The role of food hypersensitivity in the pathogenesis of atopic dermatitis (AD) and other atopic diseases has been debated for years. In the 1930s, Engman described a wheat-sensitive child who developed eczematoid skin changes following wheat ingestion, but only on areas unprotected by occlusive dressing, suggesting a role for food-induced pruritus and scratching in the development of the dermatitis. More recently studies have renewed interest in the role of food hypersensitivity in the pathogenesis of atopic dermatitis (AD) and other atopic disorders. However, questions with respect to disease definition, study design, and adequacy of controls left uncertain the importance of food in the pathogenesis of AD and other atopic diseases, such as asthma. The primary hypothesis is that food hypersensitivity reactions exhibit both immediate and late-phase components that may be recognized clinically (development of objective physical findings) and by detection of mediators characteristic of mast cells and basophils in the circulating blood. In patients having late-phase reactions additional cell types are involved and may be detected by elevation of serum eosinophil cationic protein and myeloperoxidase. A secondary hypothesis is that the late reactions (more than 12 hours after challenge) detected by other investigators are artefactual, possibly due to the open nature of the studies and the lack of objectivity of the measured outcomes. Thus, in patients undergoing a prolonged, double-blinded, placebo-controlled challenge study, no differences in symptom scores or behavioral observation scores will be detected between placebo weeks and active weeks.