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Ultra-Processed Foods, MASLD, and Cognitive Aging: A Processing-Centered Gut-Liver-Brain Axis Perspective.

Yirui Chen¹, Hongxin Gui¹, Tieniu Zhao¹

¹School of Public Health, Tianjin University of Traditional Chinese Medicine, No. 10 Poyang Lake Road, Xiqing District, Tianjin 300193, China.

|July 15, 2026

Summary

Ultra-processed foods (UPFs) may accelerate cognitive aging by disrupting gut-liver-brain communication, with metabolic dysfunction-associated steatotic liver disease (MASLD) acting as a key amplifier. This review links UPFs to liver and cognitive decline through various metabolic pathways.

Keywords:

MASLD bile acids cognitive aging dementia food processing gut microbiome gut–liver–brain axis metabolic endotoxemia neuroinflammation ultra-processed foods

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Area of Science:

Nutrition Science
Neuroscience
Hepatology

Background:

Ultra-processed foods (UPFs) are increasingly linked to adverse health outcomes, including cardiometabolic, hepatic, and neurocognitive effects.
Current understanding often overlooks how UPFs' processing characteristics, beyond nutritional content, may disrupt gut-liver-brain communication.

Purpose of the Study:

To examine metabolic dysfunction-associated steatotic liver disease (MASLD) as a potential hepatic amplifier linking UPF consumption to cognitive aging.
To synthesize evidence on the mechanisms connecting UPFs, MASLD, and cognitive aging.

Main Methods:

A structured narrative review of studies published from January 2010 to May 2026.
Searches were conducted across PubMed/MEDLINE, Web of Science, and Scopus, focusing on four key evidence modules.
Studies were prioritized based on relevance, design, validity, mechanistic specificity, and contribution to knowledge gaps.

Main Results:

Evidence links higher UPF intake to liver steatosis, MASLD/NAFLD, cognitive decline, stroke, and dementia, though causality requires further establishment.
Candidate mechanisms involve food matrix disruption, additives, gut barrier dysfunction, metabolic endotoxemia, and inflammation.
MASLD may amplify gut-derived signals relevant to brain aging, positioning UPFs as an upstream exposure.

Conclusions:

A gut-liver-brain framework integrating UPFs, MASLD, and cognitive aging offers a new perspective on metabolic-aging phenomena.
Future research should investigate UPF substitution effects using comprehensive assessments including liver imaging, microbiome analysis, and neurocognitive testing.