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Studies show that potassium becomes very deficient in the hyperthyroid state. It can become so deficient that hypokalemic paralysis results. This is a condition in which the whole body becomes rigid because of potassium deficiency. There are reports in the literature of people found in a state of hypokalemic paralysis in the street. When they are taken to the hospital and revived with potassium infusions, they are often found to have hyperthyroidism. For an unknown reason this occurs at a higher rate among Asians.  It may be genetic or dietetic (high sodium intake from soy sauce, perhaps??). There are indications that potassium deficiency may also be involved in hyperthyroidism and the rapid weight gain of hypos may be the result of potassium deficiency.

The four minerals, sodium, potassium, calcium, and magnesium are next to each other in the Periodic Table and form a square on the left side. There are strong interactions between these four minerals. The balances between these four minerals seems to be critical to health and are probably very critical for thyroid health. Excess amounts or deficiencies of any one of the four may severely disrupt thyroid function. Additionally there seem to be interactions between these four minerals and copper and zinc, which are two metallic minerals with critical thyroid functions. It seems that a copper deficiency interferes with the proper functioning of both potassium and magnesium, and zinc seems more related to sodium and calcium metabolism. Also all of these minerals seem involved in either the production, degradation, or cellular response to thyroid hormone.

Potassium, sodium, and lithium are alkaline minerals which are involved in the cellular pumps which regulate the transport of water and nutrients through the cell walls. There is evidence that a potassium deficiency can cause the cells to fill with water leading to an overall edema in the body. It's possible that edema of the brain cells from potassium deficiency may be involved in chronic headaches. It's also possible that potassium deficiency is responsible for the rapid increase in body weight seen in thyroid patients. This increase in body weight seems to occur despite calorie restriction and may be the result of swelling of all the body's cells with water.

Indications of potassium deficiency include symptoms such as muscle weakness, which is a condition reported by many thyroid patients.

You will also see below that eating licorice can deplete potassium with possible fatal consequences. I would strongly urge anyone with thyroid disease to not eat licorice.

For these reasons I think studying potassium is critically important to understanding thyroid physiology.


From the book, "Healthy Healing" by Linda Rector Page:

"Potassium--an electrolyte mineral located in body fluids. Potassium balances the acid/alkaline system, transmits electrical signals between cells and nerves, and enhances athletic performance. It works with sodium to regulate the body's water balance, and is necessary for heart health against hypertension and stroke, (people who take high blood pressure medication are vulnerable to potassium deficiency), muscle function, energy storage, nerve stability, and enzyme and hormone production."

"Potassium helps oxygenate the brain for clear thinking and controls allergic reactions. Stress, hypoglycemia, diarrhea and acute anxiety or depression generally result in potassium deficiency. A potassium broth from vegetables is one of the greatest natural healing tools available for cleansing and restoring body energy. Good food and herb sources are fresh fruits, especially kiwis and bananas, potatoes, sea vegetables, spices like coriander, cumin, basil, parsley, ginger, hot peppers, dill weed, tarragon, paprika, and tumeric, lean poultry and fish, dairy foods, legumes, seeds, and whole grains."

From the Nutrition Almanac by Kirschmann (excerpts): "...Potassium constitutes 5% of the total mineral content of the body...Potassium and sodium help regulate water balance within the body (potassium crosses over more easily); that is, they help regulate the distribution of fluids on either side of the cell walls and preserve proper alkalinity of the body fluids. Potassium also regulates the transfer of nutrients to the cells. ..."

"Potassium is necessary for normal growth enzymatic reactions. It unites with phosphorus to send oxygen to the brain and also functions with calcium in the regulation of neuromuscular activity. The synthesis of muscle protein and protein from amino acids in the blood requires potassium, as does the synthesis of nucleic acids. It aids in keeping skin healthy and in keeping a stable blood pressure."

"Potassium assists in the conversion of glucose to the form in which this substance can be stored in the liver as glycogen, and then to its useful form to do the body's work. Protein and carbohydrate metabolism are dependent upon potassium. It stimulates the kidneys to eliminate poisonous body wastes. Potassium works with sodium to help normalize the heartbeat."


The following study indicates that potassium levels are low in patients with hyperthyroidism, muscular weakness is proportionate to potassium deficiency, and correction of thyroid hormone levels results in correction of potassium levels.

Rev Neurol 1999 Sep 16-30;29(6):510-2

Title: Total body potassium in relation to thyroid hormones and hyperthyroidism.

