This narrative review summarizes current evidence on the associations between ultra-processed food (UPF) consumption, childhood and adolescent obesity, and functional gastrointestinal disorders (FGIDs), and examines the metabolic, inflammatory, microbial, and gut–brain mechanisms underlying these links. Methods: A comprehensive search of PubMed and Scopus identified articles published between January 2010 and September 2025. Eligible studies included human research in individuals aged 0–18 years; adult studies were considered when contributing relevant mechanistic insights. Of 335 records screened, 112 studies met the inclusion criteria and were synthesized narratively according to methodological appropriateness. Results: High UPF intake was consistently associated with increased adiposity, metabolic dysregulation, and greater cardiometabolic risk in youth. Children with overweight or obesity showed a higher prevalence of FGIDs compared with their normal-weight peers. Mechanistic evidence suggests that UPFs, rich in refined carbohydrates, unhealthy fats, and additives, may promote gut microbiota dysbiosis, impair intestinal barrier integrity, alter motility, and induce low-grade inflammation, thereby disrupting gut–brain signaling and contributing to FGID symptoms. Early-life and maternal UPF exposure may further increase susceptibility to metabolic and gastrointestinal disturbances through epigenetic and microbiome-mediated pathways. Conclusions: UPFs emerge as a shared etiological factor for obesity and FGIDs in childhood. This review contributes an integrated synthesis of epidemiological and mechanistic data while highlighting key research gaps, particularly the need for standardized methodologies and pediatric interventional studies to strengthen the evidence base.

Highly Processed Food and Functional Gastrointestinal Disorders in Children and Adolescents with Obesity: The Preventive Challenge-A Narrative Review

Calcaterra V;Cena H;Ferrara C;Boussetta S;Zambon I;
2025-01-01

Abstract

This narrative review summarizes current evidence on the associations between ultra-processed food (UPF) consumption, childhood and adolescent obesity, and functional gastrointestinal disorders (FGIDs), and examines the metabolic, inflammatory, microbial, and gut–brain mechanisms underlying these links. Methods: A comprehensive search of PubMed and Scopus identified articles published between January 2010 and September 2025. Eligible studies included human research in individuals aged 0–18 years; adult studies were considered when contributing relevant mechanistic insights. Of 335 records screened, 112 studies met the inclusion criteria and were synthesized narratively according to methodological appropriateness. Results: High UPF intake was consistently associated with increased adiposity, metabolic dysregulation, and greater cardiometabolic risk in youth. Children with overweight or obesity showed a higher prevalence of FGIDs compared with their normal-weight peers. Mechanistic evidence suggests that UPFs, rich in refined carbohydrates, unhealthy fats, and additives, may promote gut microbiota dysbiosis, impair intestinal barrier integrity, alter motility, and induce low-grade inflammation, thereby disrupting gut–brain signaling and contributing to FGID symptoms. Early-life and maternal UPF exposure may further increase susceptibility to metabolic and gastrointestinal disturbances through epigenetic and microbiome-mediated pathways. Conclusions: UPFs emerge as a shared etiological factor for obesity and FGIDs in childhood. This review contributes an integrated synthesis of epidemiological and mechanistic data while highlighting key research gaps, particularly the need for standardized methodologies and pediatric interventional studies to strengthen the evidence base.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/1541455
Citazioni
  • ???jsp.display-item.citation.pmc??? 3
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact