The word "arthritis" = rheumatoid arthritis = RA in this book.
It is my contention that potassium deficiency is either causing, or greatly making worse, rheumatoid arthritis, which I will shorten to "arthritis" in these articles. 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 about these 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 any experiment. This includes Exerpta Medica 1947 to 1974, and a computer search by the Central Library of the American Medical Association from 1965 on back. In addition no search of mine since has revealed an experiment.
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. 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 for 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, and it is probably an important factor in chronic fatigue syndrome (CFIDS). 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" 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.
Chapter I ---
Arthritis or rheumatism is the number one crippling disease in America, limiting activities for 7 million Americans [from a CDC article]. Those estimates probably include arthritis like diseases other than rheumatoid arthritis and estimates elsewhere are very variable, probably because the severity of the disease varies very much. A Brazilian study indicates that one half a per cent have rheumatoid arthritis as opposed to about 4% for osteoarthritis in that country, and 2% for rheumatoid has been estimated for the USA [Rasch]. The CDC says that at least 65 billion dollars are lost each year for medical costs and loss of productivity, but that figure does not a even begin to measure degradation of quality of life. 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, loss of energy, and other systemic --------- symptoms which accompany them, cause an enormous loss of productivity. 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]. Nor is a simple life a guarantee of good nutrition. 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 (including villages in Nigeria [Silman] ) and Laplanders near the Finns in Finland, as well as insane people in Massachusetts [Allander p260] and an absence of arthritis on the island of Triton da Cuhna [Kellgren]. There is no evidence of rheumatoid arthritis among early Australian aborigines [Roberts-Thompson]. The rates are very variable within regions of North America, within ethnic and economic groups, and age groups 15.2% of white people. 15.5% of black people, 11.3% of Hispanics, and 7.3% of Asian Pacific islanders have rheumatic conditions [Helmick].
Most of the people who have pains in the joints have them because of arthritis (but see symptoms of other types of joint pains). The pains usually strike first in the outer joints like wrists, carpels, 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 (or in the case of rodents possibly because they make no use of cortisol), 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 these articles will be equated with "rheumatoid arthritis" or RA) except a lower cellular potassium content than normal [LaCelle][Sambrook], and a somewhat higher plasma copper content along with a protein which binds the copper in the serum [Schubert]. However there are reports of some changes, which show up in a high proportion of arthritics. There have been reports of low potassium (the only consistent difference from normal they found) [Syrjanen], calcium, phosphorus, lysozyme, and IgA peptide in the saliva of juvenile arthritics [Siamopoulou et al] (which form of arthritis could be similar to the adult form). The sodium/potassium ATPase activity is lower in erythrocyte (red blood cell) membrane [Masoon-Yasinzai] and lower than in normal, osteoarthritis, or gout [Testa]. The steroid hormone dehydroepiandrosterone sulfate (DHEA) is statistically lower in arthritics [Dessein] as is cortisol and pregnanediol, even though ACTH is higher, as is aldosterone [Khetagurova]]. The aldosterone being higher suggests that there is something besides the low potassium itself that is involved in the cause of arthritis since aldosterone stimulates excretion of potassium and has a positive feedback. 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 and remains so today. Erythrocyte sedimentation rate (ESR) is poor for diagnosis [There are significant correlations between IgM RF and IgA immune proteins and a higher disease activity [Chen] but the correlations are not perfect. There is lower glycosylation of immune peptides (addition of sugar molecules) during arthritis [Axford]. I do not know what the significance of this is although addition of sugars may prevent the peptides from being normally active. C3 and C4 compliments are said to be the best of the other discriminators [Sari, et al]. Epithelial sodium channels, alpha and beta types are higher than normal in rheumatoid arthritis but not in osteoarthritis [Trujillo, et al]. There is high activity of collagenase and elastase in the synovial fluid of patients with rheumatoid arthritis, which is about 30 times higher than that found in the synovial fluid of patients with osteoarthritis [Bazzichi]. Arthritis sometimes has fatigue associated with it. The settling rate red blood cells is different in arthritis.
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 get adequate potassium from food from which almost every processing procedure removes potassium these days. Arthritics characteristically have poor nourishment [Morgan et al] [Stone] including magnesium, which is necessary for potassium absorption [Kremer]. One such poison, which I suspect, is the very poisonous bromine gas, since it probably affected me that way 50 years ago. It is possible that the glucocorticosteroid response modifying peptide hormone (GRMF) to be discussed in the cortisol chapter may be the system involved in the case of infection triggers.
One technique, which seemed to have some success, was the use of spas. At least their popularity would seem to indicate some success. The Dead Sea water has a reputation for healing arthritis and has been successfully investigated with healing lasting up to three months [Sukenik]. 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. Sea mud is also given credit for curative properties [Veinpalu]. The spa at Bath, England, has 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. More recently potassium supplements in connection with other drugs gave a good response [Casatta].
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 might 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. However recently improvement has been noted using a diet that had increased amounts of vegetable juice and unpolished rice [Fujita]. There also has been a study which showed a strong negative correlation with cooked vegetables in Greece [Linos] and in Italy [[LaVecchia]. Dr. Saul has described a case in which vegetable juice and vegetables healed a woman.
That diet is deeply involved in arthritis seems almost certain since when people migrate from areas with very low arthritis rates and start eating processed food, they come down with arthritis.
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 [Winegrad] all of the acetate ion or the acetate is being excreted by the kidneys before it has a chance to enter the cells 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. Kombucha, a vinegar like ferment, is said to be helpful for arthritis.
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 in Chapter II. 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 (except to people low in potassium, where it is protective against heart and kidney disease [Folis] ), some like dyes 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]. It has been proposed that vitamin D has an affect dampening the immune system. [Cantorna] although apparently this concept has not been followed up on. Those using Alexander’s diet must have had less trouble with tooth decay, tuberculosis [Wilkinson], muscle cramps, and rickets. Also vitamin D is necessary for magnesium reabsorption in the kidneys [Ritchie] which magnesium in turn is necessary for powering some of the electrolyte pumps [Grace], so it could easily be having an indirect affect on potassium in many cases. This may be the reason why women taking vitamin D have less arthritis than those who do not.[Merlino]. The optimal values in the blood are proposed as 45-50 ng/ml or 115-128 nmol/liter of vitamin D.
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. More likely is that the decline in cortisol during a potassium deficiency [Mikosha (in guinea pigs) ] stimulates the allergic response. It is also suggested by an experiment in which cortisol was increased by potassium chloride given to people [Ueda]. There is good evidence, though, of beneficial results from defeating allergy in specific cases. It is possible that allergens affect that part of the immune system involved in arthritis.
Evidence from individual case histories that I have seen myself 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 if it as much as 30% low. However there should be satisfying initial results in a month or two or even less if the other nutrition is adequate, especially magnesium [Kremer][Schoner] and maybe inositol [Charalampous] and probably less time yet if potassium is taken as the chloride (the chloride is probably not a good idea if you have high blood pressure or suffer from chronic fatigue syndrome (CFS or CFIDS).
I have been almost alone in proposing potassium as being central to rheumatoid arthritis (but see Dr. Jan de Vries' article). . Also Das has recently suggested that glucose-insulin-potassium (GIK) therapy might suppress tumor necrosis (TNF) which is thought to produce some of the symptoms of arthritis [Das]. However there is no substitute for an experiment, which has never been reported in a journal, since scientists are specialized and sometimes have trouble being interested in simple approaches, as are their funding agencies. A doctor has reported to me that potassium and magnesium had inconclusive results, but it is possible that the subjects had osteoarthritis or chronic fatigue syndrome so I am unwilling to accept this as negative evidence yet. While you are waiting patiently 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 am virtually certain that you will be healthier and will certainly have less risk of stroke, high blood pressure, and kidney stones. . I wish you good health.
REFERENCES for CHAPTER I in; http://members.tripod.com/~charles_W/arthritis.html
Chapter II ---
For years arthritis was the poor relation of medical research. Its victims did not do something dramatic like die, as they often did with pneumonia, or go insane as they did with syphilis, or bring tears to the eyes as with childhood diphtheria, or have nice bright , easily recognizable symptoms as with measles. Arthritis tended to be a disability of old folks with vague, sometimes disbelieved symptoms. That has changed and extensive, well-funded research is being done now partly because there has been a considerable increase in arthritis. Indeed, it is the leading cause of disability in the USA today. Forming the backdrop of this research are several hypotheses, some borrowed from research into other diseases, and some with a novel twist of their own.
One of the oldest of these is the stress hormone hypothesis championed by Selye [Selye 1949 & 1950 p197-198]. Roughly his contention was that hormones released by the body, especially those released by the jacket of the adrenal glands, cause an adverse reaction to the joint tissues when they are released in too large amounts or the wrong ratios under conditions of environmental stress or psychic stress. His concept was generalized and only mentioned arthritis as an unlikely possibility. The theory had some plausibility since arthritis can be produced by injecting deoxycorticosterone (DOC) into a person who has been suffering from Addisons's disease or into animals [Selye et al 1944][Turner]. Some support is given to this approach in that repressed hostility is probably correlated with rheumatoid arthritis [Cobb]. The dramatic affect that cortisone has on arthritis, removing all symptoms in a short time, would give encouragement to a scientist trying to approach this matter from Selye's viewpoint. This hypothesis has never been refuted although it has fallen into disfavor recently. This is probably because some rather severe side effects materialized eventually when medical people used cortisone for a long time. As one author put it "It is remarkable how cortisone can get a seemingly hopeless patient on his feet again. Sometimes it is so effective that he can walk all the way to the autopsy table." Cortisone changes to cortisol which reduces resistance to infection, suppresses fever, causes polyarteritis nodosa (a blood vessel disease), and suppresses collagen synthesis. Stress theories did not always emphasize steroid hormones. Histamine was suggested as possibly being involved [Eyring].
