scholarly journals Core Strategies to Increase the Uptake and Use of Potassium-Enriched Low-Sodium Salt

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3203
Author(s):  
Adefunke Ajenikoko ◽  
Nicole Ide ◽  
Roopa Shivashankar ◽  
Zeng Ge ◽  
Matti Marklund ◽  
...  

Excess sodium consumption and insufficient potassium intake contribute to high blood pressure and thus increase the risk of heart disease and stroke. In low-sodium salt, a portion of the sodium in salt (the amount varies, typically ranging from 10 to 50%) is replaced with minerals such as potassium chloride. Low-sodium salt may be an effective, scalable, and sustainable approach to reduce sodium and therefore reduce blood pressure and cardiovascular disease at the population level. Low-sodium salt programs have not been widely scaled up, although they have the potential to both reduce dietary sodium intake and increase dietary potassium intake. This article proposes a framework for a successful scale-up of low-sodium salt use in the home through four core strategies: availability, awareness and promotion, affordability, and advocacy. This framework identifies challenges and potential solutions within the core strategies to begin to understand the pathway to successful program implementation and evaluation of low-sodium salt use.

2020 ◽  
Vol 41 (35) ◽  
pp. 3363-3373 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Michael H Alderman ◽  
Adrian J B Brady ◽  
Rafael Diaz ◽  
...  

Abstract Several blood pressure guidelines recommend low sodium intake (<2.3 g/day, 100 mmol, 5.8 g/day of salt) for the entire population, on the premise that reductions in sodium intake, irrespective of the levels, will lower blood pressure, and, in turn, reduce cardiovascular disease occurrence. These guidelines have been developed without effective interventions to achieve sustained low sodium intake in free-living individuals, without a feasible method to estimate sodium intake reliably in individuals, and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with moderate intake). In this review, we examine whether the recommendation for low sodium intake, reached by current guideline panels, is supported by robust evidence. Our review provides a counterpoint to the current recommendation for low sodium intake and suggests that a specific low sodium intake target (e.g. <2.3 g/day) for individuals may be unfeasible, of uncertain effect on other dietary factors and of unproven effectiveness in reducing cardiovascular disease. We contend that current evidence, despite methodological limitations, suggests that most of the world’s population consume a moderate range of dietary sodium (2.3–4.6g/day; 1–2 teaspoons of salt) that is not associated with increased cardiovascular risk, and that the risk of cardiovascular disease increases when sodium intakes exceed 5 g/day. While current evidence has limitations, and there are differences of opinion in interpretation of existing evidence, it is reasonable, based upon observational studies, to suggest a population-level mean target of <5 g/day in populations with mean sodium intake of >5 g/day, while awaiting the results of large randomized controlled trials of sodium reduction on incidence of cardiovascular events and mortality.


1982 ◽  
Vol 63 (s8) ◽  
pp. 407s-409s ◽  
Author(s):  
T. O. Morgan

1. A group of eight patients with mild hypertension, sensitive to sodium intake, were studied. 2. Sodium chloride (70 mmol daily) caused their blood pressure to rise by 19/14 mmHg. 3. Sodium bicarbonate (70 mmol daily) caused their blood pressure to rise by 12/5 mmHg. 4. Sodium chloride given together with potassium chloride (70 mmol of each daily) caused their blood pressure to rise by 9.6 mmHg. 5. These results suggest that sodium bicarbonate causes a smaller rise in blood pressure than sodium chloride does and that potassium chloride reduces the blood pressure raising effect of sodium chloride. 6. A low sodium, high potassium and an alkaline diet may therefore be a more effective dietary method to reduce blood pressure than a diet low in sodium alone.


1985 ◽  
Vol 249 (6) ◽  
pp. F819-F826 ◽  
Author(s):  
E. Fernandez-Repollet ◽  
C. R. Silva-Netto ◽  
R. E. Colindres ◽  
C. W. Gottschalk

This study was designed to investigate the effects of bilateral renal denervation on sodium and water balance, the renin-angiotensin system, and systemic blood pressure in unrestrained conscious rats maintained on a normal- or low-sodium diet. Renal denervation was proven by chemical and functional tests. Both bilaterally denervated rats (n = 18) and sham-denervated rats (n = 15) maintained positive sodium balance while on a normal sodium intake. Both groups were in negative sodium balance for 1 day after dietary sodium restriction was instituted but were in positive sodium balance for the following 9 days. Systolic blood pressure was higher in sham-denervated (115 +/- 3 mmHg) than in denervated rats (102 +/- 3 mmHg) while on a normal diet (P less than 0.05) and remained so during sodium restriction. Plasma renin concentration (PRC) and plasma aldosterone concentration (PAC) were significantly diminished in the denervated rats during normal sodium intake (P less than 0.05). After dietary sodium restriction, PRC increased in both groups but remained significantly lower in the denervated rats (P less than 0.05). Following dietary sodium restriction, PAC also increased significantly to levels that were similar in both groups of rats. These results demonstrate that awake unrestrained growing rats can maintain positive sodium balance on a low sodium intake even in the absence of the renal nerves. However, efferent renal nerve activity influenced plasma renin activity in these animals.


