Commentary: The art and science of epidemiology: governed by the seasons?

Epidemiology is the study of ‘the distribution and determinants of health-related events in specified populations, and the application of this study to the control of health problems’.1 Observational epidemiology is bedevilled by problems of uncertainty, bias, and confounding in a world that demands certainty and clear guidance from health scientists.2 The discrepant findings between observational studies and randomized controlled trials of the associations between hormone replacement therapy and coronary heart disease (CHD), and the media and health professional responses to these discrepancies, are a particular example. Two studies3,4 published in this issue of the International Journal of Epidemiology (IJE) are, I think, important since they demonstrate examples of good epidemiological science and the art required in appropriately using epidemiological findings to affect public health policy. In 1999 Moore and colleagues undertook a study, that was published in the IJE, which showed that individuals who were born during the ‘hungry season’ in rural Gambia and who survived to at least 15 years of age had a greatly increased risk of mortality (primarily due to infectious causes) in young adulthood.5 Mortality under the age of 15 years was not affected by season of birth, and when all age groups were combined there was no overall difference in mortality by season of birth.5,6 They explored a number of possible explanations for the association between season of birth and mortality beyond the age of 15 years and excluded ‘chance’ on the basis of the strong effects and small P-values. Explanations relating to maternal or infant infectious or toxin exposures seemed unlikely. There was, however, a link between decreasing maternal weight in the last trimester of pregnancy, lower birthweight infants, and the increased risk of mortality from infectious diseases in young adulthood, all of which were related to the ‘hungry season’. The authors hypothesized that maternal, and hence fetal under-nutrition during critical periods of development, programmed abnormalities in immune function resulting in greater risk to infectious diseases in later life.5 Those findings and the suggested hypothesis were very much in line with the fetal origins of adult disease hypothesis which, until that time, had largely investigated the fetal origins of chronic degenerative adult diseases such as diabetes and cardiovascular disease in the developed world.7 Although a chance finding seemed unlikely, and the suggested explanation for the association was both plausible and backed-up by data demonstrating the associated changes in maternal weight and birthweight, the authors recognized the importance of replicating their findings. Moore and colleagues searched for other suitable datasets and in today’s IJE repeat their analyses in a rural population from Bangladesh.3 At the same time Simondon and colleagues have undertaken similar analyses in a rural population from Senegal.4 Neither study confirms the previous findings, but the fact that Moore et al. in particular recognize the importance of publishing their null findings is an example of good science. Moore and colleagues state (and demonstrate) that: