Salt and cardiovascular disease

Table salt

Salt consumption has been intensely studied for its role in human physiology and impact on human health. In particular, excessive dietary salt consumption over an extended period of time has been associated with hypertension and cardiovascular disease, in addition to other adverse health effects.[1][2][3]

Common edible salt is composed of sodium chloride.[4]

Effect of salt on blood pressure

Automated blood pressure device

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.[5]

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.

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.[6]

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.[7] 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.[8]

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.[8]

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).[8] However, this study is especially significant because participants in both the control and DASH diet group showed lowered blood pressure with decreased sodium alone.[7]

In agreement with studies regarding salt sensitivity, participants of African descent showed high reductions in blood pressure. See sodium sensitivity below.[8]

Hypertension and cardiovascular disease

There has been strong evidence from epidemiological studies, human and animal intervention experiments supporting the links between high rate of salt intake and hypertension.[2][9] A Cochrane review and meta-analysis of clinical trials showed that reduced sodium intake reduces blood pressure in hypertensive and normotensive subjects.[10][11] 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.[12] 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.[9] Several of these studies show that groups with sodium-reduced diets have lower incidences of cardiovascular disease in all demographics,[9][13] and in particular lower blood pressure.[11] One study showed lower incidence of cardiovascular disease after 15 years of sodium reduction in a randomised trial.[13]

More data is needed to support the conclusions of observational studies which suffer from design flaws.[13] Many of these studies are not large enough, nor last long enough to provide conclusions on clinical outcomes for the effect of dietary sodium intake on morbidity and mortality.[13] Previous mixed results and inconclusive interpretation of non-experimental studies may also root from the way sodium is measured in the study.[13] The study by Cook and colleagues itself was unable to isolate only a change in sodium. The techniques to reduce sodium included keeping a food diary and reading labels. Cook and colleagues listed other effects of those techniques, including a reduction in fat and calories per day (11g, 200cal), and weight loss of 1 to 3 pounds.[14] A 2014[15] Cochrane review found evidence that salt reduction prevented cardiovascular disease, but that the magnitude of the effect was uncertain and "larger than would be predicted from the small blood pressure reductions achieved."

The World Health Organization issued a 2014 fact sheet to encourage reducing global salt consumption by 30% through 2025.[16]

In 2015, the United States Centers for Disease Control and Prevention began an initiative encouraging Americans to reduce their consumption of salty foods.[17] The American Heart Association defined a daily sodium consumption limit should be 1500 milligrams (contained in less than 0.75 teaspoon of table salt).[18]

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.[19] 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.[20] 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.[17][21]

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[22] in response to a 2012 EU Salt Reduction Framework.[23]

Debate about sodium as a health problem

Despite few claims to the contrary, most physicians and clinical scientists, the European Food Safety Authority and the US Centers for Disease Control 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][3][24]

A limited group of researchers has cast doubts on the generally accepted theory that lowering sodium intake will improve the health of a given population.

Rather than create drastic salt policies based on conflicting data, Alderman and his colleague Hillel Cohen propose that the government sponsor a large, controlled clinical trial to see what happens to people who follow low-salt diets over time. Appel responds that such a trial "cannot and will not be done," in part because it would be so expensive. But unless we have clear data, evangelical antisalt campaigns are not just based on shaky science; they are ultimately unfair. "A great number of promises are being made to the public with regard to this enormous benefit and lives saved," Cohen says. But it is "based on wild extrapolations."[25]
"Taken together, our current findings refute the estimates of computer models of lives saved and health care costs reduced with lower salt intake. They do also not support the current recommendations of a generalized and indiscriminate reduction of salt intake at the population level. However, they do not negate the blood pressure-lowering effects of a dietary salt reduction in hypertensive patients."[26]

The traditional Japanese diet is very high in salt intake and yet, the Japanese had the highest rate of longevity in the world, and low rates of cardiovascular disease. ". . .we have found that the Japanese dietary pattern is associated with lower CVD mortality, despite the fact that the Japanese dietary pattern appeared to be related to higher sodium intake and high prevalence of hypertension."[27]

Other adverse cardiovascular effects

Some studies have shown that salt consumption has been found to increase the risk of myocardial infarction, stroke, arterial stiffness and heart failure.[3][28]

