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Study Disputes Link Between Increased Birthweight And Reduced Blood Pressure Later In Life (p 659)

August 28, 2002

Authors of a meta-analysis in this week's issue of THE LANCET cast doubt over the widely held belief that lower birthweight is associated with higher blood pressure in adult life.

The 'fetal origins' hypothesis proposes that impaired fetal development leading to low birthweight is associated with poorer health outcomes later in life; specifically, previous research supporting this hypothesis has suggested that a 1 kg increase in birthweight is associated with a 2-4 mmHg reduction in systolic blood pressure in adult life, with corresponding health benefits. Rachel Huxley from the Institute for International Health, Sydney, Australia, and colleagues reanalysed data from previous research to investigate whether statistical bias or inconsistencies could have been responsible for previous findings supportive of the fetal origins hypothesis.

55 studies that had reported quantitative estimates of the association between systolic blood pressure and birthweight, 48 further studies that were excluded from previous analyses, and seven studies on identical twins were included in the reanalysis. There was a clear trend towards much weaker associations between low birthweight and high adult systolic blood pressure in the larger, more informative studies. Research on identical twins (which are less prone to confounding and avoid any genetic effects) showed the same magnitude of association-around 0.6 mmHg reduction for a 1 kg increase in birthweight-as that observed in the larger studies (those involving more than 3000 participants). In addition, there was good evidence that publication bias may have contributed to previous overestimates for the size of the association, as only around a half (25 of 48) of previously excluded studies reported an association between lower birthweight and higher adult blood pressure.

Rachel Huxley comments: "The evidence reviewed here suggests that claims of a strong inverse association between birthweight and subsequent blood pressure may chiefly reflect the failure to take sufficient account of the impact of random error, the selective emphasis of particular results, the inappropriate adjustment for current body size, and inadequate adjustment for potential confounding factors such as parental blood pressure and socio-economic status. Since this association has been described previously as providing some of the strongest, and most consistent, support for the fetal origins hypothesis, it would seem prudent to subject other supporting evidence to a similar critical appraisal."

Lancet