Ultra-Processed Foods, MASLD and Cognitive Ageing: Nutrients | June 2026

• This review proposes a processing-centred gut–liver–brain axis, positioning MASLD as a metabolic amplifier between ultra-processed food exposure and cognitive decline.
• Ultra-processed foods are not simply high in sugar, fat, or salt; industrial processing disrupts the food matrix, accelerates eating, displaces fibre-rich microbial substrates, and introduces additives and processing-derived compounds.
• Higher ultra-processed food intake has been associated with hepatic steatosis, MASLD, cognitive impairment, stroke, and dementia-related outcomes, although causality remains unproven.
• Proposed mechanisms include gut microbial dysbiosis, impaired intestinal barrier integrity, metabolic endotoxaemia, altered bile acid signalling, hepatic lipotoxicity, insulin resistance, and systemic inflammation.
• The liver may amplify gut-derived signals and transmit inflammatory, vascular, endocrine, and metabolic effects to the brain.
• Altered FXR and TGR5 bile acid signalling provides a biologically plausible communication pathway connecting the microbiome, liver metabolism, and neuroimmune function.
• MASLD shares several drivers of cognitive aging, including obesity, diabetes, dyslipidaemia, endothelial dysfunction, and chronic low-grade inflammation.
• Ultra-processed foods may also promote passive overconsumption through rapid eating, hyperpalatability, altered texture, and reduced satiety.
• Many proposed pathways overlap with general cardiometabolic disease, making it difficult to isolate the independent effect of food processing itself.
• Current evidence is mainly observational and mechanistic; the review does not establish that ultra-processed foods directly cause dementia or that treating MASLD prevents cognitive decline.
• Clinically, replacing ultra-processed foods with minimally processed, fibre-rich foods may simultaneously support liver, metabolic, vascular, and cognitive health.
• Future studies should combine dietary substitution trials with liver imaging, microbiome and metabolomic profiling, bile acid and inflammatory biomarkers, neuroimaging, and longitudinal cognitive assessment.

Bottom line: Ultra-processed foods may disrupt gut–liver–brain communication, with MASLD acting as a hepatic amplifier of metabolic and inflammatory signals relevant to cognitive aging. The concept is compelling but requires prospective mechanistic and intervention studies.