2021 ◽  
Author(s):  
Rosa D Wouda ◽  
Femke Waanders ◽  
Dick de Zeeuw ◽  
Gerjan Navis ◽  
Liffert Vogt ◽  
...  

Abstract Background Angiotensin receptor blockers (ARBs) lower blood pressure (BP) and proteinuria and reduce renal disease progression in many—but not all—patients. Reduction of dietary sodium intake improves these effects of ARBs. Dietary potassium intake affects BP and proteinuria. We set out to address the effect of potassium intake on BP and proteinuria response to losartan in non-diabetic proteinuric chronic kidney disease (CKD) patients. Methods We performed a post-hoc analysis of a placebo-controlled interventional cross-over study in 33 non-diabetic proteinuric patients (baseline mean arterial pressure and proteinuria: 105 mmHg and 3.8 g/d, respectively). Patients were treated for 6 weeks with placebo, losartan, and losartan/hydrochlorothiazide, combined with a habitual (∼200 mmol/d) and low-sodium diet (<100 mmol/d), in randomized order. To analyze the effects of potassium intake, we categorized patients based on median split of 24 h urinary potassium excretion, reflecting potassium intake. Results Mean potassium intake was stable during all 6 treatment periods. Losartan and losartan/hydrochlorothiazide lowered BP and proteinuria in all treatment groups. Patients with high potassium intake showed no difference in the BP effects compared to patients with low potassium intake. The antiproteinuric response to losartan monotherapy and losartan combined with hydrochlorothiazide during the habitual sodium diet was significantly diminished in patients with high potassium intake (20% vs. 41%, p = 0.011 and 48% vs 64%, p = 0.036). These differences in antiproteinuric response abolished when shifting to the low sodium diet. Conclusions In proteinuric CKD patients, the proteinuria, but not BP-lowering response to losartan during a habitual high sodium diet was hampered during high potassium intake. Differences disappeared after sodium status change by low-sodium diet.


Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 266-274 ◽  
Author(s):  
Raquel C. Greer ◽  
Matti Marklund ◽  
Cheryl A.M. Anderson ◽  
Laura K. Cobb ◽  
Arlene T. Dalcin ◽  
...  

Use of salt substitutes containing potassium chloride is a potential strategy to reduce sodium intake, increase potassium intake, and thereby lower blood pressure and prevent the adverse consequences of high blood pressure. In this review, we describe the rationale for using potassium-enriched salt substitutes, summarize current evidence on the benefits and risks of potassium-enriched salt substitutes and discuss the implications of using potassium-enriched salt substitutes as a strategy to lower blood pressure. A benefit of salt substitutes that contain potassium chloride is the expected reduction in dietary sodium intake at the population level because of reformulation of manufactured foods or replacement of sodium chloride added to food during home cooking or at the dining table. There is empirical evidence that replacement of sodium chloride with potassium-enriched salt substitutes lowers systolic and diastolic blood pressure (average net Δ [95% CI] in mm Hg: –5.58 [–7.08 to –4.09] and –2.88 [–3.93 to –1.83], respectively). The risks of potassium-enriched salt substitutes include a possible increased risk of hyperkalemia and its principal adverse consequences: arrhythmias and sudden cardiac death, especially in people with conditions that impair potassium excretion such as chronic kidney disease. There is insufficient evidence regarding the effects of potassium-enriched salt substitutes on the occurrence of hyperkalemia. There is a need for additional empirical research on the effect of increasing dietary potassium and potassium-enriched salt substitutes on serum potassium levels and the risk of hyperkalemia, as well as for robust estimation of the population-wide impact of replacing sodium chloride with potassium-enriched salt substitutes.


2020 ◽  
Author(s):  
R Jayatissa ◽  
Y Yamori ◽  
AH De Silva ◽  
M Mori ◽  
PC De Silva ◽  
...  

