by Charles Weber, MS – isoptera at – or 828 692 5816

This article explains potassium physiology, especially in the way a deficiency affects the body’s cells, hormones and enzymes with regard to rheumatoid arthritis and gout.

CONTENTS of other chapters Back to INTRODUCTION chapter -- II. Arthritis Research -- III. Arthritis as a Potassium Deficiency (this article) -- IV. Roles of Potassium in the Body -- V. Electrolyte regulation (sodium and potassium) -- VI. Purpose of cortisol -- VII. Copper nutrition and physiology -- VIII. Nutritional Requirements -- IX. Potassium in Foods -- X. Processing Losses -- X,cont. Losses in the kitchen -- XI. Supplementation -- Side Effects and Heart Disease -- XIVPotassium and thiamin in heart disease

Strategies for chronic fatigue syndrome (CFS) and fibromyalgia-------------When Blood Potassium is too High>


POTASSIUM NUTRITION (a book by Charles Weber)

Potassium losses from perspiration, in urine, during diarrhea, from stress, poisons, and disease states are discussed in the book available here, as well as methods to supplement potassium safely, especially as involved in heart disease, gout, high blood pressure, and rheumatoid arthritis, and indirectly in diabetes. It is published by iUniverse publishing company and it is a very comprehensive book about potassium, probably much more so than any other. You may see the table of contents with chapter summaries and the introductory chapter by clicking here.

If you do not know the meaning of a word in this article, for a definition click on (Mirriam-Webster). For unknown words also see the On-Line Medical Dictionary A new dictionary is also available online at this site.

. ---------- Arthritis =rheumatoid arthritis = RA in this article

It has been determined by LaCelle that the whole body potassium is significantly lower in older arthritics. The body can sink to almost half of normal in some cases [LaCelle]. Sambrook, et al also find potassium is low in early rheumatoid arthritis [Sambrook]. These determinations were made using a whole body scintillation counter. A scintillation counter is an extremely expensive machine that can count the number of x-rays emerging from the body as a result of the radioactive decay of one of the potassium isotopes, K-40. These machines cost well over $100,000 each. Potassium in the body cells is not often determined for patients because of the enormous cost of the equipment, combined with a blind spot for potassium nutrition among doctors. Other methods for determining cell potassium involve biopsies, balance studies which must be conducted for long periods to get valid results [Lambie], isotope dilution studies which are almost as cumbersome [Jasani] and have difficulties with unreliable erratic diffusion to body components. Welt claims to be able to predict cell potassium from serum potassium if a formula is used which uses other ions, especially hydrogen ions (acid). Welt states that 0.1 pH (hydrogen ion or acidity) unit equals 0.63 millimoles of potassium per liter in the serum [Welt 1958 p217]. I am skeptical that it is always reliable. It is the case, though, that if for some reason the serum is more acid than normal, even small drops in serum potassium indicate significant lowering of cell potassium [Surawicz][Ono]. However in most cases when cell potassium is low the serum potassium is usually low also [Nickel]. Normal potassium in plasma can be half a milliequivalent lower than serum, but analysis within 30 minutes would prevent it [Bellevue]. In any case it is necessary to use plasma determinations and not serum because serum can give incorrectly high results [Ifudu]. Even with careful determination plasma potassium can be incorrectly high by 0.4 milliequivalents per liter because of potassium losses from platelets after blood is drawn during rheumatoid arthritis [Ifudu].

The National Health and Nutrition Survey-III has determined that of 39,695 people selected, there were 840 who said they had been diagnosed with rheumatoid arthritis. Of these, 691 had their serum tested for potassium. Of that number 7.8% had less than 3.6 milliequivalents per liter, 34.7% between 3.6 and 4.0, 40.7% between 4.0 and 4.4, and 18.1% above 4.4. Therefore, only 18% appeared to be in the normal range. 4.8 is the value the body attempts to achieve. The samples were refrigerated and sent out to outside contract laboratories [NHANES-III]. Refrigerating blood increases the apparent amount when it is serum that is analyzed, especially if there is a delay in the analysis. In addition to that, arthritics lose potassium from the platelets as noted above. If some were misdiagnosed, had a remission since being diagnosed, or there was a longer than usual delay in analysis, it could account for the 18% seemingly normal. So this survey showed at least most arthritics low in potassium. Many others in the survey were low in potassium also. So, unless arthritis is caused by something besides a potassium deficiency and low potassium is either a symptom or an accentuating factor, those other survey people would have to have had arthritis as well. I believe many people die of a potassium deficiency caused heart disease without being arthritic, so, if so, the first part of that last statement must be in order. Also, in a group of tuberculosis patients medicated with capreomycin, 31% developed hypokalemia [Shin] and none of them had arthritis [Shin, private communication]. Tuberculosis is a mycoplasma bacteria, and mycoplasma has been suggested as causing rheumatoid arthritis, as mentioned below. So perhaps that antibiotic solved the arthritis at the same time. In any case, a large proportion of arthritics at least, are too low for sure, some dangerously low.

A method has been developed which promises to be accurate and not too cumbersome. This involves the separation of white blood cells out and their subsequent analysis [Patrick]. So far as I know it is not used much. The red blood cells, along with the brain, heart, and liver, have modest losses for several weeks during a deficiency. The muscles suffer most of the losses, possibly due to a reversible 80% decline in pumping sites [Noergaard]. So red cell content can not be used as a criteria. The upshot is that cell potassium is largely invisible to doctors. However, there is an observation of lower potassium in the saliva of rheumatoid arthritis patients [Syrjanen] and often low serum potassium [Cockel], even though the platelets release potassium into the serum when blood is drawn [Ifudu]. There also has been developed recently a method that uses electron bombardment of a single mouth mucous cell by electrons in order to generate distinctive x-rays. It is said to cost $175 and determines other electrolytes inside the cell at the same time. This is very encouraging if it proves to be valid. An indication should be possible also by determining what percentage of a potassium supplement is retained by analysis of the daily urine total.

LaCelle's finding is very significant and has been confirmed by Nuki, et al [Nuki]. Even if one assumed that the arthritis caused the potassium content, rather than the other way around, it would seem good common sense to bring such an important mineral up to normal in view of potassium’s usual role in heart disease. It is strange that this finding has not created more interest, as a diagnostic clue if nothing else. Even if scientists are not interested, there is nothing stopping you from at least getting all the potassium that was originally in your food. When 30 mEq of potassium in a glucose solution was injected into old people for 2-3 hours it caused only one sixth the rise in aldosterone steroid hormone as it did in 35 year old people [Saruta]. I suspect that this was because the cell content of those older people was low in potassium. Red blood cell potassium averages higher in arthritics than normal. You can not take this as negative evidence since red blood cell potassium shows no correlation with plasma potassium [Ladefoged]. This may be an adaptation to avoid circulatory collapse during potassium losing diarrheas.