Edmonds CJ; Smith T
Clin Sci, 60(3):311-8 1981 Mar

1. Body weight and total body potassium were measured in 23 hyperthyroid patients before and at various stages during treatment and in 19 athyreotic patients who were being treated with high-dose L-thyroxine. 2. In the hyperthyroid patients the total body potassium rose by 23 +/- 2.8% (SEM) within a few weeks of restoring the blood thyroid hormone levels to normal. The body potassium values after treatment were close to that expected in these individuals if they were healthy indicating that a considerable loss of body potassium is usual in hyperthyroidism. 3. The gain of total body potassium in hyperthyroidism averaged 71 +/- 8 mmol for each kg of body weight gained (compared with muscle potassium concentration of about 92 mmol/kg). In contrast, weight loss produced by dietary treatment of obesity caused very little change of body potassium (maximum averaged was 14 +/- 4 mmol/kg wt. loss). 4. Among the patients with hyperthyroidism, the greatest muscular weakness was present in those with the greatest body potassium loss and these patients regained a large amount of potassium relative to weight on recovery. 5. Total body potassium changes were closely related to total plasma tri-iodothyronine concentrations but unrelated to the thyroxine levels.


The following study indicates that hyperthyroidism may be the result of potassium deficiency which may be caused or increased by physical exercise or ingestion of carbohydrates.

[No title available].

[Article in Spanish]

Carod-Artal FJ, Delgado-Villora R

Programa de Neuroclinica, Hospital Sarah, Red de Hospitales del Aparato Locomotor, Brasilia DF, Brasil.

[Medline record in process]

INTRODUCTION: Thyrotoxic hypokalemic periodic paralysis is characterized by recurrent episodes of motor weakness of variable intensity associated with thyroid overactivity. It is usually associated with low plasma potassium levels and is often precipitated by physical activity or ingestion of carbohydrates. CLINICAL CASES: We describe two men, aged 33 and 50, who complained of several episodes of muscular paralysis in the context of previously undiagnozed hyperthyroidism and associated with low plasma potassium levels. There were clearly raised levels of T3, T4 and free T4 and TSH was depressed due to hyperactive diffuse goitre. In one patient the precipitating factor was known to have been a large intake of carbohydrates and intense physical exercise. Antithyroid treatment, and the resulting correction of hyperthyroid function, prevented any further episodes of muscular weakness in both patients. CONCLUSIONS: Thyrotoxic periodic paralysis should be considered in the differential diagnosis of all acute episodes of motor paralysis in young patients. Determination of the plasma levels of potassium and thyroid hormones helps diagnosis. Early diagnosis is important so as to be able to establish antithyroid treatment and avoid further episodes of weakness.

This study shows that potassium deficiency alters the physiology of thyroid hormone activity.

Potassium deficiency enhances the effect of thyroid hormone on NaK-ATPase in liver and kidney.
Shishiba Y; Ozawa Y; Takaishi M; Eguchi N; Shimizu T
Endocrinol Jpn, 27(3):329-36 1980 Jun

In order to examine the possibility that the changes in electrolytes in tissue alter the effect of thyroid hormone on NaK-ATPase, rats were fed either synthetic K-deficient diet or synthetic K-normal diet. K-deficient diet induced a reduction in K content in serum or kidney, while that of the liver remained unchanged. When a daily dose of 2.5 micrograms T3 was administered for 7 days to k-deficient rats, both Mg- and NaK-ATPase of the homogenate of liver and kidney were elevated, while the same dose failed to influence those enzymes in K-normal rats. Furthermore, T3 dose increased the Na content of liver and kidney in K-deficient rats, resulting in a significant decrease in the K/Na ratio in those tissue. Based on the estimation from chloride space, the decrease in K/Na was deemed to have occurred mainly in the intracellular space. As the levels of serum thyroid hormone and liver T3 were not influenced by K-deficiency, the effect of K depletion is likely to be mediated not through the alteration in thyroid hormone kinetics, but through some other mechanism such as the elevation of intracellular Na. The present study demonstrates that K deficiency may sensitize NaK-ATPase to the effect of thyroid hormone.


Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.
Stedwell RE; Allen KM; Binder LS
Department of Emergency Medicine, Texas Tech University Health Sciences Center, El Paso 79905.
Am J Emerg Med, 10(2):143-8 1992 Mar

Acute hypokalemic paralysis is an uncommon cause of acute weakness. Morbidity and mortality associated with unrecognized disease include respiratory failure and death. Hence, it is imperative for physicians to be knowledgeable about the causes of hypokalemic paralysis, and consider them diagnostically. The hypokalemic paralyses represent a heterogeneous group of disorders with a final common pathway presenting as acute weakness and hypokalemia. Most cases are due to familial hypokalemic paralysis; however, sporadic cases are associated with diverse underlying etiologies including thyrotoxic periodic paralysis, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. The approach to the patient with hypokalemic paralysis includes a vigorous search for the underlying etiology and potassium replacement therapy. Further therapy depends on the etiology of the hypokalemia. Disposition depends on severity of symptoms, degree of hypokalemia, and chronicity of disease.

Title: Periodic paralysis and the sodium-potassium pump.

Author: Layzer RB

Source: Ann Neurol, 11(6):547-52 1982 Jun


Analysis of the pathophysiology of hypokalemic paralysis, as it occurs in barium poisoning, chronic potassium deficiency, and thyrotoxicosis, suggests that these disorders may have a similar mechanism. An increased ratio of muscle sodium permeability to potassium permeability reduces the ionic diffusion potential, while the resting membrane potential is sustained by an increase of Na-K pump electrogenesis. The result is that potassium entry (the sum of active and passive influx) exceeds potassium efflux; this causes a large shift of extracellular potassium into muscle until the Na-K pump turns off, leading to depolarization and paralysis. The primary defect in familial hypokalemic periodic paralysis, as in the example of barium poisoning, may be a marked reduction of muscle permeability to potassium.

The following study indicates symptoms of potassium deficiency induced by the consumption of licorice. The symptoms are muscular weakness and pain. The descriptions make me wonder if a potassium deficiency os involved in fibromyalgia.
Glycyrrhizin (licorice)-induced hypokalemic myopathy. Report of 2 cases and review of the literature.
Shintani S; Murase H; Tsukagoshi H; Shiigai T
Department of Neurology, Toride Kyodo General Hospital, Ibaraki, Japan.
Eur Neurol, 32(1):44-51 1992
Fifty-nine cases of glycyrrhizin (licorice)-induced hypokalemic myopathy (GIHM), 2 females treated in our departments (85 and 73 years old) and 57 cases reported in the literature were studied, and conditions leading to the onset, factors, clinical manifestations, laboratory assessments, muscle biopsy findings, treatment and outcome were discussed. The 59 GIHM cases comprised 32 men, 25 women and 2 patients without record of sex; the average age was 55.2 years. In many cases, conditions leading to the onset of GIHM were habitual licorice ingestion, ingestion of antituberculosis agents containing licorice and long-term ingestion of licorice-containing agents for chronic gastritis, chronic hepatitis or chronic dermatitis. The combined use of hypotensive diuretic agents increased the risk of GIHM in an overwhelming number of cases. The main clinical symptom was flaccid quadriplegia in almost all cases, with muscle pain in 32.2% and peripheral dysesthesia in the extremities, manifested mainly by numbness (27.1%). Laboratory findings included a mean serum K+ value of 1.98 mEq/l (56 GIHM cases), a mean creatine kinase of 5,385.7 IU/l (n = 30), a mean blood aldosterone concentration of 2.92 ng/dl (n = 30; normal: 2.0-13.0 ng/dl) and a mean plasma renin activity of 0.17 ng/ml/h (n = 27; normal: 0.8-4.4 ng/ml/h). Muscle biopsy was performed in 17 of the 59 cases with resultant findings of myopathic changes consisting mainly of phagocytosis, necrotic fibers, vacuolar degeneration, together with sporadic neurogenic changes. Complete cure was attained in 57 of the 59 cases of GIHM by discontinued ingestion of glycyrrhizin (licorice) and potassium supplement.


The following study indicates that a magnesium deficiency decreases the activity of the sodium-potassium cellular pumps. "It is suggested that this leads to an increase in intracellular Na+, resulting in a change in the membrane potential, and may contribute to the arrhythmias associated with magnesium deficiency." Thus magnesium deficiency may be causing irregular heat beat by its effect on the sodium-potassium pumps.

