Li Jiajun, Wan Sile, Dai Xianyu, Cui Yifeng, Lu Zhaoyang
Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Urology Department, First Hospital of Jilin University, Changchun, China.
Front Nutr. 2025 Apr 23;12:1530025. doi: 10.3389/fnut.2025.1530025. eCollection 2025.
The relationship between sodium intake and the incidence and mortality of non-alcoholic fatty liver disease (NAFLD) is underexplored in nutritional epidemiology, highlighting the need for further research.
This longitudinal cohort study analyzed data from 13,853 Participants aged 20 and older from the National Health and Nutrition Examination Survey (NHANES) (2003-2018), including 4,465 participants with NAFLD. We collected comprehensive data on mortality, dietary sodium intake, and relevant covariates. Logistic regression assessed the relationship between sodium consumption and NAFLD incidence, while Cox regression and smooth curve fitting explored sodium intake's link to all-cause mortality among Participants with NAFLD.
After adjusting for confounders, logistic regression revealed a positive association between higher sodium intake and NAFLD incidence (OR = 1.16, 95% CI = 1.11, 1.21). Adjusted odds ratios for the second (Q2), third (Q3), and fourth (Q4) quartiles of sodium intake were 0.91, 1.23, and 1.52, respectively. Smooth curve fitting and threshold analysis revealed a non-linear association between sodium intake and NAFLD risk, with an inflection point at 2.49 g/d, above which NAFLD risk significantly increased. In Cox regression, sodium intake was inversely correlated with all-cause mortality in Participants with NAFLD (HR = 0.87, 95% CI = 0.80, 0.96), with adjusted hazard ratios for Q2, Q3, and Q4 being 0.79, 0.66, and 0.63, respectively. A nonlinear model indicated a threshold effect, revealing a correlation between dietary sodium intake and mortality risk ( = 0.001). We identified a threshold intake of 3.5 grams per day (equivalent to 8.9 grams of sodium chloride): below this, each unit increase in sodium intake was associated with a 16% reduction in mortality risk (HR = 0.84, 95% CI = 0.80, 0.90). For intakes above this threshold, no significant relationship with mortality risk was observed (HR = 0.99, 95% CI = 0.90, 1.08).
This study suggests that higher sodium intake in individuals with NAFLD is associated with increased disease incidence but decreased all-cause mortality. The dose-response relationship between sodium intake and mortality risk exhibited a nonlinear pattern, with a critical inflection point around 3.5 grams per day.
在营养流行病学中，钠摄入量与非酒精性脂肪性肝病（NAFLD）的发病率和死亡率之间的关系尚未得到充分研究，这凸显了进一步研究的必要性。
这项纵向队列研究分析了来自美国国家健康与营养检查调查（NHANES）（2003 - 2018年）的13853名20岁及以上参与者的数据，其中包括4465名患有NAFLD的参与者。我们收集了关于死亡率、饮食钠摄入量和相关协变量的综合数据。逻辑回归评估了钠摄入量与NAFLD发病率之间的关系，而Cox回归和平滑曲线拟合则探讨了NAFLD参与者中钠摄入量与全因死亡率之间的联系。
在调整混杂因素后，逻辑回归显示较高的钠摄入量与NAFLD发病率呈正相关（OR = 1.16，95% CI = 1.11，1.21）。钠摄入量第二（Q2）、第三（Q3）和第四（Q4）四分位数的调整后比值比分别为0.91、1.23和1.52。平滑曲线拟合和阈值分析显示钠摄入量与NAFLD风险之间存在非线性关联，拐点为2.49克/天，高于此值NAFLD风险显著增加。在Cox回归中，钠摄入量与NAFLD参与者的全因死亡率呈负相关（HR = 0.87，95% CI = 0.80，0.96），Q2、Q3和Q4的调整后风险比分别为0.79、0.66和0.63。非线性模型表明存在阈值效应，揭示了饮食钠摄入量与死亡风险之间的相关性（P = 0.001）。我们确定的阈值摄入量为每天3.5克（相当于8.9克氯化钠）：低于此值，钠摄入量每增加一个单位，死亡风险降低16%（HR = 0.84，95% CI = 0.80，0.90）。对于高于此阈值的摄入量，未观察到与死亡风险有显著关系（HR = 0.99，95% CI = 0.90，1.08）。
本研究表明，NAFLD患者较高的钠摄入量与疾病发病率增加相关，但与全因死亡率降低相关。钠摄入量与死亡风险之间的剂量反应关系呈现非线性模式，临界拐点约为每天3.5克。
