Salt and Your Liver: Why It Matters in Fatty Liver and Cirrhosis

1. Introduction

Sodium chloride, commonly known as table salt, is a ubiquitous component of the modern diet, yet its role in metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) remains underappreciated.

While the cardiovascular effects of excess sodium are well-established (Mozaffarian et al., 2014), emerging evidence reveals a direct relationship between dietary sodium intake and the development and progression of fatty liver disease.

This chapter examines the evidence linking sodium consumption to MASLD risk, explores the role of potassium-enriched salt substitutes as a potential intervention, and provides guidance for sodium management in patients with cirrhosis.

1.1 Salt Varieties: All Essentially Sodium Chloride

A common misconception exists that certain “premium” salts, such as pink Himalayan salt, sea salt, or Celtic salt, offer health advantages over standard table salt. From a chemical standpoint, all of these varieties consist primarily of sodium chloride (NaCl), typically comprising 95-99% of their composition. The trace minerals present in specialty salts (iron, magnesium, calcium) occur in such minute quantities that they provide no meaningful nutritional benefit. For individuals concerned about liver health, the sodium content, not the salt variety, is what matters most.

Despite marketing claims, choosing pink Himalayan salt over table salt for health reasons is like choosing a designer water bottle over a regular one, the contents are essentially the same.

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2. Sodium’s Physiological Role and Portal Hypertension

Sodium is essential for maintaining fluid balance, nerve function, and cellular homeostasis. However, excessive sodium intake disrupts these processes, particularly in individuals with liver disease.

In cirrhosis, sodium retention is mediated by activation of the renin-angiotensin-aldosterone system (RAAS) and increased renal sodium reabsorption, leading to excess fluid retention and ascites (fluid accumulation in the abdomen) development (EASL, 2018). The combination of portal hypertension, increased pressure within the hepatic portal system, and sodium retention creates a perfect storm for fluid accumulation in the peritoneal cavity.

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3. Evidence Linking High Sodium Intake to NAFLD/MASLD

3.1 Systematic Reviews and Meta-Analyses

A comprehensive systematic review and meta-analysis by Shojaei-Zarghani et al. (2022) examined seven observational studies and found that high sodium intake was significantly associated with increased NAFLD risk, with an odds ratio of 1.60 (95% CI: 1.19-2.15). This analysis, which included over 6,000 participants from various populations, provides compelling evidence that high sodium consumption actively contributes to hepatic steatosis.

Another meta-analysis by da Silva (2023) looked at seven studies in humans and eight in animals and found association between high sodium intake and NAFLD.

3.2 Prospective Cohort Studies

The UK Biobank study (Chen et al., 2025), which followed 494,110 participants for a median of 13.6 years, demonstrated that individuals who sometimes, usually, and always add salt to foods have 7%, 20%, and 35% higher risk, respectively of developing MASLD compared to those who never or rarely added salt, with a clear dose-response relationship across increasing frequencies of salt use.

In the Kailuan prospective study from China involving 35,023 participants (Shen et al 2019), perceived high salt intake (≥10 g/day) was associated with significantly higher future risk of NAFLD development compared to low salt intake (<6 g/day).

3.3 Genetic Evidence

A 2025 Mendelian randomization study (Liu et al., 2025) provided causal genetic evidence linking high dietary salt consumption to MASLD development, demonstrating that genetic liability to higher salt intake causally increases MASLD risk, with no evidence for reverse causation. This study strengthens the argument that the relationship between salt and MASLD is not merely correlational but likely causal.

3.4 Objective Measures of Sodium Excretion

Using estimated 24-hour urinary sodium excretion as an objective measure, Huh et. al (2015) analyzed data from 27,433 participants in the Korea National Health and Nutrition Examination Surveys (2008-2010)and found that those in the highest sodium excretion tertile had significantly higher prevalence of NAFLD (OR 1.39-1.75 depending on the diagnostic index used), even after adjusting for body fat and hypertension.

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4. Mechanisms: How Does Sodium Contribute to NAFLD?