Effects of dietary magnesium on sodium-potassium pump action in the heart of rats.
Fischer PW; Giroux A
Nutrition Research Division, Health and Welfare Canada, Ottawa, Ontario.
J Nutr, 117(12):2091-5 1987 Dec

Sprague-Dawley rats were fed a basal AIN-76 diet containing 80, 200, 350, 500 or 650 mg of magnesium per kilogram of diet for 6 wk. Ventricular slices, as well as microsomal fractions, were prepared from the hearts and were used to determine sodium-potassium pump activity. Sodium-potassium pump activity was assessed in the microsomal membranes by determining the ouabain-inhibitable Na+, K+-ATPase activity and [3H]ouabain binding, and in the ventricular slices, by determining ouabain-sensitive 86Rb uptake under K+-free conditions. The ATPase activity increased with increasing dietary magnesium, so that in the hearts of those animals that were fed 500 and 650 mg of magnesium/kg diet, it was significantly greater than the activity in the hearts of the animals fed 80 and 200 mg/kg diet. Similarly, 86Rb uptake by heart slices from rats fed 500 and 650 mg of magnesium/kg diet was significantly greater than the uptake by heart slices from animals fed 80 and 200 mg/kg diet. [3H]Ouabain binding did not change with increasing dietary magnesium. Thus, magnesium deficiency appears to have no effect on the number of sodium-potassium pump sites, but does decrease the activity of the pump. It is suggested that this leads to an increase in intracellular Na+, resulting in a change in the membrane potential, and may contribute to the arrhythmias associated with magnesium deficiency.


Rubidium and Cesium are alkaline minerals located below potassium on the Periodic Table. There is evidence that excessive amounts of these minerals can deplete potassium. Because they are heavier minerals, it is expected that cesium and rubidium have longer half-life times in the body and very small amounts may have significant effects on potassium.

Ion effects on gating of the Ca(2+)-activated K+ channel correlate with occupancy of the pore.
Demo SD; Yellen G
Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Biophys J, 61(3):639-48 1992 Mar
We studied the effects of permeant ions on the gating of the large conductance Ca(2+)-activated K+ channel from rat skeletal muscle. Rb+ blockade of inward K+ current caused an increase in the open probability as though Rb+ occupancy of the pore interferes with channel closing. In support of this hypothesis, we directly measured the occupancy of the pore by the impermeant ion Cs+ and found that it strongly correlates with its effect on gating. This is consistent with the "foot-in-the-door model of gating, which states that channels cannot close with an ion in the pore. However, because Rb+ and Cs+ not only slow the closing rate (as predicted by the model), but also speed the opening rate, our results are more consistent with a modified version of the model in which the channel can indeed close while occupied, but the occupancy destabilizes the closed state. Increasing the occupancy of the pore by the addition of other permeant (K+ and Tl+) and impermeant (tetraethylammonium) ions did not affect the open probability. To account for this disparity, we used a two-site permeation model in which only one of the sites influenced gating. Occupancy of this "gating site interferes with channel closing and hastens opening. Ions that directly or indirectly increase the occupancy of this site will increase the open probability.
Effect of diet upon the erythrocyte Na,K pump.
DeLuise M; Izumo H; Grace EE; Flier JS
J Clin Endocrinol Metab, 56(4):739-43 1983 Apr

The number of erythrocyte Na,K-ATPase pump units has been found to be reduced in some populations of obese humans, but the effect of dietary factors upon the status of the erythrocyte pump has not been delineated. We have measured the number of Na,K-ATPase pump units by [3H]ouabain binding and the activity of the pump by ouabain-inhibitable 86rubidium uptake in response to nutritional maneuvers in several patient groups. There was no consistent change in the number or activity of Na,K-ATPase units in response to 1) an acute 600-cal meal, 2) a 3-day fast or refeeding after a fast in normal weight or obese subjects, 3) 2 weeks of hypocaloric (600 cal) feeding in obese subjects. Individuals with anorexia nervosa were also not significantly different from age- and sex-matched control subjects with respect to the erythrocyte Na,K pump. It is concluded that the circulating erythrocyte does not regulate the number or activity of Na,K pump units in response to short or medium term nutritional maneuvers. Differences between obese and thin populations with respect to the Na,K pump are not likely to be secondary to nutritional differences between the two groups.


