REVIEW URRENT C OPINION

Health effects of sodium and potassium in humans Paul K. Whelton and Jiang He

Purpose of review Review new articles that clarify the health consequences of changes in dietary sodium and potassium and that characterize adherence to sodium and potassium intake guideline recommendations. Recent findings New clinical trials meta-analyses provide additional documentation of the blood pressure (BP) lowering effects of Na reduction and K supplement, with no adverse effects of Na reduction on cholesterol in steady-state settings. BP is the leading preventable risk factor for worldwide mortality and disability-adjusted life years. A preponderance of cohort studies has identified a direct relationship between dietary sodium and cardiovascular disease (CVD), specially stroke, and an inverse relationship between dietary potassium and CVD. However, these studies are of insufficient quality to support firm conclusions. Modeling studies of sodium reduction in the general population have identified an enormous potential for health benefits. Current intake of dietary sodium and potassium fails to meet guideline recommendations. Summary There is abundant evidence that a reduction in dietary sodium and increase in potassium intake decreases BP, incidence of hypertension, and morbidity and mortality from CVD. However, there is no credible evidence that existing policies have been effective in achieving population goals for dietary sodium and potassium intake in the USA. Keywords blood pressure, cardiovascular disease, potassium, sodium

INTRODUCTION Sodium (Na) and potassium (K) are the primary cations in extracellular and intracellular fluids, respectively. They play important physiological roles, including regulation of fluid balance, membrane potential, and muscle contraction. Both Na and K have been extensively related to health effects, including blood pressure (BP), cardiovascular disease (CVD), osteoporosis, stomach cancer, asthma, kidney stones, cardiac arrhythmias, glucose intolerance, and muscle weakness. This review will focus on the relationship of Na and K to BP and CVD.

RELATIONSHIP OF Na AND K TO BLOOD PRESSURE An extensive body of information documents the presence of a direct relationship between Na and BP, and an inverse relationship between K and BP. Four meta-analyses of randomized, controlled clinical trials that studied the effect of reduced Na and increased K intake on BP were reported during the past year [1,2 –4 ]. Graudal et al. [1] updated a previous meta-analysis to report on experience by &

&

race and BP status in 167 trials. For whites, blacks, and Asians, Na reduction resulted in an overall decrement of systolic BP (SBP) of 5.18, 6.44, and 10.21 mmHg in those with hypertension and 1.29, 4.02, and 1.27 mmHg in normotensives. For the normotensives, lower Na intake resulted in a mean SBP that was decreased in 50 (70.4%) trials, unchanged in eight (11.3%), and increased in 13 (18.3%). Na reduction was associated with a significant increase in components of the renin–angiotensin–aldosterone system, plasma epinephrine, norepinephrine, and triglyceride and a small but significant increase in total cholesterol. However, the relevance of the hormonal and lipid findings is uncertain because trials of very short duration and nonphysiological abrupt wide-ranging changes in Na were included. He et al. and Aburto et al. [2 ,3 ] &

&

Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana, USA Correspondence to Paul K. Whelton, MB, MD, MSc, 440 Walnut Street, New Orleans, LA 70118, USA. Tel: +1 504 866 1786; fax: +1 504 861 3730; e-mail: [email protected] Curr Opin Lipidol 2014, 25:75–79 DOI:10.1097/MOL.0000000000000033

0957-9672 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-lipidology.com

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Nutrition and metabolism

KEY POINTS  New meta-analyses provide additional support for BP lowering effects of Na reduction and K supplementation.  A preponderance of the available cohort analyses identifies a CVD relationship between Na (direct) and K (inverse) intake. However, the reports are based on secondary analysis and are of insufficient quality to support firm conclusions.  General population modeling studies suggest Na reduction would yield major health benefits.  Only a small percentage of United States adults meet any of the recommended guidelines for Na reduction and K supplementation.  There is no evidence that general population Na reduction approaches have been effective.