A group called "Arthritis Medical Information Society" had revived this concept. They claim cures using a "balanced" regime of injected hormones, hormones which include the steroid testerone, a sex hormone. They claimed a preponderance of anabolic hormones prevent side effects. They also recommend better nutrition, which I suspect, was having the major affect.
McCord has proposed that arthritis may be caused by insufficient amounts of superoxide dismutase, an enzyme catalyzed by copper [McCord]. Copper supplements either as pharmaceuticals [Sorenson 1980] or as copper bracelets have been proposed with encouraging results. Copper as ceruloplasmin is high in the blood of rheumatoid arthritics [Zoli] [Louro] and this may be depleting copper by greater excretion through the bile. The reason why copper seemed to impact arthritis may be because a copper deficiency increases mast cells half again as much in rats [Schuschke], which increased numbers in turn increases inflammation caused by histamine release by those mast cells as stimulated by the immune peptide hormones.
Because of the dramatic successes that scientists had in their battle against bacteria and virus, it is not surprising that these men should turn their attention to finding an organism, which was responsible for arthritis. The fact that some infections could trigger an attack of arthritis must have given them encouragement. Not surprisingly infections have been searched for as causal to arthritis. I know of no infection that has been proven to chronically inhabit the joints, although lyme disease has been proposed.. Infections are known to trigger arthritis, however, and tooth abscesses can cause shoulder bursitis. Antibiotics specific against an odd bacterium species which can enter the cells called “Mycoplasma” has been said to be shown to cure many arthritics. This 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 to this site. 50% of rheumatoid arthritis patients have had mycoplasmal bacterial infections [Nicolson]. Reactive inflammatory arthritis said to be always have mycoplasma present (numerous references).Also a recent blood analysis has disclosed that rheumatoid arthritis patients have ten times as many Epstein Barr (mononucleosis) virus antibodies as normal people [Balandraud]. So it is possible that arthritis is a reaction to antibodies of that virus as the authors suggest or, more likely, to the dormant virus, at least partly.
It is possible for joints to become directly infected by pathogens, but the symptoms of this fairly rare condition are not exactly the same as arthritis. It causes skin rash, large lymph nodes, fever, and often affects the kidneys and heart [*] However an exhaustive search has not disclosed any microbe consistently present in inflamed tissue [Phillips] although some investigators believe that an amebic infection is involved. The Arthritis Trust of America and Canada is organized around the concept that killing an unknown microorganism with antibiotics will alleviate arthritis and claim to have had some good results. Also recent research has implicated bacteria called chlamydia in a disease called "reactive arthritis" which usually afflicts a few joints in the knees, ankles, or toes a few weeks or months after infection. When it affects other tissue it is called "Reiter's syndrome"
The most popular current hypothesis is the autoimmune hypothesis. This hypothesis proposes that the body's mechanism for killing disease organisms gets out of order, and starts killing connective tissue cells or perhaps dissolving the connecting tissue itself. Moderately high statistical associations between arthritis and physiological circumstances which are closely related to the immune system have given investigators all over the world encouragement. Many do not even regard the concept as a hypothesis, but as a proven theory. A much higher association of antigen HLA-B27, which is a known immunity factor, with diseases in the arthritic group such as Reiter's syndrome and ankylosing spondilitis [Mikkelsen] has tended to reinforce this feeling that they are on the right track. Investigations into the autoimmune hypothesis are well funded. Currently there is considerable effort being put into exploring the role of the increase in tumor necrosis factor (TNF or cachectin or cachexin) during arthritis. TNF is a peptide protein hormone secreted by the immune system. Encouraging results are obtained by blocking agents [Campbell] such as Remicade. However that therapy makes the patient more susceptible to infections such as tuberculosis. It probably receives some of its affect by sensitizing the pituitarv gland to secrete more ACTH and therefore stimulating the adrenals to secrete more cortisol [Staub]. It has been proposed recently that GIK solutions be used to suppress tumor necrosis factor [Das]. GIK {glucose insulin kalium) is an injection of a potassium supplement.
It would seem strange that mesenchyme tissue (tissue derived from the middle layer of the embryo) is primarily affected, that it would take so long to be destroyed, or that there would be spontaneous remissions if the auto immune hypothesis were valid. At the very least some auxiliary hypotheses would be necessary. Millman has proposed that some of the cell wall off of bacterial invaders become incorporated into the collagen [Millman]. Effects of steroid treatment may be due to inhibition of arachidonic metabolic cascade (the prostaglandin hormones) especially to leucotrienes, which are thought to activate macro white cells [Nalbandian]. The number of white cells can rise extremely high in arthritis [Meyer]. The hypothesis seems plausible but attempts to adapt it to diagnostic techniques have been unsuccessful. There have been medicines proposed which dampen the immune system, but most of them cause the joint damage to get worse in the long run. Tumor necrosis factor (TNF) inhibitors have gained recent popularity, and probably work partly by accentuatig ACTH and therefore cortisol [Staub], but dampen the immune system. Probably what happens is that the low potassium causes cortisol to decline [Mikosha]. This in turn causes superoxide dismutase (an enzyme which degrades extremely active oxides like hydrogen peroxide and superoxide radical) to decline. As a result some of the cells are killed. At the same time the enzyme which cross-links connective tissue is inhibited and this causes severe problems with blood vessels, spinal discs, and even the joints if continued a long time. There is a hypothesis that the enzymes inside the lysosome sacs inside the white cells are released because of weakness [Weissman]. This may be happening when sodium urate crystals are ingested by the white cells in gouty arthritis[*] but evidence for it in rheumatoid arthritis is inconclusive.
The hypothesis that arthritis is an allergy is in the same general category as the autoimmune hypothesis. Such a hypothesis has the advantage not shared by the autoimmune hypothesis directly of advancing an environmental factor which is almost certainly involved. The wide geographical variations already mentioned in chapter I virtually ensure this. Turnbull has had impressive percentages (50%) of arthritics improved by removing certain foods from the diet [Turnbull]. Others claim success by removing environmental poisons such as cooking gas [Randolph]. Anderson has been successful in removing a bad case of allergy by removing lustidine and sodium from his diet. However he removed sodium by adding potassium [Anderson]. Currently Mcdougall has published references to research around allergy affecting arthritis. However the diet he recommends is high in vegetables and therefore potassium and magnesium. Medical people do not pay much attention to this allergy hypothesis even as a diagnostic approach. The references on allergy often mention this, and it appears to be true of most of the literature. Zussman, who improved four arthritics this way, could not believe he was dealing with arthritis or was afraid of ridicule, and so entitled his article "Food hypersensitivity simulating rheumatoid arthritis" [Zussman]. Allergens in food is Dong's hypothesis as mentioned in Chapter I [Dong], but he has no controlled experiments to verify his contention other than the general population being a control.
Allergy is without a doubt part of the arthritis picture since arthritics have two to three times as much incidence of allergy as average [Zeller]. White cells respond to a human nuclei challenge with 3.5 times as much histamine production in arthritics as normal people [Permin]. At one time a hornet's sting caused me to break out in a rash and swell up tremendously. More recently numerous stings from wasps, yellow jackets, and a hornet caused nothing but a sharp moderate pain and irritation for a day or two resembling a mosquito bite. A genetic defect making me incompatible with hornets would surely still be with me. I put bicarbonate of soda (baking soda) on the sting immediately now, but it does not seem possible that this alkalinity would have an affect on an allergic response remote from the wound. This allergic attack preceded my bout with what was probably rheumatoid arthritis. There have been numerous experiments deleting certain foods from the diet with improvement of symptoms in a large fraction of the participants. This would seem to give considerable support to the allergic hypothesis. However in most cases the nutritional value of the diet improved as well.
Similar in practical application to the food allergic hypothesis, but probably physiologically different, is a hypothesis put forward by Childers. He maintains that poisons in the solanaceous family are causing arthritis [Childers]. This is the night shade family and includes tomatoes, potatoes, pepper, eggplant, and tobacco. He suspects a chemical similar to vitamin D in its structure, or possibly one of the solanine alkaloids. If this hypothesis proves valid, it is possible that a substance similar to deoxycorticosterone (DOC) contained in these plants will be found to be responsible [Childers]. A poison that interferes with copper metabolism is another possibility. Smoking tobacco is known to cause emphysema, which is in turn known to be often caused by a copper deficiency. Childers has had 70% of his volunteers report improvement by deleting these vegetables. However only 30% responded to his survey [Childers, private communication] so these figures could be as low as 25% and 10% respectively. Unless arthritis has more than one cause or is misdiagnosed, even 70% is too low to establish anything as a primary cause. While the causal evidence is not excellent, the evidence is good enough to persuade one to remove these vegetables from one's diet while symptoms of arthritis are still present, just in case. There are plenty of other vegetables. Also never eat green or sprouting potatoes raw. Green potatoes have a very virulent poison, virulent enough to kill some people. The poison is destroyed by frying and baking but not by boiling. Also useful to know is that most of the solanines are close to the skin and possibly the other poisons as well [Childers, inside addenda].
vitamin B-3, niacinamide, has been proposed to alleviate arthritis. There is evidence that cetyl myristoleate in food reduces the symptoms of arthritis [*].