Analysis of the effects of cesium ions on potassium channel currents in biological membranes.
Clay JR; Shlesinger MF
J Theor Biol, 107(2):189-201 1984 Mar 21

Cesium ions block potassium channels in biological membranes in a voltage dependent manner. For example, external cesium blocks inward current with little or no effect on outward current. Consequently, it produces a characteristic N-shaped current-voltage relationship. We have modeled this result by single file diffusion of ions in a narrow channel spanning the membrane with a special blocking site in the channel for cesium ions. The model enables us to make detailed comparisons of the effects of cesium on potassium channels in different types of biological membranes.

Relationship between turnover of cesium-137 and dietary potassium content in potassium-restricted mice.
Sato I; Matsusaka N; Tsuda S; Kobayashi H; Nishimura Y
Faculty of Agriculture, Iwate University, Morioka, Japan.
Radiat Res, 148(1):98-100 1997 Jul

The biological half-life of 137Cs and its organ distribution were investigated in mice fed various potassium-deficient diets. The biological half-life, which was 6.1 days in mice receiving the normal level of potassium, became longer as the dietary potassium content decreased, and 137Cs was hardly excreted from the body when dietary potassium content was restricted to 200 mg/kg or less. The muscle showed the highest concentration of 137Cs in both mice that had sufficient amounts of potassium and those that were potassium-deficient. Clearance of 137Cs from tissues was generally suppressed when mice were fed a potassium-deficient diet, but the relative distribution pattern of 137Cs was not affected by dietary potassium content. These results suggest that dietary potassium intake, which may vary with eating habits, affects the biological half-life of 137Cs in humans.



by Charles Weber

This site introduces a discussion of potassium nutrition and physiology especially as pertaining to rheumatoid arthritis.

OTHER CONTENTS II. Arthritis Research -- III. Arthritis and Potassium -- 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

It is my contention that potassium deficiency is either causing, or greatly making worse, rheumatoid arthritis which I will shorten to "arthritis" in this article. In assessing the possibility of this hypothesis people have little to go on. Virtually any textbook in the past would devote no more than a paragraph to potassium which would state that potassium is never deficient in the diet, or give one exception to the dozen or more known, or in some only under clinical conditions.

The reason for this careless treatment of potassium is probably because potassium is present in almost all foods as grown in large quantities. Professionals think about it as if it were air or water. However even air and water can be deficient and if voluminous texts are not written on their deficiencies, it is because both deficiencies can be detected by our senses. Extremely powerful emotions and instincts impel people to correct these deficiencies immediately and at any cost. Potassium is odorless, colorless, and, in the usual concentrations, tasteless. There is no way to detect a deficiency and cell content can not even easily be assessed in the body by modern analytical procedures. Whole body cell content is virtually "invisible".

There is not any indication in the literature that potassium has ever been tried by scientists as an arthritis corrective. A rather exhaustive search of the medical literature has failed to disclose an experiment. This includes Exerpta Medica 1947 to 1974, and a computer search by the Central Library of the American Medical Association from 1965 back.

I will discuss potassium physiology and nutrition and what can be done to remove an actual deficiency and thus heal any tissue which has not actually been destroyed. If you do not know the meaning of a word in this article, for a definition click on (Mirriam-Webster).

Please keep in mind, though, that potassium ramifies through every cell and process in the body, has no storage, and has a dangerous dependence on its precise control by nerve impulse transmission. This makes it a mineral to be cautious about. In particular I recommend getting as much as possible from food. Even food requires some care because it has a wide range of concentrations. You must take responsibility for your own intake and I assume no liability for the correctness of advice in this article. You use this information at your own risk.

Getting potassium from food is reasonably safe for normal people with reasonably sound kidneys. Even if you doubt my thesis of a connection between arthritis and potassium, you have nothing to lose by getting all the potassium that was originally in your food. It will even taste better. It will, in addition, help protect you from potassium's known link to heart disease. As the 12th century physician Maimonides expressed it: "A doctor should begin with simple treatments, trying to cure by diet before he administers drugs. No illness that can be treated by diet should be treated by any other means."

Anything a doctor can learn, you can also. There will be a list of definitions eventually which will make the difficult words much easier eventually. In the mean time one of the online technical dictionaries may do.


Arthritis is the number one crippler in America. The estimate for rheumatoid arthritis is 43 million men, women and children and at least 65 billion dollars lost each year currently. Two thirds of the victims are women, most of them over 45 [Rodman]. The terrible pains associated with arthritis, reminiscent of and similar to the medieval torture racks must surely be among the top causes of contemporary misery. These pains along with the actual physical disability, weak joints, and loss of energy which accompany them, cause an enormous loss of productivity, estimated to be over six billion dollars in 1978 [Arthritis Foundation]. Arthritis may be a considerable part of the cause of increasing welfare roles. Even industrial accidents are related to this monstrous and onerous burden that society carries. Small jolts and falls which should do little more than bring out some colorful language results in loss of hours and even months. It is more than just the loss of time itself. It is also the super caution that blocks even fairly healthy people from making fast, risky moves when they see some of the debacles their friends get into.

