Authors

  1. Kelly, Jaimon BSc
  2. Khalesi, Saman MSc
  3. Dickinson, Kacie APD, PhD, BNutDiet (Hons)
  4. Hines, Sonia RN, BN, GradDipEd
  5. Coombes, Jeff AEP, PhD, BAppSc, BEd (Hons), MEd
  6. Todd, Alwyn APD, PhD, PGDipDiet, BSc

Abstract

Review question/objective: The objective of this review is to establish the effect of modifying dietary sodium intake in normotensive subjects.

 

More specifically, the objectives are to identify the effect of reducing or increasing sodium intake on blood pressure in normotensive subjects with systolic blood pressure (SBP) <140mmHg, and the effect of sodium reduction or supplementation on arterial function in subjects with baseline SBP <140mmHg.

 

Background: The pressure-natriuresis relationship that was first described by Guyton1 proposes a link between dietary sodium intake and renal sodium handling. Specifically, the hypothesis states that in a normal individual, consumption of a dietary sodium load will elicit a transient rise in blood pressure that stimulates the kidney to excrete sodium. The kidney will excrete excess sodium leading to restoration of normal blood pressure. This hypothesis explains how blood pressure is maintained over the longer term even though most individuals report day-to-day variation in sodium intake.1,2

 

Following this hypothesis, intervention studies in normotensive subjects may be expected to observe a small amount of variation in blood pressure with changes to dietary sodium intake, but this variation should be small enough to be considered clinically irrelevant. Intervention studies examining the effect of dietary sodium have reported a range of different responses from significant changes,3,4 to mild, to moderate effects on blood pressure to no effect at all.5,6 Normotensive studies that report blood pressure changes over the long-term have previously documented changes in systolic blood pressure (SBP) ranging from -1mmHg7 to increases of 8.2mmHg.4

 

Previous systematic reviews of blood pressure response to dietary sodium restriction have used Cochrane Collaboration methods.8-10 One such systematic review9 has been cited over 370 times, and has been used in the development of dietary guidelines.11 Two of these reviews attempted to conduct meta-analysis by dividing subjects into normotensive and hypertensive sub-groups.8,9 Both reviews failed to specify methods for determining whether studies recruited hypertensive or normotensive subjects and included some studies in the normotensive analyses with subjects who had baseline blood pressures above 140mmHg. Due to this, a wide range of baseline blood pressure readings and responses can be observed in normotensive analyses, which is inconsistent with Guyton's pressure natriuresis hypothesis. Therefore, the validity of the findings for blood pressure changes in healthy normotensive individuals in these analyses is limited in that the majority of the included studies recruited subjects with SBP above 140mmHg.4,12-16 Subjects with hypertension (SBP >140mmHg) have been shown to respond differently to dietary sodium and hence inclusion of these studies in previous normotensive analyses may have skewed the results.9 These analyses in "normotensive" populations could be improved if studies that recruited subjects with SBP >140mmHg were excluded.

 

As well as examining blood pressure, a number of intervention studies have investigated the effects of dietary sodium intake on arterial function and found that these effects may be, at least partly, independent of blood pressure.17,18 As these effects may be key in extending our understanding of sodium intake and disease risk, they form part of the bigger picture for dietary sodium intake and chronic disease risk. It is therefore important to consider data on arterial function such as pulse wave analysis, pulse wave velocity, and flow mediated dilation in future meta-analyses of sodium restriction.

 

There is enough evidence from normotensive studies conducted in subjects with SBP<=140mmHg to conduct a separate investigation of the effects on blood pressure and arterial function. This systematic review will consider the evidence for long-term dietary sodium restriction in subjects with SBP <140mmHg on arterial function.

 

Article Content

Inclusion criteria

Types of participants

This review will consider studies that include adult subjects with systolic blood pressure <140mmHg and studies conducted in community settings (for example, free living populations) and controlled conditions (for example, metabolic ward, hospital and study centre).

 

This review will exclude studies that include subjects prescribed antihypertensive or vasoactive medications.

 

Types of interventions

This review will consider studies that evaluate dietary sodium intake for equal to or greater than four weeks duration.

 

This review will consider studies that include two study arms comprising of different levels of sodium intake.

 

This review will consider studies that modify sodium intake via dietary modification, salt reduction, and/or salt supplementation.

 

Types of outcomes

 

This review will consider studies that include the following outcome measures: systolic blood pressure, diastolic blood pressure, pulse wave velocity, pulse wave analysis, and flow mediated dilatation by Doppler ultrasound.

 

Types of studies

This review will consider any experimental study design including randomized controlled trials and non-randomized controlled trials for inclusion.

 

Search strategy

The search strategy aims to find both published and unpublished studies. A three step search strategy will be utilized in this review. An initial limited search of MEDLINE and CINAHL will be undertaken followed by analysis of the text words contained in the title and abstract and of the index terms used to describe the article. A second search using all identified keywords and index terms will then be undertaken across all included databases. Thirdly, the reference list of all identified reports and articles will be searched for additional studies. Studies published in any language will be considered for inclusion in this review, non-English publications will be translated to English. Studies published between 1980 and the present day will be considered for inclusion in this review.

 

The databases to be searched include:

 

Medline, CINAHL, ProQuest, EMBASE, Wiley InterScience, Scopus, Cochrane Library, Australia and New Zealand Clinical Trials Registry, ClinicalTrials.gov, ISRCTN, World Health Organisation International Clinical Trials Registry PlatformThe search for unpublished studies will include:

 

Proquest Dissertations and Theses Database, Dissertations and Theses International, Mednar, OpenSIGLE, EAGLE

 

Initial keywords to be used will be:

 

sodium, salt, blood pressure, normotens*, systolic, diastolic, pulse wave, controlled, endothelial function

 

Assessment of methodological quality

Papers selected for retrieval will be assessed by two independent reviewers for methodological validity prior to inclusion in the review using the standardized critical appraisal instrument, the Joanna Briggs Institute Meta-Analysis of Statistics Assessment and Review Instrument (JBI-MAStARI) (Appendix I). Any disagreements that arise between the reviewers will be resolved through discussion or through third reviewer. Where a paper lacks sufficient detail to determine if it is suitable for inclusion an attempt to contact the authors of the study and retrieve information will be made.

