David Barker’s “fetal origins” hypothesis has changed the way we think about the aetiology of adult onset diseases, such as coronary heart disease and type 2 diabetes.1 Underpinning the epidemiological evidence are recent animal data which suggest that fetal programming of these diseases by prenatal nutrition may be mediated through epigenetic mechanisms.2 If adult onset disease is partly programmed in utero, it seems even more plausible that the prenatal environment influences the inception of asthma, which may first manifest in infancy. A number of exposures during pregnancy have been implicated3^–5 and, although data are conflicting, associations with birth anthropometry prompted speculation that prenatal nutrition might programme fetal lung and immune development leading to asthma and atopy.6 Given that the diet of pregnant mothers has clearly changed considerably while asthma has been rising, the notion that it might be modified as a strategy for the primary prevention of asthma has considerable appeal.7 This has perhaps been reinforced by recent disappointments with dietary interventions aimed at secondary prevention of adult asthma.8

NUTRIENTS, FOODS OR DIETARY PATTERNS?

Trying to measure prenatal nutrition presents a major challenge for epidemiologists. Estimating maternal dietary intake in pregnancy, usually using a semiquantitative food frequency questionnaire on one occasion, leads to considerable exposure misclassification, and fetal nutrition will depend, not just on maternal intake, but also on nutrient absorption by the mother, placental transfer and fetal demand. Nutrients measured in maternal blood during pregnancy may be useful to validate dietary intake, and biomarkers measured in umbilical cord blood, cord tissue or deciduous tooth enamel may estimate fetal exposure more precisely. Furthermore, biomarkers may be the best way to capture the overall status of nutrient exposures such as vitamin D which are not exclusively determined by diet.

Initial epidemiological interest focused on the antioxidant hypothesis,9 …