There has been considerable recent broadening of basic concepts of intestinal food allergy, in particular the importance of non-IgE-mediated mechanisms. The traditional emphasis on IgE-mediated allergy now appears inappropriate in light of current studies of the basic mechanisms of oral tolerance to dietary antigen and of increasing recognition of the requirement for early infectious challenge in the prevention of allergic sensitization. This major change in emphasis has been forced both by basic scientific studies and by recognition of novel patterns of food allergic disease within the pediatric population, in which rapid increase in food-allergic sensitization has been noted in the last decade and previously rare phenomena such as multiple food allergies and sensitization of exclusively breast-fed infants to antigens eaten by the mother have become commonplace. It is thus emerging that the possession of exaggerated IgE responses may not be the direct cause of food allergic sensitization but may ensure that such sensitization is clinically obvious. Those without such immediate responses have a complex of symptoms, including diet-responsive eczema and a marked disturbance of intestinal motility. The clear demographic links with socioeconomic privilege and relative protection from gastrointestinal infarctions concord with recent murine data suggesting an obligatory input from innate immune responses to the gut flora in the establishment of oral tolerance.