One can not draw a sure conclusion from low potassium serum from the blood content alone and it is dependent on the status of hydrogen ion and chloride. The reason is that plasma can have wide swings in content. However, 80% of people with rheumatic heart disease have low blood plasma content [Sokolov]. Even cell content is not certain proof all by itself. What is needed is a controlled experiment in which only potassium is varied. There never has been such an experiment for arthritis up until recently. Rastmanesh has performed a controlled, double blind, month long, clinical trial with significant rises in cortisol and declines in pain [Rastmanesh] (see further discussion below at the end). Placebo controls have been challenged recently, but they are in order for potassium experiments because the hormone most involved in potassium excretion, aldosterone, is much increased by fear and anxiety. However there has been an experiment performed by Schick on one of the arthritic diseases of the arteries called polyarteritis nodosa, which was indicative. Unfortunately cortisone was administrated at the same time so the experiment was flawed. However, everyone given 1.5 to 3 grams of potassium supplements per day had a complete healing of all arteries [Schick]. Potassium citrate was able to prevent arterial lesions in sodium chloride loaded hypertensive dahl rats without lowering the blood pressure. Potassium chloride had a somewhat lesser protective affect [Tobian]. High blood pressure is an important risk factor in stroke. Even so, a study found that only 400 milligrams per day of potassium supplements caused a 40% reduction in stroke mortality. This effect was independent of other dietary variables, including the intake of calories, fat, protein, fiber, calcium, magnesium, and alcohol. The effect was also apparently independent of known cardiovascular risk factors, including age, sex, blood pressure, blood cholesterol level, obesity, fasting blood glucose level, and cigarette smoking [Khaw]. I suspect that these affects on the blood vessels by potassium arises because a potassium deficiency inhibits cortisol production [Ueda] [Mikosha], which cortisol deficiency inhibits lysyl oxidase, the enzyme that cross links blood vessel connective tissue. This is probably the reason why low serum potassium is a risk factor in Kawasaki disease aneurysms. [Koyanagi] and why a chief cause of death of arthritis patients is ruptured aneurysms [Matsuoka]. The rupture of aneurysms is no doubt accentuated by the high blood pressure that is associated with arthritis [Panoulas]. Vasculitis similar to polyarteritis nodosa is the most fatal of systemic complications [Hollingsworth]. Potassium chloride supplements prevent kidney damage in sodium loaded spontaneously hypertensive rats [Ellis] even though potassium as the chloride increases blood pressure, for it seems that potassium as the chloride raises blood pressure instead of lowering it in rats. Potassium deficiency damaged kidneys take several months to heal [Relmon].

There is also a single case history in which a subject was injected with various steroid hormones for a short time each to determine their effect. The only consistent change during the course of the experiment was that his daily intake of potassium was raised to 3500 milligrams per day. His arthritic symptoms showed a consistent improvement throughout the course of the experiment even though some of the hormones used increase potassium excretion [Clark]. Now an unpublished experiment has been performed by Rudin on arthritics in which potassium supplements showed favorable results on eight patients [private communication]. In an experiment unrelated to arthritis, serum potassium was not improved with 1 gram of potassium per day unless magnesium was supplemented also. This was because magnesium is necessary in order to power the potassium pumps no doubt. Potassium can not be absorbed efficiently in the presence of a magnesium deficiency probably at least partly because the body cells can not absorb potassium [Ryan, p100] (or at this site). Potassium can be impossible to absorb during a magnesium deficiency. Furthermore, a magnesium deficiency increases aldosterone secretion, which hormone increases potassium excretion. An experiment supplementing both would be in order in the future for arthritis in order to get crisper correlations. See this site for magnesium deficiency symptoms.

Spironolactone has been found to improve juvenile arthritis and other types of rheumatoid arthritis [Bendtzen] Spironolactone is a substance that inhibits the action of aldosterone, which is the hormone that stimulates potassium excretion. This is a rather ridiculous way to get cell potassium up. Nutritious food is the way to go.

One of the arthritic diseases is known as gouty arthritis in which sodium urate crystals are deposited in cartilage, especially in the feet. 90% of victims are men , perhaps because men are more likely to come in contact with lead. The crystals are thought to be ingested by white blood cells and produce inflammation by rupture of the lysosome sacs and release of their contents [Turner]. Urate is the major end product of purine (nucleoproteins) degradation in higher primates in contrast to most other mammals because of the genetic silencing of hepatic oxidative enzyme uricase. The kidney plays the dominant role in urate excretion, with the intestines accounting for about one third as much. The kidney excretes 70% of the daily urate production [Naohiko].

Lin has statistical evidence linking gout to lead poisoning [Lin 2002]. The lead poisoning makes the aldosterone system insensitive to potassium concentration and increases the potassium content of the blood plasma [Gonzalex]. The blood lead content is no indicator of toxicity and the status must be obtained with an EDTA mobilization test [Batuman]. Lead level in the body is significantly correlated with urate excretion and gout [Lin 2002]. Ethylenediaminetetraacetic acid chelator of lead has successfully increased uric acid excretion [Lin 2001]. Fluoride has been suggested to increase lead intake (see this site for a discussion of fluoride toxicity. ). Other poisons than lead may move one a little closer to gout also, such as timalol (Blocadran) combined with hydrochlorothiazide and amiloride [*] (a diuretic [Greenly]). I also suspect that toluol or some other chemical in acrylic automobile enamel may be able to trigger gout, from personal experience and I also suspect echinacea herb.

You may see an extensive discussion of gout inWikipedia along with solubility of it’s salts.I have heard of a doctor who gave his patients potassium losing diuretics and thus triggered an attack of gout. By adding a potassium supplement he was able to remove the gout. A medical doctor respondent has used potassium supplements for years for gout [private communication]. Gout can be triggered by the same agents that cause potassium losses such as fasting, surgery, and potassium losing diuretics [Rodman]. A potassium deficiency can increase urate levels in the blood [Davis] so there is a circumstantial connection. Urate kidney stones form during gout in a 10-30% of cases [Colton]. Making the urine less acid with potassium citrate or sodium bicarbonate is a current treatment for kidney stones [Shekarriz] [Rodman]. Potassium citrate has been successfully used to eliminate urate stones. I suspect that potassium bicarbonate or citrate would be preferable to potassium chloride, and there is now clinical evidence that potassium bicarbonate will remove kidney uric acid stones while sodium bicarbonate will not prevent their formation. Potassium chloride added to a junk food diet should be equivalent to adding hydrochloric acid to a nutritious diet. I have rapidly removed gout symptoms by large potassium bicarbonate supplements several times. By rapidly I mean several days. There are case histories at this site which describe removing gout by potassium bicarbonate supplements. You may see my extensive discussion in this article.

The initiating factor is probably usually lead poisoning though [Wright]. There is an association in peoples minds between gout and rich foods and lifestyle, probably because people with gout have trouble excreting nitrogen in a soluble form, which nitrogen is high in meat, and perhaps also because wine bottles and plumbing used to contain lead, which last were only available to affluent people in the distant past. Until such time as the matter is elucidated, it would be a good idea to stop eating lead, eat less proteins (especially purines), and not allow any potassium to be lost from one's food at least if you have gout. It may be that proteins from low fat dairy products may not exaggerate gout [from an inaccessible publisher URL]. Cherries have been shown to decrease urate in the urine of healthy women [Jacob], so they may have some therapeutic value. Some support to this possibility is that one half pound of cherries relieved the gout in 12 people [Blau]. It is possible that there is a substance in cherries that retards potassium excretion. There is some anecdotal evidence that celery and lettuce will relieve gout. If so, their high potassium content is probably what is involved. There is a discussion of current alternate treatment for gout online, which include black cherries. One would think that people with kidney failure that causes potassium retention would not have gout, but I know of no evidence for such a correlation. Uric acid itself is not a factor in hart disease because uric acid does not correlate with mortality from heart disease when damage to the heart and kidneys is taken into account [Lazzeri]. Orotic acid has been recommended for gout since it decreases uric acid. A dosage of 4,000 mg of Orotic Acid ((Pyrimidinecarboxylic acid, also known as vitamin B13, Animal Galactose Factor, Oro, Orodin, Oropur, Orotonin, Oroturic, Orotyl, or whey factor.) Vitamin B13 is not really recognized as a vitamin. It is manufactured in the body by intestinal flora. is normally used for a maximum of six days in Gout patients. Orotic acid is not necessarily always good in excess since it is said to bind zinc to a non-biologically active state and can damage the liver, but I would think that the 50 to 100 milligrams that has been recommended for normal supplementation should be safe. Sources of oratate are whey, yogurt, beetroot, carrots, and jerusalem artichoke.

Drinking coffee but not tea has been found to lower uric acid in the serum so this effect is not likely to be from caffeine [Kiyohara] or the potassium.

