by Charles Weber, MS

This discussion of potassium is presented in the hope that one of its readers will consider performing another experiment establishing the effect of potassium on rheumatoid arthritis (RA). There has been no report in the literature going back to 1914 of such an experiment. However, 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. 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 with the email isoptera at att.net and I will send you a copy of the article he has submitted to a journal. I can also arrange to send his curriculum vitae if you wish.

Every essential nutrient should have been explored in regard to rheumatoid arthritis before this. In view of the way hormones which are regulated by or regulate potassium, such as cortisol and DOC are involved with rheumatoid arthritis (RA), the low whole body potassium content in rheumatoid arthritis (RA), and the way potassium rich diets relieve RA, potassium especially should have been investigated before now.


Since the most serious aspect of the diarrheas is wasting of potassium, cortisol has acquired the attribute of conserving potassium by moving it into the cells when cortisol declines. Cortisol (but not corticosterone) is reduced during a potassium deficiency, and this reduction accounts for many of the symptoms of RA.

Cortisol shuts down most of the copper enzymes when it declines so that excretion of copper is increased and Lysyl oxidase inhibited. These last two attributes are proposed to account for most of the mortality from aneurysms and infections during rheumatoid arthritis (RA). Thus the urgent necessity to survive potassium loss during virulent diarrhea has set people up in the course of evolution for some of the worst symptoms of rheumatoid arthritis.


Judging by the drastic decline of mortality in babies suffering from a virulent strain of diarrhea by potassium supplements [1], potassium loss in those diseases which force cyclic AMP to excrete water into the intestines [2] must be the most serious effect of the diarrheas. I suggest that this is the reason why cortisol has acquired the attribute of moving potassium out of cells [3] and therefore into the cells upon declining. It is also undoubtedly the reason why the adrenal's cortisol secretion is inhibited by low serum potassium in vitro (in the test tube) but not corticosterone[4]. The body thus has a way of signaling for a decrease in cortisol secretion during a serious intestinal disease independently of ACTH. Thus the body inversely mobilizes its immune defenses against diarrhea through cortisol. Endotoxin bacterial diseases force the body to secrete cortisol by increasing ACTH [5] and this is probably an adaptation by the bacteria to force the body to inhibit the immune system. Glucosteroid response modifying factor (GRMF) secreted by T- cells then prevents the cortisol from having full effect on white cells other than suppresser cells [6] and thus raises the set point, as does interleukin-I [6]. Interleukin-I also stimulates cortisol secretion [7], as does cachectin (tumor necrosis factor) [8]. I suspect that this is an adaptation to provide some cortisol maintenance [9] when normal ACTH production is later cut off during endotoxin attack [10]. In other words, the immune system takes over its own regulation but at a higher set point. The role of GRMF has not yet been demonstrated for physiological processes. GRMF will probably prove to inhibit cortisol for most of those processes as well as the immune cells, surely at least for cortisol's various affects on potassium.

One of the most important of the cortisol controlled immune defenses is the mobilization of the availability of copper to the white cells, an attribute which probably arose because copper is crucial to an adequate immune defense [11]. The primary way cortisol does this is by, inversely to its concentration, shutting down production of copper-containing enzymes such as Lysyl oxidase and superoxide dismutase [12]. Lysyl oxidase catalyzes the formation of cross links in all connecting tissue including elastin [13]. Since elastin makes up the main strength of normal blood vessels [12] and has a rapid turnover, this is the most serious problem in arthritis. Ruptured aneurysms along with poor resistance to infection and heart disease are the chief terminal events in arthritis [14].

The body uses ceruloplasmin to carry copper to the immune system during infection [12]. Probably the main reason for this development is that the copper in ceruloplasmin is not in equilibrium with the serum and so is not available to pathogens. However, ceruloplasmin is also used to carry copper to the bile for excretion [15]. Therefore I submit that the rise in serum ceruloplasmin in RA [16] causes an increased excretion of copper in members of a society who, even before this, were receiving less than the minimum daily requirement.


