Smoking, birthweight, and mortality across generations

This editorial refers to ‘Cardiovascular mortality in relation to birth weight of children and grandchildren in 500 000 Norwegian families’[†][1], by O. Naess et al. , on page 3427 Beginning in the 1980s there has been considerable research into the possible role that the intrauterine environment may have in ‘programming’ adult disease— in particular, cardiovascular diseases (CVDs) and diabetes—in later life. The original ‘foetal-origins’ hypothesis was developed by David Barker and colleagues at the University of Southampton who produced a substantial number of reports detailing the possible effects that poor maternal and foetal nutrition (as measured most often by birthweight) had on cardiovascular risk factors and mortality in later life.1 This ‘foetal-programming’ was suggested to be an adaptive response made by the fetus in order to survive a suboptimal ‘intrauterine’ environment whilst simultaneously rendering the same individual at greater risk of chronic disease in adulthood. Andrew Hattersley and colleagues subsequently proposed an alternative explanation. They suggested that genetic factors were primarily responsible for both foetal growth restriction and the development of insulin resistance and other cardiovascular disorders in adult life, the ‘foetal-insulin’ hypothesis.2 However, trying to disentangle any genetic effects—‘nature’—from the impact of the maternal and foetal environment—‘nurture’—on the associations between birthweight and disease in adult life is a challenging undertaking.Naess and colleagues have now explored the relationships between offspring birthweight and CVD mortality in both parents and grandparents among half a million Norwegian families.3 By doing so, they hoped to elucidate the potential pathways—nature, nuture, or a combination thereof—that mediate the reported associations between low birthweight and … [1]: #fn-2