Systemic lupus erythmatosis (SLE or lupus) has caused such extensive damage to kidney tubules that the patients had chronic high plasma potassium which was not responsive to aldosterone [De Pronzo]. Since Lupus patients have been shown to have visibly damaged tubule in 66% of patients examined, the investigators believe that this hyperkalemia is more common than realized. Since Lupus is listed as one of the arthritic diseases and has some similar symptoms, there may be a temptation to use supplements to heal it. Not only should this probably not be attempted, but also even foods high in potassium may be undesirable in the light of this report. Maybe with some lupus victims’ potassium intake must have a narrow safe range. Research to cast light on this would be highly desirable. Several circumstances have been found to act oppositely in rheumatoid arthritis from lupus such as pregnancy, estrogen, and schizophrenia [Mawson]. Osteoarthritis can not be corrected by potassium, or at least by potassium alone [Jones].

You must be thinking that surely scientists must have created deficiencies of potassium and observed their effects. This is indeed true, at least with animals. Experiments with humans are extremely dangerous since permanent damage can be inflicted on the heart and kidneys [Rubini 1961]. I know of no long term experiments on people. Arthritis is difficult to diagnose in animals since they have no way of describing pain, and since there are no sure laboratory tests for arthritis other than potassium, which we already know is going to be low in a deficiency. Also the most common experimental animals, rodents, do not use cortisol, as will be discussed in a later chapter, and cortisol is deeply involved in arthritis.

Acute symptoms can be detected by laboratory methods. Acute symptoms can begin to materialize when as little as 15,000 milligrams (10%) out of the approximately 150,000 milligrams of potassium normally present in an adult male are missing. Numerous animal experiments have revealed the following symptoms:
The fluid (serum) of the blood becomes lower in potassium, chloride, and alkalinity [Luke][Gardner 1950]. The serum potassium declines along a curve which becomes asymptotic to the cell content axis at about 50% loss of cell content and a little over 1 mEq per liter [Scribner (with a graph)]. Scribner and Burnell use 40%, but their designation of normal is too low for humans at about 4 mEq per liter, which should be 4.8 mEq. Average in our society may be near 4.0 but 4.8 is optimum. At this -50% point much further reductions will result in death. His graph assumes normal renal function, insulin, and pH (hydrogen ion or acidity). The blood alkalinity can sometimes be corrected with hydrochloric acid, but some animals and people can only be corrected with potassium chloride [Adler p438]. This alkalinity is probably the reason why the stomach (gastric) secretions are often low in acidity in arthritics [Hartung]. Aldosterone decreases during a potassium deficiency about six fold at low sodium intake [Baumann]. The blood volume, pulse, pressure, and body weight often decline [Gann]. Low serum potassium results in a lower T wave which are rounded and prolonged, as well as slightly prolonged Q-T interval, depression of S-T segment, and possible inversion of P waves in the electrocardiogram (ECG) [American Medical Association p 455]. The ECG in general parallels the serum potassium and below 4.0 milliequivalents per liter the T-wave is decreased or inverted [Ono]. The plasma carbon dioxide, cholesterol triglycerides, urate levels [Davis], and renin [Abbrecht 1970][Sealey], which last is a hormone related to blood pressure, often rises. The stimulation of renin is thought to be due to inhibition of chloride transport in the kidney's loop of Henle [Kotchen]. The loss of pulse pressure is probably a function of potassium inside the cell, rather than serum potassium [Abbrecht 1973]. Glucose intolerance develops exclusively associated with lower insulin secretion rather than cellular response to insulin [Rowe][Gardner 1952]. It could be an adaptation to avoid low plasma potassium resulting from the potassium entering into the cell in order to associate with glycogen that would otherwise occur. Low cell potassium can inhibit the insulin response independently of serum potassium [Spergel]. Apparently the glycogen in the liver increases, though, nevertheless [Marcus]. Prostaglandin E2 hormone is inhibited by increase in plasma potassium considerably in dogs [Galvez] over a wide range of potassium concentration. The inhibition is a result of inhibition of arachidonic acid release [Zusman]. This might result in a greater allergic response during potassium deficiency, and arthritics do tend to be more allergic. Low sodium and high potassium has cured a case of urticaria (skin hives high in mast cells, urine high in histamine from allergic reaction). However serum potassium is abnormally high during hives [Welt, et al 1960][Rusk]. The ratio of cell potassium to serum potassium must be deeply involved.

The gastric secretion decreases in acidity and in potassium content, and increases in sodium content [Welt 1960 (this is an extensive review)]. This is consistent with the low cell potassium during rheumatoid arthritis since arthritics have a low secretion of stomach acid [de Witte].

The urine usually shows a reduced excretion of the organic negative ions such as citrate [Evans]. Since this excretion may be a mechanism for helping to conserve chloride, this may explain the reason for some of chloride reduction mentioned above. It may be an adaptation to avoid too much acidity when a strong base forming ion like potassium is lost. Chloride wasting starts when 20,000 milligrams of potassium out of 150,000 are gone [Garella]. Most of the chloride reabsorption is said to occur in the ascending limb of the Henle tubule via the sodium-potassium-2 chloride cotransporter and most of the chloride reabsorption in the distal tubule is by thiazide sensitive sodium - chloride cotransporter [Amlal]. These transporters are inhibited during a deficiency [there are diagrams in Amlal's reference]. Something like this would be necessary in order to prevent the chloride from making the plasma acidic when sodium entered the body's cells to take the place of potassium.

There are several enzyme systems in the kidneys that are affected by a deficiency. The enzyme which reduces the amino acid glutamine to ammonia is one of them and its activity is increased [Wohl p832][Rector][Brown][Tannen]. The ammonium ion has a positive charge and is about the same size as potassium. Therefore this may be a mechanism for helping to prevent potassium loss by substituting ammonium. The ammonium is said to be synthesized in the mitochondria of the proximal tubule cells, excreted in part by the sodium/hydrogen ion exchanger (NHE-3), then reabsorbed by the sodium-potassium-chloride cotransporter, and then brought to the collecting duct and excreted [Amlal]. I have not been able to find out which hormones regulate chloride excretion, if any. In any case, getting enough potassium from food is a much superior strategy for protecting potassium than using glutamine. Glutamine is used as a nitrogen shuttle during infection [Labow], and this may be part of the protection by potassium against infection. Fortunately getting enough potassium in food is not nearly as complicated as what happens to it after it arrives in the body.

Active excretion of potassium virtually ceases in the kidney tubules after two days on a low potassium diet [Linas]. A small part of the potassium that originally entered the kidneys through the glomerulus continues to be excreted, and potassium loss can not be completely cut off. The ability of the kidneys to conserve sodium is impaired. This is because of decline of aldosterone, no doubt.

Urinary excretion of calcium, magnesium and phosphate is higher during a potassium deficiency in Dahl rats. Increasing potassium with potassium carbonate in menopausal women who have low serum potassium results in bone uptake of calcium and phosphorus, so this circumstance must be similar in humans. It has been proposed that this bone uptake of calcium from increased potassium results partly from salt-induced volume expansion, with an increase in glomerula filtration rate, and partly to competition between sodium and calcium ions in the renal tubule that attends a low calcium intake coupled to a high salt intake [Heany]. Reduced salt or increased calcium makes the potassium reaction disappear. Frassetto, et al propose that the phenomenon is somehow associated with the acidosis that attends a low potassium intake. The concept seems to be backed up by epidemiological studies of correlation with urinary potassium in older women.

It is thought that the reduction of magnesium is what causes the association of potassium with hypertension by virtue of the affect of magnesium on the power of the potassium-sodium pumps [Potassium depletion and salt sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions.] Six months are required of magnesium supplements before complete normalization of pumps [Potassium and sodium, and potassium pumps in the skeletal muscle].