Effects of low salt consumption

In the majority of studies, reducing sodium intake lowers the risk of hypertension and associated cardiovascular disorders.[3][15][28]

In a few studies, both high (more than 7 g/day) and low salt intake (less than 3 g/day) were associated with an increased risk for cardiovascular disease[29] and increased mortality.[30]

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.[31]

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.[32]

A number of factors have been found to be associated with sodium sensitivity. Demographic factors which affect sodium sensitivity include race, gender, and age.[33] One study shows that the American population of African descent are significantly more salt sensitive than Caucasians.[34] 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.[34] Several studies have shown that the increase in age is also associated with the occurrence of sodium sensitivity.[33]

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.[33] 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.[35] Moreover, prevalence of a family history of hypertension is strongly linked with the occurrence of sodium sensitivity.

The influence of physiological factors including renal function and insulin levels on sodium sensitivity are shown in various studies.[33] One study concludes that the effect of renal failure on sodium sensitivity is substantial due to the contribution of decreasing the Glomerular filtration rate (GFR) in the kidney.[36] Moreover, insulin resistance is found to be related to sodium sensitivity; however, the actual mechanism is still unknown.[37]

Potassium and hypertension

Different salts contain different minerals contents

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.[38] However, studies have found a strong inverse association between long-term adequate to high rates of potassium intake and the development of cardiovascular diseases.[38]

The recommended dietary intake of potassium is higher than that of sodium.[39] Unfortunately, the average absolute intake of potassium of studied populations is lower than that of sodium intake.[39] According to Statistics Canada, Canadians' potassium intake in all age groups are lower than recommended, while sodium intake greatly exceed recommended intake in every age group.[40]

It has been hypothesized that the ratio of potassium to sodium intake accounts 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.[38]

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.[41]

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.[41] This change has been shown to blunt the effects of excess salt intake on hypertension and cardiovascular disease.[1][41] 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.[42]

In the food industry, processes have been developed to create low-sodium versions of existing products.[43][44] The meat industry especially have developed and fine-tuned methods to decrease salt contents in processed meats without sacrificing consumer acceptance.[41] 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.[41]

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.[41] 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.[41]

