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Meta-Analysis
. 2023 May 10;15(10):2266.
doi: 10.3390/nu15102266.

Ultra-Processed Food Intake Is Associated with Non-Alcoholic Fatty Liver Disease in Adults: A Systematic Review and Meta-Analysis

Affiliations
Meta-Analysis

Ultra-Processed Food Intake Is Associated with Non-Alcoholic Fatty Liver Disease in Adults: A Systematic Review and Meta-Analysis

Alex E Henney et al. Nutrients. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is associated with overweight/obesity, metabolic syndrome and type 2 diabetes (T2D) due to chronic caloric excess and physical inactivity. Previous meta-analyses have confirmed associations between ultra-processed food (UPF) intake and obesity and T2D. We aim to ascertain the contribution of UPF consumption to the risk of developing NAFLD. We performed a systematic review and meta-analysis (PROSPERO (CRD42022368763)). All records registered on Ovid Medline and Web of Science were searched from inception until December 2022. Studies that assessed UPF consumption in adults, determined according to the NOVA food classification system, and that reported NAFLD determined by surrogate (steatosis) scores, imaging or liver biopsy were included. The association between UPF consumption and NAFLD was assessed using random-effects meta-analysis methods. Study quality was assessed, and evidence credibility evaluated, using the Newcastle Ottawa Scale and NutriGrade systems, respectively. A total of 5454 records were screened, and 112 records underwent full text review. From these, 9 studies (3 cross-sectional, 3 case-control and 3 cohort), analysing 60,961 individuals, were included in the current review. Both moderate (vs. low) (pooled relative risk 1.03 (1.00-1.07) (p = 0.04) (I2 = 0%)) and high (vs. low) (1.42 (1.16-1.75) (<0.01) (I2 = 89%)) intake of UPF significantly increased the risk of NAFLD. Funnel plots demonstrate low risk of publication bias. Consumption of UPF is associated with NAFLD with a dose-response effect. Public health measures to reduce overconsumption of UPF are imperative to reduce the burden of NAFLD, and the related conditions, obesity and T2D.

Keywords: NOVA; non-alcoholic fatty liver disease; non-alcoholic steatohepatitis; ultra-processed food.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-reported flow diagram for study selection process.
Figure 2
Figure 2
Forest plots from a random-effects model portraying the association between (a) moderate (vs. low) ultra-processed food intake and development of NAFLD; (b) high ultra-processed food intake and development of NAFLD [24,25,26,27,34,35,36,37,38].
Figure 3
Figure 3
Bubble plot for meta-regression exploring the dose–response association between ultra-processed food intake and NAFLD. The size of circle represents the sample size of individual included the studies.
Figure 4
Figure 4
Forest plots demonstrating the association between high UPF intake and NAFLD when studies (a) directly referenced NOVA, (b) did not directly reference NOVA [24,25,26,27,34,35,36,37,38].
Figure 5
Figure 5
Forest plots demonstrating the association between high UPF intake and NAFLD when studies (a) were longitudinally designed, (b) were not longitudinally designed [24,25,26,27,34,35,36,37,38].
Figure 6
Figure 6
Forest plots demonstrating the association between high UPF intake and NAFLD when studies (a) had sample size greater than 1000 participants, (b) had sample size less than 1000 participants [24,25,26,27,34,35,36,37,38].
Figure 7
Figure 7
Funnel plots portraying risk of publication bias for studies assessing the association between (a) moderate ultra-processed food intake and development of NAFLD; (b) high ultra-processed food intake and development of NAFLD.
Figure 8
Figure 8
Graphical discussion. NAFLD = non-alcoholic fatty liver disease; IHTG = intra-hepatic triglyceride deposition; SFA = saturated fatty acids; MSG = monosodium glutamate. (a) ultra-processed foods are highly energy dense, contributing towards excess visceral adiposity and fatty liver disease; (b) ultra-processed foods are high in dietary saturated fat and refined carbohydrates which promote de novo lipogenesis and consequent intra-hepatic triglyceride deposition if consumed in excess, chronically; (c) ultra-processed foods are high in sodium salt which activates the aldose reductase-fructokinase pathway. This in turns upregulates endogenous fructose availability and downregulates leptin sensitivity, increasing hepatic adiposity; (d) ultra-processed foods are often saturated with artificial food processing ingredients in their food matrix, such as artificial sweeteners and mono-sodium glutamate, and packaging, often in the form of bisphenol a.

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