The fluid inside the cells shows a decrease in potassium, alkalinity, and phosphate [Gardner 1953] but no reduction of potassium in rat brain and liver, 18% in heart and kidneys, and 48% in muscle [Southon]. Part of the lost potassium inside the cells is replaced by sodium [Rubini 1972]. This is probably the reason why there is increased edema when potassium is repleted at first[Welt 1960 p245] since the sodium is forced out of the cells then. Arginine [Iacobellis] and lysine [Eckel], which are amino acids having a positive charge, show a marked rise in the fluid of some cells in some animals, going from almost zero to 8% of the positive ions. Adequate potassium has been shown to be necessary for protein synthesis [Cannon 1951]. There is considerably less protein metabolized in deficient chicks [Rinehart]. The positive ions, calcium and magnesium, increase inside the cells and the cell becomes more acid [Gardner 1950]. If these are adaptations to solve a potassium deficiency, such elaborate mechanisms are an indication that potassium is much more of a problem in nature than medical people think, let alone in our potassium-starved society. The diarrhea diseases are the primary problem for this in nature, no doubt. DNA synthesis inside the muscle cell is decreased during a deficiency [Truong].

An abnormal thirst is also thought to be frequently present in a deficiency. Increased water intake rises to a peak in dogs in 3 to 7 weeks, then declines to normal [Smith]

Perhaps it would be a good idea to determine as many of these circumstances as are possible without a biopsy while people are healthy so that when they become sick the potassium status can be easily estimated without expensive machinery or long time delays.

I can not be certain that all the phenomena above are caused by an acute deficiency in humans, but most are quickly and easily reversible in animals. Most of the data that do not require analysis of internal organs have been confirmed in humans.

Effects that are not easily reversible or involve structural changes in the body's cells are as follows: The part of the adrenal gland (zona glomerulosa) which synthesizes aldosterone atrophies [Cope p432]. Fat (they probably meant cholesterol) is deposited in the vascular system. This deposition is probably reversible [Davis][Strauss]. More serious is lesions of the kidneys in hypertensive salt loaded rats and permanent scarring of the kidneys which is probably irreversible [Holman]. Welt believes that the consensus is that kidney damage is reversible, however, and is largely in the distal tubules and collecting ducts [Epstein p272] with no visible changes in the glomeruli [Welt 1960 p224,225]. Calcification is prominent during phosphate loading [Welt 1960 p225]. Small particles in the cell called ribosomes have the internal structure lastingly altered. Mitochondria of the collecting tubules swell and disrupt [Kark]. Certain cells in the kidneys that have a darker color than the others increase in numbers. There is also abnormalities in the structure of other kidney cells [Rhodin][Naslund][Strauss]. Cells in the lining of the tubules are most affected in dogs [Tate]. The above is based on animal experiments. Man rarely has kidney destruction that appears the same as the rat's or dog's. Localized death of heart cells is usually found in the species observed [Rowinski][Folis][Molnar] but is not always observed in every individual [Tate]. Heart lesions from a potassium deficiency are well established. The fibers lose striations and assume a hyaline appearance. [Folis 1953]. This depend on an adequate sodium intake [Cannon 1953]. However since sodium is almost always accompanied by chloride, I am not sure that this relationship is accurately known yet since it could be the chloride which is giving part or even all of the problem, for potassium as the chloride given to rats has been shown to increase blood pressure rather than lower it as does the bicarbonate. Heart disease will be discussed at more length in the potassium supplement chapter and also here to some extent.

There is a striking, consistent alteration of the kidneys' ability to concentrate fluids in humans. This impairment reverses in one and a half to four years after relieving a deficiency, but not always [Hollander p933]. I suspect that this is to maintain urine flow by excreting water so as to reduce potassium loss that would otherwise obtain if the urine had a potassium concentration the same as serum.

Potassium is thought to be essential to defense against pathologic bacteria on the basis of increased liability to infection in deficient kidneys [Woods] that have suffered no change otherwise. It may be that the reason for this has been found. It seems that the white cell vacuole requires an alkaline medium in order to both kill and digest microbes. To achieve this it must pump potassium into the vacuole using a calcium activated (Bkca) pump. This is known because, when a chemical blocks this pump channel, microbes are not killed in spite of normal phagocytosis (engulfing of microbes) and oxidase activity [Ahluwalia]. So it seems plausible to me that, when the pump is operating normally in the absence of the above poison, a low cell potassium would make it more difficult to achieve the enhanced alkalinity. This may be the reason why potassium deficient kidneys are susceptible to infection and other infections may yet prove to be overcome with more difficulty, possibly even mycobacteria. If mycobacteria are causing arthritis as some suspect, this could explain why potassium supplements cures arthritis.

Muscular strength is directly related to potassium intake [Judge]. Paralytic blockage of the lower intestines, which sometimes attends surgery, is probably contributed to by low potassium [Lowman]. Rats have symptoms during a deficiency that include abdominal distention, lethargy, sagging organs, and loss of tone, and sometimes decreased movement of the intestines [Schrader]. A potassium deficiency seems to be most destructive to the tissues that derive from the middle layer of the embryo [Seekles]. These tissues include all the connecting tissues, the heart, the blood vessels, the kidneys and the white blood cells. A potassium deficiency causes a higher mortality during stroke. This increase is independent of age, severity of the stroke, blood pressure, history of hypertension, or smoking [Ganballa, et al].

In addition to the above phenomena, most of which have either been established beyond any doubt or have fairly substantial experience behind them (although usually based on animal experiments), it is my contention that rheumatoid arthritis is essentially a chronic potassium deficiency, or is greatly affected by one. Lending some circumstantial support to this proposal is that expression of voltage-gated K+ channels in mAb-defined T cell subsets from normal mice and mice with experimental autoimmune arthritis was studied with the patch-clamp whole-cell recording technique in combination with fluorescence microscopy. CD4+CD8- The cells from DBA/1 LacJ mice with type II collagen arthritis expressed low levels of type n K+ channels, and CD4-CD8+ T cells (cytotoxic) showed small numbers of type l or n' K+ channels, like their phenotypic counterparts in normal mice. CD4-CD8-Thy-1.2+ (double negative or DN) T cells from the diseased mice, however, displayed an abundance of type l K+ channels compared to DN T cells in normal mice. Furthermore, the aberrant expression of type l K+ channels correlated with the presence of active disease [Grissmer]. It may be that some genetic difference like sexual hormones, or differences in secretion of other hormones such as the glucocorticosteroid response modifying factors (GRMFs), or some other imbalance with other nutrients such as copper affect who and when arthritis strikes. Obviously any disease or poison that interferes with retention of potassium would increase the chance of a deficiency developing. Considering that some of the symptoms of a deficiency take a long time to heal, it seems as if a deficiency should be avoided with almost the same urgency as a water deficiency (dehydration). Also, a deficiency of, say, 40 or 50 thousand milligrams would take a fairly long time to be completely corrected by food since getting more than 3500 milligrams per day is difficult and not all of it is retained. It would probably be measured in weeks at least. Potassium as potassium chloride would be much faster. In most cases, the worst reversible symptoms would probably disappear in a week or so if a thousand milligrams were added to each meal in that case. Potassium as the chloride raises blood pressure, so such a supplement probably should not be used for those with high blood pressure, for potassium chloride has been shown to increase blood pressure in rats. This may be because of difficulty in handling hydrogen ion (acid) in some forms of high blood pressure. Support is given to this possibility since sodium bicarbonate lowered blood pressure 5 mm of mercury while sodium chloride had no affect [Luft], possibly partly because sodium chloride was already high in their diet. Both sodium and chloride are necessary for pressure augmentation [Boegshold]. This phenomenon may be involved with 18 hydroxy deoxycorticosterone steroid hormone (18OHDOC) because that hormone is raised in one of the forms of high blood pressure and that hormone is the hormone used by the body to increase acid excretion. Potassium is the main circumstance though, because vegetarians had consistently much lower blood pressure than non vegetarians in the same urban setting even though the sodium intake (and therefore chloride) of both groups was the same [Ophir]. Also limited experience makes me suspect that acids accentuate some types of headaches and potassium chloride should give the same affect as adding hydrochloric acid to a normal diet. If supplements are used, magnesium at least must be considered. Also a vitamin B-1 deficiency (beriberi) becomes very dangerous for vitamin B-1 type of heart disease (wet heart disease of beri-beri) from potassium supplements [Folis]. This last situation could be involved for those who imbibe foods that contain sulfites because sulfites destroy vitamin B-1 in the intestines. Such foods are wine, vinegar, pickles, olives, salad dressing, canned clams, fresh, frozen, canned, or dried shrimp, frozen lobster, scallops, dried cod, gelatin, pectin jelling agents, cornstarch, modified food starch, spinach pasta, gravies, hominy, breadings, batters, noodle/rice mixes, shredded coconut, vegetable juice, canned vegetables (including potatoes), pickled vegetables (including sauerkraut), dried vegetables, instant mashed potatoes, frozen potatoes, potato salad, corn syrup, maple syrup, fruit toppings, and high-fructose syrups such as corn syrup and pancake syrup, instant tea, liquid tea concentrates, beer, bottled lemon juice, some baked goods, and some dried fruits or eat unfortified refined grains. Using diuretics can cause loss of vitamin B-1 [10 Suter]. One symptom of a vitamin B-1 deficiency is lactic acid acidosis [Romanski]. The reverse would also be the case and so taking vitamin B-1 supplements should be dangerous for arthritics since heart disease is more common among rheumatoid arthritics than others, probably for this reason. Osteoarthritis is probably the same as other healthy people in this regard. So unprocessed, nourishing food high in vegetables is probably usually the best and safest way to get both potassium and vitamin B-1.