The mechanisms linking high sodium intake to NAFLD are multifactorial:

Insulin Resistance: High sodium consumption is associated with increased insulin resistance (Baudrand et al 2014), a key driver of hepatic steatosis.
Inflammation and Oxidative Stress: Animal studies (Uetake et al 2015) demonstrate that high-salt diets exacerbate NAFLD and NASH by inducing inflammation and oxidative stress.
Metabolic Syndrome: Excess sodium intake promotes multiple components of metabolic syndrome: obesity, dyslipidemia, hypertension, and diabetes (Wu et al 2023) all of which independently increase NAFLD risk.
Portal Hypertension (in advanced chronic liver disease): In patients with established liver disease, sodium retention worsens portal hypertension and contributes to decompensation.

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5. Does Limiting Salt Help Reverse NAFLD or Limit Progression?

While the evidence linking high sodium intake to NAFLD development is robust, data on whether sodium restriction can reverse established NAFLD or prevent progression is more limited. However, several considerations support sodium reduction as part of comprehensive NAFLD management:

Cardiovascular Benefits: Reducing salt intake decreases blood pressure and cardiovascular risk, which is crucial given that cardiovascular disease is the leading cause of mortality in NAFLD patients (Targher et al, 2007).
Metabolic Improvements: Sodium reduction may improve insulin sensitivity and reduce systemic inflammation, both potentially beneficial for NAFLD.
Weight Management: Lower sodium intake often has an indirect association with reduced consumption of ultra processed foods, which can help support weight loss efforts.

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6. Dietary Sodium Guidelines for NAFLD/MASLD

For individuals with NAFLD/MASLD without cirrhosis, the World Health Organization recommends limiting sodium intake to less than 2,000 mg per day (equivalent to approximately 5 grams of salt) (WHO guidelines, 2012). For context, the average American consumes 3,400 mg of sodium daily, significantly exceeding recommendations.

Practical strategies include:

Reading nutrition labels carefully (look for less than 5% Daily Value of sodium per serving)
Cooking at home using fresh ingredients
Using herbs, spices, lemon juice, and vinegar for flavor instead of salt
Avoiding processed and restaurant foods, which account for approximately 70% of sodium intake (Harnack et al, 2017).
Gradually reducing salt to allow taste adaptation

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7. Potassium-Enriched Salt Substitutes: A Promising Alternative

7.1 Composition and Mechanism

Potassium-enriched salt substitutes typically contain 75% sodium chloride and 25% potassium chloride, effectively reducing sodium intake while increasing potassium consumption, both of which contribute to blood pressure reduction.

7.2 Evidence for Blood Pressure Benefits

A meta-analysis found that replacement of sodium chloride with potassium-enriched salt substitutes lowers systolic blood pressure by an average of 5.58 mmHg and diastolic blood pressure by 2.88 mmHg (Greer et al 2020).

7.3 Cardiovascular Outcomes

The landmark Salt Substitute and Stroke Study (SSaSS), which included 20,995 participants with prior stroke or high blood pressure, demonstrated that using potassium-enriched salt (75% NaCl, 25% KCl) significantly reduced the rates of stroke, major cardiovascular events, and death from any cause.

While specific studies examining potassium-enriched salt substitutes in NAFLD patients are lacking, the blood pressure and metabolic benefits observed in other populations suggest potential advantages for NAFLD management. The blood pressure reductions observed in the SSaSS trial appear to have been driven primarily by increased potassium intake rather than sodium reduction, with majority of the benefits attributable to potassium supplementation.

7.4 Safety Considerations

The primary risk of potassium-enriched salt substitutes is hyperkalemia (dangerously high potassium levels in the blood), particularly in individuals with chronic kidney disease, those taking medications that affect potassium excretion (ACE inhibitors, ARBs, potassium-sparing diuretics), or patients with advanced cirrhosis and renal dysfunction.

Before recommending potassium-enriched salt substitutes, clinicians should:

Assess renal function
Review medications for potential potassium-elevating effects
Monitor serum potassium levels, especially during initiation
Avoid use in patients with estimated GFR (a kidney function measure based on creatinine or Cystatin C) <60 mL/min/1.73m² or known hyperkalemia

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8. Salt and Cirrhosis: Specific Guidance

8.1 Sodium Restriction in Ascites Management

For patients with cirrhosis who develop ascites, sodium restriction to 2 grams (2,000 mg) per day or less is recommended as first-line therapy, typically combined with diuretics (Kwong, et al 2024).

