Sodium and Potassium: A love story to get your heart racing.

Blood Pressure

Habitual high salt consumption has been linked to hypertension for more than a century. Yet controversy remains regarding the mechanisms by which salt influences blood pressure and in the relationship of sodium intake to cardiovascular morbidity and mortality. This is not surprising because multiple variables affect cardiovascular health including (but not limited to) genetic susceptibility, micro-nutrition, body mass, age, cardiovascular risk factors, and kidney function. In the United States, salt intake ranges between 4 g and 13 g per day leaving 24% of the adult population with hypertension. Conversely, societies with low salt intake such as the Yanomami Indians of the Amazon, have a low incidence of hypertension.

INTERSALT

The most comprehensive population-based study on the relationship between dietary salt and blood pressure involved more than 10,000 men and women between 20 and 59 years of age from 52 geographically separate test centers in 32 countries. The study looked at the association between blood pressure and 24-hour excretion of sodium ions and potassium ions in the urine. In the four centers with median values of sodium excretion less than 1.3 g per day, the populations had: a) low blood pressure, b) rare or absent hypertension, and c) no age-related rise in blood pressure. In the 48 centers where the subjects' average excretion of sodium was more than 2.4 g per day, excretion of sodium related significantly to the age-related rise in blood pressure.

Dietary Salt Restriction

Although cutting down on salt usage appears to be the simple solution to hypertension, studies to lower blood pressure through dietary salt restriction have produced mixed results. This may be explained by the fact that not all hypertensive patients are salt-sensitive and that many cases of hypertension are brought on by other causes, e.g. obesity, magnesium deficiency, potassium deficiency, vascular disease, etc. However, despite abundant epidemiological and experimental studies demonstrating a link between salt and blood pressure, skepticism remains based on the curious observation that not all individuals show changes in blood pressure after ingestion of increased or decreased amounts of salt as sodium chloride. In some hypertensive individuals, salt restriction decreases blood pressure significantly, often to levels approaching that achieved with medication. In other hypertensive patients, little or no change in blood pressure occurs, while in still others, blood pressure may actually increase with salt restriction. These diverse responses are partly influenced by age, the intake of other electrolytes (e.g. calcium, magnesium, and potassium), and certain medications. After many years of wondering and searching, genetic predisposition has finally been shown to play a substantial role.

Genetic Factors

Inherited and acquired forms of hypertension both function through a common pathway that involves sodium reabsorption in the kidney. Perturbations of this pathway have been traced to the genetic control of salt sensitivity. The fact that a genetic predisposition to hypertension exists was foretold by African Americans. This population group, in general, shows higher blood pressure earlier in life, has a greater incidence of hypertension that appears earlier, is usually more severe, and is associated with a greater risk of cardiovascular complications when compared to European Americans. This is not to say African Americans are doomed to experience high blood pressure in the face of a salty diet. Researchers have found that within every group of test subjects, whether hypertensive or not, those demonstrating sensitivity to salt and those resistant to salt intake can be identified.

Kidney Chloride Channel, CIC-Kb

The causes of the widespread salt-sensitivity observed in African Americans and salt-sensitivity observed within all ethnic and racial populations, whether hypertensive or normotensive, implies that how genes they express themselves influence blood pressure. Reabsorption of sodium ions (Na+) by the kidney can lead to the development of hypertension if the process is too efficient. Increased kidney reabsorption rates can be due to genetic disorders lead and are well-known causes of hypertension. The ClC-Kb gene is implicated. The chloride channel, ClC-Kb, is controlled by the ClC-Kb gene. It participates in salt reabsorption by the kidney. The ClC-KbT481S variant of the gene confers a strong reabsorption functionality. The presence of this T481S gene mutation is significantly higher in African populations, e.g. Ghana (22%) than in Europeans (12%). Finally, individuals carrying ClC-KbT481S have significantly higher plasma sodium concentrations and a significantly reduced ability to shed excess salt. But not all persons carrying the ClC-KbT481S gene mutation develop hypertension. This is explained by environmental complexity where inherited susceptibility must try to express itself through the influence of other predisposing factors such as diet, lifestyle, obesity, alcohol consumption, age, and stress.

DASH for Health

Dietary factors play a primary role in the control of blood pressure. Consumption of a high-fat, high sodium (salt), low-potassium, low-calcium, and/or low-magnesium diet may contribute to the development of hypertension. Therefore, lifestyle modification including weight loss, increased physical activity, moderation or reduction of alcohol consumption, and an overall healthy dietary pattern, such as the Dietary Approaches to Stop Hypertension (DASH) diet, have been recommended to help reduce blood pressure. The DASH eating plan recommends: ∑ Eating vegetables, fruits, and whole grains ∑ Including fat-free or low-fat dairy products, fish, poultry, beans, nuts, and vegetable oils ∑ Limiting foods that are high in saturated fat, such as fatty meats, full-fat dairy products, and tropical oils such as coconut, palm kernel, and palm oils ∑ Limiting sugar-sweetened beverages and sweets. Based on these recommendations, the following table shows examples of daily and weekly servings that meet DASH eating plan targets for a 2,000-calorie-a-day diet. Combining the DASH diet with reduced sodium intake produces the greatest reductions especially among older individuals. Older individuals are more susceptible to developing elevated blood pressure and will likewise respond more favorably to a DASH eating regimen with sodium restriction. The response of blood pressure to salt restriction depends significantly on age, the rigor of salt restriction, and the person‚s initial blood pressure.