If "rheumatoid arthritis" or “potassium induced heart disease” are not words describing a potassium deficiency then what is the word equivalent to "beriberi" which describes a chronic potassium deficiency? Hypokalemia or hypopotassemia are not such words. They simply are words describing a very low plasma content, with symptoms of lower T wave on the electrocardiogram, drowsiness, nausea, muscular weakness, low blood pressure, reduced digestive ability [Robinson], tachyarrhythmias, fibrillation, memory impairment, confusion, anorexia, constipation, lethargy, apathy, fatigue, depression, headache, irritability, and visual disturbance [Lindeman] (but for some reason hypokalemia induced by testosterone does not affect the electrocardiogram [Goldberger p113] ). It would seem strange to have no word that describes the degenerative disease or diseases that accompany a chronic cellular potassium deficiency. I would suggest that we find one soon.

No one has tested potassium to treat rheumatoid arthritis in the past, but now Dr. Reza Rastmanesh from Iran has recently performed a large controlled clinical trial testing potassium supplements against rheumatoid arthritis with dramatic decreases in pain in all subjects and increases of cortisol [Rastmanesh]. He would now like to continue his clinical research testing potassium in conjunction with other nutrients, especially magnesium, in an English speaking country. His credentials are impressive. If you know of any rheumatology or nutrition department able to employ him, please contact me.

continue to Chapter IV, ROLES of POTASSIUM in the BODY

Back to chapter I, ARTHRITIS


The author, Charles Weber, has a degree in chemistry and a masters degree in soil science. He has researched potassium for 50 years, primarily a library research. He has cured his own early onset arthritis (33 years old). He has published articles on allied subjects in; The Journal of Theoretical Biology (1970, 1983), The Journal of Applied Nutrition (1974) which gained the best article of the year award, Clinical and Experimental Rheumatology (1983), and Medical Hypotheses (1984, 1999, 2007, 2008) This article is solely funded by the author and no advertisements are knowingly included other than a book about potassium nutrition.

All printed rights to this article are reserved. Electronic rights are waived.

Email to; isoptera at or 1 828 692 5816 (USA)


There is an article discussing anacardic acids in cashew nuts to cure a tooth abscess that will prove useful.
There is an article that discusses copper nutrition to prevent herniated spinal discs, hemorrhoids, aneurisms, strokes, and high cholesterol.
There is also an article which proposes some speculation about diabetes amelioration as well as a chili pepper cause.
Fluoride in city water will cause fluorosis discoloration of teeth, weakened bones, damage to the kidneys an immune system, and, worst of all, damage to the nerves resembling Alzheimer’s disease. It will also cause damage to ligaments resembling arthritis.
The pioneering efforts about potassium for arthritis by Charles de Coti-Marsh enabled him to form a foundation currently active in England that promotes the use of potassium for arthritis and it has helped 3500 people.
There is a site that contains reviews of natural remedies for many diseases.

See this site for some links to health articles.
For a procedure that discusses tetrathiomolybdate for removing copper and thus preventing further solid cancer growth and Hodgkin’s, see this site. This might buy some time until you can persuade a doctor to try tumor necrosis factor or interferon or an opioid antagonist drug called Naltrexone (Naltrexone in the large 50 mg size, originally manufactured by DuPont under the brand name ReVia, is now sold by Mallinckrodt as Depade and by Barr Laboratories under the generic name naltrexone) that blocks some endorphin receptors. Said blockage is thought to cause the body to temporarily secrete more endorphins, especially after midnight at night. These endorphins are thought to stimulate the immune system, and in particular to stimulate the TH-1 or type 1 antiviral response by decreased interleukin-4 and with increased gamma interferon and interleukin-2 and a simultaneous decrease of type 2 anti bacterial response [Sacerdote]. It appears to be especially effective for minimizing symptoms and retarding progression of multiple sclerosis (MS) There are drugs listed in this site that should not be taken with low dose Naltrexone, including cortisol. Advice how to proceed if you have been taking cortisol may be seen here. (also see these sites; this site and this site and a trial) . A few doctors have had encouraging results in Crohn's Disease, and even to some extent in cancer. Low doses of Naltrexone (LDN), 1.5 to 4.5 milligrams, at bedtime is used (timing is important, and it is important not to buy slow release forms). It is said to have no known bad side effects at those doses other than insomnia the first week or two in some. There is also reports from an extensive survey in this site. and an extensive discussion at this site. I think some clinical studies on Naltrexone are in order, and it should not be a prescription drug (I have a petition to make Naltrexone an over the counter drug with the Center for Drug Evaluation and Research FDA Rockville MD 20857, Re; Docket No. 2006P-0508-CPI. Perhaps if enough people wrote supporting the petition it could be enacted). Though side effects appear unlikely, it is not proven over longer periods. If you try it (it is a prescription medicine in the USA), it seems likely that you should discontinue if you get a bacterial infection in view of its inhibition of antibacterial response. It is also being explored for AIDS by Dr. Bernard Bihari, 29 W 15th St. New York, NY 10011, 212) 929-4196 who is still prescribing Naltrexone for HIV/AIDS. (and currently Executive Director of the Community Research Initiative). Dr. Gale Guyer of Advanced Medical Center located in Zionsville, Indiana also is using it for cancer. Dr. Bihari has shown promising results for a large percentage of his cancer patients.

Olive leaf extract has shown clinical evidence of effectiveness against a wide range of viruses, including AIDS [Bihari], herpes, and cold viruses. It sometimes produces a Herxheimer or pathogen die off symptoms (from effectiveness against bacteria?). There is evidence that it is synergistic (reinforce each other) with Naltrexone. There have been a few case histories of improvement in what were probably arthritis patients and CFIDS patients. The active ingredient is said to be oleuropein or enolate. There has been very little follow up research done on it.