8.2 Compensated vs. Decompensated Cirrhosis

The European Association for the Study of the Liver (EASL) guidelines (EASL, 2018) state that prophylactic salt restriction in cirrhotic patients who have never had ascites is not supported by evidence. However, once ascites develops (grade 2 or higher), dietary sodium restriction becomes a cornerstone of management, with the goal of achieving negative sodium balance.

8.2.1 Severity-Based Recommendations

Compensated cirrhosis without ascites: No specific sodium restriction required
Grade 1 ascites (mild, detected only on imaging): Sodium restriction may be initiated, though evidence is limited
Grade 2-3 ascites: Sodium restriction to ≤2 g/day combined with diuretics is recommended
Refractory ascites: Continue sodium restriction; consider large-volume paracentesis or TIPS

8.2.2 Avoiding Excessive Restriction

Emerging evidence suggests that severe salt-restricted diets (<5 g/day total salt, equivalent to <2 g sodium) may not significantly improve ascites control (Kumar et al 2023) and could lead to complications including volume contraction, renal impairment, and hyponatremia. The key is individualized management based on urinary sodium excretion and clinical response.

8.2.3 Fluid Restriction

Fluid restriction is generally not necessary unless serum sodium falls below 125-130 mmol/L, as fluid accumulation in cirrhosis results from sodium retention, not excess water intake.

8.2.4 Monitoring

Patients with cirrhotic ascites should have regular monitoring of:

Body weight (daily)
Serum electrolytes (sodium, potassium, chloride)
Renal function
Urinary sodium excretion (when available)

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9. Practical Implementation

9.1 Reading Labels

Sodium content must be listed on food labels in the United States. Key terms include:

“Sodium-free”: <5 mg per serving
“Very low sodium”: ≤35 mg per serving
“Low sodium”: ≤140 mg per serving
“Reduced sodium”: At least 25% less sodium than the regular version
“Light in Sodium or Lightly Salted”: At least 50% less sodium than the regular product
“No-Salt-Added or Unsalted”: No salt is added during processing – but these products may not be salt/sodium-free unless stated

9.2 Hidden Sources of Sodium

Common high-sodium foods to limit:

Processed meats (deli meats, bacon, sausage)
Canned soups and vegetables
Condiments (soy sauce, ketchup, salad dressings)
Bread and baked goods
Cheese
Restaurant and fast food meals
Pickled foods

9.3 Flavor Alternatives

Enhance food palatability without sodium using:

Fresh and dried herbs (basil, oregano, thyme, rosemary)
Spices (cumin, paprika, turmeric, black pepper)
Citrus juice and zest
Vinegars
Garlic and onion
Ginger

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10. Conclusion

The evidence linking high sodium intake to NAFLD/MASLD development and progression is compelling and continues to grow. While sodium reduction alone is unlikely to reverse established NAFLD, it represents an important component of comprehensive lifestyle modification alongside weight loss, dietary improvement, and physical activity. Potassium-enriched salt substitutes offer a practical alternative for many patients, providing blood pressure and potentially metabolic benefits, though safety screening for kidney function and medication interactions is essential. For patients with cirrhosis and ascites, sodium restriction becomes a critical therapeutic intervention that must be carefully monitored and individualized. As our understanding of the sodium-liver axis continues to evolve, personalized sodium recommendations based on disease stage, comorbidities, and individual tolerance will become increasingly important.

