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]

Most forms of edible salt are composed primarily of sodium and chloride, as other minerals such as magnesium and calcium make unrefined salts bitter and therefore are rarely eaten.[3] An excessive intake of the ionic compound sodium chloride has long been suspected to increase blood pressure.[2] Sodium and chloride serum levels are both carefully controlled by the kidneys, and acute and chronic excessive intake of both ions can cause adverse health effect.[4] However, only serum sodium is thought to be strongly correlated to blood pressure levels and cardiovascular disease.

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 [4]

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 the body's needs.

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.[5]

Blood pressure may continue to increase as water is consumed hours after salt is ingested. As excess sodium is excreted by the kidneys, blood pressure drops accordingly. Diets that consistently contain high salt content will increase blood pressure over time . Fortunately, as many studies have shown, limiting salt intake in the diet can reverse these effects.[6]

Since most cases of hypertension are essential hypertension, it is unlikely that a single factor can be attributed to the cause of hypertension in most hypertensive patients.[7]

DASH-Sodium study

Main article: DASH diet

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.[8] 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.[9]

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.[9]

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

In agreement with studies regarding salt sensitivity, participants of African descent showed high reductions in blood pressure. See sodium sensitivity below.[9]

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, hypertension and cardiovascular diseases.[10] Clinical trials have shown that reduced sodium intake can prevent hypertension and facilitate control thereof,[11] and that it is related to a reduced risk of cardiovascular disease.[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.[10] Most of these studies, with a few exceptions, show statistical significance that groups with sodium reduced diets show lower incidences of cardiovascular disease in all demographics.[10][13] A study by Cook and colleagues was the first to show reduction 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 some 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."

Current trends and campaigns

According to the 2004 Canadian Community Health Survey (CCHS), Canadians in all age groups are consuming sodium between 45.1 - 98.8% above the upper limit set for their gender and age group.[16] The US Department of Agriculture claims that the average daily sodium intake for Americans over 2 years of age is 3436 mg.[17] 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.[16][18]

Evidence that high sodium levels may not be a major public health problem

A number of researchers have cast doubt recently 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."[19]
"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."[20]

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."[21]

According to at least one study, elderly people with low sodium levels (hyponatremia) have more falls and broken hips and a decrease in cognitive abilities.[22]

Other adverse cardiovascular effects

Salt consumption has been found to increase the risk of myocardial infarction, stroke, arterial stiffening and heart failure.[23]

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.[24]

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.[25]

A number of factors have been found to be associated with sodium sensitivity. Demographic factors which affect sodium sensitivity include race, gender, and age.[26] One study shows that the American population of African descent are significantly more salt sensitive than Caucasians.[27] 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.[27] Several studies have shown that the increase in age is also associated with the occurrence of sodium sensitivity.[26]

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.[26] 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.[28] 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.[26] 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.[29] Moreover, insulin resistance is found to be related to sodium sensitivity; however, the actual mechanism is still unknown.[30]

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.[31] However, studies have found a strong inverse association between long-term adequate to high rates of potassium intake and the development of cardiovascular diseases.[31]

The recommended dietary intake of potassium is higher than that of sodium.[32] Unfortunately, the average absolute intake of potassium of studied populations is lower than that of sodium intake.[32] 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.[33]

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.[31]

Salt substitutes

Main article: Salt substitute

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.[34]

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.[34] This change has been shown to blunt the effects of excess salt intake on hypertension and cardiovascular disease.[34][35] 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.[36]

In the food industry, processes have been developed to create low-sodium versions of existing products.[37][38] The meat industry especially have developed and fine-tuned methods to decrease salt contents in processed meats without sacrificing consumer acceptance.[34] 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.[34]

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.[34] 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.[34]

