI 1P4 to 5.4) for each inch (2.54 cm) increase in crown-heel length. Diastolic pressure fell by 1 9 mm Hg (95% CI 0 9 to 2.9) for each pound (454 g) gain in birth weight and by 2-4 mm Hg (95% CI 1.4 to 3.5) for each inch (2.54 cm) increase in length. Systolic blood pressure was also higher in individuals whose mother's intercristal pelvic diameter was small or whose mother's blood pressure had been raised during pregnancy but these effects were statistically independent ofthe effects of low birth weight and other measurements that indicate fetal growth retardation. Arterial compliance was lower in those who had been small at birth. Conclusion-Impairment of fetal growthis associated with raised blood pressure in adult life and decreased compliance in the conduit arteries of the trunk and legs. (Br Heart J 1995;73:116-121)