Ultra-Processed Food Consumption and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Evidence Synthesis, Methodological Appraisal, and Mechanistic Insights
- 1Metabolic Liver Disease Unit, Fondazione Italiana Fegato, 34149 Trieste, Italy
- 2Department of Life Science, University of Trieste, 34100 Trieste, Italy
- 3Department of Science and Technology, Philippine Council for Health Research and Development, Taguig 1631, Philippines
Abstract
Background/Objectives: Ultra-processed food (UPF) consumption has been associated with metabolic dysfunction-associated steatotic liver disease (MASLD), but differences in exposure definitions and liver outcomes complicate interpretation. This umbrella review synthesized existing evidence, appraised review methodology, examined primary-publication overlap, and explored proposed biological mechanisms. Methods: PubMed, Scopus, and Web of Science were searched from inception to May 2026 for systematic reviews and meta-analyses examining UPF consumption and MASLD-related outcomes in adults. The review methodology was assessed using A Measurement Tool to Assess Systematic Reviews 2 (AMSTAR 2). Primary publications were mapped across reviews, distinguishing total NOVA-defined UPF intake from selected-food and dietary-pattern proxies. Publication overlap was quantified using the corrected covered area (CCA). Findings were synthesized narratively. Results: Five systematic reviews were included, with AMSTAR 2 confidence classifications of moderate for one, low for one, and critically low for three. Mapping identified 18 distinct primary publications: 11 assessing total NOVA-defined UPF intake and seven assessing proxy exposures. Higher UPF consumption was generally associated with less favorable liver outcomes, with prospective findings proving more consistent than cross-sectional findings. Publication overlap was very high (overall CCA: 34.72%), limiting the independence of review findings. Other limitations included retrospective NOVA classification, heterogeneous liver-outcome ascertainment, and residual confounding. Proposed biological pathways included excess energy intake, visceral adiposity, insulin resistance, hepatic lipogenesis, and altered gut–liver signaling; their contribution to the observed associations remains unconfirmed. Conclusions: Existing evidence suggests an association between higher UPF consumption and adverse liver outcomes relevant to MASLD but does not establish causality or a harmful intake threshold. Future research should prioritize repeated dietary assessments, standardized MASLD ascertainment, and interventions evaluating the replacement of UPFs with minimally processed foods.
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BibTeX
@article{bernardino2026ultraprocessed,
title = {{Ultra-Processed Food Consumption and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Evidence Synthesis, Methodological Appraisal, and Mechanistic Insights}},
author = {Melvin Bernardino and Claudio Tiribelli and Natalia Rosso},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18213585},
url = {https://www.mdpi.com/2072-6643/18/21/3585},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Ultra-Processed Food Consumption and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): Evidence Synthesis, Methodological Appraisal, and Mechanistic Insights
AU - Melvin Bernardino
AU - Claudio Tiribelli
AU - Natalia Rosso
PY - 2026
DA - 2026/10/29
JO - Nutrients
DO - 10.3390/nu18213585
UR - https://www.mdpi.com/2072-6643/18/21/3585
AB - Background/Objectives: Ultra-processed food (UPF) consumption has been associated with metabolic dysfunction-associated steatotic liver disease (MASLD), but differences in exposure definitions and liver outcomes complicate interpretation. This umbrella review synthesized existing evidence, appraised review methodology, examined primary-publication overlap, and explored proposed biological mechanisms. Methods: PubMed, Scopus, and Web of Science were searched from inception to May 2026 for systematic reviews and meta-analyses examining UPF consumption and MASLD-related outcomes in adults. The review methodology was assessed using A Measurement Tool to Assess Systematic Reviews 2 (AMSTAR 2). Primary publications were mapped across reviews, distinguishing total NOVA-defined UPF intake from selected-food and dietary-pattern proxies. Publication overlap was quantified using the corrected covered area (CCA). Findings were synthesized narratively. Results: Five systematic reviews were included, with AMSTAR 2 confidence classifications of moderate for one, low for one, and critically low for three. Mapping identified 18 distinct primary publications: 11 assessing total NOVA-defined UPF intake and seven assessing proxy exposures. Higher UPF consumption was generally associated with less favorable liver outcomes, with prospective findings proving more consistent than cross-sectional findings. Publication overlap was very high (overall CCA: 34.72%), limiting the independence of review findings. Other limitations included retrospective NOVA classification, heterogeneous liver-outcome ascertainment, and residual confounding. Proposed biological pathways included excess energy intake, visceral adiposity, insulin resistance, hepatic lipogenesis, and altered gut–liver signaling; their contribution to the observed associations remains unconfirmed. Conclusions: Existing evidence suggests an association between higher UPF consumption and adverse liver outcomes relevant to MASLD but does not establish causality or a harmful intake threshold. Future research should prioritize repeated dietary assessments, standardized MASLD ascertainment, and interventions evaluating the replacement of UPFs with minimally processed foods.
SN - 2072-6643
ER -