Also it has been found that curcumin in turmeric or curry powder will inhibit several forms of cancer, including melanoma. People who live in India where these spices are eaten, have one tenth the cancer elsewhere. Here is an article with anecdotal evidence for pressurized oxygen, zinc, vitamin B6, and vitamin C after head injuries. They also claim a fair percentage of prison inmates from psychiatric disorders after head injuries.
See this site for evidence of a correlation between magnesium deficiency and cancer. The taurate is proposed as the best magnesium supplement. Taurine or 2-aminoethanesulfonic acid is an acidic chemical substance sulfonated rather than carboxylated found in high abundance in the tissues of many animals (metazoa), especially sea animals. Taurine is also found in plants, fungi, and some bacterial species, but in far less abundance. It is an amine with a sulfonic acid functional group, but it is not an amino acid in the biological sense, not being one of the twenty protein-forming compounds encoded by the universal genetic code. Small polypeptides have been identified as containing taurine, but to date there has been no report of a transfer RNA that is specifically charged with taurine [from Wikipedia]. It is essential to babies. It has been found that supplements of the amino acid, taurine, will restore the abnormal electrocardiogram present during a potassium deficiency by an unknown mechanism. This information has been used in several case histories by George Eby to control a long standing type of cardiac arrhythmia called pre atrial contractions (PACs), a benign but irritating and nerve racking heart problem, with 2.5 grams of taurine with each meal. . Taurine is said to be low in the diets of vegetarians. The 2.5 grams recommended by the American Heart Association causes diarrhea in some people and should probably be reduced in those people. Taurine has been used for high blood pressure, migraine headache, high cholesterol, epilepsy, macular degeneration, Alzheimer’s disease, liver disorders, alcoholism, and cystic fibrosis, and depression. Keep in mind that some people may have a genetic defect that limits the amount of taurine tolerated and that adequate molybdenum may desirable.

A site is available which shows. foods which are high in one nutrient and low in another (including calories). This last site should be especially useful for a quick list of foods to consider first, or for those who must restrict another nutrient because of a genetic difficulty with absorption or utilization

The very extensive USDA Handbook #8 may be seen here. To access the information you must press "enter" to search, and then divide Kcal into milligrams of potassium. This last table is very comprehensive, is used in search mode, and even lists the amino acids. There are also links in it to PDF types of printouts from the table for individual nutrients available here Just click on the “A” or “W” button for the nutrient you desire. A table that has already done the potassium calculation is here in descending concentration or in alphabetical order.

There is a free browser called Firefox, which is said to be less susceptible to viruses or crashes, has many interesting features, imports information from Iexplore while leaving Iexplore intact. You can also install their emailer. A feature that lists all the URLs on a viewed site can be useful when working on your own site.

There is a tool bar by Google that enables you to search the internet from the page viewed, mark desired words, search the site, give page rank, etc. It links to a literature search.

There is a free program available which tells on your site what web site accessed you, which search engine, statistics about which country, statistics of search engine access, keywords used and their frequency. It can be very useful.

All printed rights for sale to this article are reserved. Electronic rights are waived.


Abbrecht PH & Vander AJ 1970 Effects of chronic potassium deficiency on plasma renin activity. Journal of Clinical Investigation 49; 1510-1516.

Abbrecht PH 1972 Cardiovascular effects of chronic potassium deficiency in the dog. American Journal of Physiology 223; 555-560.

Adler S Fraley DS 1977 Potassium and intracellular pH. Kidney International, 11; 433-442.

Ahluwalia J Tinker A Clapp LH Duclien MR Abromav AY Pope S Nobles M Segal AW 2004 The large-conductance Ca2+ - activated K+ channel is essential for innate immunity. Nature 427; 853—858.

American Medical Association 1951 Handbook of Nutrition, 2nd Ed. Blakiston Co., NY.

Amlal H Wang Z & Soleimani M 1998 Potassium depletion down regulates chloride - absorbing transporters in rat kidney. Journal of Clinical Investigation 101; 1045-1054.

Batuman V Maesaka JK Landy E Haddad B Wedeen P Tepper E 1981 The role of lead in gout nephropathy. New England Journal of Medicine 304; 520-3.

Baumann K & Muller J !972 Effect of potassium intake on the final steps of aldosterone biosynthesis in the rat. Acta Endocrinol. 69; 701 & 718.

Bellevue R Dosik H Spergel G Gussof BD1975 Pseudohyperkalemia and extreme leukocytosis. Journal of Lab.Clin. Med. 85; 660-664

Bendtzen K Hansen PR Rieneck K 2003 Spironolactone inhibits prodction of inflammatory cytokines, including tumour necrosis factor-alpha and interferon-gamma, and has potential in the trearment of arthritis. Clinical and Experimental Immunology 134; 154-158.

Bihari B 1995 Efficacy of low dose Naltrexone as an immune stabilizing agent for treatment of HIV/AIDS [letter] AIDS Patient Care 9; 3.

Blau LW. Cherry diet control for gout and arthritis. Tex Rep Biol Med 1950;8:309-11.

Brown MR et al 1944 Muscular paralysis and electrocardiographic abnormalities resulting from potassium loss in chronic nephritis. Journal of the American Medical association 124; 545.

Cannon PR et al 1951 Influence of potassium on tissue protein synthesis. Metabolism 1; 49-57.

Cannon PR et al 1953 Sodium as a toxic ion in potassium deficiency. Metabolism 2; 297-312.

Clark WS et al 1956 The relationship of alterations in mineral and nitrogen metabolism to disease activity in a patient with rheumatoid arthritis. Acta Rheum. Scand. 2;193.

Cockel R, Kendall MJ, Becker JF, Hawkins CF: Serum biochemical values in rheumatoid disease. Ann Rheum Dis 1971; 30(2):166-70.

Colton RS Ward LE 1966 Uric acid, gout, and the kidney. Medical Clinics of North America 50, o. 4; 1031-1042.

Cope CL 1964 Adrenal Steroids and Disease. JB Lippincott Co., Philadelphia.

Davis WH 1970 Does potassium deficiency hold a clue to metabolic disorders associated with liability to heart disease?. South African Med. Journal 44; 1297.

de Witte TJ Geerdink PJ Lames CB Boerbooms AM van der Korst JK 1979 Hypochlorhydria and hypergastrinaemia in rheumatoid arthritis. Annals of the Rheumatic Diseases, 1979, Vol 38, 14-17.

Eckel RE et al 1954 Lysine as a muscle cation in potassium deficiency. Arch. Biochem. Biophys. 52; 293

Ellis D Banner B Janosky JE Feig PU 1992 Potassium supplementation attenuates experimental hypertensive renal injury. Journal of the American Society of Nephrology, Vol 2, 1529-1537.

Epstein FH 1960 Calcium and the kidney. Journal of Chronic Diseases 11; 255-277.

Evans BM et al 1957 Alkalosis in sodium and potassium depletion. Clinical Science 16; 53.

Folis RM et al 1942 The production of cardiac and renal lesions in rats by a diet extremely deficient in potassium. American Journal of Pathology 18; 29

Folis RH 1942 Myocardial necroses in rats on a potassium low diet prevented by thiamine deficiency. Bulletin Johns Hopkins Hosp.71; 235-241.

Folis RH, Jr. 1953 The pathology of potassium deficiency. 73; 241.

Frassetto L Morris RC Jr. Sellmeyer DE Todd K Sebastan 2001 Diet, evolution and aging The pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Europian Journal of Nutition 40 (no. 5); 200-213.

Galvez OG; Bay WH; Roberts BW; Ferris TF Source Circ Res, 40(5 Suppl 1):I11-6 1977.

Ganballa SE Robinson TG Fotherby MD 2001 Low plasma potassium on admission associated with increased death independent of age, severity, blood pressure, history of hypertension, or smoking. Journal of the American Geriatrics Society 45; (from the abstract).

Gann DS et al 1964 Control of aldosterone secretion by change of body potassium in normal man. American Journal of Physiology 207; 104.

Gardner LI et al 1950 The effect of potassium deficiency on carbohydrate metabolism. Journal Lab & Clin. Med. 35; 592-602.

Gardner LI MacLachlan EA Berman H 1952 Effect of potassium deficiency on carbon dioxide, cation, and phosphate content of muscle. Journal of General Physiology 36; 153-159.

Gardner LI 1953 Experimental potassium depletion. Journal Lancet 73; 190.

Garella S et al 1970 Saline - resistant metabolic alkalosis or chloride - wasting nephropathy. Ann. Internal Medicine 73; 31-38.

Gonzalez JJ et al 1979 Renin aldosterone system and potassium levels in chronic lead intoxication. South Med. Journal 72; 433436.

Greenly L 2003 An overview of antihypertensive medications and assessing blood pressure using the latest guidelines. Journal of Chiropractic Medicine 2; 117-123.

