Hypertension, Sodium & Potassium

Citation model. Claims grounded in AllNutrition's trust-scored library carry an inline bracketed reference [n] linking to the References section, which lists each source's evidence level and AllNutrition trust score (0–1). Where an AllNutrition query returned an overall evidence_strength and consensus_level, those labels are surfaced in the Evidence Review so readers can calibrate confidence. Only sources actually returned by the tool are cited; no trust scores are invented.

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1. Introduction

Hypertension is the single largest modifiable contributor to global cardiovascular mortality, and diet — specifically sodium, potassium, and the dietary patterns that carry them — sits at the center of both the physiology and the controversy. Few areas of clinical nutrition combine such strong mechanistic and randomized-trial evidence with such persistent public argument. On one hand, the dose-response relationship between sodium restriction and blood pressure is among the most rigorously replicated findings in all of nutrition science. On the other, a body of large observational cohorts has reported a "J-shaped" association between sodium intake and cardiovascular events, reigniting debate about whether population-wide sodium targets are correct, achievable, or even net-beneficial for everyone.

This module gives the physician-in-training the physiological vocabulary — pressure-natriuresis, the renin-angiotensin-aldosterone system (RAAS), salt sensitivity — needed to interpret that debate, and the clinical tools to counsel patients on sodium, potassium, the DASH pattern, weight, and alcohol, while safely navigating the drug-nutrient interactions (RAAS inhibitors, diuretics, licorice) that make electrolyte management in hypertensive patients a genuine safety issue rather than a lifestyle footnote.

2. Learning Objectives

By the end of this module, the learner will be able to:

1. Explain the pressure-natriuresis (Guytonian) model of long-term blood pressure control, the role of RAAS, and the vascular (endothelial/glycocalyx) mechanisms by which sodium raises blood pressure independent of volume.
2. Describe the dose-response relationship between sodium reduction and blood pressure demonstrated in DASH-Sodium and related trials.
3. Critically evaluate the sodium–cardiovascular-outcomes controversy, including the PURE study's J-curve, the methodological critiques (spot urine measurement error, reverse causation) that explain the discrepancy with RCT evidence, and where the field's consensus currently sits.
4. Summarize the evidence for dietary potassium, the sodium-to-potassium ratio, and the SSaSS trial on potassium-enriched salt substitutes — including their safety boundaries.
5. Explain the mechanisms and trial evidence for the DASH dietary pattern, weight loss, alcohol moderation, and magnesium as blood-pressure-lowering interventions, and how these compare with pharmacotherapy.
6. Identify salt-sensitive subgroups and apply guideline-based sodium/potassium targets safely, including recognizing nutrition–drug interactions with ACE inhibitors/ARBs, diuretics, and licorice.

3. Scientific Foundations

3.1 Pressure-natriuresis and renal sodium handling

The kidney is the long-term "set point" organ for blood pressure. In the classical Guytonian model, when dietary sodium intake exceeds the renal excretory threshold, plasma osmolality rises, triggering vasopressin release and thirst, expanding extracellular fluid volume and raising cardiac output; peripheral vasculature then autoregulates via vasoconstriction, and the resulting rise in systemic vascular resistance raises arterial pressure until the kidney can excrete the sodium load and restore balance — i.e., pressure forces natriuresis [1]. This volume-centric model remains foundational, but newer evidence substantially extends it: high sodium directly impairs endothelial function by reducing nitric oxide bioavailability and damaging the endothelial glycocalyx, and sodium can be stored non-osmotically in skin and muscle — independent of water retention — where it can trigger local immune activation and vascular stiffening even without measurable volume expansion [1][3]. Renal sodium handling also follows circadian rhythms, with reabsorption genes upregulated during the active phase, and hormones such as atrial natriuretic peptide (ANP) and uromodulin (which activates tubular sodium transporters NKCC2/NCC) modulate individual variability in sodium sensitivity [1][14].