Evidence can be provided for this proposal in several ways. Arthritic people should have a lower whole body potassium content than normal people. This has been proved [17]. Red blood cells have a higher potassium content than normal during RA [18]. This should not be taken as counter evidence because I suspect that this is an adaptation to help avoid circulatory collapse when dehydration reduces the blood volume during diarrhea.

There should be a lower concentration of potassium in blood plasma during RA. 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. Only 18% appeared to be in the normal range. The samples were refrigerated and sent out to outside contract laboratories [48]. 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 when blood is drawn [47]. 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 a symptom or accentuates RA, 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- a potassium deficiency must be accentuating a cause of arthritis. I suspect this cause may be a mycoplasma bacterial infection. In any case, a large proportion of arthritics, at least, are too low in potassium for sure, some dangerously low.

That accentuation statement is plausible because antibiotics (tetracyclines, especially minocycline) specific against an odd bacterium species devoid of cell walls which can enter the cells like viruses called “Mycoplasma” or mycobacteria have been said to be shown to cure many arthritics [50]. However the antibiotic is said to be only maximally affective if the patients stop eating sugars, fats, and grains. This would greatly increase potassium intake. In regard to resisting diseases, especially bacterial, there is probably another reason for keeping cell potassium normal with adequate nutrition. 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 [51]. So it seems plausible to me that, when the pump is operating normally, 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 [*]. It is conceivable that this is a problem with mycobacteria also and help explain why potassium supplements are so effective against RA. Mycobacteria as a factor in joint pain is plausible because those bacteria may well be increasing secretion of glucosteroid response modifying factors, although I have no evidence. A different spelling for the bacteria calling them mycoplasmin has also been implicated in arthritis according this reference [49]. 50% of rheumatoid arthritis patients have had other kinds of mycoplasmal bacterial infections [52].

There should be a lower incidence of RA among people on potassium supplementation or who eat Morton's Lite Salt (TM) or Stirling's Half and Half (TM). I know of no epidemiological study showing this. However, people who work in potash mines have a 25% lower incidence of heart disease than the surrounding population [19] and heart disease is more prevalent in RA. There should be a healing of RA upon starting potassium supplements. No controlled experiment has been reported which would indicate this other than Rastmanesh’s. However there is a case history of a single arthritic brought up to 3,500 milligrams per day in order to explore the effects of various steroid hormones on the body's mineral balance [20]. A total of 3,500 milligrams is about the amount an adult would obtain from unprocessed food. The subject showed consistent improvement throughout the experiment even though potassium was the only consistent change. His total body potassium slowly but consistently rose. I know of five case histories that removed RA pain by supplements. There should be a negative correlation between high potassium-caused muscle spasms and RA, but I have no supporting data. Neither do I know of a positive correlation with eating licorice (but not licorice candy, which is made of anise seeds) grapefruit, or potassium losing diuretics, each of which increase potassium loss. There should be a negative correlation between eating acids that have an indigestible anion and RA since the hydrogen ion interferes with potassium excretion [21]. I know of no good experiment or epidemiological study. However, it has been suggested from folk custom that eating vinegar [22] or cherries is efficacious. The vinegar seems doubtful since it is my understanding that acetate can be metabolized by the body [22a]. However, it is conceivable that people on a diet high in calories do not utilize all the acetate or even much of it. In any case, RA should not be present much in people who eat predominantly vegetables instead of grains. An experiment has been performed in which RA was healed in a group of people by switching to a vegetable diet [23b]. Eating bananas would increase potassium somewhat, but it is only a moderate source per calorie, about the same as potatoes.

I suspect that people with rheumatoid arthritis tend to have a poorer ability to conserve or absorb potassium than other people because of damage to their kidneys by a poison such as bromine gas (as happened to me in a college laboratory) or long term poisons in plant foods or by a mild genetic defect or by poisons excreted by pathogenic bacteria. Some bacterial infections do trigger RA. Screening some common poisons currently in food might be enlightening, both for retarding and increasing excretion. Because GRMF inhibits cortisol, it is possible that a discordance in the immune response involving GRMF in some people or some infection types (that last does happen) may accentuate RA.

If animals are used for experiments, it is futile to use rats or mice because they rely on corticosterone to regulate the immune response, not cortisol. I suspect that this developed because they have a factor in their intestinal fluid which counteracts cholera toxin [23]. They also have the ability to absorb water under cyclic AMP stimulation in part of their colon [24] instead of to excrete of water, unlike other animals. As a result of this they do not need the cortisol system against diarrhea.

Because the disturbance in copper metabolism is proposed as the most serious aspect of RA, evidence for copper's effect should be possible. Supplementing with copper should remove some of the symptoms of RA. I know of no such experiment. However, it is known that Finnish men who work in copper mines have little arthritis or susceptibility to infection. [25]. The high milk diet along with frequent saunas may be two reasons why other Finns have one of the highest rates of arthritis in the world [26], since milk is the poorest source of copper[27, p.92] and perspiration loses potassium [28]. Milk has been shown to have a high statistical correlation with cardiovascular disease, said to be as great a risk as smoking [29], which disease in turn is correlated with RA. Laplanders on a meat diet have a lower rate of RA not much further north [26]. The Masai of Africa have a higher rate of RA than the surrounding tribes [30, p768]. The Masai also use a lot of milk as well as very few vegetables, which vegetables would have increased potassium intake. Men who work in copper mines must have stronger tissues than other miners because the percentage of injuries which result in lost time is significantly lower [31], even though injuries like eye damage and burns which are not affected by strength are part of the data. Eating a lot of shellfish or liver should reduce those symptoms related to copper deficiency because they are the richest sources, but I know of no study. The same should be true of drinking acid water out of copper plumbing.

I believe that it is unwise to give cortisol to any class of people whose immune system is weak, such as arthritic people. If it is felt that cortisol should be raised in the body, why not use something relatively safe, like potassium supplements? If potassium supplements are used, be certain that vitamin B- 1 is adequate because the "wet" heart disease of beri-beri can not materialize when potassium is deficient. [32] Obviously the reverse is also true for vitamin B-1 supplementation. For this reason, If the patient has heart trouble, it is very important to determine whether it is caused or accentuated by vitamin B-1 or by potassium. If it can not be determined, it is imperative that both be supplemented.

If potassium chloride is dissolved in fruit juice it tastes good and avoids the danger to the intestines that even slow release enteric tablets may present. The chloride is the most easily retained form [33]. When the potassium is brought to normal it is necessary to switch to the bicarbonate because the chloride raises blood pressure [ http://www.wellnessresources.com/tips/articles/potassium_is_a_vital_key_for_lowering_blood_pressure/ ]. It would be better and safer yet to provide potassium from food high in potassium such as celery or bamboo shoots as Effinger proposed [34]. Not boiled, unfrozen, not canned vegetables low in starch are the richest sources [35]. However, removing a deficiency will be slower since the potassium is not associated with chloride and would take a few weeks or months longer.

A potassium deficiency can arise from diarrhea, eating processed food, reliance on grain or fatty foods [35], psychic stress stimulation of aldosterone [36] (which is the main regulator of potassium) [37], stress stimulation of cortisol (as in an operation, for instance [38]), diuretics, licorice [39] as well as probably grapefruit [39a], profuse perspiration [28], excessive vomiting [40], eating sodium bicarbonate [41], hyperventilating [42], laxatives [43], enemas [44] (especially if prolonged), shock from burns or injury [45], hostile or fearful emotions [36], and very high or very low sodium intake [46], All of these increase excretion or decrease intake of potassium and many simultaneously would be very dangerous and probably even fatal if prolonged.

