Salt and cardiovascular disease

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Salt consumption has been extensively studied for its role in human physiology and impact on human health. Chronic, high intake of dietary salt consumption is associated with hypertension and cardiovascular disease, in addition to other adverse health outcomes.[1][2][3] Major health and scientific organizations, such as the World Health Organization, US Centers for Disease Control and Prevention, and American Heart Association, have established high salt consumption as a major risk factor for cardiovascular diseases and stroke.[4][5][6] Common edible salt is the chemical compound known as sodium chloride.[7]

Effect of salt on blood pressure

Table salt

The human body has evolved to balance salt intake with need through means such as the renin–angiotensin system. In humans, salt has important biological functions. Relevant to risk of cardiovascular disease, salt is highly involved with the maintenance of body fluid volume, including osmotic balance in the blood, extracellular and intracellular fluids, and resting membrane potential.[8]

The well known effect of sodium on blood pressure can be explained by comparing blood to a solution with its salinity changed by ingested salt. Artery walls are analogous to a selectively permeable membrane, and they allow solutes, including sodium and chloride, to pass through (or not), depending on osmosis.[citation needed]

Circulating water and solutes in the body maintain blood pressure in the blood, as well as other functions such as regulation of body temperature. When salt is ingested, it is dissolved in the blood as two separate ions – Na+ and Cl. The water potential in blood will decrease due to the increase solutes, and blood osmotic pressure will increase. While the kidney reacts to excrete excess sodium and chloride in the body, water retention causes blood pressure to increase.[9]

DASH-Sodium study

The DASH-Sodium study was a sequel to the original DASH (Dietary Approaches to Stop Hypertension) study. Both studies were designed and conducted by the National Heart, Lung, and Blood Institute in the United States, each involving a large, randomized sample.[10] While the original study was designed to test the effects of several varying nutrients on blood pressure, DASH-Sodium varies only in salt content in the diet.[11]

Participants were pre-hypertensive or at stage 1 hypertension, and either ate a DASH-Diet or a diet reflecting an "average American Diet". During the intervention phase, participants ate their assigned diets containing three distinct levels of sodium in random order. Their blood pressure is monitored during the control period, and at all three intervention phases.[11]

The study concluded that the effect of a reduced dietary sodium intake alone on blood pressure is substantial, and that the largest decrease in blood pressure occurred in those eating the DASH eating plan at the lowest sodium level (1,500 milligrams per day).[11] However, this study is especially significant because participants in both the control and DASH diet group showed lowered blood pressure with decreased sodium alone.[10]

In agreement with studies regarding salt sensitivity, participants of African descent showed high reductions in blood pressure.[11]

Hypertension and cardiovascular disease

In 2018, the American Heart Association published an advisory stating that "if the U.S. population dropped its sodium intake to 1,500 mg/day, overall blood pressure could decrease by 25.6%, with an estimated $26.2 billion in health care savings. Another estimate projected that achieving this goal would reduce cardiovascular disease deaths by anywhere from 500,000 to nearly 1.2 million over the next decade."[12] There has been evidence from epidemiological studies, human and animal intervention experiments supporting the links between high rate of salt intake and hypertension.[2][13] A Cochrane review and meta-analysis of clinical trials showed that reduced sodium intake reduces blood pressure in hypertensive and normotensive subjects.[14][15] Since controlling hypertension is related to a reduced risk of cardiovascular disease, it is plausible that salt consumption is a risk factor for cardiovascular health.[16] However, to properly study the effects of sodium intake levels on risk of development of cardiovascular disease, long-term studies of large groups using both dietary and biochemical measures are necessary.[13]

As of 2019, major government research organizations, such as the US Centers for Disease Control and Prevention and the European Food Safety Authority, advise consumers to reduce their consumption of salt to lower the risk of cardiovascular diseases.[5][17] One 2016 review found that five studies were supportive of the evidence that reduced sodium intake lowers cardiovascular disease incidence and mortality, three contradicted this evidence, and two found insufficient evidence to reach a conclusion.[18] The survey found 27 primary studies and 106 letters in academic journals in support of the salt evidence, 34 primary studies and 51 letters contradicting the evidence, and 7 primary studies and 19 letters that were inconclusive.[18] There are several long-term studies which found that groups with sodium-reduced diets have lower incidences of cardiovascular disease in all demographics.[13]

Some researchers cast doubts on the link between lowering sodium intake and the health of a given population.[19]

Current trends and campaigns

Government regulatory agencies and clinical organizations, the European Food Safety Authority, the US Centers for Disease Control, and the American Heart Association recommend that consumers use less salt in their diets, mainly to reduce the risk of high blood pressure and associated cardiovascular diseases in adults and children.[2][5][12][17] The World Health Organization issued a 2016 fact sheet to encourage reducing global salt consumption by 30% through 2025.[4]

In 2015, the United States Centers for Disease Control and Prevention began an initiative encouraging Americans to reduce their consumption of salty foods.[20] The American Heart Association defined a daily sodium consumption limit of 1500 milligrams (contained in less than 0.75 teaspoon of table salt).[12][21]

According to a 2012 Health Canada report, Canadians in all age groups are consuming 3400 mg per day of sodium, more than twice as much as needed.[22] The US Centers for Disease Control and Prevention stated that the average daily sodium intake for Americans over 2 years of age is 3436 milligrams.[23] The majority of sodium consumed by North Americans is from processed and restaurant foods, while only a small portion is added during cooking or at the table.[20][24]

In the European Union, half of the member states legislated change in the form of taxation, mandatory nutrition labeling, and regulated nutrition and health claims to address overconsumption of sodium[25] in response to a 2012 EU Salt Reduction Framework.[26]

Sodium sensitivity

A diet high in sodium increases the risk of hypertension in people with sodium sensitivity, corresponding to an increase in health risks associated with hypertensions including cardiovascular disease.[27]

Unfortunately, there is no universal definition of sodium sensitivity; the method to assess sodium sensitivity varies from one study to another. In most studies, sodium sensitivity is defined as the change in mean blood pressure corresponding to a decrease or increase of sodium intake. The method to assess sodium sensitivity includes the measurement of circulating fluid volume and peripheral vascular resistance. Several studies have shown a relationship between sodium sensitivity and the increase of circulating fluid volume or peripheral vascular resistance.[28]

A number of factors have been found to be associated with sodium sensitivity. Demographic factors which affect sodium sensitivity include race, gender, and age.[29] One study shows that the American population of African descent are significantly more salt sensitive than Caucasians.[30] Women are found to be more sodium sensitive than men; one possible explanation is based on the fact that women have a tendency to consume more salt per unit weight, as women weigh less than men on average.[30] Several studies have shown that the increase in age is also associated with the occurrence of sodium sensitivity.[29]

The difference in genetic makeup and family history has a significant impact on salt sensitivity, and is being studied more with improvement on the efficiencies and techniques of genetic testing.[29] In both hypertensive and non-hypertensive individuals, those with haptoglobin 1-1 phenotype are more likely to have sodium sensitivity than people with haptoglobin 2-1 or 2-2 phenotypes. More specifically, haptoglobin 2-2 phenotypes contribute to the characteristic of sodium-resistance in humans.[31] Moreover, prevalence of a family history of hypertension is strongly linked with the occurrence of sodium sensitivity.[32]

The influence of physiological factors including renal function and insulin levels on sodium sensitivity are shown in various studies.[29] One study concludes that the effect of kidney failure on sodium sensitivity is substantial due to the contribution of decreasing the Glomerular filtration rate (GFR) in the kidney.[33] Moreover, insulin resistance is found to be related to sodium sensitivity; however, the actual mechanism is still unknown.[34]

Potassium and hypertension

Possible mechanisms by which high intakes of dietary potassium can decrease risk of hypertension and instances of cardiovascular disease have been proposed, but not extensively studied.[35] However, studies have found a strong inverse association between long-term adequate to high rates of potassium intake and the development of cardiovascular diseases.[35]

The recommended dietary intake of potassium is higher than that of sodium.[36] Unfortunately, the average absolute intake of potassium of studied populations is lower than that of sodium intake.[36] According to Statistics Canada in 2007, Canadians' potassium intake in all age groups was lower than recommended, while sodium intake greatly exceeded recommended intake in every age group.[37]

The ratio of potassium to sodium intake may account for the large difference in the occurrence of hypertension between primitive cultures eating diets made up of mostly unprocessed foods and Western diets which tend to include highly processed foods.[35]

Salt substitutes

The growing awareness of excessive sodium consumption in connection with hypertension and cardiovascular disease has increased the usage of salt substitutes at both a consumer and industrial level.[38]

On a consumer level, salt substitutes, which usually substitute a portion of sodium chloride content with potassium chloride, can be used to increase the potassium to sodium consumption ratio.[38] This change has been shown to blunt the effects of excess salt intake on hypertension and cardiovascular disease.[1][38] It has also been suggested that salt substitutes can be used to provide an essential portion of daily potassium intake, and may even be more economical than prescription potassium supplements.[39]

