4

Sodium Intake and Health Outcomes

This chapter reviews and assesses new evidence for associations between dietary sodium intake and outcomes published in the peer-reviewed literature through 2012. The health outcomes reviewed by the committee include cardiovascular disease (CVD), including stroke CVD mortality and all-cause mortality, congestive heart failure (CHF), chronic kidney disease (CKD), diabetes, cancer, and “other” outcomes, such as asthma and depression.

An estimated 76.4 million adults 20 years of age and older in the United States have high blood pressure (Roger et al., 2011). Mean dietary intake of sodium among the general U.S. population averages 3,400 mg daily, while federal nutrition policy guidance, the Dietary Guidelines for Americans 2010 (HHS and USDA, 2010a), recommends sodium intakes of less than 2,300 mg daily for adolescents and adults 14 years of age and older, and 1,500 mg daily for African Americans, individuals 51 years of age and older, and individuals with hypertension, diabetes, or CKD. Evidence underlying this recommendation can be found in a number of sources, including the report Dietary Reference Intakes for Water, Sodium, Chloride, and Sulfate (IOM, 2005), and the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010 (DGAC) (HHS and USDA, 2010b). Excess dietary sodium has been identified as a potential etiologic risk factor for CVD, based on evidence for a dose-dependent increase in blood pressure in response to increasing sodium intake, as well as evidence from studies published before 2003 of sodium intake and risk of stroke or coronary heart disease (IOM, 2005).

The DGAC report (HHS and USDA, 2010b) included a review of evi-



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4 Sodium Intake and Health Outcomes This chapter reviews and assesses new evidence for associations between dietary sodium intake and outcomes published in the peer-reviewed lit- erature through 2012. The health outcomes reviewed by the committee include cardiovascular disease (CVD), including stroke CVD mortality and all-cause mortality, congestive heart failure (CHF), chronic kidney disease (CKD), diabetes, cancer, and “other” outcomes, such as asthma and depression. An estimated 76.4 million adults 20 years of age and older in the United States have high blood pressure (Roger et al., 2011). Mean dietary intake of sodium among the general U.S. population averages 3,400 mg daily, while federal nutrition policy guidance, the Dietary Guidelines for Americans 2010 (HHS and USDA, 2010a), recommends sodium intakes of less than 2,300 mg daily for adolescents and adults 14 years of age and older, and 1,500 mg daily for African Americans, individuals 51 years of age and older, and individuals with hypertension, diabetes, or CKD. Evidence underlying this recommendation can be found in a number of sources, including the report Dietary Reference Intakes for Water, Sodium, Chloride, and Sulfate (IOM, 2005), and the Report of the Dietary Guide- lines Advisory Committee on the Dietary Guidelines for Americans, 2010 (DGAC) (HHS and USDA, 2010b). Excess dietary sodium has been identi- fied as a potential etiologic risk factor for CVD, based on evidence for a dose-dependent increase in blood pressure in response to increasing sodium intake, as well as evidence from studies published before 2003 of sodium intake and risk of stroke or coronary heart disease (IOM, 2005). The DGAC report (HHS and USDA, 2010b) included a review of evi- 57

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58 SODIUM INTAKE IN POPULATIONS dence on the impact of dietary patterns low in sodium and/or low in satu- rated fat and high in potassium (e.g., DASH [Dietary Approaches to Stop Hypertension] and Mediterranean diets) on risk of CVD, stroke, and mor- tality and concluded that plant-based, lower-sodium dietary patterns had a beneficial impact on CVD risk. However, the dietary patterns included in the evidence review included dietary modifications other than sodium reduction that have been shown to have a cumulative impact on risk of CVD and related diseases. These include increased potassium, reduced intake of saturated and trans fats, and increased intake of dietary fiber. Based on their review of the evidence, the DGAC (HHS and USDA, 2010b) concluded that reduced risk of CVD, stroke, and disease-related mortality was associated with total dietary modification. Nevertheless, decreasing sodium intake has a potential role in reducing risk of CVD, stroke, and mortality, and this was the primary focus of the committee’s review. CARDIOVASCULAR DISEASE, STROKE, AND MORTALITY As noted in Chapter 3, blood pressure is used as a surrogate indicator for CVD, stroke, and mortality risk, especially among individuals who are already at risk of disease. The committee’s review of the strength of new evidence for dietary sodium and its effects on blood pressure concurred with previously established evidence (see Chapter 3). This evidence that high sodium intakes can indirectly mediate risk of adverse health out- comes underpinned the committee’s assessment of evidence on associations between sodium intake and direct health outcomes. Taking the evidence for blood pressure effects into consideration as background, the commit- tee focused its review on new evidence on sodium intake and direct health outcomes, particularly evidence from intervention studies where available. Each outcome is discussed in turn, presenting the available data orga- nized by population group, and within each group organized alphabeti- cally by the last name of the first author. Each study is described by its population, size, and characteristics; study design, purpose, and length; sodium intake measure and method; range of intake, reference intake, and adjustments; outcome measure, confounders, and adjustments; and direc- tion and significance of effect. For each major outcome of CVD, CHF, and CKD, the committee provides a summary table evaluating each study using as criteria the generalizability of the study population to U.S. populations and the appropriateness of the methodology used to support the findings and conclusions. Finally, a summary of findings and conclusions is given on each major outcome for general populations and for population subgroups of interest as described in the statement of task, specifically those with hypertension or

