Data from epidemiological studies conducted in several countries worldwide have revealed that the prevalences of allergic conditions, including allergic rhinitis, asthma and eczema, have increased from the 1940s/50s to the 1990s. These allergic conditions involve specific IgE-mediated responses, and a few studies have demonstrated that IgE levels have increased in some communities over time in a manner similar to the incidences of allergic conditions. The predisposition for atopy appears to be determined in early life, and evidence indicates that events occurring in utero and in infancy can influence the future development of atopy. The intrauterine environment favours TH2 cell development and IgE production and could predispose to atopy. It can be hypothesized that dietary or other factors favouring TH2 proliferation might contribute to the development of atopic disease. Conversely, early infection has been found to have a negative association with the development of atopy, perhaps through promotion of a TH1 response; the reduction in infection in the very young as a consequence of modern healthcare may have contributed to the increase in atopic disease. Thus, it is a plausible hypothesis that changes in the conditions of the intrauterine environment and/or in infancy (for example, in nutrition and in rates of infection) may explain the observed increases in atopy and allergic conditions.