In the food industry, processes have been developed to create low-sodium versions of existing products.[40][41] The meat industry especially have developed and fine-tuned methods to decrease salt contents in processed meats without sacrificing consumer acceptance.[38] Research demonstrates that salt substitutes such as potassium chloride, and synergistic compounds such as phosphates, can be used to decrease salt content in meat products.[38]

There have been concerns with certain populations' use of potassium chloride as a substitute for salt as high potassium loads are dangerous for groups with diabetes, renal diseases, or heart failure.[38] The use of salts with minerals such as natural salts have also been tested, but like salt substitutes partially containing potassium, mineral salts produce a bitter taste above certain levels.[38]

See also


  1. 1.0 1.1 Barbara E Millen, Steve Abrams, Lucile Adams-Campbell, Cheryl AM Anderson, J Thomas Brenna, Wayne W Campbell, Steven Clinton, Frank Hu, Miriam Nelson, Marian L Neuhouser, Rafael Perez-Escamilla, Anna Maria Siega-Riz, Mary Story, Alice H Lichtenstein (2016). "The 2015 Dietary Guidelines Advisory Committee Scientific Report: Development and Major Conclusions". Adv Nutr. 7 (3): 438–444. doi:10.3945/an.116.012120. PMC 4863277. PMID 27184271.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  2. 2.0 2.1 2.2 Mugavero KL, Gunn JP, Dunet DO, Bowman BA (2014). "Sodium Reduction: An Important Public Health Strategy for Heart Health". J Public Health Manag Pract. 20 (101): S1–S5. doi:10.1097/PHH.0b013e3182aa659c. PMC 4450095. PMID 24322810.
  3. "Salt". National Center for Chronic Disease Prevention and Health Promotion, Division for Heart Disease and Stroke Prevention. US Centers for Disease Control. 1 June 2016. Archived from the original on 3 June 2016. Retrieved 8 June 2016.
  4. 4.0 4.1 "Salt reduction". Fact sheet. World Health Organization. 30 June 2016. Archived from the original on 11 June 2016. Retrieved 10 June 2016.
  5. 5.0 5.1 5.2 "Most Americans Should Consume Less Sodium". Centers for Disease Control and Prevention, U.S. Department of Health & Human Services. 11 July 2019. Archived from the original on 19 December 2019. Retrieved 30 September 2019.
  6. Whelton, Paul K.; Appel, Lawrence J.; Sacco, Ralph L.; Anderson, Cheryl A.M.; Antman, Elliott M.; Campbell, Norman; Dunbar, Sandra B.; Frohlich, Edward D.; Hall, John E.; Jessup, Mariell; Labarthe, Darwin R.; MacGregor, Graham A.; Sacks, Frank M.; Stamler, Jeremiah; Vafiadis, Dorothea K.; Van Horn, Linda V. (2012-12-11). "Sodium, blood pressure, and cardiovascular disease (Review)". Circulation. 126 (24): 2880–2889. doi:10.1161/cir.0b013e318279acbf. ISSN 0009-7322. PMID 23124030.
  7. "Salt reduction guide for the food industry" (PDF). Foodtech Canada. Archived (PDF) from the original on 17 April 2018. Retrieved 8 June 2016.
  8. Andersson, Bengt (1977). "Regulation of body fluids". Annual Review of Physiology. 39 (1): 185–200. doi:10.1146/ PMID 322597.
  9. Blaustein, MP (1977). "Sodium ions, calcium ions, blood pressure regulation, and hypertension: a reassessment and a hypothesis". The American Journal of Physiology. 232 (5): C165–73. doi:10.1152/ajpcell.1977.232.5.c165. PMID 324293. S2CID 9814212. Archived from the original on 2022-07-01. Retrieved 2022-03-06.
  10. 10.0 10.1 Karanja, N.; Erlinger, T P; Pao-Hwa, L.; Miller, E. R; Bray, G. A (2004). "The DASH diet for high blood pressure: from clinical trial to dinner table". Cleveland Clinic Journal of Medicine. 71 (9): 745–53. doi:10.3949/ccjm.71.9.745. PMID 15478706.