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SODIUM INTAKE AND HEALTH OUTCOMES 59 prehypertension, those 51 years of age and older, African Americans, and those with diabetes, CKD, and CHF (see Appendix F for evidence tables). Studies on General Populations The committee identified studies related to CVD from its literature search that met the criteria for inclusion described in Appendix F, Table F-1, and, on further examination, were found to be relevant to the commit- tee’s task. The cardiovascular health outcomes reviewed were CVD, stroke, stroke mortality or CVD mortality, and all-cause mortality. The committee’s summary of the evidence for each cardiovascular health outcome is shown in Tables 4-1 through 4-6. Cohen et al. (2006) Population size and characteristics Cohen et al. (2006) obtained data from participants in the National Health and Nutrition Examination Survey (NHANES) II from among the general U.S. population (n=7,154 partici- pants 30-74 years of age). Individuals with self-reported preexisting disease, as well as those who reported being on a low-sodium diet for hypertension, were excluded. Study design, purpose, and length This secondary analysis of NHANES data was carried out to assess the potential impact of dietary sodium intake on risk of CVD and all-cause mortality over a mean of 13.7 years of follow-up. Sodium intake measure and method Dietary sodium intake was assessed from a 24-hour dietary recall administered in the NHANES survey. The NHANES II dataset does not include sodium from salt added at the table. In addition, because only 1 day of intake was used, the sodium measure used in this study may not have represented the usual dietary intake of sodium at the individual level. Range of intake, reference, and adjustments Dietary sodium intake was cat- egorized as <2,300 mg [n=3,443] or ≥2,300 mg [n=3,711]; or by quartiles, corresponding to lowest to highest sodium intakes of <1,645, 1,645-2,359, 2,360-3,345, and ≥3,346 mg per day, using the highest intake quartile as reference; and also as a continuous variable (per 1,000 mg). Sodium intake was adjusted for calories and the highest and lowest 1 percent of the calo- rie intake range were excluded from the analysis. The correlation between sodium and caloric intake for most age/sex groups is greater than 0.7 (IOM, 2010, pp. 129-130).

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60 SODIUM INTAKE IN POPULATIONS Outcome measure, confounders, and adjustments Outcomes measured were CVD mortality, all-cause mortality, coronary heart disease mortality, and cerebrovascular disease mortality. All analyses were adjusted for prior hypertension and systolic blood pressure, which may be in the causal pathway. Direction and significance of effect For quartiles of sodium intake the lower sodium intake quartiles were not associated with CVD mortality (hazard ratio [HR]=1.31 [confidence interval (CI): 0.90, 1.89] p=0.14), 2 (HR=1.39 [CI: 0.91, 2.11] p=0.11), and 3 (HR=0.89 [CI: 0.64, 1.25] p=0.49). Simi- larly, no significant associations were found between sodium intake quar- tiles and all-cause or stroke mortality. However, when analyzed for intakes less than 2,300 mg per day compared to 2,300 mg per day or greater, lower sodium intake was statistically significantly associated with increased risk of all-cause mortality. Models of sodium density, expressed as a sodium-to- calorie ratio, showed a statistically significant inverse association with all- cause mortality (HR=0.89 [CI: 0.79, 1.00] p=0.05). In other words, lower sodium intake was associated with higher all-cause mortality. For dietary sodium intake measured as a continuous variable, a statistically significant inverse relationship was found between sodium intake and CVD mortality whether expressed as sodium per mg (HR=0.89 [CI: 0.80, 0.99] p=0.03) or as sodium per calorie (HR=0.80 [CI: 0.68, 0.94] p=0.008). Interactions Although data were not shown, the authors reported that they found no evidence of interactions by age, race, or prevalence of diabetes or hypertension. Cohen et al. (2008) Population size and characteristics Cohen et al. (2008) analyzed data from participants in the NHANES III survey from the general U.S. population (n=8,699 participants 30 years of age and older). Individuals with self- reported preexisting disease, as well as those who reported being on a low- sodium diet for hypertension, were excluded. Study design, purpose, and length This secondary analysis of NHANES data was carried out to assess the potential impact of dietary sodium on risk of CVD and all-cause mortality over a mean period of 8.7 years. Sodium intake measure and method Energy-adjusted dietary sodium intake was estimated from one 24-hour dietary recall. Use of added salt was deter- mined by the responses “does not add,” “adds some,” or “adds a lot.”

