Early-Life Nutrition: The Interplay of Nutritional, Microbial, Genetic, and Environmental Factors in Food Allergy Development and Prevention.

BACKGROUND: Food allergy is an important health concern, particularly during infancy and early childhood. Its development reflects complex interactions between genetic susceptibility and early-life nutritional, microbial, epithelial, immunological, and environmental factors. OBJECTIVE: To examine the role of early-life nutrition in the development and prevention of food allergy, with emphasis on its interplay with the gut microbiome, genetic and epigenetic susceptibility, epithelial barrier function, and environmental exposures. METHODS: A structured literature search was conducted primarily in PubMed, supplemented by relevant articles identified through additional bibliographic databases and literature sources. Evidence was thematically synthesized across maternal nutrition, breastfeeding, complementary feeding, allergenic food introduction, dietary diversity, micronutrients, fatty acids, gut microbiome development, genetic and epigenetic mechanisms, and environmental exposures. RESULTS: Early life represents a critical window for immune maturation and the establishment of oral tolerance. Nutritional exposures interact with the gut microbiome, epithelial integrity, and immune pathways, potentially influencing tolerance and sensitization. The most consistent evidence for primary prevention supports the timely introduction and continued ingestion of allergenic foods, particularly peanut and egg, during complementary feeding. Evidence remains insufficient or inconsistent to support maternal allergen avoidance, targeted supplementation, hydrolyzed formulas, probiotics, microbiome-directed interventions, or skin-barrier strategies as established preventive approaches. Associations involving microbiome composition, medication exposure, pollution, and other environmental factors remain heterogeneous and are largely observational. CONCLUSIONS: Food allergy reflects complex interactions among diet, microbiota, epithelial barriers, host susceptibility, and environmental exposures rather than a single causal factor.