  11. 11.0 11.1 11.2 11.3 Sacks, Frank M.; Svetkey, Laura P.; Vollmer, William M.; Appel, Lawrence J.; Bray, George A.; Harsha, David; Obarzanek, Eva; Conlin, Paul R.; Miller, Edgar R. (2001). "Effects on Blood Pressure of Reduced Dietary Sodium and the Dietary Approaches to Stop Hypertension (DASH) Diet". New England Journal of Medicine. 344 (1): 3–10. doi:10.1056/NEJM200101043440101. PMID 11136953.
  12. 12.0 12.1 12.2 "Get the Scoop on Sodium and Salt". American Heart Association. 16 April 2018. Archived from the original on 10 October 2019. Retrieved 30 September 2019.
  13. 13.0 13.1 13.2 Cappuccio, F. P (2007). "Salt and cardiovascular disease". BMJ. 334 (7599): 859–60. doi:10.1136/bmj.39175.364954.BE. PMC 1857801. PMID 17463420.
  14. Appel, L. J.; Brands, M. W.; Daniels, S. R.; Karanja, N.; Elmer, P. J.; Sacks, F. M. (24 January 2006). "Dietary Approaches to Prevent and Treat Hypertension: A Scientific Statement From the American Heart Association". Hypertension. 47 (2): 296–308. doi:10.1161/01.HYP.0000202568.01167.B6. PMID 16434724.
  15. He FJ, Li J, Macgregor GA (2013). "Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomised trials". Br Med J. 346: f1325. doi:10.1136/bmj.f1325. PMID 23558162. Archived from the original on 2022-03-07. Retrieved 2022-03-06.
  16. He, Feng J.; MacGregor, Graham A. (March 2010). "Reducing Population Salt Intake Worldwide: From Evidence to Implementation". Progress in Cardiovascular Diseases. 52 (5): 363–382. doi:10.1016/j.pcad.2009.12.006. PMID 20226955.
  17. 17.0 17.1 Turck, Dominique; Castenmiller, Jacqueline; de Henauw, Stefaan; Hirsch‐Ernst, Karen‐Ildico; Kearney, John; Knutsen, Helle Katrine; Maciuk, Alexandre; Mangelsdorf, Inge; McArdle, Harry J; Pelaez, Carmen; Pentieva, Kristina; Siani, Alfonso; Thies, Frank; Tsabouri, Sophia; Vinceti, Marco; Aggett, Peter; Fairweather‐Tait, Susan; Martin, Ambroise; Przyrembel, Hildegard; Ciccolallo, Laura; de Sesmaisons‐Lecarré, Agnès; Valtueña Martinez, Silvia; Martino, Laura; Naska, Androniki (2019). "Dietary reference values for sodium (EFSA Panel on Nutrition, Novel Foods and Food Allergens)". EFSA Journal. 17 (9): e05778. doi:10.2903/j.efsa.2019.5778. ISSN 1831-4732. PMC 7009309. PMID 32626425.
  18. 18.0 18.1 Galea, Sandro; Johns, David Merritt; Trinquart, Ludovic (2016-02-01). "Why do we think we know what we know? A metaknowledge analysis of the salt controversy". International Journal of Epidemiology. 45 (1): 251–260. doi:10.1093/ije/dyv184. ISSN 0300-5771. PMID 26888870.
  19. Melinda Wenner Moyer (Jul 8, 2011). "It is Time to End the War on Salt: The zealous drive by politicians to limit our salt intake has little basis in science". Scientific American. Archived from the original on March 10, 2022. Retrieved March 6, 2022.
  20. 20.0 20.1 "CDC's Sodium Reduction Initiative: Saving Lives and Money" (PDF). US Centers for Disease Control and Prevention. December 2015. Archived (PDF) from the original on 11 May 2016. Retrieved 9 June 2016.
  21. "Shaking the Salt Habit". American Heart Association. 2016. Archived from the original on 16 June 2016. Retrieved 9 June 2016.
  22. "Sodium in Canada". Food and Nutrition. Health Canada. 8 June 2012. Archived from the original on 10 June 2016. Retrieved 10 June 2016.
  23. "Sodium: The facts" (PDF). US Centers for Disease Control and Prevention. April 2016. Archived (PDF) from the original on 13 May 2016. Retrieved 10 June 2016.
  24. Mattes, RD; Donnelly, D (1991). "Relative contributions of dietary sodium sources". Journal of the American College of Nutrition. 10 (4): 383–93. doi:10.1080/07315724.1991.10718167. PMID 1910064.
  25. Kloss L, Meyer JD, Graeve L, Vetter W (2015). "Sodium intake and its reduction by food reformulation in the European Union — A review". Nutrition & Food Science Journal (NFS Journal). 1: 9–19. doi:10.1016/j.nfs.2015.03.001.