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SODIUM INTAKE AND HEALTH OUTCOMES 61 Range of intake, reference, and adjustments Sodium intake was categorized into quartiles of <2,060 [n=2,174], 2,060-2,921 [n=2,175], 2,922-4,047 [n=2,175], and 4,048-9,946 mg per day [n=2,175], using the highest intake quartile as reference. Intake analyses were adjusted for added table salt. Outcome measure, confounders, and adjustments Outcomes included CVD and all-cause mortality and were adjusted for blood pressure and hyper- tension, which may be in the causal pathway. Other variables examined as potential confounders included sex, age, serum cholesterol, race, treatment for hypertension, blood pressure, smoking, alcohol consumption weight, body mass index (BMI), history of diabetes, education, and added table salt. Direction and significance of effect When fully adjusted, there was a sta- tistically significant higher risk of CVD mortality (p=0.03) with the lowest vs. the highest quartile of sodium intake that was not present for all-cause mortality (p=0.17). For sodium as a continuous variable and residuals- adjusted sodium, nonsignificant inverse trends were found for both CVD and all-cause mortality. Similar trends were found using sensitivity analyses on the subset of participants (n=5,560) who reported not adding salt during cooking or at the table. Interactions Although data were not shown, the authors reported that they found no evidence of interactions by age, race, or prevalence of diabetes or hypertension. Gardener et al. (2012) Population size and characteristics Gardener et al. (2012) analyzed data from participants in the Northern Manhattan Study (n=2,657) who had no previous diagnosis of stroke, were older than 40 years of age (mean 69 ±10 years) and were ethnically diverse (21 percent white, 24 percent African American, 53 percent Hispanic). Study design, purpose, and length This multiethnic population-based pro- spective cohort study examined associations between sodium consumption and risk of stroke and combined vascular events (stroke, myocardial infarc- tion [MI], and vascular death) over a mean of 10 years. Sodium intake measure and method Dietary sodium intake was estimated using the Block National Cancer Institute food frequency questionnaire (FFQ). Average sodium intake was examined continuously.

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62 SODIUM INTAKE IN POPULATIONS Range of intake, reference, and adjustments Sodium intake was calculated from self-reported data and categorized into tertiles of ≤1,500, 1,501- 3,999, and ≥4,000 mg per day. The lowest tertile was used as the reference. Outcome measure, confounders, and adjustments The primary outcome measure was incident stroke of all subtypes; secondary outcomes were con- firmed incident of combined vascular event (combined), MI incident, and vascular death. Analytic models were adjusted for demographics, behav- ioral risk factors, and vascular risk factors (diabetes, hypercholesterolemia, hypertension, and continuous blood pressure measurements). Direction and significance of effect This study found that sodium intake was positively associated with increased risk of stroke. Using sodium as a continuous variable, stroke risk increased 17 percent for each 500 mg per day higher sodium intake (HR=1.17 [CI: 1.07, 1.27]). However, the authors noted that the relationship did not appear linear. Participants who consumed more than 4,000 mg sodium daily had a 2.5-fold increase in risk of total stroke compared to those who consumed less than 1,500 mg per day (HR=2.50 [CI:1.23, 5.07]). This difference persisted after adjustment for vascular risk factors. Those who consumed more than 1,500 but less than 4,000 mg of sodium daily had an approximate 30 percent increased risk, though this was not statistically significant. Each 500 mg per day higher sodium intake was associated with a 16 percent greater risk of isch- emic stroke. Among those who consumed more than 4,000 mg compared to those who consumed less than 1,500 mg per day (reference intake), the risk was 2.4-fold greater. Consumption of more than 4,000 mg per day also was associated with an increased risk of combined vascular events, while the results were less consistent for lower levels of sodium consumption and cardiovascular events. Interactions Although data were not reported, the authors found no evi- dence of interactions by age, race, or prevalence of diabetes or hypertension. Larsson et al. (2008) Population size and characteristics Larsson et al. (2008) analyzed data on 26,556 male smokers in Finland, 50-69 years of age, who participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention primary preven- tion trial (ATBC Cancer Prevention Study Group, 1994). Participants had smoked at least five cigarettes daily at baseline. From the original cohort, men who had evidence of disease, for example, history of cancer, and those receiving anticoagulant therapy or taking excess vitamin supplements were

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SODIUM INTAKE AND HEALTH OUTCOMES 63 excluded from the analysis, although those with a history of diabetes or coronary heart disease were included. Study design, purpose, and length This large prospective study followed a male cohort to assess relationships between magnesium, calcium, potas- sium, and sodium intake and risk of stroke for a mean of 13.6 years. Sodium intake measure and method Energy-adjusted dietary sodium intake was estimated from a self-administered, validated 276-item FFQ that included items commonly consumed in Finland. Use of cooking salt was included in the questionnaire, whereas salt added at the table was not captured. Range of intake, reference, and adjustments Median sodium intake esti- mates were divided into quintiles with means of 3,909, 4,438, 4,810, 5,212, and 5,848 mg per day, for Q1 through Q5, respectively, using the lowest quintile as the reference. Thus, the average sodium intake in the United States would be within the lowest quintile of this study. Outcome measure, confounders, and adjustments Outcome measure was first-ever stroke occurring between the date of randomization (between 1985 and 1988) and the first occurrence of stroke by the end of the study period (December 31, 2004). Strokes were classified as cerebral infarction, intracerebral hemorrhage, subarachnoid hemorrhage, or unspecified stroke, and identified from the Finnish National Hospital Discharge Register and the National Register of Causes of Death. Multivariate analysis adjusted for age, supplementation group, number of cigarettes smoked daily, BMI, systolic and diastolic blood pressure, serum total cholesterol and high- density cholesterol, as well as history of diabetes and coronary heart dis- ease, leisure-time physical activity, and intake of alcohol and total energy. Direction and significance of effect The analyses found no significant asso- ciation between dietary sodium intake and risk of any stroke subtype (p for trend for multivariate relative risk [RR]=0.99, 0.06, and 0.55 for cerebral infarction, intracerebral hemorrhage, and subarachnoid hemor- rhage, respectively). Nagata et al. (2004) Population size and characteristics Nagata et al. (2004) analyzed a cohort of Japanese adults 35 years of age and older using data collected in the Takayama population-based study. The study included 13,355 men and 15,724 women.