addressed many of these concerns by restricting their meta-analyses to trials that lasted at least 4 weeks, had a documented intervention effect (reduction in urinary Na > 40 mmol/day), included no concomitant interventions, and recruited participants with no concurrent illness other than hypertension. In an analysis of 34 trials (3230 participants) by He et al. [2 ], Na reduction resulted in an overall SBP decrement of 4.18 mmHg (95% CI, 3.18–5.18). In a meta-regression analysis, 68% of the variance in SBP decrement between the trials was explained by age, ethnicity, BP status, and change in urinary Na. In an analysis of 36 trials (49 comparisons) by Aburto et al. [3 ], reduced Na intake resulted in a significant decrement of SBP (3.39 mmHg, overall; 4.06 mmHg in hypertensives and 1.38 mmHg in normotensives). Total cholesterol was essentially unchanged (mean difference, 95% CI: 0.02, 0.03 to 0.07 mmol/l) in the 11 studies (2339 participants) with such measurements and no evidence of a change in levels was detected in the up to seven trails that reported on various components of catecholamine excretion. Changes in urinary protein excretion were consistent with a beneficial effect of Na reduction. The inclusion and exclusion criteria for the meta-analyses conducted by He et al. and Aburto et al. provide a better context for generalization to practice and to policy decision-making. Both of these meta-analyses provide lipid and catecholamine results that are reassuring. Perturbations of the renin–angiotensin– aldosterone system noted by Graudal et al. and He et al. are consistent with the expected physiologic response to Na reduction. Overall, the metaanalyses are consistent with prior knowledge that &

&

76

www.co-lipidology.com

Na reduction lowers BP and the effect is greater in older persons, African-Americans, a higher starting level of BP, and a more successful intervention. In a meta-analysis of 21 trials that lasted at least for 4 weeks, included no concomitant interventions, excluded acutely ill participants, and required 24 h urinary K measurements to estimate potassium intake, Aburto et al. [4 ] reported an overall reduction in SPB of 5.93 (95% CI, 1.70– 10.51) mmHg. Following removal of two outlier trials this was reduced to 3.49 (1.82–5.15) mmHg. The mean (95% CI) reduction was 7.16 (1.91– 12.41) mmHg in the trials where K intake was 90–120 mmol/d. There was no evidence of an adverse effect of increased K intake on catecholamine concentrations, lipid levels, or renal function. These BP findings are consistent with an earlier meta-analysis of 33 randomized controlled trials (2609 participants) by Whelton et al. [5] that reported a mean (95% CI) SBP reduction of 3.11 (1.91–4.31) mmHg, following exclusion of an outlier trial. Trends in the meta-analysis by Aburto et al. were also consistent with the findings by Whelton et al. that the BP lowering effect of increased K potassium intake is greatest in those with higher baseline levels of BP, higher levels of K intake, and higher levels of baseline urinary Na excretion. In a meta-analysis restricted to 10 trials of K supplementation in persons with a high salt intake, von Bommel and Cleophas [6] reported a pooled reduction in SBP of 9.5 (95% CI, 8.1–10.8) mmHg. &

RELATIONSHIP OF Na AND K TO CARDIOVASCULAR DISEASE The one new cohort study that related Na intake to CVD was based on experience in a 10-year prospective study in 2657 United States adults [7]. A strong, positive, and statistically significant association was noted between Na intake, assessed by food frequency questionnaire, and incident stroke. Several reviews and meta-analyses of the relationship between Na and CVD in observational studies were published during 2012 [3 ,8 ,9–10]. Although a preponderance of the reports support the presence of a direct relationship between Na and CVD (specially stroke), a substantial minority identify either null, J-shaped, or inverse relationships. A common conclusion of the reviews is that the underlying data are of insufficient quality to support firm conclusions [8 ]. All of the available reports are based on secondary analyses of datasets from studies that were not originally designed to address the association between Na and CVD. Many suffer from some combination of potential for bias (specially in the estimation of Na intake), residual confounding, reverse &

&

&

Volume 25  Number 1  February 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Health effects of sodium and potassium in humans Whelton and He

causality (specially in the studies of sick cohorts), and random error. One new meta-analysis of the relationship between K intake and CVD in nine cohort studies was published (Aburto et al. [4 ]). This study identified a significant inverse relationship between urinary K excretion and incident stroke (risk ratio 0.76, 95% CI 0.66–0.89). The risk of stroke was least when urinary potassium excretion was 90–120 mmol/d (0.70, 0.56–0.88). Nonsignificant trends in the same direction were noted for the relationship between urinary K and incident CVD and coronary heart disease. These findings were very similar to those reported for a meta-analysis of 15 cohort studies published in the preceding year (D’Elia et al. [11]). &

