Hypertension Journal

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Salt Intake and Blood Pressure Levels:Is the Concept Valid?
Salt Intake and Blood Pressure Levels:
Is the Concept Valid?
1R Chandni, 2Uday M Jadhav
1Additional Professor, 2Consultant
1Department of General Medicine, Government Medical CollegeKozhikode, Kerala, India
2Department of Cardiology, MGM New Bombay Hospital, NaviMumbai, Maharashtra, India
Correspondence Author: R Chandni, Additional ProfessorDepartment of General Medicine, Government Medical CollegeKozhikode, Kerala, India
Phone: +919447202748
e-mail: chandnidr@gmail.com
Globally, sodium intake has increased over the years, and it isseen in all ages, both genders, and in various ethnic groupsincluding Indians. High dietary salt is a major contributor tothe increasing incidence of hypertension, with an estimated30% of hypertension attributed to high salt intake. Salt intakein the developed countries largely comes from prepackagedand processed foods, shelf-stable food, and bakery items.In the Asian communities, the contributing source is in theform of added table salt and in cooking. Sodium balance ismaintained by increasing the arterial blood pressure, resultingin a pressure natriuresis and increased urinary sodiumexcretion in the presence of high sodium chloride intake.Low sodium intake to less than 3 gm/day leads to activationof renin-angiotensin-aldosterone system.
Recently, there have been reports about the deleteriouseffects of low blood sodium, and there is recognition of theconcept of a J-shaped curve. Weak research methodologieswith the use of methods like single spot urine samples andsingle 24-hour urine sodium excretion to estimate usual saltintake have been likely to influence the J curve in the studiesso far. In this context, two trials were undertaken in Trials ofHypertension Prevention (TOHP), which implemented sodiumreduction. There was no evidence of a J-shaped or nonlinearrelationship, and direct relationship with total mortality wasdemonstrated even at the lowest levels of sodium intake andconsistent with a benefit of reduced sodium and sodium/potassium intake on total mortality over a 20-year period.
This review summarizes an overview of current understandingof the concept of salt in hypertension. Dietary sodium isthe most accepted and time-tested intervention in preventionand treatment of hypertension, which needs to be implementedbut with an unresolved issue of more aggressive salt intakereduction on cardiovascular events.
Keywords: Blood pressure, Hypertension, Salt, Sodium chloride.
How to cite this article: Chandni R, Jadhav UM. Salt Intakeand Blood Pressure Levels: Is the Concept Valid? HypertensJ 2017;3(1):7-11.
Source of support: Nil
Conflict of interest: Nil


Salt has been of historic value from ancient days whenused for preserving food and meat, for trade and taxes,and played a role in rebellions and wars. High dietarysalt is a major contributor to the increasing incidence ofhypertension, with an estimated 30% of hypertensionattributed to high salt intake. Increased blood pressureand reducing dietary salt is estimated to be one of themost effective strategies to improve nation's health.1 Overthe years, the dietary sodium intake has increased from1 gm/day in the era of hunter gatherers to 9 to 12 gm/dayin the population of today's world. The World HealthOrganization recommends a maximum intake of 2 gmper day and a 30% reduction in population sodium intakeby 2025.2

An average intake of salt per adult is approximately10 gm/day (sodium 4,000 mg/day), with reported higherintakes in the Asian continent.3 Salt intake in the developedcountries largely comes from prepackaged andprocessed foods, shelf-stable food, and bakery items. Inthe Asian communities, the contributing source is discretionaryin the form of added table salt and in cooking.The nutritional transition in the third world countrieswith globalization of the food industry will increase thesalt burden in processed foods.4,5

Using a validated food frequency questionnaire,dietary profiles of 6,907 adults aged ≥20 years, from acluster of 42 villages in Kancheepuram district of TamilNadu State in Southern India, were assessed. More thanhalf (57.1%) exceeded the limit of salt intake.6