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64 SODIUM INTAKE IN POPULATIONS Study design, purpose, and length This population-based cohort study examined associations between dietary sodium intake and stroke mortality risk over a period of 7 years. Sodium intake measure and method Dietary sodium intake was estimated from a 169-item semiquantitative FFQ. The instrument included questions on use of table salt and salty condiments. Use of cooking salt was not included in the questionnaire. Range of intake, reference, and adjustments Sodium intake levels were represented by tertile for men (means 4,070, 5,209, and 6,613 mg per day) and women (means 3,799, 4,801, and 5,930 mg per day), using the lowest tertile as the reference. Sodium intake was energy-adjusted when used in analyses. Thus, the average sodium intake in the United States would be within the lowest tertile of this study. Outcome measure, confounders, and adjustments The outcome measure was stroke mortality (data obtained from National Vital Statistics for Japan). Stroke types included subarachnoid hemorrhage, intracerebral hem- orrhage, ischemic stroke, and stroke of undetermined type. Adjustment variables included age, education level, marital status, BMI, smoking, alco- hol use, and history of diabetes or hypertension. Direction and significance of effect Over the 7-year follow-up period, 43 subarachnoid hemorrhages, 59 intracerebral hemorrhage deaths, and 137 ischemic stroke deaths occurred. Among men, a 2.3-fold increased risk of stroke mortality (significantly positive for intracerebral hemorrhage and ischemic stroke death) was associated with the highest tertile of sodium intake (mean intake of 7,194 mg per day) after adjustment for other dietary variables (HR=2.33 [CI: 1.23, 4.45] p for trend=0.009). The authors also reported a borderline significant trend between high sodium intake (mean intake of 6,478 mg per day) and total stroke and ischemic stroke death among women (total stroke HR=1.70 [CI: 0.96, 3.02] p for trend=0.07); ischemic stroke (HR=2.10 [CI: 0.96, 4.62] p for trend=0.05). Stolarz-Skrzypek et al. (2011) Population size and characteristics Stolarz-Skrzypek et al. (2011) obtained data from two population-based prospective cohort studies (the Flemish Study on Environment, Genes, and Health Outcomes and the European Project on Genes in Hypertension) to examine a cohort of 2,856 partici- pants recruited from a random sample of households in several European

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SODIUM INTAKE AND HEALTH OUTCOMES 65 countries. The cohort included men and women 20-39, 40-59, and 60 or more years of age. Study design, purpose, and length This study prospectively examined asso- ciations between sodium and changes in blood pressure and risk of CVD mortality and all-cause mortality over a median of 7.9 years. Sodium intake measure and method Timed 24-hour urine samples were collected 1 week following blood pressure measurements and analyzed for sodium and potassium. Range of intake, reference, and adjustments Twenty-four-hour sodium excretion values were categorized into tertiles of low (50-126 mmol [1,150- 2,898 mg] for women; 50-158 mmol [1,150-3,634 mg] for men); medium (127-177 mmol [2,921-4,071 mg] for women; 159-221 mmol [3,657-5,083 mg] for men); and high (178-400 mmol [4,094-9,200 mg] for women; 222- 400 mmol [5,106-9,200 mg] for men). Outcome measure, confounders, and adjustments Risk of CVD events was assessed for each quartile against risk of CVD events for the whole study population. Cardiovascular outcomes, fatal and nonfatal stroke, fatal and nonfatal MI, fatal and nonfatal left ventricular heart failure, aortic aneu- rysm, cor pulmonale, and pulmonary or arterial embolism were validated by physicians against medical records. Covariables in the regression analy- ses were study population, sex, age, blood pressure level, BMI, alcohol intake, use of antihypertensive drugs, urinary potassium excretion, educa- tion, smoking status, total cholesterol, and diabetes. Direction and significance of effect Overall, the authors found that lower sodium intake was associated with higher risk of CVD mortality. In the low, medium, and high tertiles of sodium excretion the CVD mortalities were 50 (4.1% [CI: 3.5%, 4.7%]); 24 (1.9% [CI: 1.5%, 2.3%]); and 10 (0.8% [CI: 0.5%, 1.1%]) events, respectively, after adjustment for risk factors, including baseline hypertension and blood pressure level. The risk of CVD mortality was statistically significantly higher in the low versus the high tertile (HR=1.56 [CI: 1.02, 2.36] p=0.04) with a significant trend over tertiles (p=0.02). All-cause mortality showed a trend in risk of CVD mortality for low and medium tertiles, although it was not statistically significant (HR=1.14 [CI: 0.87, 1.50] and 64 (HR=0.94 [CI: 0.75-1.18]). Likewise, there was no significant effect on total CVD incidence. Analy- sis of supplemental data from this study demonstrated that individuals assigned to the low-sodium tertiles were older, less educated, had greater