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11. References

Baudrand R, Campino C, Carvajal CA, Olivieri O, Guidi G, Faccini G, Vöhringer PA, Cerda J, Owen G, Kalergis AM, Fardella CE. High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clin Endocrinol (Oxf). 2014 May;80(5):677-84. doi: 10.1111/cen.12225. Epub 2013 May 15. PMID: 23594269.
Chen H, Zhang X, Lin S, Wu Q. Adding salt to foods increases the risk of metabolic dysfunction-associated steatotic liver disease. Commun Med (Lond). 2025 Aug 8;5(1):342. doi: 10.1038/s43856-025-01074-4. PMID: 40781351; PMCID: PMC12334587. https://pubmed.ncbi.nlm.nih.gov/40781351/. This UK Biobank prospective study of nearly 500,000 participants demonstrated a dose-response relationship between frequency of adding salt to foods and MASLD incidence over 13.6 years.
Greer, R. C., Marklund, M., Anderson, C. A. M., et al. (2020). Potassium-enriched salt substitutes as a means to lower blood pressure: Benefits and risks. Hypertension, 75(2), 266-274. https://pubmed.ncbi.nlm.nih.gov/31838902/ Systematic review examining evidence for blood pressure-lowering effects of potassium-enriched salt substitutes and safety considerations, particularly regarding hyperkalemia risk.
Huang, L., et al. (2024). The contribution of sodium reduction and potassium increase to the blood pressure lowering observed in the Salt Substitute and Stroke Study. Journal of Human Hypertension, 38, 289-295. https://pubmed.ncbi.nlm.nih.gov/38379029/. Analysis demonstrating that majority of blood pressure reduction in SSaSS was attributable to increased potassium rather than decreased sodium.
Kwong AJ, Norman J, Biggins SW. Management of ascites and volume overload in patients with cirrhosis. Clin Liver Dis (Hoboken). 2024;23(1):e0115. Published 2024 Feb 9. doi:10.1097/CLD.0000000000000115. https://pmc.ncbi.nlm.nih.gov/articles/PMC10857675/. Practical guide describing sodium restriction (≤2 g/day) combined with diuretics as first-line therapy for ascites.
Liu, Q., Liu, Y., & Feng, H. (2025). High salt diet causally increases metabolic dysfunction-associated steatotic liver disease risk: A bidirectional Mendelian randomization study. Clinical Nutrition, 44(3), 799-806. https://pubmed.ncbi.nlm.nih.gov/40184888/ Mendelian randomization study providing genetic causal evidence that high dietary salt intake increases MASLD risk.
Mozaffarian, D., et al. (2014). Global sodium consumption and death from cardiovascular causes. New England Journal of Medicine, 371, 624-634. https://www.nejm.org/doi/full/10.1056/NEJMoa1304127 Large global study examining sodium consumption patterns and cardiovascular mortality across multiple countries.
Neal, B., Wu, Y., Feng, X., et al. (2021). Effect of salt substitution on cardiovascular events and death. New England Journal of Medicine, 385(12), 1067-1077. https://www.nejm.org/doi/full/10.1056/NEJMoa2105675 The landmark SSaSS trial demonstrating that potassium-enriched salt substitute (75% NaCl, 25% KCl) reduced stroke, cardiovascular events, and mortality in high-risk individuals.
Kumar R, Marrapu S. Dietary salt in liver cirrhosis: With a pinch of salt!. World J Hepatol. 2023;15(10):1084-1090. doi:10.4254/wjh.v15.i10.1084. https://pmc.ncbi.nlm.nih.gov/articles/PMC10642432/ Critical review of sodium restriction in cirrhosis, highlighting potential harms of excessive restriction and lack of evidence for very low-sodium diets.
Shojaei-Zarghani, S., Safarpour, A. R., Fattahi, M. R., & Keshtkar, A. (2022). Sodium in relation with nonalcoholic fatty liver disease: A systematic review and meta-analysis of observational studies. Food Science & Nutrition, 10(5), 1579-1591. https://doi.org/10.1002/fsn3.2781 Comprehensive meta-analysis of seven studies showing that high sodium intake is associated with 60% increased odds of NAFLD.