To Salt or Not to Salt

This does not mean salt restriction is a universal panacea for the cure of hypertension despite the apparent absence of high blood pressure among foraging horticulturalists that do not use salt. The discovery of genetically controlled salt-sensitivity and salt-insensitivity among individuals in ALL societies conversely indicates that some hypertensive patients in any salted society will not adequately improve under a salt-restricted diet. So is it a good idea to cut back on your salt intake? In general, yes. Each person is certainly biochemically unique but raised blood pressure is the most important cause of cardiovascular disease, accounting for 62% of strokes and 49% of coronary heart disease.

The protective action of dietary potassium against cardiovascular diseases

Epidemiological studies, clinical trials, and animal experiments have shown that high potassium intake protects against hypertension and cardiovascular diseases. Populations with diets rich in potassium exhibit lower rates of hypertension and have a lower incidence of cardiovascular diseases, whereas those with diets habitually low in potassium (mainly industrialized cultures) appear to have an increased incidence of cardiovascular diseases. Potassium may protect against cardiovascular diseases through these mechanisms: 1) Potassium inhibits free radical formation in endothelial cells lining blood vessels and from scavenging macrophages; 2) Potassium inhibits proliferation of vascular smooth muscle cells, blocking atherogenesis and inhibiting vascular stiffness; 3) Platelet aggregation and the risk of arterial thrombosis {blood clot) are inhibited by elevation of potassium; and 4) Vascular resistance in the kidneys is reduced and the glomerular filtration rate is increased by elevating plasma potassium, thereby enhancing sodium excretion and reducing blood pressure. By these actions, a high dietary intake of potassium provides protection against cardiovascular diseases. Whereas high sodium intake is identified as a cause of high blood pressure, and other diseases, a protective, inhibitory relationship of potassium intake with blood pressure, the incidence of stroke, and other cardiovascular diseases has been found. We do now know that potassium may be the antidote to high salt/sodium intake because: 1. Increasing potassium intake lowers blood pressure in both hypertensive and normotensive people 2. Increasing potassium intake and reducing sodium intake boosts the blood pressure-lowering effect. 3. High potassium intake reduces the risk of stroke and prevents kidney damage. 4. Increasing potassium intake reduces urinary calcium excretion, which reduces the risk of kidney stones and helps prevent osteoporosis 5. Increasing serum potassium concentrations reduces the risk of ventricular arrhythmias in patients with ischemic heart disease, heart failure, and left ventricular hypertrophy 6. The best way to increase potassium intake is to eat more fresh fruit and vegetables Increasing intake of fruits and vegetables has been found to be associated with a 27% reduction in the risk of stroke, independent of blood pressure. Indeed, abundant use of healthy fruits and vegetables in one‚s diet is associated with a lower risk of cardiovascular disease and all-cause mortality in the US population. However, other micronutrients and bioactive food substances present in fruits and vegetables may contribute to the effect. Some of them are the antioxidant polyphenols, antimicrobials, and fibers found in plants. The blood-pressure-lowering effects of potassium administration appeared to be greater in studies where participants were concurrently exposed to a high intake of sodium. This is as expected because potassium facilitates the expulsion of sodium through the kidneys and urinary tract. A total dietary modification that results in increased potassium intake decisively lowers blood pressure, particularly when potassium intake exceeds sodium intake. But in the United States, US citizens on average take in about 4000 mg per day or more of sodium while the average daily intake of potassium is approximately 2500 to 3400 mg. Our prehistoric, hunter-gatherer ancestors consumed approximately 750 to 800 mg per day of sodium and nearly 10,500 mg of potassium. Both elements are essential to life and health. Their rapid translocation across membranes of nerve cells define neurological activity. Without that activity, you won‚t walk, breathe, see or have a heartbeat. No ability to retain potassium was ever adopted into human biochemistry as potassium had always been abundant in fruits and vegetables and our ancestors consumed