GUIDELINE RECOMMENDATIONS FOR Na AND K INTAKE Based on the totality of the evidence, Whelton et al. [8 ] reaffirmed the recommendation of the American Heart Association to reduce dietary Na to less than 1500 mg/d in the United States general population. Aburto et al. [3 ] concluded that ‘The totality of the evidence suggests that most people will likely benefit from reducing sodium intake’. The World Health Organization (WHO) used the Aburto et al. [12] results and an overall review of the literature to recommend an intake of less than 2000 mg/d in adults and children. An Institute of Medicine (IOM) committee concluded that ‘when considered collectively, it indicates a positive relationship between higher levels of sodium intake and risk of CVD’ [10]. The committee decided that the data from observational risk studies were insufficient to support a recommendation to decrease Na intake to levels below 2300 mg/d. The IOM report resulted in press reports that generated confusion regarding the need and goal for sodium reduction [13–16]. Subsequently, members of the IOM committee attempted to clarify the committee’s position that the population’s intake of dietary Na is excessive and to emphasize their support for reducing the amount of Na added during the processing of foods [17 ]. Based on the entire body of evidence, the WHO recommended ‘an increase in potassium intake from food to reduce BP and the risk of CVD, stroke, and coronary heart disease in adults (strong recommendation)’ and ‘in children (conditional recommendation)’ [18]. The WHO suggested a K intake of at least 90 mmol (3510 mg)/d in adults, with an adjustment downward in children dependent on their energy requirements. This is less than the 4700 mg/d adequate intake identified in 2005 by the IOM [19] and recommended for healthy adults in the most recent federal guidelines [20]. &

&

&

POTENTIAL HEALTH BENEFITS OF REDUCING DIETARY Na INTAKE A new report from the Global Burden of Disease Study identified high BP as the leading risk factor, among 67 studied, for worldwide deaths (9.4 million, 95% CI 8.6–10.1 million) and contribution to disabilityadjusted life years (7.0%, 95% CI 6.2–7.7%) during 2010 [21 ]. Previous reports have identified BP as one of the best examples of a valid surrogate measure for CVD, specially stroke [22–24]. In the most recent reviews on this topic, the validity of BP as a CVD surrogate endpoint was reconfirmed [25,26]. In a thoughtful projection of the mortality benefits that might result from a reduction in Na intake in the United States general population, Coxson et al. employed three approaches to estimate risk reduction [direct effects of Na reduction on CVD noted during extended follow up of the Trials of Hypertension Prevention (TOHP) cohort, and indirect effects of Na reduction on CVD based on the impact of BP lowering on CVD in randomized controlled trials or based on BP as a CVD risk factor in the Framingham Heart Study] and modeled the effect of these risk reductions over a 10-year follow up using three Na reduction intervention strategies (a gradual uniform 4% annual reduction to 2200 mg/d by year 10 or instantaneous reductions, sustained over the 10 years of follow up, to 2200 mg/d or 1500 mg/d) [27 ]. Use of the TOHP risk experience and the gradual uniform 4% annual reduction in Na intake strategy predicted prevention of 505 000 deaths (516 000 due to CVD, 383 000 CHD, and 83 000 Stroke deaths). Application of the theoretical maximum effect (TOHP risk estimates with an instantaneous reduction in Na intake to 1500 mg/d) predicted the prevention of 1 215 000 deaths due to CVD (909 000 due to CHD and 190 000 due to stroke). &

&&

ADHERENCE TO GUIDELINES FOR Na AND K INTAKE &&

Cogswell et al. [28 ] used experience from adults who participated in National Health and Nutrition Examination Survey (NHANES) from 2003 to 2008 to estimate Na and K intake and adherence to guideline recommendations. The median for usual Na intake was estimated to be 3371 mg/d, with a range from the 25th to 75th percentile of 2794–4029 mg/d. The median was higher for men (3326 mg/d) compared with women (2357 mg/d). These high average intakes of dietary Na in the United States general population are consistent with prior experience, whether Na intake was estimated by 24-h dietary recall in a representative sample of the United States general population or by use of gold standard 24 h urinary excretion in nonrepresentative samples [29,30]. The