A chronic potassium deficiency must surely cause a degenerative disease. I believe it materializes in some people as RA, or at least accentuates RA. If not, then what is the name of the degenerative disease which attends a potassium deficiency ? It is not hypokalemia. This is only a word that describes low serum potassium, a marker or symptom. It is about time we found such a name.

”There is a principle which is a bar against all information, which is proof against all argument, and which cannot fail to keep man in everlasting ignorance. That principle is condemnation without investigation" (from Herbert Spencer). From the time that cod liver oil was suggested as a treatment for rickets one hundred and fifty years went by during which time cod liver oil actually declined in popularity with the medical profession. It was not until Sir Edward Mellanby established it in 1920 that it could no longer be denied. Let us hope that we do not have to wait 150 years before Dr. Rastmanesh’s clinical trial is replicated testing potassium against arthritis (see paragraph at the beginning).

REFERENCES are below

CONTENTS of other chapters about potassium
HREF="http://members.tripod.com/~charles_W/electrolyte.html">V. Electrolyte regulation (sodium and potassium) --- VI. Purpose of cortisol--- XIVPotassium and vitamin B-1 (thiamin) in heart disease --- What to do During High Blood Potassium --- Helpful strategies against CFS and fibromyalgia


The health of people in the USA is abysmal (numerous statistics), and a major part of it is poor nutrition. As the 12th century physician, trying to cure by diet before he administers drugs, said; “No illness that can be treated by diet should be treated by any other means" or as Hippocrates expressed it in 460 - 377BC; "If we could give every individual the right amount of nourishment and exercise, not too little and not too much, we would have found the safest way to health." It would seem that a healthy life style has been known for a long time. It is my belief that an unprocessed, unfrozen, not canned, high in vegetables diet would keep a large majority of people reasonably healthy and without the need for fad diets. 80% of Americans do not eat adequate vegetables, but even though 72% of Americans take vitamin or mineral supplements daily or sometimes [Sardi p148], their health is atrocious, especially old people.

I would suggest that a partial solution to the problem of poor potassium nutrition would be to place a tax on all food that has had potassium removed by food processors and completely fund all Medicare and workman’s compensation for injuries and disease that relate to rheumatoid arthritis, heart disease, and high blood pressure. This would also take the onerous tax burden now incurred for them and place it on the shoulders of those who cause the problem.

The author, Charles Weber, has a degree in chemistry and an MS 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), Clinical and Experimental Rheumatology (1983), and Medical Hypotheses (1984, 1998, 1999, 2005, 2007, 2008).

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

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


You may obtain a book about potassium nutrition at this site, along with the table of contents and first chapter. It discusses how food processing, diuretics, diarrhea, enemas, laxatives, corticosteroids, poisons, and disease states cause a deficiency and how potassium will cure heart disease, rheumatoid arthritis, gout, and hypertension. It also discusses procedures to cope with too high a blood potassium and abnormal potassium in diabetes.

There is an an article discussing cashew nuts to cure a tooth abscess Which might prove useful.
There is also an article which proposes some speculation about diabetes.
Nutrition and physiology of copper, especially relating to hemorrhoids, aneurysm, herniated discs, anemia, emphysema, and gray hair.Copper Response in Rheumatoid Arthritis:
Fluoride in city water will cause fluorosis discoloration of teeth, weakened bones, damage to the kidneys and immune system, bone cancer and, worst of all, damage to the nerves resembling Alzheimer’s disease.

There is a site that contains reviews of natural remedies for many diseases .

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 for this and other possibly other cancers until you can persuade a doctor to try tumor necrosis factor or interferon or an opioid antagonist drug called Naltrexone (Naltrexone in the large 50mg 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) (also see these sites hereand here. ) and. 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. I think some clinical studies on Naltrexone are in order, and it should not be a prescription drug. 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. There are suggestions on how to obtain Naltrexone without a prescription in this site. Naltrexone is currently being used by Dr. Enlander, a New York City doctor, but with limited success for chronic fatigue syndrome using 3 to 4.5 milligram doses for CFIDS.