It has been proposed that coeliac disease from eating gluten in wheat is more common than thought and may contribute some of Crohn’s disease and arthritis. A genetic inability to digest gluten would not strictly be an allergy, but the damage to the intestines could conceivably affect potassium nutrition and have the affect suggested. It has also been proposed that lectins, or plant proteins which bind certain carbohydrates, contribute to arthritis by enabling antigens.[Cordain]. Gluten and concavelin A are lectins.
These hypotheses are not necessarily mutually exclusive and that potassium deficiency is a common thread that runs through many of them is highly probable. Potassium is an element that is essential to every cell in the body. It and sodium are controlled by at least five steroid hormones, several peptide hormones, and some molecular hormones. It would not be surprising that more than one disease syndrome could arise from a deficiency, especially considering that in addition to that, the twenty five or more essential nutrients are often either deficient or wildly oversupplied in our society as well, in addition to numerous poisons. Considering the last statement it would not be surprising either if fuzzy, inconclusive results were obtained with both nutritional experiments and medication. With such a complicated physiological situation as potassium you must surely see why I will always recommend that nutritional solutions be attempted by eating unprocessed food rather than supplements whenever possible. Thus imbalances tend to be avoided as well as other deficiencies. In particular it is essential to have adequate magnesium in order to absorb potassium efficiently, and maybe inositol also.
The difficulty in diagnosing arthritis sets doctors up for misdiagnosis. Hemochromatosis (build up of iron in the body) was misdiagnosed as rheumatoid arthritis [Espinosa-Morales], for instance.
I will attempt to explain potassium physiology especially as it pertains to arthritis and heart disease, how it can be changed in the diet, how it may be interacting with copper, how it can be supplemented, and dangers associated with its use in succeeding chapters (see links at the beginning). I am convinced that a perceptible improvement can be had in a few weeks even with food alone and potassium can be brought to normal in a few months at most for most people. It does not have to be completely normal in order to be reasonably healthy.
Most of the recent research has centered around the autoimmune hypothesis or in developing medicines which deaden pain. Unfortunately many of these medicines have had bad effects from the medicines especially on the kidneys.
These scientific efforts are further thwarted from pursuing nutritional investigations because a certain amount of resistance to new ideas is normal in scientists. Providing the innovations have a means of being tested, there are a number of differences between medicine and pure science that can result in some medical innovations being ignored or rejected without an adequate assessment. Social-organizational factors in medicine appear to favor the acceptance of theoretically glamorous, pharmaceutical, and high technology innovations over simpler and less profitable ones [Forman] even in government research. "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 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 potassium is tested against arthritis.
Potassium has not been and is not part of any experiments. But this does not mean you can not perform what are safe experiments with food. While it is not the policy of this author to use testimonials, you may, if you wish, tell of the outcome of health strategies to a new site which archives such experiences. I am almost alone in championing the potassium hypothesis among scientists at present, although Das has suggested it in the form of glucose-insulin-potassium (GIK) salts[Das]. You hardly have to wait until the last word in research has been unraveled in order to take steps to at least get all the potassium that was originally present in your food. There could be endless debate in scientific circles as to which fang the poison came out of in snake bite, or its exact chemical composition, or its mode of action. However this should not prevent one from staying away from the head end of a snake, even a non poisonous one, until such time as the matter were resolved in detail. Potassium is known beyond any doubt at all to be essential to all life and is known to be often deficient.
REFERENCES for CHAPTER II in; http://members.tripod.com/~charles_W/arthritis2.html
Chapter III ---
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. 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. There is also a new procedure using neutron bombardment of cells.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]. In any case it is necessary to use plasma determinations and not serum because serum can give incorrectly high results [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. Only 18% appeared to be in the normal range. 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 a symptom, those other survey people would have to have had arthritis as well. I believe many people die of a potassium caused heart disease without being arthritic, so, if so, the first part of the statement must be in order. In any case, a large proportion of arthritics at least are too low for sure, some dangerously low.
Even with careful determination plasma potassium can be anonymously high because of potassium losses from platelets during rheumatoid arthritis [Ifudu]. 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 upshot is that potassium is largely invisible to doctors. However, there is an observation of lower potassium in the saliva of patients [Syrjanen]. 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.
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. 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 p6otassium 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. 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]. There is also a single case history in which a subject was injected with various steroids to determine their effect. The only consistent thing that happened during the course of the experiment was that his daily intake of potassium was raised. His arthritic symptoms showed a consistent improvement throughout the course of the experiment [Clark]. Now an as yet unpublished experiment has been performed by Rudin 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. Perhaps an experiment supplementing both would be in order in the future for arthritis in order to get crisper correlations.
One of the arthritic diseases is known as gouty arthritis in which sodium urate crystals are deposited in cartilage, especially in the feet. 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]. Low level lead 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]. Other poisons may move one a little closer to gout also, such as timalol (Blocadran) combined with hydrochlorothiazide and amiloride (Moduretic) [Laren]. I also suspect that toluol in acylic automobile enamel may be able to trigger gout, from personal experience. I have no information in the medical literature on any direct link between gout and a potassium deficiency. I have a strong suspicion that there is a link however. 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. William Ellis 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][Halla] so there is a circumstantial connection. Urate kidney stones form during gout in a fifth of the cases. Making the urine less acid with potassium citrate or sodium bicarbonate is a current treatment for stones [Shekarriz]. I suspect that potassium bicarbonate would be preferable to sodium bicarbonate, but I have no evidence. The initiating factor is probably usually lead poisoning though [Wright]. Personal experience leads me to believe that toluene in automobile enamel reducers is also a poison which can trigger gout. There is an association in peoples minds between gout and rich foods and lifestyle, probably because people with gout have trouble excreting nitrogen, which is high in meat, in a soluble form and perhaps also because wine bottles and plumbing used to contain lead. Until such time as the matter is elucidated it would be a good idea to stop eating lead, eat less proteins, and not allow any potassium to be lost from one's food. Cherries have been shown to decrease urate in the urine of healthy women [Jacob], so they may have some therapeutic value.
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.
Acute symptoms can be detected by laboratory methods. Acute symptoms can begin to materialize when as little as 15 grams (10%) out of the approximately 150 grams 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 acidity [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]. 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 [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. It has been proposed that potassium deficiency can cause hypothyroid secretion and that a severe deficiency can cause hyperthyroid secretion. If so there could be something else involved also -for I have heard of no correlation of any thyroid disease with arthritis.
The gastric secretion decreases in acidity and in potassium content, and increases in sodium content [Welt 1960 (this is an extensive review)]
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 grams of potassium out of 150 are gone [Garella]. Most of the chloride reabsorption is said to occur in the ascending limb of the Henle tubule via the sodium-potassium-2chloride 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. 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 [* I can not find the reference for this]. 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.
Urinary excretion of calcium, magnesium and phosphate is higher during a potassium deficiency in Dahl rats. 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 [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 [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 [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 society. 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 potassium-starved society. 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 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. They 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 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 a subsequent chapter.
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 of deficient kidneys that have suffered no change otherwise.
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. 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- Th 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. It would probably be measured in weeks at least. Potassium as potassium chloride would be much faster. Potassium as the chloride raises blood pressure, so such a supplement probably not be used for those with high blood pressure. 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 and a vitamin B-1 deficiency (beriberi) becomes very dangerous for vitamin B-1 type of heart disease. This last situation could be involved for those who drink sulfited wine or vinegar with their meals or eat unfortified refined grains. 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, Including others with osteoarthritis. So unprocessed, nourishing food is probably usually the best and safest way to get both potassium and vitamin B-1.
If "rheumatoid arthritis" are not words describing a potassium deficiency then what is the word equivalent to "beriberi" which describes a chronic potassium deficiency? Hypokalemia or hypopotassemia (for treatment of hypokalemia see this site) are not such words. They simply are words describing a low plasma content, with symptoms of lower T wave on the electrocardiogram, drowsiness, nausea, muscular weakness, low blood pressure, and reduced digestive ability [Robinson] (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 a chronic cellular potassium deficiency. I would suggest that we find one soon.
REFERENCES for CHAPTER III in; http://members.tripod.com/~charles_W/arthritis3.html
Chapter IV ---
MOVEMENT OF POTASSIUM ACROSS CELL MEMBRANES
The potassium probably enters the cells of higher animals by passive diffusion [Bennett][Solomon], and the active exclusion of sodium by a one way pumping mechanism has the appearance of setting up a true Donnan equilibrium [Albers]. The sodium is excluded by constantly being pumped out of the cell using metabolic energy [Hendricks] through a hollow enzyme buried in the cell wall. The pumping mechanism has been shown to be powered by adenosine triphosphate (ATP) by virtue of similar inhibitors and other parameters being similar [Post]. Lactic acid metabolism as regulated by insulin appears to be also part of the energy system [Kernan p109]. Thiamine [Sharp] and magnesium [Schoner] are also involved. There is more than one pump mechanism, and it has been suggested that sodium concentration inside the cell regulates one of them [Robinson]. The sodium pumps utilize 10% of the body's resting energy [Potts p274].
Inositol may also be involved, but probably only affects the diffusion of potassium [Charalampous]. The apparent passive diffusion is really an active simultaneous inward pumping of both potassium and sodium There is some evidence that such a pump exists on the mitochondria walls [Ulrich]. It is believed that the sodium pump acts by pumping three sodium ions out while simultaneously pumping two potassium ions out. However there is considerable variation in different animals so there must be more than one mechanism present in varying ratios of action. Yellen has written a review of the molecular mechanism known for at least three fundamentally different ways of gating potassium [Yellen].
The net action of the pumps virtually fails to operate at temperatures below 4 degrees C [Hendricks]. The rise in serum potassium that this implies is undoubtedly the reason why we feel such pain when our extremities become too cold.