0957-9672 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-lipidology.com

77

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Nutrition and metabolism

values reported by Cogswell et al. are likely to have underestimated true Na intake by close to 25% as they were derived from 24 h dietary recalls. This measurement method is known to understate Na intake by about 25% [8 ,31]. Despite this, Na intake exceeded 1500 mg/d in 99.9% of men and 98.2% of women, and exceeded 2300 mg/d in 96.9% of men and 77.6% of women. Even in the subgroups which are thought to be especially sensitive to the effects of Na, intake exceeded 1500 mg/d in 99.2% of those 50–71 years, 98.7% in non-Hispanic blacks, 99.7 and 99.1% of those with prehypertension and hypertension, 98.9% of those with diabetes, and 98.5% of those with chronic kidney disease. The median intake of dietary K was 2631 mg/d, with a range from the 25th to 75th percentile of 2164 to 3161 mg/d. The median was higher for men (3037 mg/d) compared with women (2279 mg/d). The recommended K intake of 4700 mg/d was only achieved in 1.4% of the general population and less than 1–2% of those at least 51 years, and those with prehypertension or hypertension, diabetes, or chronic kidney disease. The true situation may be even worse because dietary recall measurements tend to overestimate potassium intake by more than 15% [31]. &

Na IN PROCESSED AND RESTAURANT FOODS Studies have repeatedly demonstrated that the vast majority of Na consumed in the USA and most western countries is added during food processing or restaurant preparation [32–34]. Food labels and websites for large chain restaurants were used to compare Na content of 402 processed foods sold in supermarkets and 78 food products sold in fastfood restaurants [35 ]. There were slight nonsignificant trends for a 3.5% decline in Na content of the supermarket foods and 2.5% increase in the fastfood restaurant products but the overall finding was the absence of any appreciable change over the 6 years studied (2005–2011). In a comparison of practices by six international fast-food companies, substantial variation in Na content was noted by food category, by country for the same food category, and by company for the same food products in different countries [36 ]. For example, McDonald’s Chicken McNuggets contained 600 mg Na/g in the UK but 1600 mg Na/g in the USA. In a study of 3507 variations of 685 meals served at 26 chain sit-down restaurants in Canada, the mean (95% CI) content of Na per meal was 2269 mg (2210–2327) and was consistently above daily guideline recommendations for breakfast (2027 mg), lunch (2206 mg), and dinner (2297 mg) [37 ]. Only 1% of meals met the FDA Na criterion for a ‘healthy meal’ &

&

&

78

www.co-lipidology.com

(Na < 600 mg), with more the 50% exceeding 2300 mg and 80% exceeding 1500 mg.

CONCLUSION Publications during the past year provide additional evidence that reduced Na and increased K intake lower BP and have great potential as public health interventions to reduce the burden of CVD morbidity and mortality. Current policies and voluntary approaches aimed at meeting guideline recommendations have failed to yield any appreciable change for dietary Na and K intake in the United States general population. There is an urgent need to identify more successful approaches to achieving guideline recommendations for both dietary Na and K intake. Acknowledgements None. Conflicts of interest The authors have no conflicts of interest to declare.