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

If you use medication, you may see technical evaluations and cautions of drugs at the bottom of this site.

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.

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.


Did the Wood Roach Cause the Permian - Triassic Coal Hiatus? The ability to digest cellulose may have sparked Permian aridity and the conifer rise.
Permian Atmospheric Carbon Dioxide and Prototermite Migration A huge comet strike may have caused extinctions and spread of proto termites around the world.
Permian Phosphorus Amphibians such as dragonflies may have caused the Permian marine phosphorites and armored fish.
Termites Affect on Phosphorus in the Jurassic Sheet erosion by soil borne termites starting in late Jurassic may have caused fertile oceans and a decline of vertebrate bones and teeth on savannas from a phosphorus famine.
Paleocene and Modern Termites Evolution of termites may have contributed to the small size of vertebrates in early Paleocene.
Angiosperm Evolution Broad leafed plants may have evolved on the Ontong - Java plateau in the Permian.
Deciduous Forests from Glaze Ice It is proposed that the temperate deciduous forest zone is caused by glaze ice storms.

REFERENCES ---- [*] I have lost the reference to this statement.

1. Darrow, D.C. 1946 "Retention of Electrolyte during recovery from severe dehydration due to diarrhea," Journal of Pediat. 28; 515.

2. Mekalanos, J.J.; Swartz, D.J.; Pearson, GDN.; Harford, N.; Groyne, F.; Wilde, M. 1983. "Cholera Toxin Genes: Nucleotide Sequence, Deletion Analysis and Vaccine Developement," Nature 306; 551.

3. Bronner, F.; Comar, C.L. 1961 Mineral Metabolism Vol I, Academic Press.

4. Mikosha, A.S.; Pushkarov, I.S.; Chelnakova, I.S.; Remennikov, G.Ya. 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. ZH (Kiev) 37:60.

5. Melby J.C.; Egdahl, R.H.; Spink, W.W. 1960 "Secretion and Metabolism of Cortisol after Injection of Endotoxin." Journal of Lab. Clin. Med. 56;50.

6. Fairchild, S.S.; Shannon, K.; Kwan, E.; Mishell, R.I. 1984 "T-cell Derived Glucocorticosteroid Response Modifying Factor (GRMFt): A Unique Lymphokine Made by Normal T Lymphocytes and a T-cell Hybridoma." Journal of Immunology 132; 821.

7. Besedovsky, H.O.; Del Rey, A.; Sorkin, E. 1984 "Integration of Activated Immune Cell Products in Immune Endocrine Feedback Circuits." p. 200, Leukocytes and Host Defense Vol. 5 (Oppenheim, J.J.; Jacobs, D.M., eds). Alan R. Liss, NY.

8. Milenkovic, L.; Rettori, V.; Snyder, G.D.; Beutler, B.; McCann, S.M. 1989 "Cachectin Alters Anterior Pituitary Hormone Release by a Direct Action in Vitro." Nat. Acad. Sci. 86; 2418.

9. Finlay, G.J.; Booth, R.J.; Marbrook, J. 1979 "Antibody Responses of Human Lymphocytes in Vitro; Enhancing Effects of Hydrocortisone." Austr. Journal of Exp. Biol Med. Sci. 57; 597.

10. Jones, R.S.; Howell, E.V.; Eik-Nesk. 1959 "Inactivation by Plasma of ACTH Releasing Property of C-14 Labeled Bacterial Polysacharride." Proc. Soc. of Exper. Biol. Med. 100; 328.

11. Prohaska, J.R.; Lukaseqycz, O.A. 1981 "Copper Deficiency Suppresses the Immune Response in Mice." Science 213; 559.

12. Weber, C.E. 1984 "Copper Response to Rheumatoid Arthritis." Medical Hypotheses 15; 333.

13. Harris, E.D.; Rayton, J.K.; Baltriop, J.E.; Di Silvestro, R.A.; Garcia de Quevedo. "Copper in the Synthesis of Elastin and Collagen," p. 163, Biological Roles of Copper, Ciba Foundation Symposium No 79, Exerpta Medica NY.