AbstractBackgroundSodium intakes of different populations around the world became of interest after a positive correlation was drawn between dietary sodium intake and prevalence of hypertension. Sri Lanka has adopted a salt reduction strategy to combat high blood pressure in the population with escalation of non-communicable diseases.ObjectiveTo measure intake of salt, potassium and sodium/potassium ratio of adults in urban and rural settings.DesignA community based study of 328 adults between 30-59 years, including equal numbers from urban and rural sectors. Weight, height and waist circumference were measured. Blood pressure was measured by a standardized automated measurement system and the mean of two readings was used for analysis. 24-hour urine was collected and measured for creatinine, sodium, potassium levels.ResultsMean daily salt consumption was 8.3g (95%CI:7.9,8.8), which is 1.6 times higher than WHO recommendation. Mean daily potassium intake was 1,265g (95%CI:1191.0,1339.3), which is 2.8 times lower and sodium/potassium ratio was 4.3 (95%CI:4.2,4.5), which is 7 times higher than WHO recommendation. Daily salt consumption was significantly higher in males (9.0g;95%CI:8.3,9.8) than females (7.7g;95%CI:7.2,8.2); rural (8.9g;95%CI:8.2-9.6,) than urban (7.7g;95%CI:7.2,8.3) with increasing body mass index (8.2g;95%CI:6.1,10.2 to 10.0g;95%CI:8.5,11.6). Systolic blood pressure was significantly positively correlated with high BMI and waist circumference.ConclusionsHigh salt consumption, low potassium intake and high sodium/potassium ratio was found in this population. This information can be used to set targets to reduce salt intake in the population. Need to create awareness to enhance the consumption of potassium rich food while reducing salt intake to minimize future NCD burden.


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Jiang He ◽  
Jian-Feng Huang ◽  
Jing Chen ◽  
Ji-Chun Chen ◽  
Xiangfeng Lu ◽  
...  

Background: Blood pressure responses to dietary sodium intake vary among individuals. However, it is unknown whether sodium sensitivity and sodium resistance predict incidence of hypertension. Methods: We conducted a feeding study, including a 7-day low-sodium diet (51.3 mmol/day) and a 7-day high-sodium diet (307.8 mmol/day), among 1,718 Chinese individuals with normal blood pressure in 2003-2005 and follow-up studies in 2008-2009 and 2011-2012. Three blood-pressure measurements and 24-hour urinary sodium excretion were obtained on each of 3 days during baseline, low- and high-sodium interventions, and follow-up visits. Latent class models were used to identify subgroups that share a similar underlying trajectory in blood-pressure responses to dietary sodium intake. Results: Three trajectories of systolic blood pressure responses to dietary sodium intake were identified (Figure). Mean (standard deviation) changes in systolic blood pressure were -13.7 (5.5), -4.9 (3.0), and 2.4 (3.0) mmHg during the low-sodium intervention, and 11.2 (5.3), 4.4 (4.1) and -0.2 (4.1) mmHg during the high-sodium intervention ( P< 0.001 for group differences) in high sodium-sensitive, moderate sodium-sensitive, and sodium-resistant groups, respectively. Compared to individuals with moderate sodium sensitivity, multiple-adjusted odds ratio (95% confidence intervals) for incident hypertension were 1.44 (1.03 to 1.99) for those with high sodium sensitivity and 1.42 (1.02 to 1.97) for those with sodium resistance ( P <0.001 for quadratic trend). Furthermore, a J-shaped association between systolic blood pressure responses to high sodium intake and incident hypertension was identified ( P <0.001). Similar results were observed for diastolic blood pressure. Conclusions: Individuals with either high sodium sensitivity or sodium resistance are at an increased risk for developing hypertension.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lieke Gijsbers ◽  
James Dower ◽  
Marco Mensink ◽  
Johanna M Geleijnse

Introduction: We performed a 12-week randomized placebo-controlled crossover study to examine the effects of sodium and potassium supplementation on blood pressure (BP) and arterial stiffness in untreated (pre)hypertensive individuals on a low-sodium, low-potassium diet. Methods: During the study, subjects were on a fully controlled diet that provided on average 2.4 g/d of sodium (equals 6 g/d of salt) and 2.2 g/d of potassium. After a 1-week run-in period, 37 subjects received capsules with supplemental sodium (3 g/d, equals 7.5 g/d of salt), supplemental potassium (3 g/d), or placebo, for four weeks each (not separated by wash-out), in random order. Fasting office BP, 24-h ambulatory BP, and measures of arterial stiffness (SphygmoCor®) were assessed at baseline and after each treatment. Results: Subjects had a mean pre-treatment BP of 145/81 mmHg and 68% (25 of 37) had systolic BP (SBP) ≥140 mmHg. In 36 subjects who completed the study, sodium supplementation increased urinary sodium by 97.6 mmol/24h (2.2 g/d) and potassium supplementation increased urinary potassium by 62.9 mmol/24h (2.5 g/d), compared to placebo (Table). Sodium supplementation significantly increased office BP by 7.5/3.3 mmHg, 24-h BP by 7.0/2.1 mmHg and central BP by 8.5/3.6 mmHg. Potassium supplementation significantly reduced 24-h BP by 4.0/1.7 mmHg. Measures of arterial stiffness did not change. Conclusion: Increasing the intake of sodium has a strong adverse effect on BP in untreated (pre)hypertensive individuals. Increased potassium intake, however, lowers BP even when people are on a reduced sodium diet. Short-term changes in sodium and potassium intake have little effect on arterial stiffness. Trial registration: ClinicalTrials.gov Identifier: NCT01575041


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