PO:02:027 | Fast food, slow damage: ultra-processed foods, western diet and inflammatory arthritis - a systematic scoping review

Background: Western dietary patterns, characterized by high intake of ultra-processed foods (UPFs), added sugars, and saturated fats, have been increasingly implicated in promoting systemic inflammation and disrupting gut microbiota composition. These mechanisms may influence the onset, progression, and comorbidities of chronic inflammatory arthritides. This systematic scoping review aimed to summarize current evidence on the association between Western diet (WD) or UPF consumption and the risk, activity, and related outcomes in rheumatoid arthritis (RA), axial spondyloarthritis (axSpA), and psoriatic arthritis (PsA). Methods: We conducted a systematic review including randomized controlled trials, observational studies (cohort, case-control, cross-sectional), and preclinical models assessing the relationship between WD or UPF intake and disease-related outcomes in RA, axSpA, or PsA. Exclusion criteria comprised narrative reviews, editorials, case reports, and studies not specifically addressing both the dietary exposure and relevant disease outcomes. A comprehensive literature search was conducted in PubMed, Embase, Scopus, Web of Science, and the Cochrane Library, with the final search on May 18, 2025 and no time limit applied. Reference lists were manually screened, and forward citation tracking was performed using Google Scholar. Risk of bias was not formally assessed, consistent with the exploratory nature of this scoping review. Data were synthesized narratively and tabulated by dietary exposure, outcomes, and key findings. Results: During screening, we assessed 165 papers. Only 10 studies involving over 244,000 individuals were included. Eight studies addressed RA, comprising 7 clinical and 1 preclinical investigation. Across these, greater UPF consumption or adherence to WD was consistently associated with adverse outcomes. Cohort studies reported an increased RA incidence with adjusted hazard ratios between 1.04 and 1.17; case-control analyses found odds ratios up to 1.84. Inflammatory markers were elevated, including CRP (+0.01 to +0.097 mg/L), ESR (+2 to +3.985 mm/h), and HbA1c (+0.02% to +0.04%). Effects on disease activity were variable (DAS28: +0.01 to +0.49; SJC: up to +0.6 joints). Cardiometabolic risk indicators, such as Framingham score, glucose, insulin, and visceral fat, also worsened with higher UPF intake. Alterations in gut microbiota were documented in both clinical and murine RA models. For axSpA, 1 prospective study (n=140) found no significant association between UPF intake and disease activity. No eligible clinical studies were found for PsA, though one preclinical model demonstrated that WD exposure exacerbated joint and skin inflammation and induced dysbiosis. Discussion: Current evidence supports a detrimental association between WD or UPF intake and inflammatory and metabolic outcomes in RA. Data on axSpA are scarce and inconclusive, and clinical evidence in PsA is lacking. These findings underscore the need for targeted dietary research in spondyloarthritis and support the incorporation of nutritional assessment into comprehensive rheumatologic care.