Sodium intake around the world is well in excess ofphysiological need (i.e., 10-20 mmol/day). Most adultpopulations have mean sodium intake >100 mmol/day,and for many (particularly the Asian countries) meanintake is >200 mmol/day.7 Human dietary salt intake hasincreased tenfold over the last few hundred years.8,9 Insodium-deficient states, salt consumption is driven by saltappetite - an innate and motivated behavioral responsethat drives a human or animal to seek and ingest saltcontainingfoods and fluids.10-12 Salt appetite is a statewhere normally aversive concentration of salt is readilyconsumed. Many animals have evolved specializedmechanisms for detecting and ameliorating deficits in body sodium. However, under usual circumstances, theambient salt diet is in excess of physiological need, andin humans, it has been difficult to distinguish innate saltappetite and salt need from salt preference.13 The hungerfor salt is also influenced by taste, culture, social custom,the widespread availability of salt, and habit independentof the need for salt.14 Heterogeneity exists in the humanblood pressure response to alterations in sodium andextracellular fluid balance and the mechanisms that havebeen invoked for them.3

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R Chandni, Uday M Jadhav


Reducing dietary salt has been shown to lower bloodpressure and the risk of cardiovascular disease (CVD).3,4,Salt has the potential to increase arterial pressurethrough various neural, endocrine/paracrine, and vascularmechanisms.4 When there is a high NaCl intake,sodium balance is maintained by increasing the arterialblood pressure, resulting in a pressure natriuresis andurinary sodium excretion increases. The physiologicalconsequence of low sodium intake to less than 3 gm/dayis activation of renin-angiotensin-aldosterone system.Interestingly, hyperinsulinemic state also stimulatesthe resorption of sodium,8 and glycemia contributes toan sustained antinatriuretic action of insulin. This mayhave relevance in the developing countries with highprevalence for diabetes.

The role of sodium in CVD and salt restriction in themanagement of hypertension has become a little controversialin recent times, and it has been pointed in somestudies that stringent salt restriction may be detrimental.Data from 23 cohort studies and 2 follow-up studies ofrandomized controlled trials concluded that both low andhigh sodium intakes are associated with increased mortality,consistent with a U-shaped association betweensodium intake and health outcomes. The hazard ratios(HRs) of total mortality and CVD for low vs usual sodiumintake were 1.10 [confidence interval (CI), 1.01-1.22] and1.11 (CI, 1.01-1.22) respectively. The corresponding HRsfor high vs usual sodium exposure were 1.16 (1.03-1.30)and 1.12 (1.02-1.24).5 Moreover, 24-hour collection ofurine is considered to be the best assessment of salt intake, and a high sodium intake is typically defined by urinarysodium excretion of more than 150 mmol per day.
The study by Graudal et al5 extends 2013 Instituteof Medicine report by identifying a specific range ofsodium intake (2645-4945 mg) associated with the mostfavorable health outcomes, within which variation insodium intake is not associated with variation in mortality(Table 1).


Large body of observational studies is increasinglycomplemented by well-designed randomized trials thathave shown the benefits of lower salt intake.18

Dietary Approaches to Stop Hypertension
Sodium Trial19

This trial is the most often quoted trial for the effectof reduced sodium intake to very low levels less than1.5 gm/day over 30 days, adhering to low salt specifiedmeals. Despite being a small study, it effectively showeda blood pressure reduction.


This is a multicentric study of electrolyte excretion andblood pressure that reported blood pressure change of0.94/0.03 mm Hg/1 gm of 24-hour urinary sodium excretion.20 INTERSALT data also showed a correlation betweensalt consumption and the rise in blood pressure with age.INTERSALT failed to demonstrate a significant associationwhen the primitive societies of Yanomamo Indians andtribes in Africa with low life expectancy were excluded.

International Study on Micronutrient
and Blood Pressure (INTERMAP)

Lower salt intake and smaller sodium/potassium ratioresulted in lowering blood pressure in population.21


In the South Asian urban population, the mean dietarysalt intake (8.5 gm/day)22 was positively associated with hypertension on multiregression analysis. Reductionof 3 gm/day predicted a fall in blood pressure of 3.6 to5.6/1.9 to 3.2 mm Hg (systolic/diastolic) in hypertensivesand 1.8 to 3.5/0.8 to 1.8 mm Hg in normotensives.