There is very little chance that potassium is transported actively by an exclusive pump independently of sodium, however. Such a valuable mechanism would surely have ramified throughout the body by this time. It would, for instance, be priceless in the absorption mechanism during a deficiency. Since it is not transported actively independently of sodium, it follows then that all the movement of potassium in the body must actually or in effect be by passive diffusion as a counter current to sodium. This is not a simple ion exchange. Since it is powered by metabolic energy, a considerable number of interactions are theoretically possible, depending on the organ, direction of motion, and which facing wall the various pumps are on.
This dependence on sodium is probably the reason why electrolyte steroid hormones such as aldosterone affect the status of both sodium and potassium. It is also probably the reason why these two elements affect each other's excretion. It is also undoubtedly the reason why the excretion of potassium can not be cut off [Tarail]. It is thought that potassium in the urine can decline to almost half the amount in the serum [Fourman]. It must be done by excretion of water after the potassium has been reabsorbed. Sodium can be concentrated against a concentration gradient of 10,000 to 1 (by the toad's bladder, for instance) [Ulrich]. There is nothing even remotely resembling such an efficiency for potassium.
OSMOTIC PRESSURE
Since sodium and Potassium are the primary soluble positive ions in the body, they must be the primary regulators of osmotic pressure. Precisely how all the mechanisms interact is not known yet with perfect clarity. The cell must be kept in perfect balance osmotically with the blood plasma, or it would either shrivel up or swell and burst. If one system fails, the others tend to take up the slack, and attempt to keep the situation at a reasonably normal level [Davis]. The various ions have various affects on each other, but ultimately excretion of each has to be independent of the others, since intake is very variable.
BLOOD PRESSURE
Part of the regulatory system involves blood pressure. The sodium pump in the toad's bladder probably operates at two different sites, one affected by aldosterone, the other by vasopressin (a protein peptide hormone), and using a different energy system [Sharp]. Since the effort of the regulators of the various systems to counteract a failure or overload of one of the other regulators could involve disadvantageous compromises, it would seem wise to put no strain on them which could have been avoided by proper diet. For instance high blood pressure is thought to be caused by at least three different causes [Meneely] (maybe even 4 or 5). One of them may be involved with a potassium deficiency and at least that should not be allowed to contribute to the difficulty. Hypertension will be discussed a little further in a subsequent chapter (Chapter VII).
ACID - BASE REGULATION
Since potassium makes up so large a part of the cell's osmotic pressure` it is indirectly involved with regulation of the acid - base balance. During a potassium deficiency, potassium migrates out of the cell and causes the cell fluid to become acidic (lower pH) [Davis][Halla]. This is probably related to the circumstance that sodium does not take up the full slack [Rubini], coupled with a rise in weak base forming anions such as positively charged amino acids [Eckel] (which should really be called amino bases in this case). The buffering action of the negatively charged ions of weak acid forming anions such as phosphate is the chief innate regulator of the acid - base balance. however, some of the above alterations would tend to overwhelm it. Since enzyme systems are often sensitive to acidity, this drift toward acidity could easily be the cause of some of the symptoms from a potassium deficiency, and therefore also of arthritis.
The kidneys have enzymes which makes ammonium ion, using glutamine as a precursor. Phosphate-dependent glutaminase enzyme splits off an ammonium ion. Then in a second step, glutamine dehydrogenase enzyme splits off another ammonium ion from the glutamate which had resulted from the first step to form alpha ketogluterate [Tannen]. This enables the kidneys to excrete more acid [Harper p217] and to do so at a site which interferes with potassium excretion. The above enzymes become more active when the cell's fluid becomes more acidic [Rector]. Glutamine itself is an essential amino "acid", at least in the sense that it must ultimately be present. This may be an adaptation primarily for the purpose of conserving potassium even though ammonium excretion itself may be directly related to hydrogen ion (acid or low pH) and not to potassium concentration [Tannen]. Potassium depletion has been shown to increase ammonia production by the kidneys from both glutamine and glutamate, decrease glutamate conversion to glutamine, and increase ammonium removal from aspartate [Tannen]. The ammonium ion and potassium are the same charge and size, and they are handled at the same site in the kidneys. Berliner, Kennedy, and Orloff believe that hydrogen ion and potassium compete at the same site in the kidney's distal tubules [Berliner]. It is possible that 18hydroxy deoxycorticosterone steroid is the hormone which regulates the handling of ammonium. In any case potassium excretion is quite sensitive to hydrogen ion concentration (acidity). Injecting sodium bicarbonate or even hyperventilating (breathing rapidly beyond need) can triple potassium excretion [Kilburn]. The diurnal rhythm for potassium and hydrogen ion excretion show a rather close inverse relationship [Mills], which gives additional circumstantial support to the supposition that they compete at a common site.
It is obvious that a potassium deficiency puts an increased drain on glutamine, and would presumably be disadvantageous to someone not getting enough protein. It also seems likely that eating baked goods which have been risen with sodium bicarbonate, or stomach antacids would worsen a deficiency. There is a possibility that fruits which contain acids which acids can be absorbed but not metabolized would have a conserving effect on potassium. I am aware of no investigation which would substantiate this. However there is a report of cherries having a beneficial effect on arthritis [*].
NERVE TRANSMISSION
One of the most important roles for potassium in animals having a nerve net work is as a counter flow for sodium's function in nerve transmission. When a neuron decides to fire, the cell wall suddenly becomes permeable to sodium ions, and sodium ions near the cell wall suddenly move into the cell, followed a microsecond later by a flow of thousands [Yellen] of potassium ions in the opposite direction [Fuhrman]. This change in permeability shoots down the nerve fiber as a wave at about 100 meters per second powered by 1/10 of a volt of concentration differential [Baker]. This is approximately the speed of a thrown baseball.
Half the metabolic energy supplied to nerve cells is required to move the sodium back out of the cell [Potts p37] in order to recharge it. For this system to work the potassium in the plasma has to be kept as close as possible to 187 milligrams per liter (4.8 milliequivalents per liter) [Lans (complete with graph)]. If it rises above 400 (9 or 10 milliequivalents) or falls below about 80 (2 milliequivalents or more) death is almost certain from failure of the nerves leading to vital organs to fire. Rising above 400 is the greatest risk because excessive loading of plasma is quite possible from supplements, metabolic shock, and various hormone failures. On the other hand , it is quite unlikely that excessive potassium could be suddenly lost from the plasma, but even if it were lost, replete cells provide an enormous reservoir of potassium to replenish the plasma's potassium in case the lower limit were approached. A sudden rise in potassium, then, ranks high among the most dangerous physiological events which can happen to a person. Some of the implications of this will be elaborated further in the supplements chapter.
ENZYME ACTIVATION
Potassium is known to be the activator for several enzyme systems [Suelter]. Since only minute amounts are needed for most of them, there could never be a deficiency which would inactivate the majority of them. The amount needed for activation is usually about 40 milligrams per liter [Kernan p127], and no cell could ever get this low and live. One exception is transport of d-amino isobutyric acid which is permanently disrupted at a cellular level which is still well over the amount needed to stay alive. [Charalampous]. It is probable that no other enzymes are inactivated directly by a low potassium whole body count (cell content).
COLLAGEN
I suspect that a large part of the weakened connective tissue is manifesting itself by virtue of the indirect effect a continuing potassium deficiency is having on the the copper metabolism especially as it pertains to the copper catalyzed lysyl oxidase enzyme.
Healthy collagen ranks with steel in strength of individual fibers [*]. Healthy bone, which is essentially an ossified connective tissue, has a strength which approaches that of cast iron [45]. Such theoretical strengths are above the strengths which are observed in most people, and would be very advantageous in solving everyday problems. Such strengths would give people considerably less apprehension about injuries. There should be no reason why these strengths can not be obtained. It is my belief that the strength of connecting tissue and its ability to regenerate are of considerable importance, not only in clear cut cases of arthritis, but also very likely in a large number of degenerative diseases which affect modern society such as susceptibility to sprains and shaving cuts, aneurysms of blood vessels, ruptures, weak bones, varicose veins, sagging organs, slipped discs, and bleeding while breast feeding. I further believe that one of the common threads running through many of these difficulties is potassium deficiency, and that the carelessness of modern processing is causing far more problems in ruined lives, inexplicable accidents, marginal loss of efficiency, and needless fear than the raw statistics of arthritis, strokes, and other mesoderm tissue [Lamont-Havers] disasters would indicate. It would be a good idea to get all the potassium originally present in your food. If someone succeeded in defrauding you of 30% of your after taxes paycheck, you would probably scream in anguish. Perhaps it is time to scream about losses in nutrition of this much or more.
REFERENCES for CHAPTER IV in; http://members.tripod.com/~charles_W/arthritis4.html
Chapter V ---
Sodium and are proposed to be regulated by varying secretion of aldosterone, DOC, 18 OH-DOC, and 16 alpha 18 dihydroxy 11 deoxycorticosterone in response to the nutritional load. The first two steroids are for high potassium and the second two for low potassium intake, the potassium effects of the third indirect via affects on hydrogen ion (acidity). The first and third steroids are for low sodium intake.
Examination of the results of past experiments on the mineralocorticoid hormones seems to say that they exert their control over kidneys for the purpose of keeping blood serum sodium and potassium content constant through at least three and possibly four or more steroid hormones. I believe that aldosterone's role is fairly clear, and well accepted. The others are largely speculations of mine.
