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Food additives, emulsifiers, microplastics, and ultra-processed foods in rheumatic disease pathogenesis
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Researchers reviewed how ultra-processed food components — including emulsifiers, synthetic colorants, excess sodium, and microplastic contaminants from packaging — may disrupt gut barrier integrity, reshape the microbiome, and activate inflammatory pathways that overlap with mechanisms implicated in rheumatoid arthritis and related autoimmune conditions.
PURPOSE OF REVIEW: Dietary patterns have changed significantly over time, with ultra-processed foods now comprising a large proportion of daily energy intake in many countries. Ultra-processed foods (UPFs) contain numerous additives and may also increase exposure to processing- and packaging-related contaminants that could influence immune function. This review summarizes why UPFs have drawn growing attention and evaluates their potential relevance to autoimmune inflammation, with a focus on rheumatoid arthritis (RA) and related disorders. RECENT FINDINGS: Population studies suggest that higher UPF intake is associated with an increased risk of RA after adjustment for obesity and lifestyle factors. Experimental and translational studies suggest that components common in UPF-rich diets (e.g., emulsifiers, thickeners, synthetic colorants, added sugars, excess sodium, and some nonnutritive sweeteners), as well as microplastic exposures, may disrupt gut barrier integrity, remodel the microbiome, and promote low-grade inflammation. These mechanisms overlap with pathways implicated in RA and systemic inflammation, including dysregulation of Treg/Th17 balance, loss of mucosal tolerance, endotoxemia, and innate immune activation. SUMMARY: Overall, evidence supports biologically plausible mechanisms and epidemiologic associations linking UPF-rich dietary patterns to immune dysregulation relevant to rheumatic disease, but direct RA-specific interventional and mechanistic clinical data remain limited. Dietary exposures may represent modifiable risks; however, stronger longitudinal studies with validated RA phenotyping and pragmatic dietary interventions are needed before firm clinical recommendations can be made.
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