Table 1: Guideline recommendations
Salt Intake and Blood Pressure Levels:Is the Concept Valid?
AHA: American Heart Association; ACC: American College of Cardiology; JNC: Joint National Committee

Salt Intake and Blood Pressure Levels: Is the Concept Valid?


For each 1 gm increase in mean sodium intake, systolicblood pressure increased by 2.63, 1.72, and 0.71 mm Hgfor sodium intakes of >5, 3 to 5, and < 3 gm/day respectively.23 The PURE study demonstrated a U-shaped curvefor salt intake and events.

In a prospective population study, involving 3,681participants without CVD, systolic blood pressure, butnot diastolic pressure, changes over time aligned withchange in sodium excretion, but this association didnot translate into a higher risk of hypertension or CVDcomplications. Lower sodium excretion was associatedwith higher CVD mortality.24

Coronary heart disease (CHD) policy model has beenused to quantify the benefits of potentially achievable,population-wide reductions in dietary salt of up to 3 gm(1200 mg of sodium) per day. Reducing dietary salt by3 gm per day is projected to reduce the annual number ofnew cases of CHD by 60,000 to 120,000, stroke by 32,000to 66,000, and myocardial infarction by 54,000 to 99,000and to reduce the annual number of deaths from anycause by 44,000 to 92,000. All segments of the populationwould benefit, with blacks benefiting proportionatelymore, women benefiting particularly from stroke reduction,older adults from reductions in CHD events, andyounger adults from lower mortality rates.25

  • Food and Salt Industry competing commercial financialinterests
  • Likelihood of study bias due to both random andsystematic errors of hidden sodium in processed foods
  • Day-to-day variation in diet may negatively impact a24-hour diet question chart
  • Reverse causation theory. Inclusion criteria in studiesinvolve subjects with existent diseases like diabetesmellitus and hypertension, who may consume lowsalt, which may influence morbidity and mortality
  • Weak research methodology with the use of methodslike single spot urine samples to estimate usual saltintake


In context with the above evidence limitations, twotrials, phase I (1987-1990), with 741 participants over 18 months, and phase II (1990-1995), with 2,382 participantsover 36 months, were undertaken in TOHP,which implemented sodium reduction but withoutcontrol intervention.26,27

Researchers estimated that three 24-hour collectionswould improve accuracy to 75% compared with sodiumingestion and that seven would be needed to improveaccuracy to 92%.

The Trials of Hypertension Prevention (TOHP) studyused up to seven excretion measurements from prehypertensiveadults 30 to 54 years of age. A total of 251 deathsoccurred, representing a nonsignificant 15% lower risk inthe active intervention (possibly due to insufficient power)as compared with 272 deaths in those not assigned to anactive sodium intervention. There was a linear associationbetween average sodium intake and mortality, with an HRof 0.75, 0.95, 1.00, and 1.07 (p trend ¼ 0.30) for < 2,300, 2,300to < 3,600, 3,600 to <4,800, and >4,800 mg/24 hour respectively;and with an HR of 1.12 per 1,000 mg/24 hours. Therewas no evidence of a J-shaped or nonlinear relationship.

The study concluded a direct relationship with totalmortality, even at the lowest levels of sodium intake andconsistent with a benefit of reduced sodium and sodium/potassium intake on total mortality over a 20-year period.The TOHP trial participants did not previously havecomorbid conditions like hypertension, diabetes, or CVD,and these reduced the problem of reverse causation.Evidence of the safety or efficacy of low sodium intake(< 2.3 gm/day) was not commented upon, as low sodiumintake was not achieved in the intervention group.