The three discussed here, besides aldosterone, are deoxycorticosterone (also called cortexone, 11 desoxycorticosterone, DOCA, or DOC), 18 hydroxy 11 deoxycorticosterone (also designated 18 OH-DOC), and 16 alpha 18 dihydroxy 11 deoxycorticosterone which I will designate DOH-DOC.
They all must conserve sodium in order to be called a mineralocorticoid. Sodium makes up most of the cations of blood plasma. Plasma is filtered through the glomerulus of the kidneys in enormous amounts, about 180 liters per day [Potts p261]. Thus 580 grams of sodium and 36 grams of potassium are filtered each day. All but the 1-10 grams of sodium and the 1-3 grams of potassium likely to be in the diet must be reabsorbed. Sodium must be reabsorbed in such a way as to keep the blood volume exactly right and the osmotic pressure correct; potassium must be absorbed in such a way as to keep serum concentration as close to 4.8 mEq [Lans] (about 190 mg) per liter as possible. Therefore, the sodium pumps must always operate to conserve sodium. Potassium must sometimes be conserved also, but since the amount of potassium in the serum is very small and the pool of potassium in the cells is fifty times as large, the situation is not so critical for potassium. Since potassium is moved passively [Bennett] [Solomon] in counter flow to sodium in response to a Donnan equilibrium [Kernan p40, 48] the urine can never sink below the concentration of potassium in serum except sometimes by actively excreting water at the end of the processing. Potassium is secreted twice and reabsorbed three times before the urine reaches the collecting tubules. [Wright] At that point, it usually has about the same concentration as plasma with respect to potassium. If potassium were removed from the diet, there would remain a minimum obligatory kidney excretion of about 200 mg per day when the serum declines to 3.0-3.5 mEq/1 in about one week, [Squires] and can never be cut off completely. Because it cannot be cut off completely, death will result when the whole body potassium declines to the vicinity of one-half normal. At the end of the processing, potassium is secreted one more time if the serum potassium is too high. The potassium moves passively through "gates" and probably through one of the pumps which also pumps sodium. Even so, the net apparent effect is active in the tubules. In addition to the kidneys, the gastric glands, salivary glands, colon, perspiration glands, and maybe the red cells are target organs for the mineralocorticoids [Turner]. For an elaborate chart of what scientists think the pumps may look like on a molecular scale, see this site
I believe I now see how the regulation of sodium and potassium is organized by the mineralocorticoids.
Aldosterone has been shown to be the primary steroid used to control the force and direction of the pumps under this circumstance [O'Malley]. When potassium in the serum is higher than 4.8 mEq/1, the zona glomerulosa [Brown] of the adrenal jacket secretes more aldosterone [Lans] and potassium is excreted into the end of the tubules and the collecting ducts [Peterson & Wright]. Aldosterone also reverses potassium out flow in the last part of the colon only [Fraser] and increases sodium absorption throughout the colon. In the first part of the colon chloride enters with the sodium while in the last part there is only a potassium - sodium exchange [Dolman]. All this was in rats which make poor experimental animals as discussed below. The amount of aldosterone secreted is a function of the serum potassium [Bauer & Gauntner] [Linas]as probably determined by sensors in the carotid artery [Gann , Cruz & Casper], pressure in the carotid artery [Gann, Mills, & Bartter], the inverse of the sodium intake as sensed via osmotic pressure [*], anxiety [Vening], and of the angiotensin II formation [Brown][Dluhy][Williams & Dluhy], which last is a peptide hormone for increasing blood pressure by constricting the arteries just ahead of the capillary bed [Haddy]. Angiotensin II is regulated by the rennin (a peptide hormone) from the kidneys. Depletion of either potassium [Albrecht] or sodium activates secretion of rennin, but in potassium depletion aldosterone is suppressed [Sealed]. If blood pressure has to be increased by constricting capillaries, which is what angiotensin II does [Encyclopedia], it is an indication that the body needs more sodium in order to expand blood volume or more potassium to strengthen the heart beat. That is undoubtedly the reason why angiotensin is involved in regulating aldosterone and is the core regulation [Williams & Dluhy]. Angiotensin II acts synergistically with potassium, and the potassium feedback is virtually inoperative when no angiotensin II is present [Pratt]. A portion of the regulation resulting from angiotensin II must take place indirectly from decreased blood flow through the liver due to constriction of capillaries [Messerli]. When the blood flow decreases so does the destruction of aldosterone by liver enzymes. However, the primary regulation is acting directly on aldosterone production because angiotensin II acts synergistically with potassium, and the potassium feedback to aldosterone is virtually inoperative when no angiotensin is present [Pratt][Williams & Dluhy]. Such an arrangement tends to be fail safe. If anything happens to send the blood pressure spiraling upward out of control, when angiotensin II drops out in order to correct the situation, it leaves behind a somewhat enhanced potassium serum concentration which also tends to reduce pressure at serum contents of potassium [Haddy] above 4.8 mEq/liter of potassium, and causes sodium to start to decline by the same failure to stimulate aldosterone.
ACTH, a pituitary peptide, also has some stimulating effect on aldosterone probably by stimulating DOC formation which is a precursor of aldosterone [Brown]. I suspect that this is an adaptation to inversely help protect the body during diarrhea assuming that the primary purpose of ACTH is to inversely mobilize the body's defenses against intestinal disease [Weber 1998]. Aldosterone is increased by blood loss [Ruch p1099], pregnancy [Farrell], and possibly by other circumstances such as physical exertion, endotoxin shock,, and burns [Glas & Vecsei p209]. The aldosterone production is also affected to one extent or another by nervous control which integrates the inverse of carotid artery pressure [Gann, Mills, & Bartter], pain, posture [Farrell], and probably emotion (anxiety, fear, and hostility) [Venning 1956, 1957](including surgical stress) [Davson p715] to produce an unknown messenger hormone which stimulates aldosterone secretion [*]. I suspect the main reason why emotion is factored in, especially anxiety, is that the aldosterone operates by diffusing to the nucleus to produce a messenger RNA and the various steps take about an hour to come completely on stream [Sharp]. Thus, there is an advantage in an animal anticipating a future need from interaction with a predator since too high a serum content of potassium has very adverse effects on nervous transmission [Rechcigl]. Anxiety's effect can be discordant. People with an anxiety neurosis can have as high as four times the secretion as normal and people with schizophrenia have a low secretion [Lamson].
This system has been well studied and its major features are not subject to much doubt. Potassium feedback is the main regulation of aldosterone in normal diet and health, and the other features of aldosterone's regulation are for the purpose of fine tuning and forestalling future circumstances.
The slope of the response of aldosterone to serum potassium is almost independent of sodium intake [Dluhy]. Aldosterone is much increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum is not much lower at high sodium intakes than it is at low. Feedback by aldosterone concentration itself of a non morphological character (that is other than changes in the cells' number or structure) is poor so the electrolyte feedbacks predominate short term [Glaz & Vecsei]. Thus, the potassium is strongly regulated at all sodium intakes by aldosterone when the supply of potassium is adequate, which it usually is in primitive diets. The known stimulation by aldosterone of the sodium pump which secretes potassium into the distal loop of the tubules [Stanbury], along with the nature of the potassium feedback already mentioned, make aldosterone certainly a hormone for unloading potassium. As much as 26 grams of potassium can be unloaded per day by healthy people accustomed to a large intake [Peterson CG]. Aldosterone is heavily relied on during high plasma potassium for the aldosterone secretion rises seven fold between 5 milliequivalents and six milliequivalents of potassium in the blood [Braley]. That aldosterone makes available the sodium in the bones which contain nearly half the body's sodium is circumstantial evidence that the body depends considerably on aldosterone to keep the serum sodium retained and normal [Davson p717] and aldosterone keeps the sodium and potassium normal in mononuclear leucocytes [Wheling].
The question is "What hormones are involved when a different diet or disease makes necessary a different excretion pattern?" I suggest that at least three other mineralocorticoids may be involved. Aldosterone is designated CASE #1.
Such a case would obtain when well fed primitive humans have a clam bake or find a salt lick. It is still necessary to unload potassium, but sodium retention must be less strenuous. I suspect that DOC is used for this purpose. DOC stimulates the collecting tubules (the tubules which branch together to feed the bladder) [O'Neil] to continue to excrete potassium in much the same way that aldosterone did but not like aldosterone in the end of the looped tubules (distal) [Peterson & Wright]. At the same time it is not nearly so rigorous at retaining sodium as aldosterone [Ellinghaus], more than 20 times less [Brommer]. In addition to its inherent lack of vigor there is an escape mechanism controlled by an unknown non steroid hormone [Pearce] which overrides DOC's conserving power after a few days just as aldosterone is overridden also [Schacht]. This hormone may be the peptide hormone kallikrein which is augmented by DOC and suppressed by aldosterone [Bonner]. If sodium becomes very high, DOC also increases urine flow [O'Neil]. DOC has about 1/20 of the sodium retaining power of aldosterone [Oddie] and is said to be as little as one per cent of aldosterone at high water intakes [Desaulles]. Since DOC has about 1/5 the potassium excreting power of aldosterone [Oddie] it probably must have aldosterone's help if the serum potassium content becomes too high. DOC's injections do not cause much additional potassium excretion when sodium intake is low [Bauer & Gauntner]. This is probably because aldosterone is already stimulating potassium outflow. When sodium is low DOC probably would not have to be present, but when sodium rises aldosterone declines considerably, and DOC probably tends to take over.