3.2 The renin-angiotensin-aldosterone system (RAAS)

RAAS is the principal hormonal regulator of blood pressure and fluid balance, and its overactivity is a major driver of primary hypertension, particularly with obesity, diabetes, and insulin resistance [1]. Dietary sodium and RAAS exist in an inverse feedback loop: high sodium intake suppresses plasma renin and angiotensinogen, while sodium restriction activates RAAS as a compensatory sodium-conserving response [1]. This has a direct pharmacologic consequence: sodium restriction "primes" RAAS-inhibiting drugs (ACE inhibitors, ARBs), amplifying their antihypertensive effect, whereas high sodium intake blunts RAAS-inhibitor efficacy and contributes to treatment resistance [1][2]. A separate "potassium switch" pathway means potassium deficiency itself activates renal sodium retention pathways, effectively mimicking high sodium intake and worsening salt sensitivity regardless of actual sodium intake [1].

3.3 Vascular mechanisms and renal sodium handling in disease

Beyond RAAS and volume, chronic RAAS/sodium-driven activation produces vascular inflammation, arterial stiffening, and target-organ damage independent of blood pressure elevation per se; a longitudinal multiorgan transcriptomic analysis found that high salt intake causes organ damage through parallel molecular pathways distinct from blood-pressure elevation alone, implying that BP normalization does not fully reverse salt-induced vascular injury [1][3]. Uromodulin is emerging as a biomarker of salt sensitivity in chronic kidney disease (CKD), where higher levels predict a stronger BP rise with sodium loading [14].

3.4 Sodium reduction and blood pressure: the DASH-Sodium dose-response

DASH-Sodium-type evidence demonstrates a linear dose-response: moving from high (~3,300 mg/day) to intermediate (~2,400 mg/day) to low (~1,500 mg/day) sodium intake produces progressively greater blood pressure reductions, with the greatest reductions achieved at the lowest sodium level combined with the DASH dietary pattern; this pattern is consistent across age and baseline blood pressure [4]. Population-wide, each 100 mmol reduction in urinary sodium excretion is associated with roughly 6.8 mmHg systolic and 3.85 mmHg diastolic reduction [1][2], though other pooled estimates in guideline consensus documents report smaller effects (2.6–4.3 mmHg systolic) depending on population and methodology [2].

3.5 The sodium–cardiovascular-outcomes controversy: PURE, the J-curve, and reverse causation

Large observational cohorts, notably the PURE study, report a J-shaped relationship between estimated sodium intake and cardiovascular events — risk rising at both very high (>5–6 g/day) and very low (<3 g/day) intakes — which conflicts with RCT evidence (e.g., Trials of Hypertension Prevention, TOHP) showing a linear, monotonic benefit of sodium reduction with no lower-bound harm signal [5]. The dominant explanation is methodological, not biological: most large cohorts estimate sodium from single spot urine samples using predictive equations that systematically overestimate excretion at low intakes and underestimate it at high intakes, artificially generating a J-shape; self-reported dietary recall further underestimates intake relative to urinary biomarkers [1][7]. Reverse causation compounds this: chronically ill, frail individuals eat less food — and therefore less sodium — as a consequence of their illness, not its cause, producing a spurious association between low sodium and mortality [1][7]. When individualized, repeated 24-hour urine collections are used, the sodium–cardiovascular relationship is more consistently linear across a wide range of intakes [1]. Major bodies (WHO, AHA, NASEM) continue to recommend reduction targets on this basis, while acknowledging the debate is not fully resolved and that some experts now argue for targeted, salt-sensitivity-based strategies rather than uniform population mandates [1][7].

3.6 Potassium, the sodium-to-potassium ratio, and vascular effects

Potassium lowers blood pressure via renal natriuresis, vasodilation, and blunted vascular sensitivity to angiotensin II and catecholamines; RCT evidence shows that increasing potassium intake by ~2.4 g/day lowers blood pressure by roughly 3.9/1.6 mmHg and improves flow-mediated dilation (a marker of endothelial function) [6]. Higher potassium intake is associated with an estimated 21% reduction in stroke risk per 1.64 g/day increment in some pooled analyses [6]. Increasingly, the evidence supports evaluating the sodium-to-potassium ratio rather than either mineral in isolation, since a lower Na:K ratio is more consistently associated with cardiovascular benefit than isolated sodium restriction [1][20].