Recent studies have invited substantive controversyand have drawn significant criticism from the scientificcommunity for many limitations in research design andmethods, misinterpretation of study results, and potentialconflicts of interest of the authors.28 Uncertainties existson whether reducing sodium intake below 2300 mg/dayeither decreases or increases CVD risk in the general population.28 For these reasons, the World Hypertension Leagueand supporting organizations have made an urgent callfor quality research on salt intake and health and listedimportant issues that could be addressed in setting standardsfor research on sodium (salt) intake and health.29


Excess salt consumption leads to increase in blood pressure,which in turn increases the CVD and translatesto mortality. The lowering of salt intake from high tomoderate level is definitely beneficial in people withhypertension. The current available evidence does notsupport aggressive population-based strategies for lowsaltdiet. In this context, two trials were undertaken inTOHP, which implemented sodium reduction. Therewas no evidence of a J-shaped or nonlinear relationship and direct relationship with total mortality was demonstrated,even at the lowest levels of sodium intake andconsistent with a benefit of reduced sodium and sodium/potassium intake on total mortality over a 20-year period.
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R Chandni, Uday M Jadhav

Table 2: What is the existent knowledge?
Salt Intake and Blood Pressure Levels:Is the Concept Valid?

Larger studies comparing varying levels of salt intaketo blood pressure and CV outcome are needed to clarifyand understand the optimal sodium intake to preventCV events (Tables 2 and 3).

  1. Campbell NR, Neal BC, MacGregor GA. Interested in developinga national programme to reduce dietary salt? J HumHypertens 2011 Dec;25(12):705-710.
  2. Campbell NR, Lackland DT, Niebylski ML, Orias M,Redburn KA, Nilsson PM, Zhang XH, Burrell L, Horiuchi M,Poulter NR. 2016 dietary salt fact sheet and call to action: theWorld Hypertension League, International Society of Hypertension,and the International Council of CardiovascularPrevention and Rehabilitation. J Clin Hypertens (Greenwich)2016 Nov;18(11):1082-1085.
  3. Panel on Dietary Reference Intakes for Electrolytes and Water,Standing Committee on the Scientific Evaluation of DietaryReference Intakes, Food and Nutrition Board, Institute ofMedicine. Dietary reference intakes for water, potassium,sodium, chloride, and sulfate. Washington, DC: NationalAcademies Press; 2005.
  4. Kotchen, TA. Hypertensive vascular disease. Harrison'sprinciples of internal medicine. 19th ed. New York: McGrawHill Education; 2015.
  5. Graudal N, Jurgens G, Baslund B, Alderman MH. Comparedwith usual sodium intake, low- and excessive-sodium dietsare associated with increased mortality: a meta-analysis. AmJ Hypertens 2014 Sep;27(9):1129-1137.
  6. Sowmya N, Lakshmipriya N, Arumugam K, Venkatachalam S,Vijayalakshmi P, Ruchi V, Geetha G, Anjana RM, Mohan V,Krishnaswamy K, et al. Comparison of dietary profile of arural south Indian population with the current dietary recommendationsfor prevention of non-communicable diseases(CURES 147). Indian J Med Res 2016 Jul;144(1):112-119.
  7. Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes aroundthe world: implications for public health. Int J Epidemiol 2009Jun;38(3):791-813.
  8. Lawes CM, Vander Hoorn S, Rodgers A. Global burden of bloodpressure-related disease, 2001. Lancet 2008 May;371(9623):1513-1518.

Table 3: What is new?
Salt Intake and Blood Pressure Levels:Is the Concept Valid?