 

Data collection

Data will be extracted from papers included in the review using the standardized data extraction tool from JBI-MAStARI (Appendix II). The data extracted independently by two reviewers (JK and SK) and will include specific details about the interventions, populations, study methods and outcomes of significance to the review question and specific objectives.

 

Data synthesis

Quantitative data will, where possible, be pooled in statistical meta-analysis using JBI-MAStARI. All results will be subject to double data entry. Effect sizes, expressed as odds ratio (for categorical data) and weighted mean differences (for continuous data), and their 95% confidence intervals will be calculated for analysis. Heterogeneity will be assessed statistically using the standard Chi square. Where statistical pooling is not possible the findings will be presented in narrative form including tables and figures to aid in data presentation where appropriate. Sensitivity analysis will be conducted if the results of an individual study appear to be heterogeneous with the results of other included studies, or when the methodology of included studies may present an element of bias in the context of this review for example when studies exclude subjects who should otherwise be included if this was an original research study of "normotensive' subjects). Sub-group analyses will be undertaken on studies recruiting subjects with SBP <130mmHg, studies achieving a 40mmol or greater reduction in urinary sodium excretion, studies conducted in subjects of different ethnicities, and studies conducted in those with and without a diagnosis of diabetes.

 

Conflicts of interest

Nil

 

References

 

1 Guyton A. The surprising kidney-fluid mechanism for pressure control-its infinite gain! Hypertension. 1990; 16(6): 725-30. [Context Link]

 

2 Guyton AC. Blood pressure control-special role of the kidneys and body fluids. Science. 1991; 252(5014): 1813-6. [Context Link]

 

3 Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med. 2001; 344(1): 3-10. [Context Link]

 

4 Cappuccio FP, Markandu ND, Carney C, Sagnella GA, MacGregor GA. Double-blind randomised trial of modest salt restriction in older people. Lancet. 1997; 350(9081): 850-4. [Context Link]

 

5 Todd AS, Macginley RJ, Schollum JB, Williams SM, Sutherland WH, Mann JI, et al. Dietary sodium loading in normotensive healthy volunteers does not increase arterial vascular reactivity or blood pressure. Nephrology. 2012; 17(3): 249-56. [Context Link]

 

6 Ruppert M, Overlack A, Kolloch R, Kraft K, Gobel B, Stumpe KO. Neurohormonal and metabolic effects of severe and moderate salt restriction in non-obese normotensive adults. J Hypertens. 1993; 11(7): 743-9. [Context Link]

 

7 The Trials of Hypertension Prevention Collaborative Research Group. Effects of weight loss and sodium reduction intervention on blood pressure and hypertension incidence in overweight people with high-normal blood pressure. The Trials of Hypertension Prevention, phase II. Arch Intern Med. 1997; 157(6): 657-67. [Context Link]

 

8 Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev. 2011; 9(11). [Context Link]

 

9 He FJ, Li J, Macgregor GA. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials. BMJ. 2013; 3(346). [Context Link]

 

10 Aburto NJ, Ziolkovska A, Hooper L, Elliott P, Cappuccio FP, Meerpohl JJ. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013; 3(346). [Context Link]

 

11 National Health and Medical Research Council. Australian Dietary Guidelines. Canberra: National Health and Medical Research Council; 2013. [Context Link]

 

12 Mascioli S, Grimm R, Launer C, Svendsen K, Flack J, Gonzalez N, et al. Sodium chloride raises blood pressure in normotensive subjects. The study of sodium and blood pressure. Hypertension. 1991; 17(1 Suppl): I21. [Context Link]

 

13 Puska P, Iacono JM, Nissinen A, Korhonen HJ, Vartianinen E, Pietinen P, et al. Controlled, randomised trial of the effect of dietary fat on blood pressure. Lancet. 1983; 1(8314-5): 1-5. [Context Link]

 

14 Schorr U, Distler A, Sharma AM. Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial. J Hypertens. 1996; 14(1): 131-5. [Context Link]

 

15 Watt GC, Foy CJ, Hart JT, Bingham G, Edwards C, Hart M, et al. Dietary sodium and arterial blood pressure: evidence against genetic susceptibility. BMJ. 1985; 291(6508): 1525-8. [Context Link]

 

16 Cobiac L, Nestel PJ, Wing LM, Howe PR. A low-sodium diet supplemented with fish oil lowers blood pressure in the elderly. J Hypertens. 1992; 10(1): 87-92. [Context Link]

 

17 Todd AS, Macginley RJ, Schollum JB, Johnson RJ, Williams SM, Sutherland WH, et al. Dietary salt loading impairs arterial vascular reactivity. Am J Clin Nutr. 2010; 91(3): 557-64. [Context Link]

 

18 Dickinson KM, Keogh JB, Clifton PM. Effects of a low-salt diet on flow-mediated dilatation in humans. Am J Clin Nutr. 2009; 89(2): 485-90. [Context Link]

Appendix I: Appraisal instruments

 

MAStARI appraisal instrument[Context Link]

Appendix II: Data extraction instruments

 

MAStARI data extraction instrument[Context Link]

 

Keywords: sodium; salt; blood pressure; normotens*; systolic; diastolic; pulse wave; controlled; endothelial function