3.7 The DASH dietary pattern: mechanisms beyond sodium

The DASH pattern lowers blood pressure through mechanisms independent of its sodium content: potassium-driven natriuresis and vasodilation; magnesium and calcium acting as natural vascular smooth-muscle relaxants (magnesium functions partly as a natural calcium-channel blocker and stimulates nitric oxide and prostaglandin E synthesis); inorganic nitrates from leafy vegetables converted to vasodilatory nitric oxide; antioxidant and anti-inflammatory polyphenols and vitamin C/folate reducing oxidative stress and arterial stiffness; and fiber-driven favorable shifts in gut microbiota [4]. In RCTs where sodium was not restricted, weight was not lost, and exercise was not increased, DASH alone still reduced systolic blood pressure by roughly 4.25 mmHg and diastolic by 2.27 mmHg [4].

4. Clinical Relevance

Hypertension management sits at the intersection of nutrition counseling and pharmacotherapy, and physicians must be fluent in both. Patients ask about salt substitutes, "natural" alternatives to medication, and whether low-sodium diets are actually dangerous — questions shaped by genuinely conflicting headlines rooted in the observational/RCT discrepancy above. Clinicians also must recognize when dietary potassium optimization (a genuinely evidence-based, high-value intervention) becomes dangerous — specifically in patients on RAAS inhibitors, potassium-sparing diuretics, or with reduced kidney function, where a "healthy" salt substitute can precipitate life-threatening hyperkalemia. Equally, under-recognized dietary causes of resistant hypertension (excess licorice, alcohol, sodium-heavy processed foods) are frequently missed in standard histories.

5. Evidence Review

Established (high confidence):

• Reducing sodium intake lowers blood pressure in a linear, dose-dependent manner (DASH-Sodium-type evidence); greatest reductions occur at the lowest sodium levels, and effects are more pronounced in hypertensive and salt-sensitive individuals. AllNutrition evidence_strength: strong, consensus_level: moderate [1][4].
• The DASH dietary pattern lowers blood pressure through mechanisms (potassium, magnesium, nitrates, antioxidants) independent of sodium reduction. evidence_strength: strong, consensus: moderate [4].
• The SSaSS trial (potassium-enriched salt substitute, 75% NaCl/25% KCl) significantly reduced stroke, major cardiovascular events, and all-cause mortality in a high-risk rural Chinese population, without a significant excess of serious hyperkalemia events in the overall trial population. evidence_strength: strong, consensus: moderate [1][8][9].
• Weight loss and alcohol moderation produce clinically meaningful blood pressure reductions (~8.5 mmHg systolic per 3 kg/m² BMI reduction; ~5.5 mmHg systolic per 50% alcohol reduction). evidence_strength: strong, consensus: moderate [10].
• Licorice (glycyrrhizin, >100 mg/day, particularly beyond 30 days) causes pseudohyperaldosteronism via 11β-HSD2 inhibition, producing hypertension and hypokalemia. evidence_strength: moderate, consensus: moderate [11].

Probable:

• A lower dietary sodium-to-potassium ratio is a better predictor of cardiovascular risk than either mineral considered alone. evidence_strength: strong, consensus: mixed [1][20].
• Magnesium intake/supplementation modestly lowers blood pressure, particularly at higher baseline BP or BMI, with possible synergy with vitamin D. evidence_strength: strong, consensus: moderate [16][17].
• Structured lifestyle intervention (DASH/Mediterranean/Nordic patterns, combined with exercise and weight management) is recommended as first-line therapy for 3–6 months in low-risk Stage 1 hypertension before adding pharmacotherapy, per 2025 AHA/ACC-referenced consensus guidance. evidence_strength: strong, consensus: moderate [2].

Emerging:

• Salt sensitivity is being reframed as a progressive, mechanistically heterogeneous trait (renal transporter genetics, insulin resistance, aging-related nephron loss, uromodulin biomarkers) rather than a fixed binary phenotype, pointing toward future personalized sodium/potassium prescribing. evidence_strength: moderate, consensus: moderate [1][14].
• Non-osmotic tissue sodium storage and endothelial glycocalyx injury as BP-independent mechanisms of sodium-related vascular damage. evidence_strength: strong, consensus: mixed [1][3].

Controversial:

• Whether the PURE study's J-shaped sodium–mortality association reflects true biological harm from low sodium intake, or is an artifact of spot-urine measurement error and reverse causation; RCT evidence favors the latter interpretation, but the debate — and its implications for whether universal versus targeted sodium reduction is optimal policy — remains unresolved. evidence_strength: moderate, consensus: mixed [1][5][7].
• An apparent inverse association between high salt intake and mortality in adults over 50 in some observational data, plausibly confounded by frailty-driven reverse causation, illustrates how age-stratified sodium epidemiology can appear to contradict trial evidence. evidence_strength: moderate, consensus: mixed [7][15].

