SODIUM AND HEALTH
Blood pressure–related diseases (eg, coronary heart disease, stroke, heart failure, and chronic kidney disease) are leading causes of morbidity and mortality worldwide. The strong relationship between excessive sodium intake and high blood pressure forms the basis for recommendations to reduce sodium intakes. Numerous authoritative scientific bodies and professional health organizations have issued current population sodium intake recommendations, all of which are at least 1000 mg/d lower than the average American sodium intake of 3478 mg/d1 (Table).
Sodium recommendations are based on results from animal studies, epidemiological studies, clinical trials, and meta-analyses of trials that demonstrate the adverse health effects of excess sodium intake. Feeding studies evaluating sodium intake ranging from 1500 to 2300 mg/d demonstrate blood pressure–lowering effects.2,3 They also indicate that the relationship is direct and progressive, but nonlinear. For example, decreasing sodium intake by a given amount can reduce blood pressure more when starting sodium intake is lower, compared with when sodium intake is decreased by the same amount from a higher starting sodium intake.4–6 Several trials that evaluated long-term effects of sodium reduction on blood pressure demonstrated a consistent trend for fewer cardiovascular disease (CVD) events and/or mortality among those on a reduced sodium intervention.7
The impact of sodium reduction on blood pressure is greater in people with hypertension, but people with blood pressure in nonhypertensive ranges also benefit.5 The GenSalt feeding study2 and DASH (Dietary Approaches to Stop Hypertension)-Sodium are 2 trials that demonstrated blood pressure–lowering effects of sodium reduction in people without clinically defined hypertension. Furthermore, the effect of sodium reduction is greater in older versus younger study participants, and in the DASH-Sodium trial, effects of sodium reduction are increased when it occurs in tandem with good diet quality such as the DASH diet.8
In addition to a study that observed an inverse relationship of sodium intake and blood pressure,9 other studies have suggested that sodium intakes in the range recommended by authoritative scientific bodies and professional health organizations are more harmful than higher sodium intakes.10,11 These studies are inconsistent with findings from the majority of observational studies and randomized clinical trials. In addition, possible explanations for these inverse findings include measurement error from assessment tools that rely on self-report, reverse causality, and lack of adjustment for total kilocalorie intake or other nutrients that influence blood pressure.
In addition to the strong science on the effects of sodium on blood pressure, excess sodium has also been linked to kidney stones, asthma, osteoporosis, and gastric cancer.12 Emerging research suggests that higher sodium intakes may be a risk factor for development of autoimmune diseases,13 and preliminary research has also associated higher sodium intakes with increased adiposity and inflammation in healthy adolescents, independent of calorie intake.14
WHY POPULATION SODIUM REDUCTION?
Hypertension is a major public health problem affecting nearly 78 million US adults (about 1 in 3) and more than 40% of African Americans, and nearly half of those affected have uncontrolled hypertension.15 Easing the burden of blood pressure–related disease warrants a comprehensive approach of both treating diagnosed hypertension and addressing underlying causes of high blood pressure in the population, such as a poor diet, to prevent future cases.
Average sodium intakes in the United States for those 2 years or older is 3478 mg/d, at least 1000 mg higher than any of the recommendations given by expert groups.
Given the significant number of people in the United States who would benefit from blood pressure lowering, reducing sodium intake in the American population is expected to have widespread benefits. People with hypertension, diabetes, and chronic kidney disease, as well as middle- and older-aged persons and African Americans, tend to exhibit a greater blood pressure response to reduced sodium intake than their healthier, younger, white counterparts.16 These populations represent approximately 50% of the US population 2 years or older.17 In addition, the blood pressure–raising effects of excess sodium are more pronounced in overweight and obese people, who comprise nearly 70% and 32% of the US adult and child/youth populations, respectively.15 Furthermore, lowering dietary sodium can significantly blunt the rise in blood pressure that occurs with age.4 This is important given that 90% of all Americans are expected to develop high blood pressure in their lifetime.18
INSTITUTE OF MEDICINE 2013 REPORT: WHAT IT DID AND DIDN’T SAY
A 2013 Institute of Medicine (IOM) report on Sodium Intake in Populations examined evidence published since 2003 concerning the potential benefits and adverse effects on health outcomes of sodium intake, particularly intakes of 1500 to 2300 mg/d.19 The health outcomes examined included CVD, heart failure, myocardial infarction, diabetes, mortality, stroke, bone disease, fractures, falls, headaches, kidney stones, skin reactions, immune function, thyroid disease, and cancer but did not include intermediate outcomes such as blood pressure. The IOM committee did not conclude that blood pressure is not an acceptable surrogate for health outcomes, and blood pressure was characterized as a valid surrogate marker in a 2010 IOM report.20 The Food and Drug Administration also recognizes blood pressure as a valuable biomarker for increased CVD risk.21
The IOM report generated much interest and debate, and some news stories contained inaccuracies and misrepresentations about its conclusions. Some stories suggested that sodium reduction was unnecessary or harmful, which likely created consumer confusion. An editorial authored by several committee members was published in the Journal of the American Medical Association,22 and it summarized key points from the report including the following:
- There is a positive relationship between sodium intake of 2300 mg/d or greater and risk of CVD, supporting efforts to reduce current population sodium intakes.