See also

References

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  2. 1 2 3 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. PMC 4450095 Freely accessible. PMID 24322810. doi:10.1097/PHH.0b013e3182aa659c.
  3. 1 2 3 4 "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. Retrieved 8 June 2016.
  4. ↑ "Salt reduction guide for the food industry" (PDF). Foodtech Canada. Retrieved 8 June 2016.
  5. ↑ Andersson, Bengt (1977). "Regulation of body fluids". Annual Review of Physiology. 39 (1): 185–200. PMID 322597. doi:10.1146/annurev.ph.39.030177.001153.
  6. ↑ 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. PMID 324293.
  7. 1 2 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. PMID 15478706. doi:10.3949/ccjm.71.9.745.
  8. 1 2 3 4 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. PMID 11136953. doi:10.1056/NEJM200101043440101.
  9. 1 2 3 Cappuccio, F. P (2007). "Salt and cardiovascular disease". BMJ. 334 (7599): 859–60. PMC 1857801 Freely accessible. PMID 17463420. doi:10.1136/bmj.39175.364954.BE.
  10. ↑ 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. PMID 16434724. doi:10.1161/01.HYP.0000202568.01167.B6.
  11. 1 2 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. PMID 23558162. doi:10.1136/bmj.f1325.
  12. ↑ 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.
  13. 1 2 3 4 5 Cook, N. R; Cutler, J. A; Obarzanek, E.; Buring, J. E; Rexrode, K. M; Kumanyika, S. K; Appel, L. J; Whelton, P. K (2007). "Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP)". BMJ. 334 (7599): 885–8. PMC 1857760 Freely accessible. PMID 17449506. doi:10.1136/bmj.39147.604896.55.
  14. ↑ "Feasibility and Efficacy of Sodium Reduction in the Trials of Hypertension Prevention, Phase I". Hypertension. 22: 502–512. 1993. doi:10.1161/01.hyp.22.4.502.. Retrieved from http://hyper.ahajournals.org/content/22/4/502.full.pdf
  15. 1 2 Adler, AJ; Taylor, F; Martin, N; Gottlieb, S; Taylor, RS; Ebrahim, S (18 December 2014). "Reduced dietary salt for the prevention of cardiovascular disease.". The Cochrane database of systematic reviews. 12: CD009217. PMID 25519688. doi:10.1002/14651858.CD009217.pub3.
  16. ↑ "Salt reduction". Fact sheet. World Health Organization. September 2014. Retrieved 10 June 2016.
  17. 1 2 "CDC’s Sodium Reduction Initiative: Saving Lives and Money" (PDF). US Centers for Disease Control and Prevention. December 2015. Retrieved 9 June 2016.
  18. ↑ "Shaking the Salt Habit". American Heart Association. 2016. Retrieved 9 June 2016.
  19. ↑ "Sodium in Canada". Food and Nutrition. Health Canada. 8 June 2012. Retrieved 10 June 2016.
  20. ↑ "Sodium: The facts" (PDF). US Centers for Disease Control and Prevention. April 2016. Retrieved 10 June 2016.
  21. ↑ Mattes, RD; Donnelly, D (1991). "Relative contributions of dietary sodium sources". Journal of the American College of Nutrition. 10 (4): 383–93. PMID 1910064. doi:10.1080/07315724.1991.10718167.
  22. ↑ 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.
  23. ↑ "Survey on Members States’ Implementation of the EU Salt Reduction Framework" (PDF). European Commission. 2012. Retrieved 10 June 2016.
  24. ↑ "EFSA provides advice on adverse effects of sodium". European Food Safety Authority. 22 June 2005. Retrieved 8 June 2016.
  25. ↑ "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 Jul 8, 2011. Melinda Wenner Moyer.
  26. ↑ "Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion" Journal of the American Medical Association. Stolarz-Skrzypek, et al. May 4, 2011.
  27. ↑ Shimazu Taichi; et al. "Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study". International Journal of Epidemiology. 36: 600–609. doi:10.1093/ije/dym005.
  28. 1 2 Susic, D; Frohlich, ED (February 2012). "Salt consumption and cardiovascular, renal, and hypertensive diseases: clinical and mechanistic aspects.". Current Opinion in Lipidology. 23 (1): 11–6. PMID 22123673. doi:10.1097/MOL.0b013e32834d9c52.
  29. ↑ Mente Andrew; et al. "Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies". The Lancet. 388: 465–75. PMID 27216139. doi:10.1016/S0140-6736(16)30467-6.
  30. ↑ Graudal N., Jürgens G., Baslund B., Alderman M.H. (Sep 2014). "Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis". Am. J. Hypertens. 27: 1129–1137. PMID 24651634. doi:10.1093/ajh/hpu028.
  31. ↑ 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.
  32. ↑ 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, Theory and practice. 14 (6): 1037–49. PMID 1424217. doi:10.3109/10641969209038191.
  33. 1 2 3 4 Weinberger, MH (1996). "Salt sensitivity of blood pressure in humans". Hypertension. 27 (3 Pt 2): 481–90. PMID 8613190. doi:10.1161/01.hyp.27.3.481.
  34. 1 2 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. PMID 9931076. doi:10.1161/01.hyp.33.1.18.
  35. ↑ 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. PMID 3653973. doi:10.1161/01.hyp.10.4.443.
  36. ↑ 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. PMID 7040224. doi:10.1161/01.HYP.4.2.190.
  37. ↑ 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. PMID 10775552. doi:10.1161/01.HYP.35.4.864.
  38. 1 2 3 Young, DB; Lin, H; McCabe, RD (1995). "Potassium's cardiovascular protective mechanisms". The American journal of physiology. 268 (4 Pt 2): R825–37. PMID 7733391.
  39. 1 2 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. PMID 4036845.
  40. ↑ 2004 Canadian Community Health Survey - Nutrition.http://www.statcan.gc.ca/pub/82-003-x/2006004/article/sodium/4148995-eng.htm
  41. 1 2 3 4 5 6 7 Desmond, E (2006). "Reducing salt: A challenge for the meat industry". Meat Science. 74 (1): 188–96. PMID 22062728. doi:10.1016/j.meatsci.2006.04.014.
  42. ↑ Sopko, J. A.; Freeman, RM (1977). "Salt substitutes as a source of potassium". JAMA. 238 (7): 608–10. PMID 577961. doi:10.1001/jama.238.7.608.
  43. ↑ 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.
  44. ↑ 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. PMID 9022569.
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