Unsupported / overstated:

• The claim that potassium-based salt substitutes are safe for all patients regardless of renal function or RAAS-inhibitor/diuretic use; trial and real-world safety data explicitly exclude or caution against use in patients with impaired potassium excretion [1][8][9][12].
• The claim that dietary sodium restriction alone can substitute for pharmacotherapy in Stage 2 hypertension or in high 10-year cardiovascular risk patients — guideline consensus reserves lifestyle-only trials for low-risk Stage 1 disease [2].

6. Practical Clinical Applications

Targets. For general blood pressure management: sodium <2,000 mg/day (some guidance to <1,500 mg/day for those with hypertension, or as low as ~1,000 mg/day for additional benefit), and potassium 3,500–4,700 mg/day from food, unless contraindicated [1][2]. CKD stage 3–5 patients typically require tighter sodium limits (<2.0 g/day per contemporary guideline recommendations) and potassium capped near 2.4–3.0 g/day for advanced disease — always individualized [1][2].

When lifestyle-first is appropriate. A 3–6 month trial of lifestyle intervention alone (DASH-style diet, sodium reduction, weight loss, alcohol moderation, exercise) is reasonable for Stage 1 hypertension (SBP 130–139 or DBP 80–89 mmHg) in patients without established cardiovascular disease, diabetes, or CKD, and with low estimated 10-year cardiovascular risk [2].

When not to rely on diet alone. Stage 2 hypertension (≥140/90 mmHg), or Stage 1 hypertension with existing cardiovascular disease, diabetes, CKD, or elevated 10-year risk, warrants concurrent pharmacotherapy alongside lifestyle change, not lifestyle-only trials [2].

Nutrition–antihypertensive drug interactions — the highest-yield safety teaching point in this module:

• ACE inhibitors/ARBs + potassium-based salt substitutes or high-potassium diets: risk of hyperkalemia is real and clinically significant; SSaSS-type trials that demonstrated net benefit largely excluded or closely monitored patients with impaired potassium excretion, and real-world hyperkalemia-management data show meaningful reductions in hyperkalemia-related hospitalization with proactive management (e.g., potassium binders) in RAAS-inhibitor-treated patients [1][8][9][12][13]. Screen renal function and current medications before recommending potassium-based salt substitutes.
• Diuretics: thiazide and loop diuretics both increase urinary magnesium and potassium losses (thiazides act at the distal convoluted tubule, loop diuretics at the thick ascending limb), producing dose-dependent hypomagnesemia and hypokalemia risk that can itself provoke arrhythmia and, per emerging data, calcium pyrophosphate arthritis; potassium-sparing diuretics conversely raise hyperkalemia risk when combined with RAAS inhibitors or potassium supplementation [18][19].
• Licorice: counsel patients on chronic licorice tea/candy/supplement use (>100 mg/day glycyrrhizin, especially beyond 30 days) as a reversible cause of treatment-resistant hypertension and hypokalemia via pseudohyperaldosteronism; management is discontinuation, potassium repletion, and, if needed, a mineralocorticoid receptor antagonist such as spironolactone [11].

7. Clinical Pearls

• A patient on an ACE inhibitor or ARB who starts using a potassium-based salt substitute needs a basic metabolic panel check — don't assume "natural" means risk-free.
• Unexplained hypokalemia plus resistant hypertension: ask about licorice (tea, candy, supplements) before ordering an aldosterone/renin panel.
• The PURE study's J-curve is a measurement-and-confounding story, not proof that sodium restriction is harmful — but it is a legitimate reason to individualize rather than universally mandate very-low sodium targets.
• DASH lowers blood pressure even without sodium restriction; sodium restriction plus DASH is additive, not redundant.
• Thiazide and loop diuretics deplete magnesium as reliably as they deplete potassium — think beyond potassium when a patient on chronic diuretics reports muscle cramps or arrhythmia symptoms.
• Weight loss (~8.5 mmHg systolic per 3 kg/m² BMI reduction) is among the single most powerful nutrition-adjacent interventions available for blood pressure — comparable to or exceeding many single dietary changes.

