Purpose of review
Food-induced anaphylaxis continues to be an important cause of hospital admissions, particularly in children. This review outlines recent advances in understanding the epidemiology of IgE-mediated food allergy and potential mechanisms for its rise in prevalence.
The rise in food allergy prevalence in Western countries has happened more quickly than changes to the genome can occur; thus, environmental changes are likely to be important. Recent studies, however, suggest that genetic risk determines responses to environmental risk factors. Environmental peanut exposure has been associated with increased peanut allergy risk in individuals with filaggrin null mutations, consistently with sensitization occurring through a damaged skin barrier. Reduced microbial and vitamin D exposure is also leading candidates for risk factors for food allergy in the context of genetic susceptibility. In addition, HLA-DR and HLA-DQ gene region variants appear to play a role in peanut allergy, although no studies have yet assessed their susceptibility to environmental cues. Finally, findings from observational cohorts and the first large-scale intervention trials for food allergy prevention support early oral allergen exposure to reduce the prevalence of specific food allergies, which is informing changes in public health guidelines at the population level. Further research will be required to assess the impact of these guideline changes on the population prevalence of food allergy.
New studies are providing important insights into the prevalence, causes, and mechanisms of food allergy. Recent findings are informing changes to population health guidelines in developed countries, which have the potential to halt or reverse the increase in food allergy prevalence. By contrast, food allergy in the developing world remains understudied.