DOC has a similar feedback with respect to potassium as aldosterone. A rise in serum potassium causes a rise in DOC secretion [Brown], which is the correct response for this thesis. However, sodium has little effect [Schambelan & Biglieri], and what effect it does have is direct [Oddie}. Angiotensin (the blood pressure hormone) has little effect on DOC [Brown], but DOC causes a rapid fall in rennin, and therefore angiotensin I, the precursor of angiotensin II. [Grekin]. Therefore, DOC must be indirectly inhibiting aldosterone since aldosterone depends on angiotensin II. Sodium, and therefore blood volume, is difficult to regulate internally. That is, when a large dose of sodium threatens the body with high blood pressure, it cannot be resolved by transferring sodium to the intracellular (inside the cell) space. The red cells would be possible, but that would not change the blood volume. Potassium, on the other hand, can be moved into the large intracellular space, and apparently, it is by DOC [Grekin] in rabbits since DOC injections lowered serum potassium but did not alter excretion [Law]. Thus, a problem in high blood potassium can be resolved somewhat without jettisoning too much of what is sometimes a dangerously scarce mineral. Movement of potassium into the cells would intensify the sodium problem somewhat because when potassium moves into the cell, a somewhat smaller amount of sodium moves out [Rubini]. Thus, it is desirable to resolve the blood pressure problem as much as possible by the fall in rennin above, therefore avoiding loss of sodium which was usually in very short supply on the African savannas where humans probably evolved.
The resemblance of the pattern of the electromotive forces produced by DOC in the kidney tubules to normal potassium intake, and the total dissimilarity of their shape as produced by potassium deficient tubules, [Helman & O'Neil] would tend to support the above view. The above attributes are consistent with a hormone which is relied upon to unload both sodium and potassium.
DOC's action in augmenting kallikrein, the peptide hormone thought to be the sodium "escape hormone," and aldosterone's action in suppressing [Bonner][Wright & Davis] it is also supportive of the above concept.
ACTH has more effect on DOC than aldosterone. I suspect that this is to give the immune system control over the electrolyte regulation during diarrhea [Weber 1998] since during dehydration, aldosterone virtually disappears any way even though rennin and angiotensin rise high [Gyton WB]. It is for this reason that potassium supplements are very dangerous during dehydration. DOC's primary purpose is to regulate electrolytes. It has other effects on copper enzymes, proteins and connective tissue which I believe is used by the body to survive during potassium wasting intestinal diseases. Most of the DOC is secreted by the zona fasciculata of the adrenal cortex which also secretes cortisol, and a small amount by the zona glomerulosa which secretes aldosterone.
The greater efficiency of DOC in permitting sodium excretion (or perhaps it should be expressed as inefficiency at retention) must be partly through morphological changes in the kidney cells because escape from DOC sodium retention takes several days to materialize, and when it does, these cells are much more efficient at unloading it if sodium is then added than cells accustomed to a prior low intake [*]
Someone living on the Savanna, profusely perspiring and confined to eating nuts, or worse yet nothing at all, could find himself in this situation. When potassium becomes low, the first thing that happens is that excretion of potassium from the far end of the kidney tubules and collecting tubules declines. This happens within 24 hours and virtually stops in 2 day s. [Bauer & Gauntner]. The large decline in aldosterone secretion [Bauer & Gauntner] is undoubtedly a large part of it. However, it is still necessary to rigorously conserve sodium, and I tentatively propose that this is the function of 18 OH-DOC. I have no direct evidence for this yet, but there is strongly suggestive circumstantial evidence. Under low sodium intake 18 OH DOC is increased in serum [Williams, Braley & Underwood]. There is a marked increase in serum 18 OH DOC after injection of insulin [Sparano] [Hiatt] and this may be due to the hypokalemic (low serum potassium) tendency after a rise in insulin [Flatman] which in turn would make the serum more acidic.
!8 OH-DOC lowers urine pH but has no affect on potassium excretion [Nicholls]. This would seem to indicate that 18 OH-DOC's primary purpose is to stimulate hydrogen ion or ammonium excretion. If so, its use by the body to conserve potassium would be indirect by virtue of hydrogen ion's interference with potassium excretion and perhaps strongly dependent on the potassium cell or plasma content. It would also hint that the large affect that ACTH has on 18OH DOC revolves primarily around keeping immune enzymes at a low pH during infection. Perhaps additional experimentation will cast some light on 18 OH-DOC. Insulin is used by the body to counter high serum potassium only at low potassium intakes. At high intakes the affect of insulin stays normal [Knochel].
It is possible that the 18OH DOC does not act directly on electrolytes, but, in addition to the above hydrogen ion affect, through a synergistic or blocking action on other hormones. I suspect that 18 OH DOC acts primarily by blocking aldosterone's effect on potassium, and must have aldosterone to assist it. Nichols, et al, have been able to show that injection of 18 OH-DOC, which raised blood levels of this hormone ten times, were more retentive of sodium than a similar amount of aldosterone. At the same time, the ratio of sodium to potassium declined very little for 18 OH-DOC, while for aldosterone, the ratio fell to as little as 1/3 that of control men [Nichols]. This implies a considerable sparing of potassium by 18 OH-DOC. If the original aldosterone could have been removed from the serum first, it is possible that the difference would have been greater yet.
Angiotensin II has very little effect on 18 OH-DOC and is ambiguous nor does serum potassium above 4.8 mEq/litter (187 mg) [Biglieri & Lopez].- This last is not surprising since 18 OH DOC would not be used at high serum potassium. Under low sodium intake, 18 OH-DOC rises in the serum [Williams GH], which is the correct response for the proposed purpose. ACTH causes a marked increase in 18 OH-DOC [Moore] up twenty fold [Melby, Dale & Wilson], probably by a generalized affect on the zona fasciculata of the adrenal cortex where 18 OH-DOC is synthesized . I believe that the decline in 18 OH-DOC when ACTH declines implied by this is part of the defense against diarrhea already mentioned because of the dehydration that ensues then and the need to preserve osmotic pressure by unloading sodium. Also it is possible that it is related to a necessity of immune enzymes to operate more vigorously at lower pH (higher acidity). Large amounts of ACTH have a greater affect on 18 OH-DOC than on cortisol [May]. When ACTH drops to zero, 18 OH-DOC does also [*]. I have not seen evidence so far that cholera enterotoxin, or any other aspect of digestive disease except dehydration [Aguilera] directly affects ACTH yet. If this hypothesis is correct, some aspect of diarrhea should affect ACTH
More important to know would be the effect of 18 OH-DOC has on angiotensin II because at low serum potassium situations, the intracellular (inside the cells) potassium is usually decreased and this depresses heart contraction. I suspect that 18 OH-DOC will be found to stimulate angiotensin II rather than the reverse if it has an affect because the intracellular potassium is much more important than serum potassium on the strength of heart contractions [Libretti][Biglieri & Lopez]. So when heart contraction strength decreases from low potassium status, it should be imperative to contract the capillaries in order to make sure that blood pressure does not drop. This is likely because the relaxation of capillaries by potassium between 4 and 8 mEq/l serum content [*] is some kind of an adaptive circumstance rather than an inherent characteristic of pre capillary blood vessels. Whether the above stimulation has evolved or not, I don't know since I know of no experimental data. However angiotensin II apparently does cause a drop in 18 OH-DOC [Williams GH] which might be a negative feedback kind of phenomenon. If this hunch is correct, the low sodium status in this case would reinforce its evolution because low serum sodium's effect on volume also decreases blood pressure. While direct evidence is not available to me, it has been demonstrated that there is more of a marked rise in rennin and therefore angiotensin II at low potassium intake than at any other electrolyte status [Douglas]. In any case, 18 OH-DOC is deeply involved in one of the at least three forms of hypertension [Melby 1972 p323].
Any of our progenitors who managed to find a salt lick, nothing but nuts or nothing at all would find themselves in this circumstance. Modern man eating only starchy, salty refined food would also be there. Someone with diarrhea would probably also be because the dehydration creates a serum artificially high in sodium concentration and because when water can't be absorbed in the lower intestinal tract, potassium can't be either and is lost. For this situation, I propose DOH-DOC. DOH-DOC increases the sodium to potassium ratio in urine slightly when injected into rats. This slight increase takes place even when small amounts of aldosterone are injected at the same time. That amount of aldosterone injected alone lowered the ratio slightly. [Fuller]. Unfortunately, rats are not good experimental animals for experiments on a hormone possibly used during diarrhea because rats have something in their digestive fluid which neutralizes cholera enterotoxin. [Donowitz]. Also, their ascending colon increases water absorption under c-AMP stimulation, opposite the effect in the descending colon and in other animals.[Hornyck]. Thus, the enterotoxin of diarrhea undoubtedly has much less effect on them. DOH-DOC combined with aldosterone is more retentive of sodium than either alone. [[Melby & Dale 1976]. DOH-DOC does not displace aldosterone in general. [Fuller]. DOH-DOC must act in conjunction with aldosterone. If both are secreted together, sodium would be drastically conserved. If aldosterone drops out, there would be a precipitous loss of sodium retention since DOH-DOC alone has no affect on sodium [Melby & Dale 1976 (both)], while at the same time, if my contention is correct, potassium would cease to be excreted in the tubules. I suspect that DOH-DOC has its greatest effect on sodium in the colon because it is here where it would be most advantageous to unload sodium in order to keep water loss in the kidneys at a minimum. I know of no evidence for the colon effect. Its affect on potassium excretion would be most valuable in the kidneys, and this may be why it interferes with DOC's potassium excretion stimulation in the kidneys [Linas]. Conversion of 18 OH DOC to DOH-DOC is greatly increased in the kidneys of low renin patients [Melby & Dale 1977]. under such a circumstance sodium could be much more strongly retained as long as aldosterone was present and potassium more retained in any case. Not many experiments have been performed on DOH DOC, so more assured conviction that this is the hormone for case #4 will have to wait.