- An association between sodium intake and CVD outcomes persisted after adjusting for blood pressure in some studies, suggesting that other factors (such as potassium intake) could mediate the relationship.
- Studies on direct health outcomes were of inconsistent quality and insufficient quantity to conclude whether sodium intakes less than 2300 mg/d were associated with greater or lesser risk for CVD. This statement does not convey that there is no benefit to further sodium reduction; rather, better-quality studies are needed before a more definitive conclusion can be drawn about these intake levels and direct health outcomes. Research is needed to determine associations between sodium intakes of 1500 to 2300 mg/d and health outcomes in the general population and in individuals with various health conditions (eg, diabetes and chronic kidney disease).
The IOM committee was not tasked with identifying a target sodium intake level (and the report explained that the heterogeneity of the available data precluded the committee from doing so), although its report fueled much debate on this topic. These debates highlighted the importance of focusing on the totality of the evidence base: Americans are consuming much more sodium than any public health recommendation, and lowering current intakes confers benefits on blood pressure and CVD.
A J-SHAPED RELATIONSHIP BETWEEN SODIUM AND CVD COULD RESULT FROM METHODOLOGICAL LIMITATIONS IN OBSERVATIONAL STUDIES
Recently published observational epidemiologic studies suggest that sodium intakes less than 2300 mg/d may increase risk of adverse outcomes, particularly in individuals with some health conditions (eg, diabetes and chronic kidney disease). These findings have led to disagreements among some in the public health and medical community about recommended sodium intake targets and ultimately about the importance of any reduction from current levels.
Interpreting the results of observational studies is challenging because they can be highly dependent on the types of data collected (and not collected) and the statistical analytic approach. For example, a recent large observational study that assessed sodium intake by analyzing spot urines found greater risk of death and cardiovascular events with sodium intakes of less than 3000 mg/d (or >6000 mg/d),11 whereas another recent long-term follow-up study that assessed sodium intake by multiple 24-hour urine collections documented a reduced risk of CVD with intakes less than 3000 mg/d.23
A number of methodological issues may account for the inconsistency of results in observational studies examining the relationship between sodium intake and CVD, many of which use data sets that were not specifically designed to test the relationships between sodium intake and CVD. Key issues include the following:
- Use of unreliable measures of sodium intake, such as spot urines. A single urine sample is not an ideal measure to predict health outcomes that occur decades later. Because of intraindividual variation in day-to-day sodium intake and diurnal sodium excretion, multiple 24-hour urine collections are the criterion standard for assessing sodium intake. These collections place a greater burden on the investigator and study participants, so inferior measures are often used. Recent evidence suggests that there are major variations in urinary sodium output in tightly controlled settings where dietary intake is known,24 underscoring the importance of using multiple 24-hour urine collections for greater accuracy.
- Reverse causality, that is, inclusion of sick people who may have reduced their sodium intake in response to medical orders to limit sodium or who decreased overall food/calorie intake as a result of medication use or because of their disease state. The low sodium levels in these groups may not be the cause of their adverse health outcomes; instead, the low sodium intakes are prompted by the comorbid conditions.
- An insufficient number of cardiovascular events to definitively support the conclusion that a low-salt diet increases a person’s chances of dying of heart disease.
Methodological issues are common. An empirical analysis of methodological issues in 26 cohort studies that found a mix of direct, inverse, null, and J-shaped associations between sodium intake and CVD detected an average of 3 to 4 methodological problems per study.25 Many of these studies were recently included in a meta-analysis that concluded that sodium intakes less than approximately 2500 mg/d increase health risk,10 but averaging lower-quality studies does not improve quality or strengthen inferences.
Methodological concerns limit the usefulness of these observational studies in setting dietary recommendations. It has been recommended that until well-designed cohort studies in a representative sample of the population are available, it remains appropriate to base recommended levels of sodium intake on the robust body of evidence linking sodium with elevated blood pressure and the few existing general population trials of sodium reduction on CVD.25
Feasibility concerns explain the lack of randomized controlled trials showing improved health outcomes as a result of reducing sodium intake from current average intakes to recommended levels in the 1500- to 2300-mg/d range. It is unlikely that this evidence will be available soon because trials that examine clinical end points are notoriously expensive, requiring large numbers of participants and taking years to achieve an adequate number of study outcomes.