da Silva Ferreira G, Catanozi S, Passarelli M. Dietary Sodium and Nonalcoholic Fatty Liver Disease: A Systematic Review. Antioxidants (Basel). 2023 Feb 28;12(3):599. doi: 10.3390/antiox12030599. PMID: 36978847; PMCID: PMC10045331. https://pubmed.ncbi.nlm.nih.gov/36978847/. Comprehensive systematic review examining both human and animal studies on sodium intake and NAFLD, finding evidence for both high and very low sodium intake being associated with adverse liver outcomes in a U or J-shaped relationship.
Shen X, Jin C, Wu Y, Zhang Y, Wang X, Huang W, Li J, Wu S, Gao X. Prospective study of perceived dietary salt intake and the risk of non-alcoholic fatty liver disease. J Hum Nutr Diet. 2019 Dec;32(6):802-809. doi: 10.1111/jhn.12674. Epub 2019 Jun 18. PMID: 31209928. https://pubmed.ncbi.nlm.nih.gov/31209928/. Kailuan prospective study of 35,023 Chinese participants showing dose-response relationship between perceived salt intake and NAFLD development.
Huh JH, Lee KJ, Lim JS, Lee MY, Park HJ, Kim MY, Kim JW, Chung CH, Shin JY, Kim HS, Kwon SO, Baik SK. High Dietary Sodium Intake Assessed by Estimated 24-h Urinary Sodium Excretion Is Associated with NAFLD and Hepatic Fibrosis. PLoS One. 2015 Nov 16;10(11):e0143222. doi: 10.1371/journal.pone.0143222. PMID: 26571018; PMCID: PMC4646649. https://pubmed.ncbi.nlm.nih.gov/26571018/ Korean study using objective 24-hour urinary sodium estimates demonstrating association between high sodium excretion and both NAFLD prevalence and advanced fibrosis.
Targher G, Arcaro G. Non-alcoholic fatty liver disease and increased risk of cardiovascular disease. Atherosclerosis. 2007 Apr;191(2):235-40. doi: 10.1016/j.atherosclerosis.2006.08.021. Epub 2006 Sep 12. PMID: 16970951. https://pubmed.ncbi.nlm.nih.gov/16970951/
Uetake Y, Ikeda H, Irie R, et al. High-salt in addition to high-fat diet may enhance inflammation and fibrosis in liver steatosis induced by oxidative stress and dyslipidemia in mice. Lipids Health Dis. 2015;14:6. Published 2015 Feb 13. doi:10.1186/s12944-015-0002-9. https://pmc.ncbi.nlm.nih.gov/articles/PMC4337194/. Animal study demonstrating that high-salt diet combined with high-fat diet stimulated oxidative stress production and inflammatory reactions in the liver, leading to NASH development.
World Health Organization. (2012). Guideline: Sodium intake for adults and children. WHO. https://www.who.int/publications/i/item/9789241504836 Official WHO guidelines recommending <2g sodium per day for adults.
Wu, W., et al. (2023). The role of dietary salt in metabolism and energy balance: Insights beyond cardiovascular disease. Diabetes, Obesity and Metabolism, 25(4), 927-939. https://pubmed.ncbi.nlm.nih.gov/36655379/ Comprehensive review discussing how high salt intake promotes overproduction of fructose, leptin resistance, insulin resistance, and reduces key metabolic hormones, contributing to obesity and metabolic syndrome.
Harnack LJ, Cogswell ME, Shikany JM, Gardner CD, Gillespie C, Loria CM, Zhou X, Yuan K, Steffen LM. Sources of Sodium in US Adults From 3 Geographic Regions. Circulation. 2017 May 9;135(19):1775-1783. doi: 10.1161/CIRCULATIONAHA.116.024446. PMID: 28483828; PMCID: PMC5417577. https://pubmed.ncbi.nlm.nih.gov/28483828/
European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018 Aug;69(2):406-460. doi: 10.1016/j.jhep.2018.03.024. Epub 2018 Apr 10. Erratum in: J Hepatol. 2018 Nov;69(5):1207. doi: 10.1016/j.jhep.2018.08.009. PMID: 29653741.
U.S. Food and Drug Administration. (2024). Sodium in your diet. FDA. https://www.fda.gov/food/nutrition-education-resources-materials/sodium-your-diet

Other Supporting References

Heller B, Reiter FP, Leicht HB, Fiessler C, Bergheim I, Heuschmann PU, Geier A, Rau M. Salt-Intake-Related Behavior Varies between Sexes and Is Strongly Associated with Daily Salt Consumption in Obese Patients at High Risk for MASLD. Nutrients. 2023 Sep 12;15(18):3942. doi: 10.3390/nu15183942. PMID: 37764734; PMCID: PMC10534674. Study examining salt intake behaviors in MASLD patients, finding mean daily intake of 7.3 g in men and 5.3 g in women.

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