REFERENCES AND RECOMMENDED READING Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest && of outstanding interest 1. Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low-sodium diet vs. high-sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cocherane Review). Am J Hypertens 2012; 25:1–15. 2. He FJ, Li J, MacGregor GA. Effect of longer term modest salt reduction on & blood pressure: Cochrane systematic review and meta-analysis of randomized trials. BMJ 2013; 346:f1325. Meta-analysis of 34 randomized controlled clinical trials, relevant to clinical practice and public health, which documents the BP lowering effect of Na reduction and identifies factors that modify the response. 3. Aburto NJ, Ziolkovska A, Hooper L, et al. Effect of lower sodium intake on & health: systematic review and meta-analyses. BMG 2013; 346:f1326. Meta-analysis of 36 randomized controlled trials, relevant to clinical practice and public health, which documents the BP lowering effect of Na reduction, identifies no adverse effect on total cholesterol or catecholamine, and suggests a beneficial effect on renal protein excretion. This study served a major resource in setting the new WHO guidelines for Na intake. 4. Aburto NJ, Hanson S, Gutierrez H, et al. Effect of increased potassium on & cardiovascular risk factors and disease: systematic review and meta-analyses. BMJ 2013; 346:f1378. Meta-analysis of 21 randomized controlled trials, relevant to clinical practice and public health, which documents the BP lowering effect of K supplementation and identifies no adverse effect on lipid levels, catecholamines, or renal function. This study served a major resource in setting the new WHO guidelines for K intake. 5. Whelton PK, He J, Cutler JA, et al. Effect of oral potassium on blood pressure. Meta-analysis of randomized controlled clinical trials. JAMA 1997; 277: 1624–1632. 6. van Bommel E, Cleophas T. Potassium treatment for hypertension in patients with high salt intake: a meta-analysis. Int J J Clin Pharmacol Ther 2012; 50:478–482. 7. Gardner H, Rundek T, Wright CB, et al. Dietary sodium and risk of stroke in the Northern Manhattan Study. Stroke 2012; 43:1200–1205. 8. Whelton PK, Appel LJ, Sacco RL, et al. Sodium, blood pressure, and cardio& vascular disease. Further evidence supporting the American Heart Association sodium reduction recommendations. Circulation 2012; 126:2880–2889. This review highlights the challenges of interpreting the available observational studies that relate Na intake to CVD and provides a summary of the evidence supporting the American Heart Association’s recommendations for Na reduction.

Volume 25  Number 1  February 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Health effects of sodium and potassium in humans Whelton and He 9. Kotchen TA, Cowley AW, Frohlich ED. Salt in health and disease: a delicate balance. N Engl J Med 2013; 368:1229–1237. 10. Strom BL, Yaktine AL, Oria M, editors. Sodium intake in populations: assessment of evidence. Washington, DC: The National Academies Press; 2013. 11. D’Elia L, Barba G, Cappuccio FP, Strazzullo P. Potassium intake, stroke, and cardiovascular disease. A meta-analysis of prospective studies. J AM Coll Cardiol 2011; 57:1209–1210. 12. WHO. Guideline: sodium intake for adults and children. Geneva: World Health Organization (WHO); 2012. 13. Young S. Report questions benefits of salt reduction. The Chart. CNN Health. http://thechart.blogs.cnn.com/2013/05/14/report-questions-benefits-of-saltreduction/. [Accessed 10 August 2013] 14. Kolata G. No benefit seen in sharp limits on salt in diet. The New York Times, May 14, 2013. http://www.nytimes.com/2013/05/15/health/panel-findsno-benefit-in-sharply-restricting-sodium.html?pagewanted=all. [Accessed 10 August 2013] 15. Fontenot B. Do you really have to cut back on salt? MORE for women of style and substance. http://www.more.com/health/healthy-eating/do-you-reallyhave-cut-back-salt. [Accessed 10 August 2013] 16. Neravetla SR. Media spin of IOM Report out of control. Health Books Now. ‘It’s time to stop killing ourselves’ http://www.healthnowbooks.com/2013/05/ media-spin-of-iom-report-out-of-control/. [Accessed 10 August 2013] 17. Strom BL, Anderson CAM, Ix JH. Sodium reduction in populations. Insights & from the Institute of Medicine Committee. JAMA 2013; 310:31–32. This brief article summarizes the findings and conclusions of the 2013 IOM report on observational studies that have investigated the CVD health consequences of Na reduction. 18. WHO. Guideline: potassium intake for adults and children. Geneva: World Health Organization (WHO); 2012. 19. Institute of Medicine Panel on Dietary Reference Intakes for Electrolytes and Water. Dietary reference intakes for water, potassium, sodium, chloride and sulfate. Washington, DC: The National Academies Press; 2005. 20. US Department of Agriculture and US Department of Health and Human Services. Dietary guidelines for Americans. 7th ed. Washington, DC: US Government Printing Office; 2010. 21. Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment of burden of & disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012; 380:2224–2260. This report provides a comparative risk assessment from the Global Burden of Disease Study that identifies BP as the leading risk factor for worldwide mortality and burden from disability-adjusted life years. 22. Temple R. Are surrogate markers adequate to access cardiovascular disease drugs? JAMA 1999; 282:790–795. 23. Desai M, Stockbridge N, Temple R. Blood pressure as an example of a biomarker that functions as a surrogate. AAPS J 2006; 8:E146–152. 24. Micheel CM, Ball JR, editors. Evaluation of biomarkers and surrogate endpoints in chronic disease. Washington, DC: The National Academies Press; 2010. 25. Fleming TR, Powers JH. Biomarkers and surrogate endpoints in clinical trials. Statist Med 2012; 31:2973–2984.