14. Matsuoka, Y.; Obana, M.; Mita, S.; Kohno, M.; Irimajiri, S.; Fujimori, I.; Fukuda, J. "Studies of Death in Autopsied Cases with Rheumatoid Arthritis," p. 27, New Horizons in Rheumatoid Arthritis. ( Shiokawa, Y.; Abe, T.; Yamauchi, Y., eds.) Excerpta Medica Internat. Cong. Series #535.

15. Frieden, E. 1981 "Ceruloplasmin: A Multifunctional Metalloprotein of Vertebrate Plasma." Metal Ions and Biological Systems, Vol. 13, p. 117 (Sigel, H.; Sigel, B., eds.) Marcel Dekker, NY & Basel.

16. Aiginger, P.; Kolarz, G.; Wilvonseder, R. 1978 "Copper in Ankylosing Spondylitis and Rheumatoid Arthritis." Scand. Journal of Rheumatol. 7; 75.

17. LaCelle, P.L., et al. 1964 "An Investigation of Total Body Potassium in Patients with Rheumatoid Arthritis." Proc. Ann. Meeting of the Am. Rheumatism Assoc. Arth. Rheum. 7; 321.

18. Knudsen, E.T.; Thomas, M.J. 1957 "Erythrocyte Potassium Level in Rheumatoid Arthritis." Lancet 272; 251.

19. Waxweiler, R.J., et al. 1973 "Mortality of Potash Workers." J. Occup. Med. 15; 486.

20. Clark, W.S, 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.

21. Berliner, R.W, et al. 1951 "Relationship between Acidification of the Urine and Potassium Metabolism." Amer. Journal Med. 11; 274.

21a. Mills, J.H.; Stanbury, S.W. 1954 "A Riciprocal Relationship between K+ and H+ Excretion in the Diurnal Excretory Rhythm in Man." Clin. Sci. 13; 177.

22. Jarvis, D.C. 1960 "Arthritis and Folk Medicine." Pan Books Ltd. London.

22a. Winegrad AT Reynold AE 1958 Effects of insulin on the metabolism of glucose, pyruvate, and acetate. Journal of Biol. Chem. 233; 267.

22b. Kjeldsen-Kraw, J. 1991 Lancet Oct. 12; 899.

22d 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.

23. Donowitz, M.; Binder, H.J. 1976 "Effect of Enterotoxins of Vibrio Cholerae, Escherichi coli, & Shigelladienteriae Type 1 on Fluid and Electrolyte Transport in Colon." Journal of Infect. Dis. 134; 135.

24. Hornyck, A.; Meyer, P.; Milliez, P. 1973 "Angiotensin, Vasopressin, and Cyclic AMP: Effects of Sodium & Water Fluxes in Rat Colon." Am Journal of Physiol. 224; 1223.

25. Sorrenson, JRJ;. Hangarter, W. 1977 "Treatment of Rheumatoid and Degenerative Diseases with Copper Complexes." Inflammation 2; 217.

26. Kellgren, J.H. 1966 "Epidemiology of RA" Arh. Rheum. 9; 658.

27. Underwood, E.J. 1972 "Trace Elements in Human and Animal Nutrition." Academic Press NY.

28. Consolazio, C.F., et al. 1963 "Excretion of Sodium, Potassium, Magnesium, and Iron in Human Sweat and the Relation of Each to Balance and Requirements." Journal of Nutr. 79; 407.

29. Seely, S. 1981 "Diet and Coronary Disease: A Survey of Mortality Rates and Food Consumption Statistics of 24 Countries." Med. Hypotheses. 7; 907.

30. Best, C.H.; Taylor, N.B. 1950 The Physiological Basis of Medical Practice, 5th ed. Williams and Wilkins Co., Baltimore (p. 768).

31. U.S. Dept. of Labor, Mine Safety and Health Administration. 1981 "Injury Experience in Metallic Mineral Mining," IR 1142 Table # 6. pp. 24 & 58.

