Atopic Dermatitis and Food Allergy in Infants: Decoding the Bidirectional Relationship and Implications for Early Intervention

Abstract

Atopic dermatitis (AD) represents one of the most common chronic inflammatory skin conditions in infancy and early childhood, affecting 15%–30% of children globally with a significant impact on quality of life for patients and families. Recent evidence has fundamentally challenged traditional paradigms regarding the relationship between AD and food allergy, revealing a complex bidirectional interaction where early-onset AD significantly increases the risk of developing food allergies through epicutaneous sensitization. The “dual-allergen exposure hypothesis” proposes that cutaneous exposure to food allergens through a disrupted skin barrier in AD promotes allergic sensitization, whereas early oral introduction may induce tolerance. This paradigm shift has profound implications for preventive strategies and clinical management in pediatric populations. This narrative review synthesizes current evidence on the mechanistic links between AD and food allergy, examining epidemiological data demonstrating that infants with moderate-to-severe AD have substantially elevated risks for developing immunoglobulin E-mediated food allergies, particularly to eggs, peanuts, and milk. We explore the role of filaggrin mutations and other genetic factors, environmental influences, including the skin microbiome, and the impact of topical therapies on food allergy prevention. Recent landmark studies, including PETIT, EAT, and LEAP trials, have transformed clinical recommendations regarding the timing of allergenic food introduction. The review examines practical screening approaches for identifying high-risk infants, evidence-based management strategies for optimizing skin barrier function, controversies surrounding prophylactic food allergen avoidance, and emerging therapeutic interventions targeting the atopic march. Understanding these interconnections enables pediatricians and dermatologists to implement evidence-based preventive strategies that may interrupt the progression from AD to systemic allergic diseases.