An increasing number of studies have evaluated the association between ultra-processed foods (UPF) consumption and metabolic disorders. However, the association between UPF intake and non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, we analyzed data from 6545 participants who were recruited in National Health and Nutrition Examination Surveys (NHANES) 2011–2018. UPF were defined in light of the NOVA food classification system and divided into quartiles based on its proportion of total weight intake. Complex logistic regression models were used to assess the association between UPF and NAFLD. Mediation analyses were conducted to reveal underlying mediators. We found that NAFLD patients consumed more UPF than controls (925.92 ± 18.08 versus 812.70 ± 14.32 grams/day, P <0.001). Dietary intake of UPF (% weight) was negatively related to the Healthy Eating Index-2015 (HEI-2015) score (Spearman r = -0.32, P<0.001). In the multivariable model, the highest quartile compared with the lowest, the ORs (95% CIs) were 1.83 (1.33–2.53) for NAFLD (OR per 10% increment: 1.15; 95% CI: 1.09–1.22; P for trend <0.001) and 1.52 (1.12–2.07) for insulin resistance (OR per 10% increment: 1.11; 95% CI: 1.05–1.18; P for trend =0.002). Mediation analyses revealed that poor diet quality, high saturated fat and refined grain intake partly mediated the association between UPF and NAFLD. In conclusion, high UPF intake was associated with an increased risk of NAFLD in US adults. Further prospective studies are needed to verify these findings.

Large longitudinal studies exploring the role of dietary patterns in the assessment of long-term outcomes of NAFLD are still lacking. We conducted a prospective analysis of 128,695 UK Biobank participants. Cox proportional hazards models were used to estimate the risk associated with two dietary patterns for long-term outcomes of NAFLD. During a median follow-up of 12.5 years, 1925 cases of end-stage liver disease (ESLD) and 12,466 deaths occurred in patients with NAFLD. Compared with patients in the lowest quintile, those in the highest quintile of the diet quality score was negatively associated with the risks of ESLD and all-cause mortality (HRQ5vsQ1: 0.76, 95% CI: 0.66–0.87, p < 0.001; HRQ5vsQ1: 0.84, 95% CI: 0.79–0.88, p < 0.001, respectively). NAFLD patients with high-quality carbohydrate patterns carried a 0.74-fold risk of ESLD and a 0.86-fold risk of all-cause mortality (HRQ5vsQ1: 0.74, 95% CI: 0.65–0.86, p < 0.001; HRQ5vsQ1: 0.86, 95% CI: 0.82–0.91, p < 0.001, respectively). For prudent dietary patterns rich in vegetables, fruits and fish, the adjusted HR Q5vsQ1 (95% CI) was 0.87 (0.76–0.99) and 0.94 (0.89–0.99) for ESLD and all-cause mortality of NAFLD patients. There was a U-shaped association between the meat-rich dietary pattern and all-cause mortality in patients with NAFLD. These findings suggest that a diet characterized by a high-quality, high intake of vegetables, fruits, fish and whole grains as well as an appropriate intake of meat, was associated with a lower risk of adverse outcomes of NAFLD.

Background and Aims:The association of serum uric acid (SUA) levels with liverrelated morbidity and mortality remains undetermined. Therefore, we aimed to explore the association of SUA levels with liver-related morbidity and mortality. Methods:The present cohort study included 459 619 adults from the UK Biobank.Multivariable Cox proportional hazards models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations of SUA levels with morbidity and mortality of overall liver disease. Mendelian randomization (MR) analyses were conducted to explore the underlying causality. A polygenic risk score was generated to assess whether there was a gene-exposure interaction.Results: During a median follow-up of 12.6 years, 14 302 nonfatal and 609 fatal cases of overall liver disease were identified. Compared to individuals in the lowest quartile, the HRs (95% CI) of incident overall liver disease were 1.08 (1.02-1.14), 1.13 (1.07-1.20) and 1.44 (1.36-1.53) for individuals with SUA levels in quartiles 2, 3 and 4 respectively. Similarly, the HRs (95% CI) of liver disease-associated mortality were 1.09 (0.78-1.52), 1.55 (1.14-2.13) and 1.96 (1.42-2.69) for individuals with SUA levels in quartiles 2, 3 and 4 respectively. The MR results did not support the causal association of SUA levels with liver disease. In addition, there was a significant modification effect of the polygenic risk score on the association of SUA levels with incident overall liver disease (p interaction = .003).Conclusions: Higher SUA levels were significantly associated with an increased risk of overall liver disease morbidity and mortality.

Afamin is a member of the hepatokine that are strongly associated with various metabolic diseases. The relationship between afamin and nonalcoholic fatty liver disease (NAFLD) remains unclear. This study aimed to explore the correlation between serum afamin levels and NAFLD. We analyzed 88 NAFLD patients and 88 age- and sex-matched healthy controls who took their health examinations at the First Affiliated Hospital, Zhejiang University School of Medicine. The association was further confirmed in 22 biopsy-confirmed NAFLD patients and 36 healthy controls. Serum afamin levels were evaluated using an enzyme-linked immunosorbent assay (ELISA). NAFLD patients had significantly higher serum afamin levels than the healthy controls (14.79 ± 5.04 mg/L versus 10.83 ± 3.24 mg/L; P < 0.001 ). Serum afamin levels were positively correlated with metabolic parameters including the body mass index, waist circumference, systolic blood pressure, liver enzymes, and lipid profiles. A multiple regression analysis showed that serum afamin levels were independently related to the risk of NAFLD (OR: 1.289, 95% CI, 1.141–1.456; P < 0.001 ). The receiver operating characteristic (ROC) analysis showed that the area under curve (AUC) of serum afamin plus the BMI for detecting NAFLD was 0.878. In participants with liver biopsies, the serum afamin plus the BMI detected NAFLD with an AUC of 0.758. In conclusion, serum afamin levels were positively associated with prevalence and risk of NAFLD, and serum afamin plus the BMI had a high diagnostic performance for NAFLD. This study provides epidemiological evidence of afamin in NAFLD.