32. Folis, R.H. 1942 "Myocardial Necrosis in Rats on a Potassium Low Diet Prevented by Thiamine Deficiency." Bull. Johns-Hopkins Hospital 71; 235.

33. DeLand, E.C., et al. 1979 "A Theoretical and Experimental Study of Ionic Shifts Induced by K Depletion and Replacement." Journal of Theor. Biol. 76; 31.

34. Eppinger, H. 1939 "Einiges Uber Dietetische Therapie." Ztschr. F. Artzl. Fortbild. 36; 672 & 709.

35. Weber, C.E. 1974 "Potassium in the Etiology of Rheumatoid Arthritis and Heart Infarction." Journal of Applied Nutrition. 26; 41 (Bibliography published separately).

36. Glaz, E.; Vecsei, P. 1971 "Aldosterone." Pergamon Press NY (p 209).

37. Weber, C.E 1983 "Corticosteroid Regulation of Electrolytes." Journal of Theor. Biol. 104; 443.

38. Elman, R., et al. 1952 "Intracellular and Extracellular Potassium Deficits in Surgical Patients." Ann. Surgery 136; 111.

39. Stormer, FC, Reistad, R, Alexander, J 1993 Glycyrrizic acid in licorice - evaluation of health hazard. Food Chem. Toxicol 31; 303-312.

39a. Lee YS, Lorenzo, BJ, Koufis, T, Reidenberg, MN 1996 Grapefruit juice and its flavenoids inhibit 11 beta - hydroxy steroid dehydrogenase. Clin. Pharmacol. Ther. 59; 62-71.

40. Barter, F.C. 1980 "Clinical Problems of Potassium Metabolism, Contributions to Nephrology." p. 21, Disturbances of Water and Electrolyte Metabolism. Bahlmann, J.; Brod, J., eds. S. Karger, Basel.

41. Berliner, R.W, et al. 1951 "Relationship between Acidification of the Urine and Potassium Metabolism." Amer. Journal of Med. 11; 274.

42. Kilburn, K.H. 1966 "Movements of Potassium during Acute Respiratory Acidosus and Recovery." Journal of Applied Physiol. 21; 679.

43. Schwartz, W.B.; Relman, M.B. 1953 "Metabolic and Renal Studies in Chronic Potassium Depletion Resulting from Overuse of Laxatives." Journal of Clin. Invest. 32; 58.

44. Dunning, M.F.; Plum, F. 1956 "Potassium Depletion by Enemas." Amer. Journal of Med. 20; 789.

45. Fox, C.L.; Baer, H. 1947 "Redistribution of Potassium, Sodium, and Water in Burns and Trauma and Its Relation to Phenomena of Shock." Am. Journal of Physiol. 151.

46. Williams, G.H.; Dluhy, R.G. 1972 "Aldosterone Biosynthesis: Interrelationship of Regulatory Factors." Am. Journal of Med. 53; 595.

47. Ifudu O Markell MS Friedman EA 1992 Unrecognized pseudohyperkalemia as a cause of elevated potassium in patients with renal disease. American Journal of Nephrology12; 102-104.

48. 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.

49. Ramírez AS Rosas A Hernández-Beriain JA Orengo JC Saavedra P de la Fe C Fernández A Poveda JB 2005 Relationship between rheumatoid arthritis and Mycoplasma pneumoniae: a case–control study. Rheumatology 44(7):912-914;

50. Poehlmann KM 2002 Rheumatoid Arthritis the Infection Connection. Satori Press, 904 Silver Spur Road #323, Rolling Hills Estates, CA 90274.

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

52. Nicolson, GL. Nasralla, MY, De Meirleir K, Gan, R., Haier J 2003 Evidence for Bacterial and Viral Co-Infections in Chronic Fatigue Syndrome Patients. Journal of Chronic Fatigue Syndrome 2003; 11(2):7-20.

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