Dietary fiber intake and non-alcoholic fatty liver disease: The mediating role of obesity

Background and aimsDietary pattern rich in fiber is negatively associated with the risk of non-alcoholic fatty liver disease (NAFLD). Meanwhile, obesity is a known predisposing factor for NAFLD. Nutrient-focused research can enhance the mechanistic understanding of dietary effects. We thus hypothesized that higher dietary fiber intake was associated with lower risk of NAFLD through the mediating role of obesity.MethodsIn this nationwide cross-sectional study, dietary fiber was surveyed using two 24-h recalls. NAFLD and clinically significant fibrosis (CSF) were determined by vibration-controlled transient elastography. Multivariable logistic and linear regression were applied to investigate the association of dietary fiber with NAFLD, CSF, and liver function parameters. We used counterfactual-based mediation analysis to estimate the direct and indirect effect of dietary fiber on NAFLD.ResultsOf the 3,974 participants, ~36.86% and 7.78% of participants were diagnosed with NAFLD and CSF. Compared with participants among the lowest tertile, the highest tertile of dietary fiber consumption was associated with lower odds of NAFLD (OR = 0.81; 95% CI: 0.66–0.98; Poverall = 0.019). Dietary fiber intake appeared to be linked with lower odds of CSF (ORTertile3vs.Tertile1 = 0.81; 95% CI: 0.58–1.14; Poverall = 0.107). Mediation analysis showed that obesity fully mediated the association of dietary fiber with NAFLD. Dietary fiber was associated with improved hepatic parameters.ConclusionsThe findings indicated that increasing dietary fiber intake could confer a greater benefit to protect against NAFLD. Translating these findings regarding dietary fiber into dietary advice might be an attractive strategy for NAFLD prevention

Higher Adherence to Healthy Lifestyle Score Is Associated with Lower Odds of Non-Alcoholic Fatty Liver Disease

Growing evidence supports that individual lifestyle factors contribute to the development of non-alcoholic fatty liver disease (NAFLD) without considering the coexistence and synergistic effect of lifestyle factors. Our aim is to derive a healthy lifestyle score (HLS) and estimate its association with NAFLD. In this nationwide cross-sectional study, we derived a five-item HLS including dietary pattern, body mass index, physical activity, cigarette smoking, and sleep duration. NAFLD and clinically significant fibrosis (CSF) were assessed based on vibration-controlled transient elastography (VCTE). Liver function parameters were also tested. Multivariable logistic and linear regressions were applied to investigate the association between HLS and liver diseases. Of the 3893 participants with VCTE examination, approximately 14.1% of participants possessed zero or one healthy lifestyle, 62.5% possessed two or three healthy lifestyles, and 23.4% possessed four or five healthy lifestyles. Compared with participants with a low HLS (0–1 score), the adjusted odds ratios and 95% confidence intervals for those with a high HLS (4–5 score) were 0.25 (0.19~0.33, Ptrend < 0.001) for NAFLD and 0.30 (0.18~0.50, Ptrend < 0.001) for CSF. HLS was positively associated with albumin, total protein, and total bilirubin (all Ptrend ≤ 0.001), and was inversely associated with globulin, alanine aminotransferase, and gamma-glutamyl transaminase (all Ptrend ≤ 0.003). Higher adherence to HLS is associated with lower odds of NAFLD and CSF and may improve liver function. Strategies for the promotion of a healthy lifestyle should be considered as part of NAFLD prevention