Nor is arthritis confined to North America. Countries at such extremes of latitude as Finland and Jamaica have even higher rates than we do [Kellgren]. The simple life is not any guarantee against misery either. The Masai tribesmen of Africa have high rates [Best p768]. Political or economic ideologies are not barriers. Arthritis crosses the iron curtain, is also present in nomadic hunters, and cave men, cave bears, and ancient Egyptians are thought to have had it [Bach][Crain]. It shows no obvious clear association with any culture even though it is very variable, with low rates in tribes near the Masai and Laplanders near the Finns in Finland, as well as insane people in Massachusetts {Allander p260].

Most of the people who have pains in the joints have them because of arthritis. The pains usually strike first in the outer joints like fingers or joints with a history of injury. Load bearing joints are also vulnerable. The pain is most likely in the early morning. It is often accompanied by stiffness. It is not to be assumed that the disease is localized because the pain is, Arthritis is present throughout the body and can affect kidneys, pericardium of the heart, and connecting tissue [Strukov][Ropes]. It is a disease largely associated with humans [LaMont-Havers], probably partly because animals can not talk, but I suspect primarily because animals usually do not have access to refined food. Arthritis has few externally observable symptoms, especially in early stages. There are no known consistent biochemical changes in arthritis (which word in this article will be equated with "rheumatoid arthritis") except a much lower cellular potassium content than normal [LaCelle], and a higher copper content along with a protein which binds the copper in the serum [Schubert]. There has been an effort to use changes in some of the body's other proteins in diagnosis, but with limited success so far, although some of the other rheumatic diseases can be almost diagnosed from blood proteins alone [Waller]. As nearly as I can tell this seemed to be the consensus for arthritis at the 1982 Pan American Conference on Arthritis. There are significant correlations between IgM RF and IgA immune proteins and a higher disease activity [Chen] but the correlations are not perfect. C3 and C4 compliment are said to be the best of the other discriminators.[Sari, et al]. Arthritis sometimes has fatigue associated with it.

In the past arthritis was associated with old age in people's minds and there was a tendency to suffer it stoically as inevitable. While the medical profession has intellectually abandoned an assumption that only people in old age are affected, many laymen still assume this is the case. The concept that this is "old age" is pervasive, even creeping into common cultural media as modern as "Star Trek". This is not to indicate that the victims did not often attempt to do something. Arthritis has a long history of quack nostrums and screwball procedures. These quack remedies were assisted by the numerous spontaneous remissions that occur with arthritis or by pain deadening chemicals. It was not necessary to cure everyone, since those who were "cured" were very grateful and those who were not were fatalistic, since their doctors could do nothing either.

It is my contention that arthritis is either a potassium deficiency or is strongly affected by one. I suspect that some poison or some infections or decline in kidney function with age degrades our ability to concentrate potassium and thus makes it impossible to eat the food from which almost every processing procedure removes potassium these days. Arthritics characteristically have poor nourishment {Morgan et al]. One such poison which I suspect is the very poisonous bromine gas, since it probably affected me that way 50 years ago.

One technique which seemed to have some success was the use of spas. At least their popularity would seem to indicate some success. That king sized spa, the ocean, has been given credit for anti-arthritic tendencies also. This is plausible because the ocean contains potassium in about the same concentration as blood fluid. The spa at Bath, England, has a potassium content less than one tenth that of ocean water [Riley]. If it is typical of spas, then unless they were drinking the water, it is hard to see how it could have helped.

There have been closer associations with potassium. At one time sulfurated potash was used to combat arthritis [Osol p1092]. It is not surprising that it fell into disfavor associated with such a poisonous anion. An anion is a negatively charged substance which neutralizes the positive charge of an ion like potassium. The first person to definitively link potassium to arthritis in no uncertain terms was DeCoti-Marsh in a book published in England in 1957 [deCoti-Marsh]. He claimed numerous case histories. He recommended a whole pot-pouri of anions to go with the potassium, some of them not nutritional, and some even poisonous. He attributed magical properties to these anions. His approach was reminiscent of the writings of ancient alchemists.