  1. Eaton SB, Konner M. Paleolithic nutrition. A considerationof its nature and current implications. N Engl J Med 1985Jan;312(5):283-289.
  2. Daniels D, Fluharty SJ. Salt appetite: a neurohormonal viewpoint.Physiol Behav 2004 Apr;81(2):319-337.
  3. Morris MJ, Na ES, Johnson AK. Salt craving: the psychobiologyof pathogenic sodium intake. Physiol Behav 2008Aug;94(5):709-721.
  4. Leshem M. Biobehavior of the human love of salt. NeurosciBiobehav Rev 2009 Jan;33(1):1-17.
  5. Weinberger MH. Salt sensitivity of blood pressure in humans.Hypertension 1996 Mar;27(3 Pt 2):481-490.
  6. He FJ, MacGregor GA. Effect of longer-term modest saltreduction on blood pressure. Cochrane Database Syst Rev2004;(3):CD004937.
  7. World Health Organization. Sodium intake for adults andchildren. Geneva, World Health Organization (WHO), 2012.Available from: http://www.who.int/nutrition/publications/guidelines/sodium_intake_printversion.pdf last accessed on10/02/2017.
  8. Eckel RH, Jakicic JM, Ard JD, Hubbard VS, de Jesus JM, Lee IM,Lichtenstein AH, Loria CM, Millen BE, Miller NM, et al. 2013AHA/ACC guideline on lifestyle management to reducecardiovascular risk. Available from: http://circ.ahajournals.org/content/129/25_suppl_2/S76.full.pdf
  9. James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, Lackland DT, LeFevre ML,MacKenzie TD, Ogedegbe O, et al. 2014 evidence-based guidelinefor the management of high blood pressure in adults:report from the panel members appointed to the Eighth JointNational Committee (JNC 8). JAMA 2014 Feb;311(5):507-520.
  10. He FJ, Li J, Macgregor GA. Effect of longer term modest saltreduction on blood pressure: Cochrane systematic review andmeta-analysis of randomised trials. BMJ 2013 Apr;346:f1325.
  11. He FJ, MacGregor GA. How far should salt intake be reduced?Hypertension 2003 Dec;42(6):1093-1099.
  12. INTERSALT: an international study of electrolyte excretionand blood pressure. Results for 24 hour urinary sodium andpotassium excretion. Intersalt Cooperative Research Group.BMJ 1988 Jul;297(6644):319-328.
  13. Stamler J, Elliott P, Dennis B, Dyer AR, Kesteloot H, Liu K,Ueshima H, Zhou BF; INTERMAP Research Group. INTERMAP:background, aims, design, methods, and descriptivestatistics (nondietary). J Hum Hypertens 2003 Sep;17(9):591-608.
  14. Radhika G, Sathya RM, Sudha V, Ganesan A, Mohan V.Dietary salt intake and hypertension in an urban south Indian population - [CURES - 53]. J Assoc Physicians India2007 Jun;55:405-411.


Salt Intake and Blood Pressure Levels: Is the Concept Valid?

  1. Mente A, O'Donnell MJ, Rangarajan S, McQueen MJ, Poirier P,Wielgosz A, Morrison H, Li W, Wang X, Di C, et al; PUREInvestigators. Association of urinary sodium and potassiumexcretion with blood pressure. N Engl J Med 2014 Aug;371(7):601-611.
  2. Stolarz-Skrzypek K, Kuznetsova T, Thijs L, Tikhonoff V,Seidlerova J, Richart T, Jin Y, Olszanecka A, Malyutina S,Casiglia E, et al; European Project on Genes in Hypertension(EPOGH) Investigators. Fatal and nonfatal outcomes,incidence of hypertension, and blood pressure changesin relation to urinary sodium excretion. JAMA 2011 May4;305(17):1777-1785.
  3. Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A,Lightwood JM, Pletcher MJ, Goldman L. Projected effect of dietary salt reductions on future cardiovascular disease.N Engl J Med 2010 Feb;362(7):590-599.

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  3. Institute of Medicine. Sodium intake in populations: assessmentof evidence. Washington, DC: National Academies Press; 2013.
  4. Campbell NR, Appel LJ, Cappuccio FP, Correa-Rotter R,Hankey GJ, Lackland DT, MacGregor G, Neal B, Niebylski ML,Webster J, et al. Policy Statement from The World HypertensionLeague. A call for quality research on salt intake and health:from the World Hypertension League and supporting organizations.J Clin Hypertens (Greenwich) 2014 Jul;16(7):469-471.

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