The fetal origins of adult diseaseBMJ 2001; 322 doi: https://doi.org/10.1136/bmj.322.7283.375 (Published 17 February 2001) Cite this as: BMJ 2001;322:375
No longer just a hypothesis and may be critically important in south Asia
- Roger Robinson, associate editor
David Barker pioneered the idea that the 20th century epidemic of coronary heart disease in Western countries might have originated in fetal life.1
Paradoxically, the epidemic coincided with improved standards of living and nutrition, yet in Britain its greatest impact was in the most deprived areas. Barker observed that early in the 20th century these areas had the highest rates of neonatal mortality and by inference the highest rates of low birth weight. He postulated that impaired fetal growth might have predisposed the survivors to heart disease in later life. The first world congress on the fetal origins of adult disease in Mumbai earlier this month provided an opportunity to assess the state of the hypothesis and consider its implications for future research and policy.
Barker's group originally examined cardiovascular mortality in men born in Hertfordshire, England, in the early decades of the century, on whom good records had been kept of size at birth and growth in infancy. Deaths from ischaemic heart disease were indeed commoner in men who had been small at birth and at 1 year. This kind of retrospective cohort study depends on anthropometric measurements in infancy having been preserved. At least seven such studies have shown that lower birth weight is associated with higher risks of later ischaemic heart disease and diabetes or impaired glucose tolerance. These …
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