26. Lassere Mn, Johnson KR, Schiff M, Rees D. Is blood pressure reduction a valid surrogate endpoint for stroke prevention? An analysis incorporating a systematic review of randomized controlled trials, a by-trial weighted errors-invariables regression, the surrogate threshold effect (STE) and the biomarkersurrogacy (Biosurrogate) evaluation schema (BSES). BMC Med Res Methodol 2012; 12:27. 27. Coxon PG, Cook NR, Joffres M, et al. Mortality benefits from US population&& wide reduction in sodium consumption. Projections from 3 modeling approaches. Hypertension 2013; 61:564–570. This paper is a thoughtful and careful analysis that identifies the potential CVD health consequences of three different approaches to Na reduction. 28. Cogswell ME, Zhang Z, Carriquiry AL, et al. Sodium and potassium intakes && among US adults: NHANES 2003-2008. Am J Clin Nutr 2012; 96:647–657. This study estimates adherence to Na reduction guidelines by United States adults. It suggests very poor adherence to any of the guideline recommendations, even in population subgroups who are most likely to benefit from a reduced intake of dietary Na. 29. Briefel RB, Johnson CL. Secular trends in dietary intake in the United States. Annu Rev Nutr 2004; 24:401–431. 30. Bernstein AM, Willett WC. Trends in 24-h urinary sodium excretion in the United States, 1957-2003: a systematic review. Am J Clin Nutr 2010; 92:1172–1180. 31. Espland MA, Kumanyika S, Wilson AC, et al. Statistical issues in analyzing 24-h dietary recall and 24-h urine collection data for sodium and potassium intakes. Am J Epidemiol 2001; 153:996–1006. 32. James WP, Ralph A, Sanchez-Castillo CP. The dominance of salt in manufactured food in the sodium intake of affluent societies. Lancet 1987; 1:426– 429. 33. Sanchez-Castillo CP, Warrender S, Whitehead TP, James WP. An assessment of the sources of dietary salt in a British population. Clin Sci 1987; 72:95–102. 34. Anderson CAM, Appel LJ, Okuda N, et al. Dietary sources of sodium in China, Japan, the United Kingdom, and the United States, women and men 40 to 59 years: the INTERMAP Study. J Am Diet Assoc 2010; 110:736–745. 35. Jacobson MF, Havas S, McCarter R. Changes in sodium levels in processed & and restaurant foods, 2005 to 2011. JAMA Intern Med 2013; 173:1285– 1291. This report identifies an absence of any appreciable change in the Na content of processed and restaurant foods in the USA between 2005 and 2011. 36. Dunford E, Wester J, Woodward M, et al. The variability of reported salt levels & in fast foods across six countries: opportunities for salt reduction. CMAJ 2012; 184:1023–1028. This study documents wide variability in the content of Na in fast foods within country and across country, even for identical food products being sold by the same company. It highlights the opportunity for reducing the Na content of fast food products. 37. Scourboutakos MJ, Semnani-Azad Z, L’Abbe MR. Restaurant meals: almost a & full day’s worth of calories, fats, and sodium. JAMA Intern Med 2013; 173:1373–1374. This report of the Na content of meals served in Canadian sit-down restaurants indicates that only 1% of meals meet the FDA criterion for a healthy meal.

0957-9672 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-lipidology.com

79

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Health effects of sodium and potassium in humans.

Review new articles that clarify the health consequences of changes in dietary sodium and potassium and that characterize adherence to sodium and pota...
194KB Sizes 0 Downloads 0 Views