Consuming ultra-processed foods is associated with an increased risk of developing non-alcoholic fatty liver disease

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In a recent study published in the Nutrients Journal, researchers performed a meta-analysis to determine the contribution of ultra-processed food (UPF) intake to the risk of developing the non-alcoholic fatty liver disease (NAFLD).

Study: Ultra-Processed Food Intake Is Associated with Non-Alcoholic Fatty Liver Disease in Adults: A Systematic Review and Meta-Analysis. Image Credit: Evan Lorne/Shutterstock.comStudy: Ultra-Processed Food Intake Is Associated with Non-Alcoholic Fatty Liver Disease in Adults: A Systematic Review and Meta-Analysis. Image Credit: Evan Lorne/Shutterstock.com

Background

The spectrum of NAFLD ranges from fat accumulation and inflammation in the liver to end-stage fibrosis, cirrhosis, and hepatocellular carcinoma.

UPF diets have poor nutritional profiles, comprising high content of high energy density, total fat, saturated fat, refined carbohydrates, and salt, and low mineral, vitamin, and fiber content.

NAFLD is associated with obesity, type 2 diabetes mellitus (T2D), and metabolic syndrome (MetS) due to excessive chronic calorie intake. Previous studies have reported that consuming UPFs enhances the risk of T2D and obesity.

About the study

Researchers quantitatively assessed the association between UPF consumption and NAFLD prevalence in the present meta-analysis. As a secondary analysis, they investigated whether the two are associated in a dose-response manner.

Data were searched on the Web of Science and Medline databases for relevant studies on December 5, 2022. Additional studies were identified by searching the references of the included studies and contacting field experts.

The team included studies of observational type (including retrospective and prospective cohort study designs, cross-sectional, and case-control studies); studies assessing UPF exposure using the NOVA classification; studies assessing the relationship between UPF intake and NAFLD risk; studies including adult participants; and studies reporting results as hazard ratios (HR), relative risks (RR), odds ratios (OR), or β coefficients, or providing data for calculating the effect size;

In the included studies, NAFLD was defined using the Controlled Attenuation Parameter (CAP) or Fatty Liver Index (FLI) scores, imaging [ultrasonography, transient elastography, computed tomography (CT) or magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS)] or hepatic tissue biopsies. Studies defining NAFLD based on only hepatic enzymatic molecules were excluded.

In addition, the team excluded animal studies, in vitro studies, secondary research articles, including reviews, and studies on pediatric individuals. The secondary outcome was assessed based on the differences in NAFLD prevalence rates among individuals with low UPF intake compared to individuals with moderate-high UPF intake.

Two reviewers independently performed data screening, and disagreements were resolved by discussion between the two. Random-effects modeling was performed to calculate the relative risks (RR) and determine the relationship between UPF intake and NAFLD.

The team assessed the quality of the included studies using the Newcastle-Ottawa Scale (NOS) and the credibility of the evidence obtained using the NutriGrade scoring system.

The team generated Begg’s funnel plots to determine the publication bias. In addition, sensitivity analyses were performed for longitudinal versus non-longitudinal studies, with NOVA-classified versus non-NOVA-classified reported UPF intake, a sample size of less than 1,000 versus greater than 1,000 individuals, and limiting the analysis to continents such as Asia, Europe, and North America.

Results and discussion

Of the 5,454 studies initially identified, 500 duplicate articles were removed, and only 112 underwent full-text screening, following which the team excluded 67 studies where the NOVA classification was not used, 21 studies with inadequate data for meta-analysis; 12 studies that did not report results as ORs, HRs, RRs, or beta coefficients; four studies with other study designs; six studies with other outcomes; one study not published in English; and one study including a non-adult population.

As a result, nine studies, including three cross-sectional studies, three case-control studies, and three cohort-based studies, were considered for the final analysis, including a total of 60,961 individuals. Both moderate (versus low, pooled RR 1.0) and high (versus low, RR 1.4) UPF intake significantly enhanced NAFLD risks.

UPF consumption was related to NAFLD in a dose-response manner, and largely symmetrical funnel plots were obtained, indicating low risks of publication bias. All the included studies were of high quality, with NOS scores ranging between 7.0 and 9.0, and showed high credibility of the evidence, with a mean NutriGrade score of 8.0.

In the sensitivity analyses, the relationship between the intake of UPFs and the prevalence of NAFLD remained significant when only including studies that did not use the NOVA system (RR 1.6).

Likewise, the associations remained significant using non-longitudinal studies (RR 1.6) and those with sample sizes of less than 1,000 individuals (RR 1.7). Moreover, the analysis yielded significant results, including studies conducted in Europe (RR 1.5) or other continents (RR 1.4).

The underlying mechanisms of the increase in NAFLD prevalence among individuals with high UPF intake are as follows:

  1. UPF foods have a high energy density, resulting in greater total daily caloric intake and excessive adiposity;
  2. the high content of macronutrients and refined carbohydrate overfeeding, leading to de novo lipogenesis and an increase in saturated fatty acid (SFA) levels;
  3. the high dietary content, which increases triglyceride deposition in the liver;
  4. the high salt content in UPFs activates the aldose reductase-fructokinase pathway, leading to enhanced fructose availability and lowered leptin sensitivity and the resultant increase in hepatic adiposity;
  5. the food processing procedures involve the addition of artificial sweeteners, monosodium glutamate (MSG), and packaging materials that contain bisphenol A, which increases the risk of NAFLD.

Conclusion

Overall, the study findings showed that UPF consumption significantly increased the risk of NAFLD, directly proportional to the quantity of UPF consumption.

The study findings indicate that health authorities must formulate policies to lower UPF intake and promote physical exercise to decrease the burden of NAFLD and associated conditions such as T2D and obesity.

Journal reference:
Pooja Toshniwal Paharia

Written by

Pooja Toshniwal Paharia

Pooja Toshniwal Paharia is an oral and maxillofacial physician and radiologist based in Pune, India. Her academic background is in Oral Medicine and Radiology. She has extensive experience in research and evidence-based clinical-radiological diagnosis and management of oral lesions and conditions and associated maxillofacial disorders.

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