It may yet be found that angiotensin II or rennin do not increase DOH-DOC, but that DOH-DOC decreases angiotensin II in the vicinity of 4.8 mEq/l and then considerably increases it if the intracellular (cell interior) potassium becomes low. If the mechanism is such that both trends are not possible, then only the second should obtain, for in matters of regulation it is the extreme circumstances which should prevail if a compromise becomes necessary, those circumstances when an animal is fighting for its life.
When DOC is injected into people, it creates malaise, headache, loss of appetite, insomnia and muscle cramps [Relman & Schwartz]. It is possible that some of these symptoms are actually arising from increased internal secretion of DOH-DOC which may be resulting from retention of sodium and loss of potassium implied in the use of DOC injections. It is unlikely that the DOC is causing these symptoms directly because they do not appear when a diet high in sodium and potassium raises DOC in the body. The body may be using DOH-DOC to create some of those symptoms and feelings in order to help to protect it from excessive action during diarrhea. Some of the damaging effects of DOC injections on the heart [Melby, et al 1972] may arise this way also. The loss of appetite, if it exists, would be especially valuable during diarrhea.
If DOH-DOC is important during diarrhea as I suspect, it could be that ACTH inhibits it, and thus stimulates it upon ACTH's decline, or at least ACTH has no effect. I know of no information on this.
By secreting various ratios of the above steroids in conjunction with rennin, the angiotensins, ADH water retaining hormone, thirst and unknown supporting hormones, fairly accurate fine tuning should be possible of sodium, potassium, serum volume, osmotic pressure, hydrogen ion, and blood pressure. The cell status is maintained largely by controlling the serum [*].
I suspect that the distant ancestors of man evolved primarily as fruit, nut and leaf eaters of broad leafed plants, using meat as a fortuitous supplement. The tooth design is almost conclusive evidence of a herbivore, the salivary gland which dissolves starch is strongly suggestive of nuts, and the present day eating preferences of most people is supportive of broad leafed (dicotyledon) plants. Such a diet is low in sodium and fairly high in potassium [Abernethy]. If so, and I am right about the above, we are organized around aldosterone. I suspect that when we depart from this possibly ideal state for any length of time, we lay ourselves open to the statistical chance of degenerative diseases because our other physiological processes are geared to this hormone balance.
I suspect that Case #2 may be associated with the form of hypertension which is hard to reverse. The reason I suspect this is that DOC is associated with increased synthesis of collagen [*] and it is possible that tends to increase the thickness of artery walls [Cox] with time and decrease their elasticity. The much greater tendency to grow excess connective tissue when foreign bodies such as silica are imbedded in the skin during DOC injections [Desaulles] [Pospisilova] would give circumstantial support to such an explanation.
Case #3 is probably furnishing some of the symptoms of rheumatoid arthritis since there is a consistently low whole body potassium content in this disease [LaCelle] aldosterone is low in arthritics [Cope & Llaurado] [Gonall], and personal experience is supportive[Weber 1974]. Indicative is that arthritis has been produced by DOC injections [Selye]. I have no information on the status of 18 OH DOC in arthritis. Anyway, it is probable that the bulk of the symptoms manifest themselves through cortisol status and its response modifying factors because this hormone is reduced in its secretion by the effect of low potassium on the zona fasciculata [Mikosha] and because cortisol removes many of the symptoms of arthritis. The amount of potassium to heal rheumatoid arthritis must usually be 3.5 grams/day or more because this is the amount which permitted slow improvement of a man across a three month time span [Clark], assuming his sodium intake was normal. Black people receive 1.5 grams/day and white people 2.0 grams/day in Georgia [Grim] which intake would probably not replenish potassium if something caused a deficiency, since two grams is less than the minimum daily requirement (MDR). There is also circumstantial evidence from nutritional experiments using vegetables [Eppinger][Kjeldsen-Kraw]. An unpublished experiment performed on eight subjects has revealed beneficial results from potassium supplements [Rudin MV, private communication].
I suspect that most of the people who have rheumatoid arthritis, especially young onset, have had their kidneys damaged by poison or disease in such a way as to make them less efficient at retaining potassium or too efficient at excreting it. I suspect bromine gas as one possibility, for instance since it probably affected me that way. Childers has proposed poisons in tomatoes, potatoes, egg plant, and peppers [Childers] although it has not been established to date. Some infectious diseases may have a similar effect. In addition some people's immune system may be more sensitive to a potassium deficiency than others.
Case #4 may prove to be associated with degeneration of heart and kidneys, but based primarily on nutritional statistics. It is also possible that it plays a role in suppressed rennin hypertension, since there is increased secretion of DOH-DOC in all cases of that last disease [Melby & Dale 1976]. There is no evidence I know of that the DOH-DOC itself causes the damage. Drifting back and forth between case #3 and #4 may make one more susceptible to heart attacks and periarteritis nodosa, because arthritics have a low cell content to start with, so that this is superimposed on the harmful effects of high sodium intake, whatever they are, the situation could be much worse than when starting from a healthy body. The higher death rate in arthritics from heart attacks is indicative. When arthritics finally die, the usual terminal events are heart attacks, infections, and ruptured blood vessels [Matsuoka]. We have become so accustomed to these distorted statistics, that we fail to perceive their oddity. Indians in El Salvador have a heart disease rate one per cent of ours [World Health Organization]. There is very little chance for such a wide disparity not to have an environmental cause, especially nutrition. A possible reason for the infection and ruptures are discussed in a copper article. How to increase copper in food may be seen here.
Pregnant women increase their DOC secretion 10 times by the end of the pregnancy [Parker 1980] and have a markedly higher secretion before the onset of menstruation [Parker 1981]. It may be that the larger secretion of progesterone which takes place at these times [Parker 1981] makes necessary the enhanced secretion of DOC by virtue of progesterone's interference with DOC's primary purpose [Gornall]. This erratic secretion may have something to do with the much larger rate of arthritis among women. It is not difficult to envision a problem if such large swings became even a little misregulated or had to handle odd electrolyte intakes of sodium and potassium.
Modern nutritional professionals are all convinced that potassium is adequate in all diets and that a deficiency never materializes except occasionally clinically. Past nutritional texts reflect this view both in the amount of space devoted to potassium and its content, which content will usually list only one of the many causes of a deficiency (for instance [Robinson] ). When potassium supplements are prescribed, they get around the discordance between their convictions and practice semantically by calling the supplements "salt substitutes," "polarizing solutions," "pharmaceutical effects," "ORT salts (oral rehydration therapy for diarrhea)", or similar terms. A deficiency is further defined out of existence by defining the blood serum content is normal at a 4.2 mEq/liter when the actual figure is 4.8 [Scribner].
Nevertheless, there are numerous circumstances which can cause potassium to be ominously low in the diet or cause excessive excretion (with references). I have already mentioned diarrhea, the most common and dangerous circumstance in nature. Potassium supplements to babies brought mortality from a virulent strain of diarrhea from 35% to 5% [Darrow]. Numerous experiments have shown that potassium supplements are very important for recovery from heart disease [Kadaner]. It is not possible to produce heart disease in animals with any known poison unless potassium is also deficient [Prioreschi]. It is important to know whether the heart disease is caused by potassium deficiency or vitamin B-1 deficiency because heart disease cannot materialize in rats if both are deficient [Folis]. Therefore, it is probable that potassium supplements or a high potassium diet to a patient with the "wet" heart disease of beri-beri would kill him. This may be one reason why results with potassium against heart disease have been statistically fuzzy in the past.
Psychic stress stimulation of aldosterone, profuse perspiration, excessive vomiting, eating sodium carbonate or bicarbonate (because hydrogen ion is excreted at the same site as potassium), laxatives, diuretics, licorice, hyperventilating, enemas, shock from burns or injury, hostile or fearful emotions, and very high or low sodium intakes all increase potassium losses, some massively. All together would probably be lethal in a fairly short time. Reliance on grain (especially white flour) or fatty foods, boiling vegetables, use of chemicals (soft drinks, for instance) instead of food, and use of most processed foods including frozen and canned permit considerable reduction of intakes. So does the reduced appetite associated with a sedentary life.
To speak of potassium deficiency as an aberration when enormous numbers of people are affected by these circumstances is not logical. Even if a serious degenerative disease does not materialize, an adequate intake is desirable to forestall future disasters and to permit one to operate at optimum. Some of the manifestations of the placebo effect become understandable in light of the effect of emotions on hormones. However, we cannot always be assured of a placebo being available, certainly not on the firing line, but not even for that matter in the quiet of a hospital where even nurses can be testy at times.
While understanding the hormonal basis for electrolyte control will not always have a practical nutritional application, it is nevertheless important that it be well understood. Unless the medical establishment understands the physiological basis for nutritional strategy, it will never accept programs with any ardor based on vague nutritional statistics alone. Also, even if it did, some patients would slip through the cracks as we have seen in the potassium vs. vitamin B-1 interaction. Also, sometimes clinical intervention is essential for genetic or cancer malfunctions of the hormonal systems or to help correct massive assaults of poison or injury. It is well to realize clearly what is happening. The abandonment of aldosterone for DOC may not prove logical for all cases, for instance. Excess potassium is the main problem in metabolic shock [Fox], yet previous texts about shock did not even so much as mention potassium. Our nutritional strategy and even our philosophy of life is entwined with understanding hormones.
