Potential role of inflammation in relation to dietary sodium and β-carotene with non-alcoholic fatty liver disease: a mediation analysis

BACKGROUND: High sodium intake has been linked to the prevalence of non-alcoholic fatty liver disease (NAFLD), but the underlying mechanism remains unclear. This study aims to explore the role of chronic inflammation in the association between sodium and NAFLD, and to examine whether β-carotene, which has strong anti-inflammatory effects, lowers the odds of NAFLD. METHODS: Mediation analyses assessed the mediating effects of C-reactive protein (CRP) and red cell distribution width (RDW) on the relationship between dietary sodium and NAFLD defined by the hepatic steatosis index (HSI) and the fatty liver index (FLI). RESULTS: Among 6725 participants, compared with the high sodium–low carotene group, those in the high sodium–high carotene group had 16% and 26% lower odds of HSI- and FLI-defined NAFLD, respectively. There were positive indirect effects of dietary sodium on HSI-defined NAFLD (indirect effect: 0.0057, 95% CI: 0.0021–0.0091, P < 0.0001) and FLI-defined NAFLD (indirect effect: 0.0081, 95% CI: 0.0024–0.0162, P < 0.0001) when CRP was considered a mediator. Mediating effects were attenuated after adjusting for dietary β-carotene. Similar results were found for RDW as a mediator in the HSI-defined NAFLD analysis. CONCLUSIONS: Higher sodium intake increases the odds of NAFLD by upregulating inflammation. Dietary β-carotene may attenuate this association by downregulating inflammation.