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N R Poulter a Cardiovascular Studies Unit, Department of Clinical
Pharmacology, Imperial College School of Medicine, St Mary's Campus,
London W2 1PG, b Twin Research and Genetic
Epidemiology Unit, St Thomas's Hospital, Guy's and St Thomas's
Hospital Trust, London SE1 7EH
Correspondence to: N R Poulter
n.poulter{at}ic.ac.uk
Objectives:
To evaluate the associations in twins
between within pair differences in birth weight and subsequent blood
pressures as adults thereby removing the impact of potential parental
confounding variables.
Design:
Historical cohort study.
Setting:
St Thomas's UK adult twin register, June
1992 to September 1995.
Participants:
492 pairs of female twins (mean age 54 years).
Main outcome measures:
Mean within pair differences in
adult blood pressure in each of four strata of within pair differences
in birth weight (0, 1-500 g, 501-1000 g, >1000 g). Differences in blood pressure were analysed before and after adjustment for potential confounders between adult twins, after exclusion of those twin pairs
including at least one twin taking antihypertensive drugs, and by zygosity.
Results:
Reported mean birth weights of heavier and lighter twins were 2.51 (SD 0.61) v 2.12 (0.59) kg
respectively. A graded inverse relation between strata of within pair
differences in birth weight and differences in adult blood pressure was
apparent, with an adjusted blood pressure range of 8.7/5.1 mm Hg across the four strata (test for trend: systolic, P=0.05; diastolic, P=0.09).
After excluding those women taking antihypertensive drugs the
significance of the association was similar (systolic, P=0.04; diastolic, P=0.10). When differences in blood pressure were stratified for zygosity similar but non-significant trends were apparent.
Conclusion:
It would seem that birth weight is
inversely associated with adult blood pressure and that this
association is independent of parental confounding variables probably
including, in view of the findings in monozygotic twins, genetic
factors. The observed blood pressure differences are likely to result
from retarded intrauterine growth due to placental dysfunction rather than inadequate maternal nutrition.
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