Grissmer S, Hanson DC, Natoli EJ, Cahalan MD, Chandy KG. 1990 CD4-CD8- T cells from mice with collagen arthritis display aberrant expression of type l K+ channels. J Immunol. Oct 1;145(7):2105-9.

Hartung EF Steinbrocker O 1935 Gastric acidity in chronic arthritis Ann. Intern. Med. 9; 252-257.

Heaney RP 2006 Role of Dietary Sodium in Osteoporosis. Journal of the American College of Nutrition 25, No. 90003, 271S-276S.

Hollander W Blythe WB 1971 Nephropathy of potassium depletion. in; Diseases of the Kidney, II, (Strauss MB & Welt LG, editors) p933 Little Brown & Co., Boston.

Hollingswort JW Saykaly RJ 1977 Systemic complications of rheumatoid arthritis. Med. Clinics of North America 61; 217-258.

Holman RL et al ---- Arterioscelerosis - the lesion. American Journal of Clinical Nutrition 8; 85-94.

Iacobellis M et al 1956 Free amino acid patterns of certain tissues from potassium and/or protein - deficient rats. Amer. Journal Physiology 185 ;275.

Ifudu O Markell MS Friedman EA 1992 Unrecognized pseudohyperkalemia as a cause of elevated potassium in patients with renal disease. American Journal of Nephrology 12; 102-104.

Jacob RA, Spinozzi GM, Simon VA, Kelley DS, Prior RL, Hess-Pierce B, Kader AA. 2003 Consumption of cherries lowers plasma urate in healthy women. J Nutr. 2003 Jun;133(6); 1826-9.

Jasani BM & Edmond CJ 1971 Kinetics of potassium distribution in men using isotope dilution and whole body counting. Metabolism 20; 10991106.

Jones NF et al Inappropriate production of vasopressin, potassium deficiency and heart disease. American Journal of Medicine 45; 474-479.

Judge TG & Cowan NR 1971 Dietary potassium intake and grip strength in older people. Gerontol. Clin. 13; 221.

Kark RM 1958 Some aspects of nutrition and the kidney. American Journal of Nutrition 25; 698-707.

Khaw K-T Barrett-Connor E 1987 Dietary potassium and stroke associated mortality. 316; 235-249.

Kiohara C, et al 1999 Inverse association between coffee drinking and serum uric acid concentration in middle - aged Japanese males. British Medical Journal 82; 125-130.

Kohvakka A Luurila O Gordin A & Sundberg S 1989 Magnesium. Magnesium 8; 71-76.

Kotchen TA Guthrie GP Jr. Galla JH Luke RG Welch WJ 1983 Effects of NaCl on renin and aldosterone responses to potassium depletion. American Journal of Physiology 244; (2) E164-169.

Koyanagi H Nakamura Y Yanagawa H 1998 Lower level of serum potassium and higher level of C-reactive protein as an independent risk factor for giant aneurysms in Kawasaki disease. Acta Paediatrica 87; 32-36.

Labow BI Soula WW 2000 World Journal of Surgery 24; 1503.

LaCelle PL 1964 An investigation of total body potassium in patients with rheumatoid arthritis. Proceedings of the Annual Meeting of the American Rheumatism Association, Arthritis and Rheumatism 7; 321.

Ladefoged K Hagen K 1986 Correlation between concentrations of magnesium, zinc, and potassium in plasma, erythrocytes and muscles. Clin. Chim. Acta 177; 157-166.

Lambie AT 1964 Renal mechanisms of potassium depletion. Proceedings Nutr. Soc. 24; 63-73.

Lazzeri C Valente S Chlostri M Picariello C Gencini GF 2010 Uric acid in the early risk stratification of ST-elevation myocardial infarction. Internal and Emergency Medicine published online Jan. 15.

Lin JL, Yu CC, Lin-Tan DT, Ho HH 2001 Lead chelation therapy and urate excretion in patients with chronic renal diseases and gout. Kidney Int. Jul;60(1):266-71.

Lin JL, Tan DT, Ho HH, Yu CC 2002 Environmental lead exposure and urate excretion in the general population. Am J Med. 2002 Nov;113(7):563-8.

Linas SL Peterson LN Anderson RJ Aisenbrey GA Simon FR Berl T 1979 Mechanism of renal potassium conservation in the rat. Kidney International 15; 601-611

Lindeman RO Pederson JA 1983 Hypokalemia in Potassium: Its Biological Significance. Aikawa JK, ed. CRC Press inc., Boca Raton FL.

Lowman MD 1971 The potassium depletion states and post - operative ileus - editorial. Rad. 98; 691.

Luft FC Zemel MB Sowers JA Fineberg NS Weinberger MH 1990 Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man. Journal of Hypertension 8; 663-670.

Luke RG Wright FS Fowler N Kashgarian M & Giebisch GH 1978 Effect of potassium depletion on renal tubular chloride transport in the rat. Kidney International 14; 414-427.

Marcus DF et al 1968 A comparative study of various hyperglycemic agents in potassium deficient rats. Proceedings of the Society Experimental Biol. Med. 127; 533-538.

Matsuoka Y Obana M Mita S Kohno M Irimajiri S Fujimori I & Fukuda J1981 :: Studies of death in autopsied cases with rheumatoid arthritis, p 27. in; New Horizons in Rheumatoid arthritis, (Shiokawa Y Abe T & Yamauchi Y, eds.). exerpta Medica International Congress Series #535.

Mawson AR 1985 Are rheumatoid arthritis and systemic lupus erythmatosis inversely related diseases? Medical Hypotheses 18; 377-386.

Melby JC, Dale SL, Grekin RJ, Gaunt R, Wilson TE. 18-hydroxy 11 deoxycorticosterone (18 OH-DOC) secretion in experimental and human hypertension. Recent Progress in Hormone Resarch. 28: 287-351, on p 323 1972.

Mikosha, A.S.; Pushkarov, I.S.; Chelnakova, I.S.; Remennikov, G.Y.A. 1991 "Potassium Aided Regulation of Hormone Biosynthesis in Adrenals of Guinea Pigs Under Action of Dihydropyridines: Possible Mechanisms of Changes in Steroidogenesis Induced by 1,4, Dihydropyridines in Dispersed Adrenocorticytes." Fiziol. [Kiev] 37: 60,.

Molnar Z et al 1962 Cardiac changes in the potassium depleted rat. Arch. Pathol. 74; 339-347.

Muehrcke RC & McMillan JC 1963 The relationship of chronic pyelonephritis of chronic potassium deficiency. Ann Int. Med 59; 427

Naohiko Anzai, Atsushi Enomoto and Hitoshi Endou 2005 Renal Urate Handling: Clinical Relevance of Recent Advances. Current Rheumatology Reports 7; 227-234.

Naslund PH & Hultin T 1971 Structural and functional defects in mammalian ribosomes after potassium deficiency. Biochem. Biophys. Acta 254; 104.

NHANES-III, Catalog #77560, U.S. Department of Health and Human Services (DHHS). National Center for Health Statistics. Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III Laboratory Data File (CD-ROM). Public Use Data File Documentation Number 76200. Hyattsville, MD.: Centers for Disease Control and Prevention, 1996. Available from; National Technical Information Service (NTIS), Springfield, VA. Acrobat. PDF format; includes access software: Adobe Systems, Inc. Acrobat Reader 2.1.

Nickel JF et al 1953 Renal function during sodium deprivation. Journal of Clinical Investigation 32; 68-79.

Noergaard A Kjeldsen K Clausen T 1981 Potassium depletion decreases the number of 3H-oubain binding sites and active Na-K transport in skeletal muscle. Nature 293; 739-741.

Nuki G et al 1975 Potassium metabolism in patients with rheumatoid arthritis - effects of treatment with depot tetracosactrin spirono-lactone and oral supplements of potassium chloride. Annals of the Rheumatic Dis. 34; 506-514.