8. Common Misconceptions

• "The PURE study proves low sodium is dangerous." The weight of RCT and biomarker-based evidence attributes the J-curve primarily to spot-urine measurement error and reverse causation, not a true biological floor effect [1][5][7].
• "Salt substitutes are safe for everyone." They are well-studied and net-beneficial in general and even CKD populations under appropriate monitoring, but trials establishing safety specifically excluded or closely monitored patients with impaired potassium excretion or RAAS-inhibitor/potassium-sparing-diuretic use — this caveat is frequently dropped in lay reporting [1][8][9][12].
• "DASH works because it's low in sodium." RCT evidence shows DASH lowers blood pressure substantially even when sodium is not restricted, through potassium, magnesium, nitrate, and antioxidant mechanisms [4].
• "Diuretics only affect potassium." Both thiazide and loop diuretics also meaningfully deplete magnesium, a clinically under-recognized interaction [18][19].
• "Herbal and food-based remedies for blood pressure are inherently safe." Licorice is a well-documented, dose-dependent cause of pseudohyperaldosteronism-driven hypertension and hypokalemia [11].

9. Summary

Blood pressure is set over the long term by the kidney's pressure-natriuresis relationship and modulated acutely by RAAS, with sodium and potassium acting as the dominant dietary levers on both systems — sodium via volume, RAAS suppression/activation, and direct vascular (endothelial, glycocalyx) injury; potassium via natriuresis, vasodilation, and counter-regulation of sodium's effects. The DASH-Sodium dose-response and multiple RCTs establish a robust, linear benefit of sodium reduction, while the PURE study's J-curve reflects the limits of observational sodium epidemiology (measurement error, reverse causation) more than a true biological floor of harm. Potassium-enriched salt substitutes (SSaSS), the DASH pattern, weight loss, alcohol moderation, and magnesium all have meaningful trial-level evidence for lowering blood pressure — but each carries drug-interaction caveats, chiefly the hyperkalemia risk of potassium interventions in patients on RAAS inhibitors or with reduced renal function, and the electrolyte-depleting effects of diuretics. Licorice remains an underappreciated, fully reversible dietary cause of resistant hypertension. The physician's task is to apply guideline-based sodium and potassium targets while individualizing for salt sensitivity, renal function, and concurrent pharmacotherapy — treating diet not as a replacement for medication in high-risk patients, but as a first-line strategy in low-risk Stage 1 disease and an essential adjunct at every stage.

10. References

Ordered by evidence strength / relevance. Evidence level and AllNutrition trust score (0–1) as returned by the tool.