Physiological Response to Reduced Sodium Intake
Dr Heaney states that continual deployment of the renin-angiotensin-aldosterone system in response to reduction in sodium intake leads to increased risk of myocardial infarction and cardiac death.26 The renin-angiotensin-aldosterone system response is known to be greater with large and abrupt changes in sodium intake, but this may not be relevant to the gradual, sustained sodium reductions that are advocated.27,28 It is not known with certainty how much and for what duration various degrees of sodium reduction increase renin or aldosterone levels, or the clinical relevance of modest increases in plasma renin activity (whether acute or sustained) resulting from sodium reduction.29 Renin also rises in response to blood pressure–lowering therapies that reduce CVD risk. There is greater certainty of the rise in blood pressure as a biomarker for future CVD than how the rise in renin affects CVD.28
Feasibility of Achieving Sodium Intake Recommendations
Education and counseling to promote individual behavior change are important, but reducing the sodium in the food supply is critical. Nearly 80% of Americans’ sodium intake comes from sodium added to packaged and restaurant foods.29 This food environment makes it challenging for people to attain recommended sodium levels unless they prepare much of their food from scratch, in contrast to trends in preferences for convenience foods and meals.30 Less sodium pre-added to consumers’ food purchases would help them decrease sodium intake and provide more control over their sodium intake.
While the numerous roles sodium plays in foods contribute to the complexity of the issue, sodium reduction can be achieved by industry and be accepted by consumers.31 Some progress may occur by simply reducing salt, and beyond that, there is opportunity for innovation with new food manufacturing technologies and culinary techniques. The broad span of sodium content within similar food categories indicates that reduction to lower levels is feasible. A recent survey showed remarkable variability of sodium content in the same branded foods across countries. No single country consistently had the highest salt products; thus, regional taste preferences may not be responsible for the variation in salt content.32
Taste is an important driver of food choices, but is a malleable trait. Because most people eat considerably more salt than the body needs, salt preference appears to drive consumption rather than physiological need. Preferred levels are likely the result of the normative levels in the food supply. People who begin eating lower-sodium diets acclimate to prefer the lower levels, even eventually finding previously enjoyed foods to taste too salty. If the sodium they eat decreases gradually, they are usually not able to detect a difference in taste. Although more sensory research is still needed, it seems likely that consumers’ preferences for salty foods will shift downward without a decline in taste enjoyment if sodium in the US food supply is reduced gradually in a stepwise fashion.29 Stepwise reduction will likely take several years to achieve average American sodium intake that is within the range of what is acceptable to the public health community.
Standards for sodium levels in each food category would provide a level playing field for the industry, because all companies would have a common target as they reduce sodium in their products. This would help mitigate the potential for a given company to lose a competitive edge if they reduce sodium in their products while other companies do not. Such standards have been implemented in the United Kingdom, which recently observed a reduction in blood pressure, heart disease and stroke events, and deaths at the same time that sodium was reduced in the food supply by 15%.33
A comprehensive approach to cardiovascular health promotion and disease prevention must be multifactorial. In addition to a healthy diet, it should include regular physical activity, maintaining a healthy body weight, managing blood pressure and cholesterol, controlling blood sugar, and avoiding tobacco. Sodium reduction is not an isolated recommendation; it is an important component of a healthy dietary pattern that emphasizes intake of vegetables, fruits, and whole grains; includes low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts; and limits intake of sweets, sugar-sweetened beverages, and red meats.6 Diets aligned with this pattern will likely have less sodium and more potassium, magnesium, and calcium than standard American diets. Combined, these factors will decrease CVD risk.
Successful sodium reduction requires action and partnership at all levels—individuals, healthcare providers, professional organizations, public health agencies, governments, and industry. Health and nutrition professionals must consider that public health recommendations are made after weighing all of the evidence, including studies of greater and lesser strength of design and some with conflicting results. To echo the conclusion of more than 30 leading nutrition scientists in a June 2014 statement: “Population-wide reduction of sodium intake is an integral approach to reducing CVD events and mortality in the United States.”34
1. US Department of Agriculture ARS. Nutrient Intakes From Food and Beverages: Mean Amounts Consumed per Individual, by Gender and Age, What We Eat in America, NHANES 2011–2012. Beltsville, MD: USDA Agricultural Research Service, Food Surveys Research Group; 2014.
2. He J, Gu D, Chen J, et al. Gender difference in blood pressure responses to dietary sodium intervention in the GenSalt study. J Hypertens. 2009; 27( 1): 48–54.
3. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet. N Engl J Med. 2001; 344( 1): 3–10.