  26. "Survey on Members States' Implementation of the EU Salt Reduction Framework" (PDF). European Commission. 2012. Archived (PDF) from the original on 3 August 2016. Retrieved 10 June 2016.
  27. Morimoto, A; Uzu, T; Fujii, T; Nishimura, M; Kuroda, S; Nakamura, S; Inenaga, T; Kimura, G (1997). "Sodium sensitivity and cardiovascular events in patients with essential hypertension". The Lancet. 350 (9093): 1734–7. doi:10.1016/S0140-6736(97)05189-1. PMID 9413464. S2CID 25794555.
  28. Wedler, B; Wiersbitzki, M; Gruska, S; Wolf, E; Luft, FC (1992). "Definitions and characteristics of salt-sensitivity and resistance of blood pressure: should the diagnosis depend on diastolic blood pressure?". Clinical and Experimental Hypertension, Part A. 14 (6): 1037–49. doi:10.3109/10641969209038191. PMID 1424217.
  29. 29.0 29.1 29.2 29.3 Weinberger, MH (1996). "Salt sensitivity of blood pressure in humans". Hypertension. 27 (3 Pt 2): 481–90. doi:10.1161/01.hyp.27.3.481. PMID 8613190.
  30. 30.0 30.1 Morris Jr, RC; Sebastian, A; Forman, A; Tanaka, M; Schmidlin, O (1999). "Normotensive salt sensitivity: effects of race and dietary potassium". Hypertension. 33 (1): 18–23. doi:10.1161/01.hyp.33.1.18. PMID 9931076.
  31. Weinberger, MH; Miller, JZ; Fineberg, NS; Luft, FC; Grim, CE; Christian, JC (1987). "Association of haptoglobin with sodium sensitivity and resistance of blood pressure". Hypertension. 10 (4): 443–6. doi:10.1161/01.hyp.10.4.443. PMID 3653973.
  32. Castiglioni, Paolo; et al. (2016). "Hemodynamic and Autonomic Response to Different Salt Intakes in Normotensive Individuals". Journal of the American Heart Association. 5 (8). doi:10.1161/JAHA.116.003736. Archived from the original on 2022-03-06. Retrieved 2022-03-06.
  33. Koomans, HA; Roos, JC; Boer, P; Geyskes, GG; Mees, EJ (1982). "Salt sensitivity of blood pressure in chronic renal failure. Evidence for renal control of body fluid distribution in man". Hypertension. 4 (2): 190–7. doi:10.1161/01.HYP.4.2.190. PMID 7040224. Archived from the original on 2022-07-01. Retrieved 2022-03-06.
  34. Suzuki, Masaaki; Kimura, Y; Tsushima, M; Harano, Y (2000). "Association of Insulin Resistance With Salt Sensitivity and Nocturnal Fall of Blood Pressure". Hypertension. 35 (4): 864–8. doi:10.1161/01.HYP.35.4.864. PMID 10775552.{{cite journal}}: CS1 maint: url-status (link)
  35. 35.0 35.1 35.2 Young, DB; Lin, H; McCabe, RD (1995). "Potassium's cardiovascular protective mechanisms". The American Journal of Physiology. 268 (4 Pt 2): R825–37. doi:10.1152/ajpregu.1995.268.4.R825. PMID 7733391.
  36. 36.0 36.1 AW Caggiula; Wing, RR; Nowalk, MP; Milas, NC; Lee, S; Langford, H (1985-09-01). "The measurement of sodium and potassium intake". The American Journal of Clinical Nutrition. 42 (3): 391–8. doi:10.1093/ajcn/42.3.391. PMID 4036845.
  37. "Sodium (Survey from 2004 updated to July 2007)". Statistics Canada. 2007. Archived from the original on 2018-02-24. Retrieved 2022-03-06.
  38. 38.0 38.1 38.2 38.3 38.4 38.5 38.6 Desmond, E (2006). "Reducing salt: A challenge for the meat industry". Meat Science. 74 (1): 188–96. doi:10.1016/j.meatsci.2006.04.014. PMID 22062728.
  39. Sopko, J. A.; Freeman, RM (1977). "Salt substitutes as a source of potassium". JAMA. 238 (7): 608–10. doi:10.1001/jama.238.7.608. PMID 577961.
  40. Sofos, John N. (1985). "Influence of Sodium Tripolyphosphate on the Binding and Antimicrobial Properties of Reduced NaCl-Comminuted Meat Products". Journal of Food Science. 50 (5): 1379–83. doi:10.1111/j.1365-2621.1985.tb10481.x.
  41. A Engstrom; Tobelmann, RC; Albertson, AM (1997-02-01). "Sodium intake trends and food choices". The American Journal of Clinical Nutrition. 65 (2): 704S–707S. doi:10.1093/ajcn/65.2.704S. PMID 9022569.