Prevention of Food Allergy and Atopic Disease

Food allergy, with a prevalence of 4-6% in childhood, represents a major and potentially life-threatening burden to our children. Studies on the natural history of food allergy document that clinical allergy to foodstuffs such as milk, egg and soy frequently remit while allergy to peanut, nuts, and fish typically persists during childhood. Avoidance of foodstuffs after sensitization and food allergy development appear to hasten tolerance; however, the mechanism for the development of clinical tolerance to one group of food allergens and not another is poorly understood. An urgency exists today to identify and develop effective strategies to prevent food allergy and other allergic afflictions owing to their epidemic worldwide increase in prevalence and morbidity. Though genetic, and particularly immunological, engineering hold promise for food allergy and atopy prevention, environmental strategies which promote food allergen and aeroallergen avoidance provide an avenue for prevention at the present time. These latter efforts rely on active efforts to reduce the allergenic load and exposure of atopic-prone infants and children to allergenic foodstuffs and aeroallergens. Moreover, allergy prevention can be directed at three potential stages of allergic sensitization and disease manifestation including: (1) primary prevention which inhibits IgE and other immunological sensitization; (2) secondary prevention which abrogates disease expression subsequent to immunological sensitization; and (3) tertiary prevention which suppresses symptoms after and despite disease expression1. Strategies to promote allergen avoidance have met with great difficulty at all of these stages due to limitations in knowledge, societal compliance and resources. Though primary prevention of allergy is optimal, secondary prevention may be a necessary adjunct to the former or serve as a fall-back option to families uninterested in allergy prevention until real markers of atopic risk are identified in their offspring. Tertiary prevention, the arena most familiar to practising allergists and paediatricians, is generally instituted after manifestations of allergy are recognized, often long after clinical disease has been expressed and suffering experienced. These stages must be integrated into any programme to prevent the consequences of atopic disease. The success of allergen prevention strategies must be judged by the degree to which they satisfy specific criteria including the ability to: (1) predict the high-risk infant and child; (2) demonstrate effectiveness of the intervention strategy; (3) utilize acceptable interventions; (4) minimize adverse effects; and (5) generate cost effective outcomes. To date, no allergen avoidance intervention study has met all of these requisites. A critical period appears to exist early postnatally in which the genetically programmed atopic-prone infant may be at an increased risk to become sensitized to exposed/ encountered allergens. Prompt perinatal identification of such at-risk neonates would be important should preventive efforts prove efficacious, safe and cost-effective. Many genetic linkage markers2 and immunological factors/ markers (elevated cord blood and infancy IgE levels, egg specific-IgE, lower gamma-interferon/IL-4 ratio, etc.) have been determined to be significantly associated with the subsequent development of allergic disease; however, none possesses greater sensitivity or specificity than atopic family history for the practical screening of at risk neonates for primary allergy prevention3. With respect to the institution of anti-allergy measures, certain major atopic risk factors such as atopic heredity, male gender and non-white ethnicity are not modulatable, while other factors such as birth month, low socioeconomic status, and urban residences are poorly modulatable. Possible ways to modulate atopic risk factors include (1) raising low atopic health consciousness; (2) delaying introduction of allergenic foods during infancy; (3) reducing household dust mite, cockroach and dander levels; and (4) reducing environmental pollution and environmental tobacco exposure (ETS). Table 1 presents a strategy for both the identification of high-risk infants and institution of preventive measures directed at all three stages of allergy prevention4.