Abstract
INTRODUCTION AND OBJECTIVES: While excessive sodium intake is associated with hepatic steatosis, its precise role in metabolic dysfunction-associated steatotic liver disease (MASLD) remains underexplored. This study investigated the relationship between different measures of sodium intake and the risk of MASLD.
MATERIALS AND METHODS: The complete data of 286,073 participants on their self-reported frequency of adding salt to food and estimated 24-h urinary sodium excretion from the UK Biobank were analyzed. Cox proportional hazards models quantified hazard ratios (HRs) for incident MASLD, cirrhosis or liver cancer, and liver-related mortality. Mediation analyses evaluated potential mediating between sodium intake and MASLD. Energy-adjusted dietary sodium intake was evaluated in a sub-cohort of 119,073 participants with ≥2 dietary recalls.
RESULTS: During a median follow-up of 13.3 years, 3147 MASLD, 1354 cirrhosis or liver cancer, and 523 liver-related mortality cases were identified. After adjusting for confounders, participants who reported “always” adding salt had an increased risk of MASLD (HR=1.36, 95 % CI=1.19-1.56). Higher urinary sodium excretion was also associated with incident MASLD (HR=1.62, 95 % CI=1.53-1.72), displaying a J-shaped nonlinear relationship with the threshold point at 1.93 g/d. Inflammatory dysregulation, insulin resistance and renal function impairment partly mediated this association. In the sub-cohort, every 1 g increase in energy-adjusted dietary sodium intake conferred a 14 % higher risk of MASLD (HR=1.14, 95 % CI=1.01-1.28).
CONCLUSIONS: The habit of always adding salt to food, a 24-h urinary sodium excretion above 1.93 g/day, and energy-adjusted dietary sodium intake above 1.49g/d increased the risk of MASLD, partly mediated through inflammation, insulin resistance, and renal dysfunction. It is recommended that public health strategies target reducing MASLD risk based on these findings.