4. Appel LJ, Frohlich ED, Hall JE, et al. The importance of population-wide sodium reduction as a means to prevent cardiovascular disease and stroke: a call to action from the American Heart Association. Circulation. 2011; 123( 10): 1138–1143.
5. Whelton PK, Appel LJ, Sacco RL, et al. Sodium, blood pressure, and cardiovascular disease: further evidence supporting the American Heart Association sodium reduction recommendations. Circulation. 2012; 126( 24): 2880–2889.
6. Eckel RH, Jakicic JM, Ard JD, et al. 2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014; 129( 25 suppl 2): S76–S99.
7. He FJ, MacGregor GA. Salt reduction lowers cardiovascular risk: meta-analysis of outcome trials. Lancet. 2011; 378( 9789): 380–382.
8. Bray GA, Vollmer WM, Sacks FM, et al. A further subgroup analysis of the effects of the DASH diet and three dietary sodium levels on blood pressure: results of the DASH-Sodium Trial. Am J Cardiol. 2004; 94( 2): 222–227.
9. McCarron DA, Henry HJ, Morris CD, et al. Blood pressure and nutrient intake in the United States. Science. 1984; 224: 1392–1398.
10. Graudal N, Jurgens G, Baslund B, et al. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens. 2014; 27( 9): 1129–1137.
11. O’Donnell M, Mente A, Rangarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014; 371( 7): 612–623.
12. He FJ, MacGregor GA. A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. J Hum Hypertens. 2009; 23( 6): 363–384.
13. Kleinewietfeld M, Manzel A, Titze J, et al. Sodium chloride drives autoimmune disease by the induction of pathogenic TH
17 cells. Nature. 2013; 496( 7446): 518–522.
14. Zhu H, Pollock NK, Kotak I, et al. Dietary sodium, adiposity, and inflammation in healthy adolescents. Pediatrics. 2014; 133( 3): e635–e642.
15. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics— 2014 update: a report from the American Heart Association. Circulation. 2014; 129( 3): e28–e292.
16. Dietary Guidelines Advisory Committee. Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010, to the Secretary of Agriculture and the Secretary of Health and Human Services. Washington, DC: US Department of Agriculture, Agricultural Research Service; 2010.
17. Centers for Disease Control and Prevention (CDC). Usual sodium intakes compared with Dietary Guidelines. MMWR Morb Mortal Wkly Rep. 2011; 60( 41): 1413–1417.
18. Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-aged women and men: the Framingham Heart Study. JAMA. 2002; 287( 8): 1003–1010.
19. Institute of Medicine. Sodium Intake in Populations: Assessment of Evidence. Washington, DC: The National Academies Press; 2013.
20. Institute of Medicine. Evaluation of Biomarkers and Surrogate Endpoints in Chronic Disease. Washington, DC: The National Academies Press; 2010.
22. Strom BL, Anderson CM, Ix JH. Sodium reduction in populations: insights from the Institute of Medicine committee. JAMA. 2013; 310( 1): 31–32.
23. Cook NR, Appel LJ, Whelton PK. Lower levels of sodium intake and reduced cardiovascular risk. Circulation. 2014; 129( 9): 981–989.
24. Rakova N, Jüttner K, Dahlmann A, et al. Long-term space flight simulation reveals infradian rhythmicity in human Na+
balance. Cell Metabolism. 2013; 17( 1): 125–131.
25. Cobb LK, Anderson CA, Elliott P, et al. Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes: a science advisory from the American Heart Association. Circulation. 2014; 129( 10): 1173–1186.
26. Heaney RP. Making sense of the science of sodium. Nutrition Today. 2015; 50( 2): 63–66.
27. Sagnella GA, Markandu ND, Buckley MG, et al. Plasma atrial natriuretic peptide, aldosterone, and plasma renin activity responses to gradual changes in dietary sodium intake. Am J Hypertens. 1990; 3( 11): 863–865.
28. Aburto NJ, Ziolkovska A, Hooper L, et al. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013; 346: f1326.
29. Institute of Medicine. Strategies to Reduce Sodium Intake in the United States. Washington, DC: The National Academies Press; 2010.
30. International Food Information Council Foundation. Food & Health Survey: The Pulse of America’s Diet: From Beliefs to Behaviors. Washington, DC: International Food Information Council; 2014.
31. Antman EM, Appel LJ, Balentine D, et al. Stakeholder discussion to reduce population-wide sodium intake and decrease sodium in the food supply: a conference report from the American Heart Association Sodium Conference 2013 Planning Group. Circulation. 2014; 129( 25): e660–e679.
33. He FJ, Pombo-Rodrigues S, MacGregor GA. Salt reduction in England from 2003 to 2011: its relationship to blood pressure, stroke and ischaemic heart disease mortality. BMJ Open. 2014; e004549. doi:10.1136/bmjopen-2013-004549.