A more successful technique was the raw vegetable diet described by Holbrook in Europe during the forties [Holbrook]. This diet became quite popular, even though most people must have found it fairly unpalatable. Eppinger hinted that the success of this diet may have been due to its high potassium content [Eppinger]. It might have become more popular if a recommendation to use fried vegetables, soup, or to drink the boil water had been made, which would have permitted the same potassium intake. There have been experiments with vegetarian diets in recent years but they have been changed merely by removing meat from the diet which is probably why only moderate success has been attained.

At the present time there are several books relating diet to arthritis. Jarvis stresses honey and vinegar in his book [Jarvis]. Since honey is extremely low in potassium, it would be counter productive. The vinegar could be very beneficial if well fed people are failing to metabolize all of the acetate ion because the acid hydrogen ion interferes with potassium at the excretion site as will be developed later. I know of no tests reported in the literature testing this concept. Jarvis hints at other dietary changes also, which if followed, would increase potassium intake inadvertently.

Dong and Banks prescribe a diet free of chemicals, milk, meat and sugar, and low in fat [Dong]. If his diet were followed it would definitely increase potassium intake, especially since he stresses unprocessed vegetables. However, he attributes its success to freedom from allergens and chemicals, so that philosophically he tends to be in the same general physiological category as the autoimmune hypothesis is in, to be discussed later. I am fairly certain that those who have success with his diet do so because of the lucky quirk that potassium increases at the same time. I think a good case could be made for keeping chemicals out of food. Some, like sulfite which destroys vitamin B-1 are known to be harmful, some like dyes and nitrites are fraudulent and\or harmful. I doubt if removing them would have more than a small affect on arthritis though. Alexander recommends vitamin D against arthritis. However like Dong he also speaks of low sugar and raw vegetables [Alexander]. I doubt if the vitamin D had much affect on arthritis, although those using his diet must have had less trouble with tooth decay, tuberculosis, and rickets.

Allergy has been proposed as a possible cause but stressing allergens naturally present in food. It is quite conceivable that allergens damage the kidneys' ability to retain potassium. However, no one has established this yet. There is good evidence, though, of beneficial results from defeating allergy in specific cases.

Evidence from individual case histories and the known characteristics of potassium physiology supports the proposal that arthritis is either a potassium deficiency or that a deficiency is its most important symptom. The replete body contains about 75 times as much potassium or more as is usually in the processed diet, so if it is increased, it will still take quite awhile to come up to normal. However there should be satisfying initial results in a month or two or even less.

I have been almost alone in proposing potassium as being central to rheumatoid arthritis (but see Dr. Jan de Vries' article). . However there is no substitute for an experiment, which has never been done. While you are waiting for such an experiment there is nothing stopping you from eating nutritious food and making sure you do not lose any of the potassium by your own preparations. I wish you good health.

Low potassium levels seem to occur more at night and in the hotter months of the year. This seems to coincide with the times when hypers have more hyperthyroid storms.
QJM 1996 Jun;89(6):463-8

Thyrotoxic periodic paralysis in a Chinese population.

Ko GT, Chow CC, Yeung VT, Chan HH, Li JK, Cockram CS

Department of Medicine, Chinese University of Hong Kong, Shatin.

We retrospectively evaluated the characteristics of adult patients admitted with thyrotoxic hypokalaemic periodic paralysis in Hong Kong. From 1984 to 1993, 45 Chinese adult patients were admitted with acute limb weakness, plasma potassium < or = 3.5 mmol/l and thyrotoxicosis confirmed by laboratory investigations. All but one were male. Seventy-five percent of attacks occurred between 9pm and 9am. Half of the attacks occurred between July and October (49.1%), most commonly in August (20%). Mean (+/- SEM) plasma potassium on admission was 2.17 +/- 0.08 mmol/l (range 1.1-3.5). In 15 episodes (27.3%), plasma potassium on recovery exceeded 5.0 mmol/l, while in three episodes (5.5%), potassium exceeded 6.0 mmol/l. No patient had a positive family history of thyrotoxic periodic paralysis. Only 28.9% had a known history of thyrotoxicosis before their first presentation with periodic paralysis. Twenty-seven (60%) had clinical evidence of thyrotoxicosis. Although all were biochemically thyrotoxic, 11.4% had only a mild degree of thyrotoxicosis (suppressed thyroid-stimulating hormone, high free thyroxine, but normal free triiodothyronine). One quarter of the patients had a normal erythrocyte zinc concentration, indicating either a short history of thyrotoxicosis or transient thyrotoxicosis. The diagnosis of thyrotoxic hypokalaemic paralysis should always be considered in Chinese patients with acute muscle weakness, especially in young males. Absence of clinical thyrotoxicosis does not exclude the diagnosis. Plasma potassium should be monitored carefully during treatment to prevent rebound hyperkalaemia.


