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Failure to realise growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men

^a Epidemiology Unit, London School of Hygiene and Tropical Medicine, London WC1E 7HT, ^b Institute for Geriatrics, Uppsala University, PO Box 609, S-751 25 Uppsala, Sweden, ^c Swedish Institute for Social Research, University of Stockholm, S-10691 Stockholm, Sweden

Correspondence to: Dr Leon.

Abstract

Objectives: To clarify the type of fetal growth impairment associated with increased blood pressure in adult life, and to establish whether this association is influenced by obesity and is mediated through impairment of insulin action.
Design: Cross sectional survey with retrospective ascertainment of size at birth from obstetric archives.
Subjects: 1333 men resident in Uppsala, Sweden, who took part in a 1970 study of coronary risk factors at age 50 and for whom birth weight was traced.
Main outcome measures: Systolic and diastolic blood pressure at age 50.
Results: In the full study population for a 1000 g increase in birth weight there was a small change in systolic blood pressure of -2.2 mm Hg (95% confidence interval -4.2 to -0.3 mm Hg) and in diastolic blood pressure of -1.0 mm Hg (-2.2 to 0.1 mm Hg). Much stronger effects were observed among men who were born at term and were in the top third of body mass index at age 50, for whom a 1000 g increase in birth weight was associated with a change of -9.1 mm Hg (-16.4 to -1.9 mm Hg) systolic and -4.2 mm Hg (-8.3 to -0.1 mm Hg) diastolic blood pressure. Men who were light at birth (<3250 g) but were of above median adult height had particularly high blood pressure. Adjustment for insulin concentrations reduced the associations of birth weight with systolic and diastolic blood pressure.
Conclusions: A failure to realise growth potential in utero (as indicated by being light at birth but tall as an adult) is associated with raised adult blood pressure. Impaired fetal growth may lead to substantial increases in adult blood pressure among only those who become obese. Metabolic disturbances, possibly related to insulin resistance, may provide a pathway through which fetal growth affects blood pressure.

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