See also

References

  1. ↑ Dietary reference intakes for water, potassium, sodium, chloride, and sulfate. Washington, D.C: National Academies Press. 2005. ISBN 0-309-53049-0.
  2. 1 2 Klaus, D; Böhm, M; Halle, M; Kolloch, R; Middeke, M; Pavenstädt, H; Hoyer, J (May 2009). "Die Beschränkung der Kochsalzaufnahme in der Gesamtbevölkerung verspricht langfristig großen Nutzen" [Restriction of salt intake in the whole population promises great long-term benefits]. Deutsche Medizinische Wochenschrift (in German) 3: S108–18. doi:10.1055/s-0029-1222573. PMID 19418415.
  3. ↑ Ann Louise Gittleman, Sodium is essential to life. Total health magazine, vol 22, no 2.
  4. 1 2 Andersson, Bengt (1977). "Regulation of body fluids". Annual Review of Physiology 39 (1): 185–200. doi:10.1146/annurev.ph.39.030177.001153. PMID 322597.
  5. ↑ 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.
  6. ↑ Morgan, T (May 2003). "Renin, angiotensin, sodium and organ damage.". Hypertension research : official journal of the Japanese Society of Hypertension 26 (5): 349–54. doi:10.1291/hypres.26.349. PMID 12887125.
  7. ↑ Carretero, OA; Oparil, S (2000). "Essential hypertension. Part I: definition and etiology.". Circulation 101 (3): 329–35. doi:10.1161/01.CIR.101.3.329. PMID 10645931.
  8. 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. doi:10.3949/ccjm.71.9.745. PMID 15478706.
  9. 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. doi:10.1056/NEJM200101043440101. PMID 11136953.
  10. 1 2 3 Cappuccio, F. P (2007). "Salt and cardiovascular disease". BMJ 334 (7599): 859–60. doi:10.1136/bmj.39175.364954.BE. PMC 1857801. PMID 17463420.
  11. ↑ 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.
  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. doi:10.1136/bmj.39147.604896.55. PMC 1857760. PMID 17449506.
  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. ↑ 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.
  16. 1 2 2004 Canadian Community Health Survey — Nutrition. Retrieved from http://www.statcan.gc.ca/pub/82-003-x/2006004/article/sodium/4148995-eng.htm December 2nd, 2010
  17. ↑ U.S. Department of Agriculture. What we eat in America. Available from http://www.ars.usda.gov/service/docs.htm?docid=15044
  18. ↑ 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.
  19. ↑ "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.
  20. ↑ "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.
  21. ↑ Dietary patterns and cardiovascular disease mortality in Japan: a prospective cohort study. International Journal of Epidemiology Taichi Shimazu, et al. Volume 36, pp. 600-609.
  22. ↑ "Hyponatremia in the Elderly: Risk Factors, Clinical Consequences, and Management"Geriatrics/ 2009.
  23. ↑ 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. doi:10.1097/MOL.0b013e32834d9c52. PMID 22123673.
  24. ↑ 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.
  25. ↑ 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. doi:10.3109/10641969209038191. PMID 1424217.
  26. 1 2 3 4 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.
  27. 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. doi:10.1161/01.hyp.33.1.18. PMID 9931076.
  28. ↑ 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.
  29. ↑ Koomans, HA; Roos, JC; Boer, P; Geyskes, GG; Mees, EJ (03/01/1982). "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. Check date values in: |date= (help)
  30. ↑ Suzuki, Masaaki; Kimura, Y; Tsushima, M; Harano, Y (04/01/2000). "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. Check date values in: |date= (help)
  31. 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.
  32. 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.
  33. ↑ 2004 Canadian Community Health Survey - Nutrition.http://www.statcan.gc.ca/pub/82-003-x/2006004/article/sodium/4148995-eng.htm
  34. 1 2 3 4 5 6 7 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.
  35. ↑ US Dept of Health and Human Services, 2005 US Department of Health and Human Services (2005). 2005 Dietary guidelines for Americans. Available from <http://www.health.gov/dietaryguidelines/dga2005/document>.
  36. ↑ 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.
  37. ↑ 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.
  38. ↑ 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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