Salt and cardiovascular disease: insufficient evidence to recommend low sodium intake

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.

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3232
Author(s):  
Andrew Mente ◽  
Martin O’Donnell ◽  
Salim Yusuf

Several health organizations recommend low sodium intake (below 2.3 g/day, 5.8 g/day of salt) for entire populations, on the premise that lowering of sodium intake, irrespective of its level of intake, will lower blood pressure and, in turn, will result in a lower incidence of cardiovascular disease. These guidelines were developed without effective interventions to achieve long term sodium intakes at low levels in free-living individuals and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with average levels of intake). In this review, we examine whether advice to consume low amounts of sodium is supported by robust evidence. We contend that current evidence indicates that most people around the world consume a moderate range of dietary sodium (3 to 5 g/day), that this level of intake is associated with the lowest risk of cardiovascular disease and mortality, and that the risk of adverse health outcomes increases when sodium intakes exceeds 5 g/day or is below 3 g/day. While the current evidence has limitations, it is reasonable, based upon prospective cohort studies, to suggest a mean target of below 5 g/day in populations, while awaiting the results of large randomized controlled trials of sodium reduction on cardiovascular disease and death.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Alissa Stevens ◽  
Elizabeth Courtney-Long ◽  
Dianna Carroll ◽  
Cathleen Gillespie ◽  
Brian Armour

Introduction: While hypertension is a key treatable risk factor for cardiovascular disease, it is not controlled in an estimated 36 million US adults. Previous research has shown that nearly half of adults with disabilities have hypertension and that adults with disabilities are more likely to have hypertension than those without disabilities. However, no study has documented the prevalence of uncontrolled hypertension among the disability population. Our objectives were 1) to determine the prevalence of uncontrolled hypertension among adults with a disability, and 2) estimate the prevalence of awareness, treatment with blood pressure (BP)-lowering medication, and lifestyle factors among adults with disabilities who have uncontrolled hypertension. Methods: Using nationally-representative data from the 2001-2010 National Health and Nutrition Examination Survey for 10,805 participants aged ≥20 years with a disability (self-reported limitation in cognition, hearing, vision, or mobility), we examined the prevalence of hypertension (measured systolic BP ≥140, diastolic BP ≥90 or self-reported use of BP-lowering medication) and uncontrolled hypertension (systolic BP ≥140 or diastolic BP ≥90). Among those with uncontrolled hypertension, we estimated the prevalence of awareness (ever told by a doctor that had hypertension), treatment (self-reported use of BP-lowering medication), and lifestyle factors (measured body mass index and dietary sodium intake and self-reported aerobic physical activity and cigarette smoking). Results: Nearly 38% of US adults have a disability. Overall 46.0% (nearly 37 million) of US adults with disabilities have hypertension. Of those, nearly 20 million (52.4%) had uncontrolled hypertension. Over half of those with uncontrolled hypertension were aware and treated (52.9%), 13.6% were aware but untreated, and 33.4% were unaware. Among those with uncontrolled hypertension 40.5% were obese, 52.1% were physically inactive (had no bouts of aerobic physical activity per week that lasted ≥10 minutes), 18.2% were current smokers, and 62.0% had an average sodium intake of ≥2,300 mg per day. Conclusion: Over half of the 37 million adults with disabilities who have hypertension do not have it controlled; and of those, one third are unaware they have hypertension. This study highlights the need to regularly measure and monitor blood pressure among adults with disabilities. It also identifies adults with disabilities as an important population to include in public health efforts that support and encourage healthy behaviors that might improve BP control and lower risk for cardiovascular disease.


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.