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66 SODIUM INTAKE IN POPULATIONS comorbidities, lower urine volume, and lower serum creatinine than those in higher-sodium tertiles. Takachi et al. (2010) Population size and characteristics Takachi et al. (2010) examined data from the Japan Public Health Center-based Prospective Study, conducted in two cohorts. Cohort I and II participants were 40-59 and 40-69 years of age, respectively. Those with a history of cancer or coronary heart disease were excluded, leaving a final study population of 77,500 (35,730 men and 41,770 women). Study design, purpose, and length The objective of this prospective study was to assess associations between sodium and salted food consumption and risk of either cancer or CVD. Participants were followed from the beginning in 1990 (cohort I) or 1993 (cohort II) until December 31, 2004. Sodium intake measure and method Dietary sodium intake data were deter- mined from a 138-item FFQ that included cooking salt, soy sauce, table salt, and other salty condiments. Range of intake, reference, and adjustments Energy-adjusted sodium intake per day was categorized by quintile: medians were 3,084, 4,005, 4,709, 5,503, and 6,844 mg per day for Q1 through Q5, respectively. Thus, the average sodium intake in the United States would be close to the lowest quintile of this study. Outcome measure, confounders, and adjustments Cardiovascular outcomes included diagnosis of MI and diagnosis of stroke confirmed by computed tomography (CT) scan and/or magnetic resonance imaging (MRI) from medical records. Adjustment variables for analysis were sex and age, with additional adjustment for BMI, smoking status, alcohol consumption, phys- ical activity, and quintiles of energy, potassium, and calcium. Direction and significance of effect Adjusted multivariate analysis found a significant positive association between sodium consumption at the highest compared to the lowest quintile and risk of stroke (HR=1.21 [CI: 1.01, 1.43] p for trend=0.03) and between use of cooking and table salt and risk of stroke (HR=1.21 [CI: 1.02, 1.44] p for trend=0.05), but not between use of dried salted fish and risk of stroke. Increased intake of dried and salted fish was associated with lower risk of MI. The risk of the composite CVD endpoint was elevated in the highest quintile of sodium (HR=1.19 [CI: 1.01, 1.40] p for trend=0.06). The results also showed correlation with

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SODIUM INTAKE AND HEALTH OUTCOMES 67 other variables, such as dried and salted fish, although the impact of those variables on the outcomes is unknown. Umesawa et al. (2008) Population size and characteristics Umesawa et al. (2008) examined data from participants in the Japan Collaborative Cohort Study for Evaluation of Cancer Risks (23,119 men and 35,611 women) 40-79 years of age. Study design, purpose, and length This large prospective study examined associations between dietary sodium intake and mortality from stroke; stroke related to subarachnoid hemorrhage, intraparenchymal hemorrhage, or ischemic stroke; coronary heart disease; and total CVD over a mean follow-up period of 12.7 years. Sodium intake measure and method Energy-adjusted dietary sodium intake was estimated from responses to a 35-item FFQ and the results were cali- brated against a previous validation study that included items from the FFQ and four 3-day dietary records. Range of intake, reference, and adjustments Dietary sodium intake was categorized into quintiles from lowest to highest with Q1=101 ±30 (2,323 ±690), Q2=146 ±11 (3,358 ±253), Q3=182 ±11 (4,186 ±253), Q4=220 ±12 (5,060 ±276), and Q5=272 ±36 (6,256 ±828) mmol (mg) per day. The calibrated sodium intake based on a validation study was twice as high in all five quintiles in which median values were assigned for each quintile and the significance of the variables was tested. Outcome measure, confounders, and adjustments Outcome measures were stroke (including ischemic stroke), CVD, or CHD mortality derived from data obtained from death certificates for targeted populations in each study locale. Adjustments were made for CVD risk factors, including hyperten- sion, and for potassium intake. Direction and significance of effect The authors found an association between greater dietary sodium intake and greater mortality from total stroke, ischemic stroke, and total CVD. Multivariable hazard ratios were strongest with the highest compared to the lowest quintiles of sodium intake: HR=1.55 (CI: 1.21, 2.00) for total stroke, HR=2.04 (CI: 1.41, 2.94) for ischemic stroke, and HR=1.42 (CI: 1.20, 1.69) for total CVD mortal- ity. The positive associations found between dietary sodium intake and mortality risk of total and ischemic stroke and CVD were independent of

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108 SODIUM INTAKE IN POPULATIONS General Population Based on its assessment of the evidence, the committee found, first, the evidence reviewed on specific adverse health outcomes consistently indicates an association in the general population between excessive sodium intakes and increased risk of CVD, particularly for stroke. In particular, data from studies using FFQs generally supported an association between high sodium intake and increased risk of CVD, particularly stroke (Gardener et al., 2012; Nagata et al., 2004; Takachi et al., 2010; Umesawa et al., 2008), although not consistently (Larsson et al., 2008). Several of these studies evaluated populations with sodium intakes much higher than the average U.S. intake of 3,400 mg per day (Nagata et al., 2004; Takachi et al., 2010; Umesawa et al., 2008). Gardener et al. (2012), however, found an effect on stroke with sodium intakes starting at 1,500 mg per day (HR=1.17 per 500 mg increase in sodium). Sodium intake data from FFQs, however, are limited by errors in estimating discretionary sodium intake (salt added in cooking or at the table), which accounts for an estimated 11 percent of sodium intakes (Mattes and Donnelly, 1991). The committee found, in contrast, that the evidence from the current literature is inconsistent with regard to associations with sodium intakes below 2,300 mg per day, with results ranging from lower, similar, or higher risk of CVD, stroke, or mortality, including all-cause mortality. All of the studies identified have limitations of different types. The evidence in some cases is suggestive, however, of associations between lower sodium intake (below 2,300 mg per day) and potential increased risk of adverse health outcomes, though reverse causation, confounding, and systematic measure- ment error cannot be ruled out. For example, studies using data from NHANES III (which is represen- tative of the general U.S. population) used 24-hour recall data to estimate sodium intake, which, as discussed in Chapter 2, could introduce consider- able error in the measurement of sodium levels. In addition, such studies showed inconsistent results, depending on the methodological approach. Two studies (Cohen et al., 2006, using NHANES II; Cohen et al., 2008, using NHANES III) found an increased risk of CVD at lower sodium levels, while one study (Yang et al., 2011, also using NHANES III) found a lower risk of all-cause mortality at lower sodium intake levels. These studies, however, are limited by the sodium intake measurement used. In addition, they differ on the corrections made for sodium measurements as well as for calorie intake adjustment. Additionally, Cohen et al. (2006, 2008) did not adjust for within-individual day-to-day variation in intake, whereas that adjustment was made in Yang et al. (2011) As another example, Stolarz- Skryzpek et al. (2011), in a general population, also reported higher CVD outcomes in the lower sodium intake group. However, Stolarz-Skryzpek

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SODIUM INTAKE AND HEALTH OUTCOMES 109 et al. (2011) were limited by the possibility of unmeasured confounding and undercollection of urine specimens in the lowest sodium tertile. Population Subgroups Some studies addressed questions related to associations between sodium intake and health outcomes in population subgroups. The commit- tee evaluated one large (O’Donnell et al., 2011) and six small (Arcand et al., 2011; Dong et al., 2009; Ekinci et al., 2011; Heerspink et al., 2012; Kono et al., 2011; Tikellis et al., 2013) prospective cohort studies in patients with preexisting CHF, stroke, MI, CKD, and diabetes, using various methods of sodium assessment. The outcomes estimates were extremely heterogeneous, with HR values ranging between 0.11 (Dong et al., 2009) and 3.54 (Arcand et al., 2011). Because these populations are typically advised to reduce their sodium intake, reverse causation cannot be ruled out as a factor in the relationship. In contrast, two related observational studies (Cook et al., 2007, 2009) used three to seven 24-hour urine collections, the best available method, to measure sodium intake levels. Both of these studies were conducted in prehypertensive individuals. Cook et al. (2007), an observational follow-up of the TOHP I and II sodium reduction trials, found a 25 percent reduction in CVD incidence, as well as a nonsignificant 20 percent reduction in total mortality when average levels of sodium intake decreased from approxi- mately 3,600 to 2,300 mg per day in the intervention group in TOHP I and from 4,200 to 3,200 mg per day in TOHP II. Cook et al. (2009), also an observational study that followed participants in the TOHP I and II tri- als, found a linear increase in the risk of total CVD events with increasing sodium intake levels after adjusting for potassium intake. However, there were relatively few outcomes in the lowest ranges of sodium intake, lead- ing to unstable estimates in those ranges. The committee found that these studies suggest an association between a decrease in CVD event rates and sodium intakes down to 2,300 mg per day, and perhaps below, although based on small numbers. The committee identified and evaluated three RCTs and two cohort studies that examined associations between sodium intake at low, moder- ate, and high levels and health outcomes in study participants with CHF at various levels of severity. Although the results from the effects of dietary sodium on outcomes in these participants appear inconsistent, several fac- tors might have contributed to the disparate findings. Three RCTs with a similar sodium reduction protocol from a single site in Italy consistently demonstrate higher adverse events (hospital readmission and mortality) associated with lower-sodium diets. Treatment regimens in the three RCTs (Parrinello et al., 2009; Paterna et al., 2008, 2009) included low rates of

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110 SODIUM INTAKE IN POPULATIONS beta blocker use and high-dose furosemide diuretic use combined with significant fluid restriction, which does not reflect contemporary U.S. man- agement of patients with CHF.3 However, the committee could not identify weaknesses in the study designs. Further, the uniformity of the results even under very different basic treatments suggests a need for additional trials to be conducted by other investigators with participants under treatments similar to those used in the United States. The observational studies may suggest a difference in the effect of lower sodium consumption depending on the degree of compensation of the CHF patients (NYHA I/II vs. III/IV), but this was not observed in the Paterna trials (one trial was done in NYHA II and one in decompensated CHF NYHA Class II to IV). Additional difficulty comparing the trials and the observational studies may arise from the differences in CHF patients after hospital discharge (e.g., the Paterna trials) and stable outpatients with heart failure (e.g., the observational studies in CHF clinics in Lennie et al. [2011] and Arcand et al. [2011]). Lastly, adjustment for different potential confounders may have influenced the outcomes observed in the cohort studies, leading to different interpretations. For example, while Arcand et al. (2011) controlled for caloric intake, none of the studies controlled for education, which has been shown to be associated with better health out- comes and lower sodium intake. In contrast to the Italian studies, which show consistency in the results, the results from Arcand et al. (2011) are inconsistent in that the number of hospital readmissions is largest in the middle sodium intake category (66 percent), although it has the lowest mortality (0 percent). Importantly, CHF is the only health outcome for which RCTs exist. Therefore, although differences in disease management preclude a definitive assessment of the effects of low sodium intake (i.e., 1,840 mg per day) for CHF patients in the United States, the evidence suggests that low sodium intakes may lead to higher risk of adverse events in mid- to late-stage CHF patients with reduced ejection fraction receiving aggressive therapeutic regi- mens. In addition, a cohort study in a population including individuals with 3  The Guidelines for Heart Failure patients of the Heart Failure Association of America de- scribes therapies appropriate for the different stages of a patient’s health (e.g., decompensated heart failure, reduced ejection fraction, end of life). For patients with reduced ejection fraction (≤40 percent), the guideline recommends ACE inhibitors, ARBs (when ACE inhibitors are not tolerated by patients or in post-MI or chronic heart failure patients), beta blockers, and aldosterone antagonists (unless creatinine is >2.5 mg/dL or serum potassium is >5 mmol/L). In addition, diuretic therapy is recommended in certain patients to restore normal volume. For example, the recommended initial daily dose of furosemide is 20-40 mg once or twice per day for a maximum total daily dose of 600 mg. The guideline states that to minimize fluid retention, sodium intake should be limited to 2,000-3,000 mg per day and fluid should be restricted to less than 2,000 ml.

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SODIUM INTAKE AND HEALTH OUTCOMES 111 CVD supports the conclusion reached by the Italian studies. That is, low sodium intake levels might result in increased CHF episodes (O’Donnell et al., 2011). However, O’Donnell et al. (2011) used spot urine collection, and the relationship between low sodium intakes and higher CVD risk appeared limited to the outcome of CVD death and CHF, with no apparent relationship between low sodium and risk of MI or stroke. Nevertheless, three randomized trials in CHF patients (Parrinello et al., 2009; Paterna et al., 2008, 2009) found that a sodium intake of 1,840 (vs. 2,870) mg per day was associated with increased mortality in this popula- tion subgroup. These trials, however, were limited to patients with mid- to late-stage CHF and reduced ejection fraction. In addition, patients were receiving aggressive therapeutic regimens that were very different from current standards of care, and thus, the results may not be generalizable. Finally, the committee found that overall, the paucity of evidence in the general population and population subgroups strongly points to the need for further research to better define relationships between sodium intake and risk of CVD, stroke, and mortality, particularly at the lowest levels of sodium intake within the U.S. population. STUDIES ON KIDNEY DISEASE Two studies explored the relationship between sodium intake and CKD (Heerspink et al., 2012; Thomas et al., 2011). Collectively, the commit- tee found these studies lacking in clarity about the risk of kidney disease progression or ESRD associated with sodium intake. Both of the studies reviewed evaluated populations with diabetes who had macroalbuminuria. These two studies show conflicting results about either benefits or risks associated with sodium intake in diabetic patients with macroalbuminuria. Thomas et al. (2011) demonstrated an inverse association of sodium intake with ESRD risk, which suggests that lower sodium intake may increase ESRD risk. On the other hand, the study by Heerspink et al. (2012) sug- gests that use of renin-angiotensin-aldosterone system (RAAS)-blocking agents may be more beneficial in patients with low sodium intake. RAAS blockade is the first-line therapy for treatment of diabetic nephropathy (Arauz-Pacheo et al., 2003; NKF, 2007) and has consistently been shown to delay progression of diabetic nephropathy into ESRD. Thus, Heerspink et al. (2012) suggest that sodium restriction may be beneficial rather than harmful in preventing kidney disease progression in kidney disease patients with diabetes and macroalbuminuria. Overall, the studies published since 2003 reviewed by the committee provide inconsistent data about the relationship of sodium intake levels and kidney disease progression in patients with type 2 diabetes and mac- roalbuminuria, and some evidence suggests that low sodium intake may be

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112 SODIUM INTAKE IN POPULATIONS harmful in this population. The committee found no studies published since 2003 evaluating the risk of ESRD among individuals with kidney disease at baseline, who had nondiabetic forms of CKD, or in individuals with diabetes but without macroalbuminuria. Some studies suggest that lower sodium intake may lead to lower proteinuria, and that proteinuria is a strong risk factor for CKD progression (described in Chapter 3). However, recent large-scale clinical trials demonstrate that decrements in proteinuria are not always associated with slower progression of CKD (Mann et al., 2008; Parving et al., 2012). For these reasons, to reach its conclusions, the committee relied primarily on data evaluating relationships between sodium level and CKD progression and dialysis initiation rather than changes in proteinuria. STUDIES ON METABOLIC SYNDROME, DIABETES, AND GASTRIC CANCER The committee identified from its literature search two cross-sectional studies that examined associations between sodium intake and risk of metabolic syndrome (Rodrigues et al., 2009; Teramoto et al., 2011). The committee also identified two prospective cohort studies that examined associations between sodium intake and risk of developing diabetes (Hu et al., 2005; Roy and Janal, 2010) and one study that examined the role of genetic polymorphisms linked to sodium intake in risk of diabetes (Daimon et al., 2008). These studies did not meet the committee’s criteria for further evaluation of the strengths and weaknesses of the study and its relevance to the committee’s task. The committee identified seven prospective cohort studies (Murata et al., 2010; Peleteiro et al., 2011; Shikata et al., 2006; Sjodahl et al., 2008; Takachi et al., 2010; Tsugane et al., 2004; van den Brandt et al., 2003) and five case-control studies (Lazarević et al., 2011; Lee et al., 2003; Pelucchi et al., 2009; Strumylaite et al., 2006; Zhang and Zhang, 2011) that exam- ined associations between sodium intake and risk of gastric cancer. These studies had a number of limitations, including that the reported intakes of the populations studied were not relevant to intake levels in the United States. Overall, the prospective cohort studies showed conflicting results for risk of gastric cancer and the case-control studies were potentially biased due to recall bias. Another possible effect modifier is infection with H. pylori. There is no agreement in the published literature, however, about whether the relationship between infection and sodium intake modifies risk of gastric cancer (Lee et al., 2003; Peleteiro et al., 2011). Taken together, the limitations in these studies precluded further evaluation. Although some evidence suggests that high sodium intake may be associated with increased

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SODIUM INTAKE AND HEALTH OUTCOMES 113 risk of gastric cancer, the committee found that evidence was not definitive for an effect at low intake ranges. Details about the design, characteristics, and outcomes for each of these studies are tabulated in Appendix F. ADDITIONAL HEALTH OUTCOMES In addition to the more commonly studied health outcomes above, the committee identified studies that examined outcomes related to ascites and reflux (Aanen et al., 2006; Gu et al., 2012; Nilsson et al., 2004), pul- monary function, including asthma and pulmonary hyperresponsiveness (Gotshall et al., 2004; Hirayama et al., 2010; Mickleborough et al., 2005; Sausenthaler et al., 2005), genitourinary symptoms, including kidney stone formation and urinary tract symptoms (Eisner et al., 2009; Maserejian et al., 2009; Meschi et al., 2012; Yun et al., 2010), depression (Song, 2009), and quality of life (Ramirez et al., 2004). The studies identified were incon- sistent in methodological approach and results and, for the majority of spe- cific outcomes, only one study was found for a given outcome. For example, although three studies addressed the potential association of sodium dietary intake and stone formation (Eisner et al., 2009; Meschi et al., 2012; Yun et al., 2010), the results were inconsistent. Meschi et al. (2012) found a positive correlation between sodium intake and calcium nephrolithiasis in a retrospective study of Italian women and Yun et al. (2010) found that in a cohort of stone formers, those with hypernatriuresis were more likely to develop stones in 3-year follow-up. The role of sodium intake in the risk of stone formation is not clear, and some authors suggest that while an increase in dietary sodium intake might increase urine calcium, it also might increase urine volume and decrease the urinary supersaturation of calcium oxalate (Eisner et al., 2009). In addition, these studies mirror many of the limitations of other studies reviewed in this chapter, including inconsistent and inadequate sodium intake assessment. Although the evidence was insuf- ficient for the committee to draw conclusions about associations between sodium intake and these health outcomes it recognizes that other studies are ongoing and may be useful in the future. REFERENCES Aanen, M. C., A. J. Bredenoord, and A. J. P. M. Smout. 2006. Effect of dietary sodium chlo- ride on gastro-oesophageal reflux: A randomized controlled trial. Scandinavian Journal of Gastroenterology 41(10):1141-1146. AHA (American Heart Association). 2011. Classes of heart failure. http://www.heart.org/ HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_ UCM_306328_Article.jsp (accessed March 15, 2013).

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