Subj: Re: [hyperthyroidism] Recently diagnosed with hyperthyroidism [Canada]
Date: 2/20/01 10:01:36 AM Pacific Standard Time
From: Penny


I can't wait for the website to be repaired. I've been dying to talk to you about this potassium thing. Thanks, by the way, for your recent potassium article at the site.

Anyway, you know I'm hypo, and I'd also been feeling that potassium was something I needed to look into. Thanks to your research, I've been experimenting with approximately 1,000 mgs a day (more when I can manage it) and every time I do, I see a huge improvement in my strange heart sensations. However, I also KNOW that I'm deficient in magnesium, because of muscle twitching and spasms etc. so I'm still taking that as well. I just don't feel right if I don't take it. Does this make sense, to need both? 

I'm definitely liking the effect of the potassium especially since I've been feeling hyper lately, and pretty sure that I'm going to be going down to 25 mcg of hormone as soon as I get the results of my last blood test (if you remember, I started at 150 over a year ago). So I can vouch for the effectiveness of the supplements! Even more remarkable is that I'm hypo, and doctors tell us that it's impossible to get off the hormone!

One other note. Since I've been feeling so hyper, I've been experiencing the breathing difficulties again. I tried B-1 all alone, (200-400 mgs) and my breathing normalizes within 20 minutes. It's wonderful! 

Thanks John, (oh yeah, in case you forgot, which is completely understandable, the main question here was about taking the potassium and magnesium together. I'm just excited!)



Subj: potassium 
Date: 8/11/02 12:25:39 PM Pacific Daylight Time
Sent from the Internet (Details)

Hi John,

I don't have thyroid problems but I came across your website while investigating isothiocyanates and goitrogens.  I was interested in your information on potassium because many years ago I did a study in which potassium supplementation was used to eliminate symptoms of PMS. 

 I do not know if you know this but magnesium is the metal that is the coenzyme for the Na-K ATPase pump located on all cell membranes used to concentrate potassium inside of cells, where over 98% of the mineral is located.  A magnesium deficiency in the presence of a potassium deficiency makes the potassium deficiency even worse.  Replenishing just the magnesium will go some way into helping with the potassium deficiency because it will help concentrate it inside of the cell.  Potassium supplements must be used to replenish a potassium deficiency because the acid-base balance that is usually messed up in a potassium deficiency must also be corrected in order for the body to retain the potassium.  Using foods alone will not adequately correct a potassium deficiency.  I never found any ratio that needed to be followed between the magnesium and potassium, just that both deficiencies needed to be corrected in the case of potassium deficiencies due to the role of magnesium in the Na-K ATPase pump.  I did find however, that in order for the potassium to work on PMS (it took 3 months of daily potassium supplementation (600-1200 mgs/day) for the symptoms to go gradually away over this time) you could not touch phosphorous-free calcium or it was as if the potassium was not being replenished or working.  Taking this form of calcium during this critical 3-month time would cause the complete return of symptoms and then you had to start the 3 month time period over.  You could take dairy products, or any calcium naturally found in foods and this was fine.  After the PMS is gone, taking phosphorus-free calcium was fine and symptoms did not return. 

I did a hair analysis on myself throughout the time I was discovering this, about two years prior to the study I did, and it showed a very low potassium and a screeching high calcium.  This was over 20 years ago but as I recall after correcting the potassium, my calcium values went down to normal.  There is a study showing that use of calcium reduces PMS symptoms by 50%.  Prior to discovering the potassium effects I had been on calcium and found this to be true.  To me it was as if alot of PMS had to do with calcium balance, but that it could not occur in the presence of a potassium deficiency (whether due to the acid-base imbalance effecting the distribution of ionized/protein boiund calcium or some other reason I do not know).  Correcting the potassium deficiency corrected the calcium imbalance.

Anyways, thought you might be interested. 


Beckie Takacs