2015 ◽  
Vol 39 (1-3) ◽  
pp. 16-20 ◽  
Author(s):  
Paul K. Whelton

Background/Aims: National and international agencies recommend a reduction in dietary sodium intake. However, some have questioned the wisdom of these policies. The goal of this report was to assess the findings and quality of studies that have examined the relationship between dietary sodium and both blood pressure and cardiovascular disease. Methods: Literature review of the available observational studies and randomized controlled trials, including systematic reviews and meta-analyses. Results: A large body of evidence from observational studies and clinical trials documents a direct relationship between dietary sodium intake and the level of blood pressure, especially in persons with a higher level of blood pressure, African-Americans, and those who are older or have comorbidity, including chronic kidney disease. A majority of the available observational reports support the presence of a direct relationship between dietary sodium intake and cardiovascular disease but the quality of the evidence according to most studies is poor. The limited information available from clinical trials is consistent with a beneficial effect of reduced sodium intake on incidence of cardiovascular disease. Conclusions: The scientific underpinning for policies to reduce the usual intake of dietary sodium is strong. In the United States and many other countries, addition of sodium during food processing has led to a very high average intake of dietary sodium, with almost everyone exceeding the recommended goals. National programs utilizing voluntary and mandatory approaches have resulted in a successful reduction in sodium intake. Even a small reduction in sodium consumption is likely to yield sizable improvement in population health. Video Journal Club ‘Cappuccino with Claudio Ronco' at www.karger.com/?doi=368975.


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.


2013 ◽  
Vol 124 (10) ◽  
pp. 617-626 ◽  
Author(s):  
Chris Tikellis ◽  
Raelene J. Pickering ◽  
Despina Tsorotes ◽  
Valma Harjutsalo ◽  
Lena Thorn ◽  
...  

It is recommended that individuals with diabetes restrict their dietary sodium intake. However, although salt intake is correlated with BP (blood pressure), it also partly determines the activation state of the RAAS (renin–angiotensin–aldosterone system), a key mediator of diabetes-associated atherosclerosis. apoE KO (apolipoprotein E knockout) mice were allocated for the induction of diabetes with streptozotocin or citrate buffer (controls) and further randomized to isocaloric diets containing 0.05%, 0.3% or 3.1% sodium with or without the ACEi [ACE (angiotensin-converting enzyme) inhibitor] perindopril. After 6 weeks of study, plaque accumulation was quantified and markers of atherogenesis were assessed using RT–PCR (reverse transcription–PCR) and ELISA. The association of sodium intake and adverse cardiovascular and mortality outcomes were explored in 2648 adults with Type 1 diabetes without prior CVD (cardiovascular disease) from the FinnDiane study. A 0.05% sodium diet was associated with increased plaque accumulation in diabetic apoE KO mice, associated with activation of the RAAS. By contrast, a diet containing 3.1% sodium suppressed atherogenesis associated with suppression of the RAAS, with an efficacy comparable with ACE inhibition. In adults with Type 1 diabetes, low sodium intake was also associated with an increased risk of all-cause mortality and new-onset cardiovascular events. However, high sodium intake was also associated with adverse outcomes, leading to a J-shaped relationship overall. Although BP lowering is an important goal for the management of diabetes, off-target actions to activate the RAAS may contribute to an observed lack of protection from cardiovascular complications in patients with Type 1 diabetes with low sodium intake.


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.


Proceedings ◽  
2019 ◽  
Vol 37 (1) ◽  
pp. 42
Author(s):  
Borderon ◽  
Eyles ◽  
Mhurchu ◽  
Young ◽  
Bradbury

High dietary sodium intake increases blood pressure, a major risk factor for cardiovascular disease. [...]


2020 ◽  
Author(s):  
Henrique Cotchi Simbo Muela ◽  
Mujimbi José Viana ◽  
António Gerson Bastos Francisco ◽  
Isaura da Conceição Almeida Lopes ◽  
Valeria Aparecida Costa-Hong

Increased salt consumption is believed to induce high blood pressure (BP)-mediated organ damage, although it is not yet clear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. Exceeding dietary sodium intake is acknowledged to be the main modifiable environmental risk factor for cardiovascular events that accounts for an increase in blood pressure and induces hypertension (HTN)-related target organ damage. Arterial stiffness is well known as an independent cardiovascular risk factor, and sodium intake may be a determinant of arterial stiffness. Even so, the studies that investigated the effect of dietary sodium reduction intake on arterial stiffness in humans provided inconclusive results. Therefore, we aim to perform a review of the available evidence of salt restriction and arterial stiffness and its impact on hypertensive patients.


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.


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