Abstract
In recent years, the prevalence of immunoglobulin E (IgE)-mediated food allergy appears to be rising. Our ability to confirm this epidemiologic trend is limited. Over the past several decades, multiple cohorts have been established to investigate the etiologic risk factors and natural history of asthma and allergic diseases.1 The allergic (atopic) march includes the development of eczema, food allergy, allergic rhinitis, and asthma. One of the great tools of clinical epidemiology, the longitudinal cohort, has been successful in describing the allergic march, but this approach has been severely underutilized to study food allergy.
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