Evidence map›Paper›PMID 40336965›Full record

ArticleFrontiers in nutrition2025

The relationship between dietary sodium intake and all-cause mortality in patients with non-alcoholic fatty liver disease: a cohort study from NHANES 2003-2018.

Jiajun Li, Sile Wan, Xianyu Dai, Yifeng Cui, Zhaoyang Lu

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Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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3citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jiajun Li *Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Sile Wan *Department of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Xianyu DaiUrology Department, First Hospital of Jilin University, Changchun, China.
Yifeng CuiDepartment of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhaoyang LuDepartment of Hepatic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: 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. Methods: 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. Results: 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 ( Conclusion: 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.

Indexed as

all-cause mortalitydose-response relationshipNational Health and Nutrition Examination Surveynon-alcoholic fatty liver diseasesodium intake

Identifiers

PMID40336965
PMCPMC12055778

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.