Answers are grounded in this paper and cite their sources.
Childhood diet may shape immune and inflammatory trajectories through interacting metabolic, microbial, and developmental pathways, but the long-term human evidence remains heterogeneous. This scoping review mapped longitudinal studies examining dietary exposures from birth to 18 years in relation to subsequent immune, inflammatory, allergic, autoimmune, gastrointestinal, immunometabolic, hepatic, neurocognitive, and endocrine–immunometabolic outcomes. The review was conducted in accordance with Joanna Briggs Institute guidance and reported according to PRISMA-ScR principles. A total of 403 studies were included. Evidence was concentrated in infancy and early childhood and predominantly addressed allergic and atopic outcomes; evidence on other immunological outcomes and on middle childhood and adolescence was more limited. Thirty studies provided relatively direct immunometabolic evidence, 149 contributed mechanistically indirect evidence, and 224 primarily reported longitudinal clinical diet–outcome associations. The principal mechanistic axes involved allergic sensitization and immune tolerance, lipid and fatty-acid metabolism, micronutrient and antioxidant pathways, cytokine signaling, gut microbiome and metabolite pathways, and human-milk-derived bioactive signals. Dietary diversity and overall diet quality intersected with several of these pathways. Associations were frequently context-dependent, varying according to developmental timing, host susceptibility, genetic background, immune state, and feeding context. Mechanistic interpretation rests on convergence across complementary studies rather than on complete pathways demonstrated within individual cohorts. Overall, the evidence is compatible with a proposed life-course nutritional immunology framework in which childhood diet acts as a dynamic developmental exposure interacting with microbial, metabolic, and immune processes; however, this framework derives mainly from early-life exposures and allergic and atopic outcomes, and the persistence of effects beyond early childhood remains insufficiently demonstrated. Limitations include restriction to English-language publications, marked methodological heterogeneity, residual confounding, and the absence of a formal risk-of-bias assessment.
No takes yet. Share an insight, caveat, or question.
Cristun et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: