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Structured Abstract
Objectives:
This systematic review synthesized the evidence regarding the effects of interventions to decrease sodium intake or increase potassium intake on cardiovascular and renal disease outcomes and related risk factors, as well as evidence from prospective cohort studies on the associations between sodium, potassium, or sodium to potassium ratio and these outcomes. The purpose of the review is to provide a future Dietary Reference Intakes (DRI) Committee with the evidence on chronic disease endpoints for consideration in reviewing the DRIs for sodium and potassium.
Data sources:
PubMed®, Embase®, the Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, CINAHL®, Web of Science, references of prior reviews, hand searches of gray literature, and expert recommendations.
Review methods:
Two reviewers independently screened citations and full-text publications. Eligible studies included randomized controlled trials (RCTs), nonrandomized controlled trials, and prospective observational studies published through 2017 that enrolled healthy populations or those with pre-existing hypertension, cardiovascular disease (CVD), diabetes, or obesity and that assessed blood pressure (BP), incident hypertension, achievement of prespecified blood pressure goals, all-cause mortality, CVD morbidity and mortality, coronary heart disease morbidity and mortality, stroke, myocardial infarction, renal morbidity and mortality, kidney stones, and adverse events. We extracted data, assessed risk of bias (RoB, or study quality), summarized and synthesized results, and evaluated the strength of the evidence (SoE) supporting the conclusions separately for conclusions based on controlled trials and those based on prospective cohort studies.
Results:
We identified 15,912 unique citations, of which 257 publications reporting on 171 studies were deemed eligible for the review.
Moderate-strength evidence from 48 RCTs supports a significant BP-lowering effect of dietary sodium reduction in adults (e.g., a decrease of 3.23 mm Hg [95% confidence interval 2.41 to 4.06] in systolic blood pressure with a 42 mmol weighted mean decrease in sodium intake), but sodium reduction interventions do not appear to show statistically significant effects on BP in children (low SoE). Comparing the findings of studies of adults with hypertension with those in adults with normal BP showed that sodium reduction has a greater BP-lowering effect in adults with hypertension than in normotensive adults (moderate SoE). Sodium reduction may also increase the proportion of study participants who achieve a prespecified BP goal (low SoE), but the evidence is unclear regarding the effect of reducing sodium intake on the incidence of hypertension (because of the small number of trials). Prospective cohort studies suggest an association between lower urinary sodium excretion and reduced risk for hypertension (low SoE because of high RoB and lack of consistency).
Only a small number of RCTs assessed the effects of sodium reduction on longer term chronic disease outcomes: Sodium reduction decreased the risk for the combined outcome of CVD mortality/morbidity and a composite outcome of any CVD events (low SoE). Although sodium levels appear to be associated with all-cause mortality (low SoE), the shape of this relationship could not be determined (insufficient SoE), and evidence from prospective cohort studies was insufficient to draw conclusions regarding associations with combined CVD morbidity/mortality and stroke risk.
Use of potassium salt substitutes in place of sodium chloride and increasing potassium intake itself through the use of supplements significantly decrease BP (moderate SoE), but evidence is insufficient to assess their effect on risk for hypertension, kidney stones, or longer term outcomes, including all-cause mortality or CVD, stroke, or renal morbidity or mortality, or the potential moderating effects of other factors, and whether these effects are moderated by changes in sodium intake. Evidence from prospective cohort studies suggests potassium intake may be associated with decreased risk for kidney stones but is insufficient to assess associations of potassium intake with other outcomes of interest.
Conclusions:
Reducing sodium intake, increasing potassium intake, and use of potassium-containing salt substitutes in the diet significantly decrease BP, particularly among those with hypertension. Limited evidence also suggests that sodium intake is associated with risk for all-cause mortality, and that reducing sodium intake may decrease the risk for CVD morbidity and mortality.
Contents
- Key Messages
- Preface
- Acknowledgments
- Technical Expert Panel
- Peer Reviewers
- Evidence Summary
- Introduction
- Methods
- Criteria for Inclusion/Exclusion of Studies in the Review
- Other Exclusions Applying to All Key Questions
- Searching for the Evidence
- Data Abstraction and Data Management
- Assessment of Methodological Risk of Bias of Individual Studies
- Data Synthesis/Analysis
- Grading the Strength of Evidence (SoE) for Major Comparisons and Outcomes
- Assessing Applicability
- Peer Review and Public Commentary
- Results
- Introduction
- Results of Literature Searches
- Key Question 1. Effect of Interventions To Reduce Sodium Intake on Blood Pressure
- Key Question 1b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 1c. Subpopulations Defined by Hypertension, Diabetes, and Obesity Health Status
- Key Question 1a. Effect of Other Minerals on Effect of Sodium (Reduction)
- Key Question 2. Association Between Sodium Intake and Blood Pressure
- Key Question 2a. Subpopulations Defined by Sex, Race/Ethnicity, and Age
- Key Question 2b. Subpopulations Defined by Hypertension, Diabetes, and Obesity Health Status
- Key Question 3. Effects of Interventions To Reduce Sodium Intake on CVD and Kidney Disease Morbidity and Mortality, and on Total Mortality, in Adults
- Key Question 3b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 3c. Subpopulations Defined by Hypertension, Diabetes, Obesity, and Renal Health Status
- Key Question 3a. Effect of Other Minerals on Effect of Sodium
- Key Question 4. Association Between Sodium Intake and CVD, CHD, Stroke, and Kidney Disease Morbidity and Mortality, and Between Sodium Intake and Total Mortality, Among Adults
- Key Question 4a. Effect of Other Minerals on Association With Sodium
- Key Question 4b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 4c. Subpopulations Defined by Hypertension, Diabetes, Obesity, and Renal Health Status
- Key Question 5. Effect of Interventions To Increase Potassium Intake on Blood Pressure and Kidney Stone Formation
- Key Question 5b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 5c. Subpopulations Defined by Hypertension, Diabetes, Obesity, and Renal Health Status
- Key Question 5a. Effect of Other Minerals on Effect of Potassium
- Key Question 6. Association Between Potassium Intake and Blood Pressure and Kidney Stone Formation
- Key Question 6a. Subpopulations Defined by Sex, Race/Ethnicity, and Age
- Key Question 6b. Subpopulations Defined by Hypertension, Diabetes, and Obesity Health Status
- Key Question 7. Effect of Interventions To Increase Potassium Intake on CVD and Kidney Disease Morbidity and Mortality, and on Total Mortality, Among Adults
- Key Question 7a. Effect of Other Minerals on Effect of Potassium
- Key Question 7b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 7c. Subpopulations Defined by Hypertension, Diabetes, Obesity, and Renal Health Status
- Key Question 8. Association Between Dietary Potassium Intake and CVD, CHD, Stroke, and Kidney Disease Morbidity and Mortality, and Between Dietary Potassium and Total Mortality, Among Adults
- Key Question 8a. Effect of Other Minerals on Potassium
- Key Question 8b. Subpopulations Defined by Sex, Race/Ethnicity, Age, and Reproductive Status (for Women)
- Key Question 8c. Subpopulations Defined by Hypertension, Diabetes, and Obesity Health Status
- Discussion
- References
- Abbreviations/Acronyms
- Appendix A. Search Methodology
- Appendix B. List of Excluded Studies
- Appendix C. Evidence Tables for All Included Studies
- Appendix D. Subgroup Tables for All Included Studies
- Appendix E. Quality of Included Studies
- Appendix F. Strength of Evidence
- Appendix G. List of Systematic Reviews Reference Mined
- Appendix H. Results From the Observational Studies (Key Question 4)
- Appendix I. Sensitivity Analyses Removing High and Unclear Risk of Bias Studies
Suggested citation:
Newberry SJ, Chung M, Anderson CAM, Chen C, Fu Z, Tang A, Zhao N, Booth M, Marks J, Hollands S, Motala A, Larkin JK, Shanman R, Hempel S. Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and Risks. Comparative Effectiveness Review No. 206. (Prepared by the RAND Southern California Evidence-based Practice Center under Contract No. 290-2015-00010-I.) AHRQ Publication No. 18-EHC009-EF. Rockville, MD: Agency for Healthcare Research and Quality; June 2018. Posted final reports are located on the Effective Health Care Program search page. DOI: https://doi.org/10.23970/AHRQEPCCER206.
This report is based on research conducted by the RAND Southern California Evidence-based Practice Center under contract to the Agency for Healthcare Research and Quality (AHRQ), Rockville, MD (Contract No. 290-2015-00010-I). The findings and conclusions in this document are those of the authors, who are responsible for its contents; the findings and conclusions do not necessarily represent the views of AHRQ. Therefore, no statement in this report should be construed as an official position of AHRQ or of the U.S. Department of Health and Human Services.
None of the investigators have any affiliations or financial involvement that conflicts with the material presented in this report.
The information in this report is intended to help health care decisionmakers—patients and clinicians, health system leaders, and policymakers, among others—make well informed decisions and thereby improve the quality of health care services. This report is not intended to be a substitute for the application of clinical judgment. Anyone who makes decisions concerning the provision of clinical care should consider this report in the same way as any medical reference and in conjunction with all other pertinent information, i.e., in the context of available resources and circumstances presented by individual patients.
This report is made available to the public under the terms of a licensing agreement between the author and the Agency for Healthcare Research and Quality. This report may be used and reprinted without permission except those copyrighted materials that are clearly noted in the report. Further reproduction of those copyrighted materials is prohibited without the express permission of copyright holders.
AHRQ or U.S. Department of Health and Human Services endorsement of any derivative products that may be developed from this report, such as clinical practice guidelines, other quality enhancement tools, or reimbursement or coverage policies, may not be stated or implied.
This report may periodically be assessed for the currency of conclusions. If an assessment is done, the resulting surveillance report describing the methodology and findings will be found on the Effective Health Care Program Web site at www.effectivehealthcare.ahrq.gov. Search on the title of the report.
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