almost 3.2 pounds of plant material each day. Sodium, on the other hand, was scarce in ancient diets, so a mechanism to carefully re-absorb sodium through the kidneys as it tried to exit the body evolved to assure that we would always have enough to keep nerves firing and life sustained. So do you really need a bratwurst hot off the grill, smothered in sauerkraut, with some mustard on top? Not really. But if you do indulge in that decadent summertime delight, just be sure to balance it with a full plate of green salad, some roasted vegetables, and perhaps a banana, strawberries, and some cherries for dessert. Oliver WJ, Cohen EL, Neel JV. Blood pressure, sodium intake, and sodium related hormones in the Yanomamo Indians, a "no-salt" culture. Circulation. 1975 Jul;52(1):146-51. Rodriguez BL, Labarthe DR, Huang B, Lopez-Gomez J. Rise of blood pressure with age. New evidence of population differences. Hypertension. 1994 Dec;24(6):779-85. Weinberger MH. Salt sensitivity of blood pressure in humans. Hypertension. 1996 Mar;27(3 Pt 2):481-90. Luft FC, Weinberger MH. Heterogeneous responses to changes in dietary salt intake: the salt-sensitivity paradigm. Am J Clin Nutr. 1997 Feb;65(2 Suppl):612S-617S. Lifton RP, Gharavi AG, Geller DS. Molecular mechanisms of human hypertension. Cell. 2001 Feb 23;104(4):545-56. Weinberger MH, Hypertension in African Americans: the role of sodium chloride and extracellular fluid volume. Semin Nephrol. 1996 Mar;16(2):110-6 Lifton RP. Molecular genetics of human blood pressure variation. Science. 1996; 272: 676‚ì680. Warnock DG. Liddle syndrome: genetics and mechanisms of Na+ channel defects. Am J Med Sci. 2001; 322: 302‚ì307. Jeck N, Waldegger S, Lampert A, Boehmer C, Waldegger P, Lang PA, Wissinger B, Friedrich B, Risler T, Moehle R, Lang UE, Zill P, Bondy B, Schaeffeler E, Asante-Poku S, Seyberth H, Schwab M, Lang F. Activating mutation of the renal epithelial chloride channel ClC-Kb predisposing to hypertension. Hypertension. 2004 Jun;43(6):1175-81. Reusser ME, McCarron DA., Micronutrient effects on blood pressure regulation. Nutr Rev. 1994 Nov;52(11):367-75. Op. cit. Sacks FM, et.al. N Engl J Med. 2001 Jan 4;344(1):3-10. Vollmer WM, Sacks FM, Ard J, Appel LJ, Bray GA, Simons-Morton DG, Conlin PR, Svetkey LP, Erlinger TP, Moore TJ, Karanja N; DASH-Sodium Trial Collaborative Research Group. Effects of diet and sodium intake on blood pressure: subgroup analysis of the DASH-sodium trial. Ann Intern Med. 2001 Dec 18;135(12):1019-28. Op. cit. Reusser ME, McCarron DA., Nutr Rev. 1994 Young DB, Lin H, McCabe RD. Potassium's cardiovascular protective mechanisms. Am J Physiol. 1995 Apr;268(4 Pt 2):R825-3 Stamler J., The INTERSALT Study: background, methods, findings, and implications. Am J Clin Nutr. 1997 Feb;65(2 Suppl):626S-642 He FJ, MacGregor GA. Fortnightly review: Beneficial effects of potassium. BMJ. 2001 Sep 1;323(7311):497-501. Venneman K, Huybrechts I, Gunter MJ, Vandendaele L, Herrero R, Van Herck K., The epidemiology of Helicobacter pylori infection in Europe and the impact of lifestyle on its natural evolution toward stomach cancer after infection: A systematic review. Helicobacter. 2018 Jun;23(3):e1248 Bazzano LA, He J, Ogden LG, Loria CM, Vupputuri S, Myers L, Whelton PK Fruit and vegetable intake and risk of cardiovascular disease in US adults: the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study. Am J Clin Nutr. 2002 Jul;76(1):93-9. Whelton PK1, He J.,Potassium in preventing and treating high blood pressure. Semin Nephrol. 1999 Sep;19(5):494-9. Harsha DW, Lin PH, Obarzanek E, Karanja NM, Moore TJ, Caballero B. Dietary Approaches to Stop Hypertension: a summary of study results. DASH Collaborative Research Group. J Am Diet Assoc. 1999 Aug;99(8 Suppl):S35-9. Eaton SB, Eaton SB 3rd, Konner MJ. Paleolithic nutrition revisited: a twelve-year retrospective on its nature and implications. Eur J Clin Nutr. 1997 Apr;51(4):207-16. DISCLAIMER: This information is not intended as a substitute for advice provided by a competent health care professional. You should not use this information in diagnosing or treating a health problem. No claim or opinion in this blog is intended to be, nor should be construed to be, medical advice. If you are now taking any drugs, prescribed or not, or have a medical condition, please consult a competent physician who is aware of herb/drug interactions before taking any herbal supplements. The information presented herein has not been evaluated by the FDA or the Department of Health and is not intended to diagnose, prevent, cure, mitigate or treat any disease or illness.

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