1. Pathophysiological Mechanisms and Clinical Controversies of Sodium-Induced Hypertension: A Multi-Systemic Perspective. Nutrients (2026). Review — trust 0.85.
2. Consensus on the management of hypertension in individuals with diabetes by Asian-Pacific Society of hypertension (APSH) & Diabetes Asia Study Group (DASG). Journal of Human Hypertension (2026). Guideline — trust 0.90.
3. Longitudinal multiorgan transcriptomic atlas of salt-induced hypertension. JCI Insight (2026). Observational — trust 0.912.
4. Effects of the Dietary Approach to Stop Hypertension (DASH) diet on cardiovascular risk factors: a systematic review and meta-analysis. British Journal of Nutrition (2015). Systematic review — trust 0.682. (Supplemented by companion DASH-mechanism sources below.)
5. Rethinking the Impact of Dietary Sodium and Potassium on Blood Pressure to Advance Public Health. American Journal of Clinical Nutrition (2026). Review — trust 0.777.
6. Effects of sodium and potassium supplementation on endothelial function: a fully controlled dietary intervention study. British Journal of Nutrition (2015). RCT — trust 0.642.
7. Comparison of Measured 24-Hour Urinary Salt Excretion With Spot Urine and 24-Hour Dietary Recall Estimates Among Adolescents and Parents. JMIR Public Health and Surveillance (2026). Observational — trust 0.662.
8. Efficacy and safety of potassium-containing low-sodium salt substitutes for cardiovascular disease prevention in mixed adult populations: an umbrella review. medRxiv (2026). Review — trust 0.642.
9. Estimated health and economic effects of different salt reduction strategies on cardiovascular disease in Brazil: a microsimulation analysis. Scientific Reports (2026). Observational — trust 0.802.
10. The effects of multimodal lifestyle interventions on blood pressure, body weight, and waist circumference in hypertensive patients: a network meta-analysis. Frontiers in Public Health (2026). Systematic review — trust 0.857.
11. Pseudo-Hyperaldosteronism After the Ingestion of Licorice Tea: A Case Report. Cureus. Observational — trust 0.588.
12. Impact of Duration of Outpatient Sodium Zirconium Cyclosilicate Therapy on Hyperkalemia-Related Health Care Resource Utilization: A Matched Cohort Analysis. Kidney Medicine (2026). Observational — trust 0.752.
13. Mineralocorticoid receptor antagonists in dialysis patients after ACHIEVE and ALCHEMIST: updated systematic review and meta-analysis of 14 randomized trials. Renal Failure (2026). Systematic review — trust 0.79.
14. Effects of urine uromodulin levels on the association between sodium intake and ambulatory blood pressure in individuals with chronic kidney disease. European Journal of Internal Medicine (2026). Observational — trust 0.77.
15. High salt intake and its dual impact on obesity and cardiovascular mortality in individuals over 50: a paradoxical relationship. BMC Public Health (2025). Observational — trust 0.698.
16. Hypomagnesemia: A Clinical and Nutritional Update. Current Nutrition Reports (2026). Review — trust 0.73.
17. Potential synergistic influence of magnesium and vitamin D supplementation on blood pressure reduction: a narrative review. Nutrition Research (2026). Review — trust 0.675.
18. Diuretic-Induced Hypomagnesemia May Play a Key Role in the Development of Calcium Pyrophosphate Arthritis. Rheumatology and Therapy (2026). Observational — trust 0.752.
19. Influence of Daily Salt Intake on Blood Pressure and Atrial Natriuretic Peptide Levels in Patients Treated with Sacubitril/Valsartan. Internal Medicine (2025). Observational — trust 0.735.
20. Sodium, potassium, and blood pressure regulation in Latin American populations: a critical narrative review of multifactorial determinants. Frontiers in Cardiovascular Medicine (2026). Review — trust 0.73.

Supporting sources also surfaced: Increased fluid intake and blood pressure in healthy children, a randomized controlled trial (Pediatric Nephrology 2025, RCT, trust 0.817); The Dietary Management of Sodium in Children with Kidney Diseases (Pediatric Nephrology 2025, guideline, trust 0.907); Which is more effective in hypertension?: Salt-free diet vs DASH diet (Medicine 2025, RCT, trust 0.795); Remote dietitian counseling with short-term meal delivery improves DASH diet adherence (American Heart Journal 2026, RCT, trust 0.853); Effects of Caloric Restriction Diet on Arterial Hypertension and Endothelial Dysfunction (Nutrients 2021, review, trust 0.85); Multi-pronged biobehavioural intervention strategies for prevention and control of hypertension (SAGE Open Medicine 2026, systematic review, trust 0.842); Trends of Global Burden of Cardiovascular Diseases Attributable to High Sodium Intake From 1990 to 2021 (Journal of Clinical Hypertension 2025, observational, trust 0.767); New evidence linking lifestyle factors to blood pressure: Focus on 2024 findings (Hypertension Research 2026, review, trust 0.765); The impact of adherence to a DASH diet pattern on pharmacotherapy initiation in stage 1 hypertension (American Journal of Preventive Cardiology 2026, observational, trust 0.752); Is the effect of antihypertensive drug therapy associated with dietary sodium-potassium ratio? NHANES study (Frontiers in Cardiovascular Medicine 2026, observational, trust 0.752); Short-term high sodium intake increases nocturnal blood pressure but not arterial stiffness in Black adults (European Journal of Nutrition 2026, observational, trust 0.752); Association between DASH diet adherence and mortality in non-diabetic adults with and without CKD (Nutrition & Metabolism 2026, observational, trust 0.77); Reduced antihypertensive treatment with maintained ambulatory blood pressure control following weight loss in type 2 diabetes (Blood Pressure 2026, observational, trust 0.688); Sufficient Magnesium Intake Reduces Retinal Vein Occlusion Risk (Nutrients 2025, observational, trust 0.693); Broadening Primary Aldosteronism Screening: Alignment Across Contemporary Guidelines (Hypertension 2026, guideline, trust 0.928); Consumo de sodio: evidencias, controversias y recomendaciones prácticas (Nutrición Hospitalaria 2026, review, trust 0.725).