Ono I Hukuoka T & Onodera I 1964 The effects of varying dietary potassium on the electrocardiogram and blood electrolytes in young dogs. Jap. Heart Journal 5; 272.

Ophir O Peer G Gilad J Blum M Aviram A 1983 Low blood pressure in vegetarians: the possible role of potassium. American Journal of Clinical Nutrition 37;755-762.

Panoulas VF, G. S. Metsios, A. V. Pace, H. John, G. J. Treharne, M. J. Banks and G. D. Kitas 2008 Hypertension in rheumatoid arthritis Rheumatology 47(9):1286-1298.

Patrick J & Bradford b 1971 A comparison of leucocyte potassium content with other measurements in potassium - depleted rabbits. Clinical Science 42; 415-421.

Rastmanesh R 2008 A pilot study of potassium supplementation in treatment of hypokalemic patients with rheumatoid arthritis: a randomized, double-blinded, placebo controlled trial. The Journal of Pain 9; 722-731.

Rector FC Jr. et al 1955 The mechanism of ammonia excretion during ammonium chloride acidosis. Journal of Clinical Investigation 34; 20.

Relmon AS Schwartz WB 1956 The nephrology of potassium depletion: depletion a clinical and pathological entity. New England Journal of Medicine.255; 195-203.

Rinehart KE et al 1968 Effect of dietary deficiency of potassium on protein synthesis in the young chick. Journal of Nutrition 95; 627-632

Rhodin JAG 1971 Structure of the kidney. in; Diseases of the Kidney (Strauss MB & Welt LG, editors) Little Brown & Co., Boston.

Robinson CH & Lawler MR 1972 Normal and therapeutic nutrition, Macmillan & Co. New York.

Rodman JS 2002 Intermittant versus continuous alkaline therapy for uric acid stones and uretal stones of uncertain composition. Urology 60; 378-382.

Romanski SA, McMahon MM. 1999 Metabolic acidosis and thiamine deficiency. Mayo Clin Proc. 1999 Mar;74(3):259-63.

Rowe JW et al 1980 Effect of experimental potassium deficiency on glucose and insulin metabolism. Metabolism 29; 448-502.

Rowinski P 1960 Potassium in the animal organism - Proceedings of the 6th Congress of the International Potash Institute, Amsterdam, p381-433.

Ryan MP Whang R 1983 Interrelationships between potassium and magnesium. In; Potassium: Its Biologic Significance. CRC Press, Boca Raton, FL.

Rubini ME 1961 Water excretion in potassium - deficient man. Journal of Clinical Investigation 40; 2215-2224.

Rubini ME & Chojnacki RE 1972 Principles of parenteral therapy. Am. Clin. Nutr. 25; 96-113.

Rusk HA Weichselbaum TE 1939 Changes in serum potassium in certain allergic states. JAMA 112, No. 23; 2395-2398.

Sambrook PN Ansell BM Foster S Gumpbell JM Hesp R Reeve J Zanelle JM 1985 Bone turnover in early rheumatoid arthritis: Biochemical and kinetic indexes. Annals of the Rheumatic Diseases 44; 575-579.

Saruta T Suzuki A Hayashi M Yasui T Eguchi T Kato E 1980 Mechanism of age-related changes in renin and adrenocortical steroids. Journal of the American Geriatrics Society 28; 210-214.

Schrader GA et al 1937 Symptomology and pathology of potassium and magnesium deficiencies in the rat. Journal of Nutrition. 14; 85-109.

Scribner BH & Burnell JM 1956 . Metabolism 5; 468-479.

Sealey JE et al 1970 Potassium balance and the control of renin secretion. Journal of Clinical Investigation 49; 2119-2127.

Seekles L 1960 Potassium in the animal organism. Proceedings of the 6th Congress of the Intl. Potash Institute, Amsterdam 349-379.

Shekarriz B, Stoller ML 2002 Uric acid nephrolithiasis: current concepts and controversies. J Urol. 2002 Oct;168(4 Pt 1):1307-14.

Shick RM 1957 Periarteritis nedosa and temporal arteritis. Collected Papers of the Mayo Clinic 49; 381.

Shin S, Furin J, Alcántara F, Hyson A, Joseph K, Sánchez E, Rich M. 2004 Hypokalemia among patients receiving treatment for multidrug-resistant tuberculosis. Chest. Mar;125(3):974-80.

Smith SG & Lasater TE 1950 Diabetes insipidus like condition produced in dogs with potassium deficient diet. Proc. Soc. Exptl. Biol. Med. 74; 427-431.

Sokolov EI 1966 Disorders of electrolyte metabolism in cases of rheumatic valvular heart disease (Russian). VOP. Revmatizma 1; 55-58 from; Arthritis and Rheumatic Diseases Abstracts 3; 526, 96.

Southon S Heaton FW 1981 Changes in cellular and subcellular composition during potassium deficiency. Comparative Biochemistry and Physiology 72a; 415-419.

Spergel et al 1967 Potassium on the impaired glucose tolerance in chronic uremia metabolism. Metabol. Clin. Ex. 16; 581-585.

Strauss MB & Welt LG, editors 1971 Diseases of the kidney, Vol II, Little Brown & Co., Boston.

Surawicz B 1968 The role of potassium in cardiovascular therapy. Med. Clins. N. Am. 52; 1103-1113.

Syrjanen S, Lappalainen R, Markkanen H 1986 Salivary and serum levels of electrolytes and immunomarkers in edentulous healthy subjects and in those with rheumatoid arthritis. Clin Rheumatol. Jan;5(1):49-55.

Tannen RL 1977 Relationships of renal ammonia production and potassium homeostasis. Kidney International 11; 453-465.

Tate CL Bagdon WJ & Bokelman DVM 1978 Morphological abnormalities in potassium - deficient dogs. American Journal Pathology 93; 103-116.

Tobian L MacNeill D Johnson MA Gagul MC & Iwai J 1984 Potassium protection against lesions of the renal tubules, arteries, and nephron loss in salt loaded hypertensive dahl S rats. Hypertension, supplement I 6: 170-176.

Truong L et al 1973 Influence of dietary protein on skeletal muscle growth of normal and potassium - chloride depleted young rats. Nutr. Reports Int. 7; 655-664.

Turner RA Counts GB Treadway WJ Holt DA Agudelo CA 1981 Rheumatoid factor and monosodium urate crystal-neutrophil interactions in gouty inflammation. Inflammation 5; 353-361.

Ueda Y, Honda M, Tsuchiya M, Watanabe H, Izumi Y, Shiratsuchi T, Inoue T, Hatano M. 1982 Response of plasma ACTH and adrenocortical hormones to potassium loading in essential hypertension. Jpn Circ J. 1982 Apr;46(4):317-22.

Welt LG et al 1958 The prediction of muscle potassium from blood electrolytes in potassium depleted rats. Tr. A. Am Physicians 71; 750.

Welt LG et al 1960 Consequences of potassium depletion. Journal of Chronic Dis. 11; 213-254.

Winegrad AT Reynold AE 1958 Effects of insulin on the metabolism of glucose, pyruvate, and acetate. Journal of Biol. Chem. 233; 267.

Wohl MG Goodhart RS 1968 Modern Nutrition in Health and Disease, 4th edition. Lea & Febiger.

Woods JW Welt LG Hollander W Jr. 1961 Susceptibility of rats to experimental pyelonephritis during potassium depletion. Journal of Clinical Investigation 40; 599-602.

Wright, LF; Saylor, RP; Ceere, FA (1984) Occult lead intoxication in patients with gout and kidney disease. Journal of Rheumatology. 11, no. 4; 517-520.

Zhu K Devine A Prince RL 2004 The effects of high potassium consumption on bone mineral density in a prospective cohort study of elderly postmenopausal women. Osteoporosis International 20 (no. 2); 336-340.

Zusman RM Keiser HR 1980 Regulation of prostaglandin E2 synthesis by angiotensin II, potassium, osmolality, and dexamethasone. Kidney International 17; 277-283.

This article was updated in April 2014
This page has been visited times