It is especially important that nutrition be established by experiment. Currently, every one in the medical establishment is convinced that potassium deficiency cannot be involved in rheumatoid arthritis, but this without an experiment ever having been performed. It simply is not possible to predict the outcome of an experiment with certainty without performing it. It would be desirable to determine the effect of every food common in commerce not only on arthritis, but on all the degenerative diseases. Some foods known to be poisonous to animals or have poisonous related species in the wild have been used for thousands of years without ever having been tested. This is undoubtedly due to a universal quasi religious conviction or instinct that foods our parents taught us to eat or taste good could not possibly be harmful. This is not necessarily the case. Such experiments could have another advantage in that they might uncover foods which have a beneficial effect. Even small effects would be worth knowing about. The above conviction (or instinct) is so strong that most people will not eat nutritious food if tastier, less nutritious food is available. Their instincts override their intellect not only in their eating habits, but in their scientific efforts. These scientific efforts are further thwarted from pursuing nutritional investigations because medical science stresses pharmaceuticals and glamour theories [Forman]
You may see the complicated series of chemical steps by which the body synthesizes steroids from precurser molecules at http://www.nsac.ns.ca/envsci/jhoyle/students/jhealy/Biosynthesis%20of%20Steroids.htm
REFERENCES for CHAPTER V in; http://members.tripod.com/~charles_W/electrolyte.html
Chapter VI ---
It is proposed that the primary purpose of the glucocorticoids, including cortisol (hydrocortisone), is to mobilize the body to resist infection. They do so by normally altering processes which increase pathogens' growth or their adverse effects and then declining when under attack. Cortisol is for intestinal disease (diarrhea) and corticosterone serum disease. Glucocorticoid mobilization for fight or flight is an adjunct, made possible because most processes which resist infection impair fight or flight. A different hormone controls those which do not.
Potassium loss is the most serious aspect of intestinal diseases, so the electrolyte capabilities of cortisol, but not corticosterone, are oriented toward conserving potassium. Low cell potassium reduces adrenal synthesis of cortisol, but not corticosterone. Sodium, water, glucose, amino acids, chloride, hydrogen ion, copper , and numerous others are controlled by cortisol such as to survive during intestinal disease.
Some gram negative bacteria have an endotoxin which subverts this strategy by forcing the secretion of huge amounts of ACTH, which is the chief mediator of cortisol. A glucocorticoid response modifying factor (GRMF) and interleukin-1, raises the effective set point of cortisol. The immune cells thus take over their own regulation, using interleukin-1 to mediate production of cortisol via ACTH.
This paper will propose that the primary purpose of cortisol (hydrocortisone) and corticosterone in mammals is to mobilize the body's physiological processes against infection and its adverse effects, cortisol against potassium wasting intestinal disease and corticosterone against serum disease. These steroids control a large number of enzymes, hormones, and processes, most of which could enhance growth of pathogens or make the adverse symptoms worse. The few which do not, do not affect immunity either, and are probably opportunistic adaptations of these hormones to peripheral functions. Extinction of juvenile play traits is an example.
Glucocorticoids mobilize immunity by declining their serum concentration. This inverse style is highly desirable, otherwise a pathogen could easily overwhelm the immunity defenses simply by evolving an enzyme which could degrade steroids. Some circumstances controlled inversely enhance an animal's survival from the adverse effects of bacterial poisons or the animal's own defenses. Such a defense would be control of blood pressure. This control, I suspect, is largely to protect infection damaged and copper starved blood vessels from hemorrhage.
Please keep in mind as you read this, that cortisol's functions to inhibit or stimulate become the reverse, to stimulate or inhibit, upon decline respectively. This concept will be handled by use of the phrases "inversely stimulates" or "inversely inhibits" respectively as cortisol declines.
Cortisol is controlled by the pituitary peptide ACTH. 1 ACTH is in turn controlled by the hypothalamic peptide, corticotrophin releasing factor [CRF], 2 under nervous control. CRF is synergistic with arginine vasopressin, angiotensin II, and epinephrine. 2 Therefore ACTH and CRF cannot be overwhelmed by bacterial degradation either. ACTH probably controls cortisol by controlling movement of calcium into the cortisol secreting target cells. 1
Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1 (IL-1), and unable to produce the T-cell growth factor. 4 That cortisol often increases during infection does not make this hypothesis invalid because when activated macrophages start to secrete IL-1, which synergistically with CRF increase ACTH, 5 T-cells also secrete glucosteroid response modifying factor [GRMF] as well as IL-1, both of which increase the amount of cortisol required to inhibit almost all the immune cells. 6 Thus immune cells take over their own regulation, but at a higher set point. Even so, the rise of cortisol in diarrheic calves is minimal over healthy calves and drops below with time. 7 The cells do not lose all of the fight or flight override because of interleukin-1's synergism with CRF. Cortisol even has a negative feedback effect on interleukin-1 5 which must be especially useful against those diseases which gain an advantage by forcing the hypothalamus to secrete CRF, such as the endotoxin bacteria to be discussed later.
The suppressor cells are not affected by GRMFs, 6 so that the effective set point for the immune cells may be even higher than the set point for physiological processes. It may be that the GRMFs have a different spectrum of effects for each of the physiological processes in order to fine tune the immune response in order to optimize the attack against different organisms.
It seems to me that resources diverted to immunity or denied to non-viral pathogens usually diminish an animal’s performance when fighting or fleeing. Therefore, the cortisol system can be overridden by perceived danger. This is no doubt made desirable because it takes several hours or more for pathogens to rise to dangerous levels, but only a few seconds for a predator to kill an animal. Anxiety is also factored in because, I suggest, cortisol operates by changing the nucleus commands to send RNA for production of enzymes, etc. in almost every case and the various diffusion steps take an hour or more to complete. Therefore, an anticipation of danger would be very desirable.
The desirability of inhibiting activity during infection is no doubt the reason why cortisol is responsible for creating euphoria, 8, p.736 as does aldosterone, 9 and presumably the reverse upon declining. The desirability of not disturbing tissues weakened by infection or of not cutting off their blood supply could explain the inverse stimulation of pain widely observed for cortisol. These neural mechanisms as geared to stress have been emphasized in concepts concerning glucocorticoids as pioneered by Selye up to now. Nevertheless, when a process must move in the same direction for both immunity and fight or flight, a different hormone system controls it for stress. An example is release of ceruloplasmin by the liver, which is controlled for purposes of stress by epinephrine and by an unknown hormone for immunity to be discussed later.
The most dangerous digestive diseases produce a protein poison which stimulates cyclic adenosine monophosphate [c-AMP] hormone in such a way that the intestines cannot remove water from their contents10 and thus cause diarrhea. Since potassium in food and the 2.5 grams or so secreted with digestive fluids can only move into the blood stream passively, 11 this causes a large loss of potassium. Judging by the reduction of the death rate in babies with virulent diarrhea from 34% to 6% by potassium supplements12 in spite of the danger of hyperkalemia (high serum potassium) during dehydration, the loss of potassium implied is the most serious consequence of diarrhea. When this poison first evolved, it must have been catastrophic to terrestrial vertebrates. Even today, after what was probably a major evolutionary transformation of cortisol, the diarrheas are among the most important causes of mortality in the tropics, especially cholera 12a and diarrhea was the third leading cause of death 100 years ago in the USA, ahead of heart disease. It must have been imperative to evolve mechanisms to surmount those pathogens. In most mammals, a wide range of processes are stimulated by cortisol, each of which would make an animal less able to resist potassium and water wasting intestinal disease. Rodents have very little cortisol, which may be related to a marked inhibition of the effect of cholera toxin by rodents' intestinal contents. 13 Also, c-AMP increases water absorption in their ascending colon, opposite to the effect in their descending colon. 14 This makes rodents dubious for experiments on the hypothalamic-adrenal axis and perhaps for any experiments.
POTASSIUM
The greatest urgency during diarrhea is to prevent loss of potassium, since there is no storage of potassium in any cell. In cells, 88% of the potassium is in free solution. 11 Indeed, one of cortisol's functions conserves potassium. It has been suggested that cortisol tends to move potassium inversely into the cells [cortisone]. 15 If this is the case, potassium is inversely conserved by lower secretion of cortisol (dexamethasone). 16 In order for potassium to move into the cell, cortisol inversely moves out an equal number of sodium ions. 15 It can be seen that this should make pH regulation much easier, unlike the normal potassium deficiency situation in which about 2 sodium ions move in for each 3 potassium ions that move out17, p.445 which is closer to the DOC effect. 15 This is probably the reason why the cell becomes acid during a deficiency caused by low potassium intake. 18 Nevertheless, cortisol consistently causes alkalosis of the serum [inversely acidosis] while in a deficiency pH does not change. I suspect that this is for the purpose of bringing serum pH to a value most optimum for some of the immune enzymes.
Potassium is also inversely inhibited from loss in the kidneys somewhat by cortisol [9 alpha fluorohydrocortisone]. 19 Potassium is primarily blocked from loss in the kidneys by a drastic decline of aldosterone during dehydration. 20 Aldosterone acts on the last part of the kidney tubules and the lower colon. 21 In the colon, aldosterone reverses the normal inward flow of potassium, or at least stops its reabsorption22 and so inversely conserves potassium there. Aldosterone is directly controlled by potassium and inversely by osmotic pressure20 while angiotensin II is required. Thus as osmotic pressure rises during dehydration; aldosterone undergoes a drastic decline. Aldosterone also backs up cortisol by possibly inversely moving potassium into muscle cells somewhat. 22
To be useful in combating a potassium wasting disease, it would be necessary for cortisol to decline at such a time. A high potassium media, which stimulates aldosterone secretion in vitro, also stimulates cortisol secretion from the fasciculata zone of dog adrenals. 23 and potassium loading increases ACTH and cortisol in people [101]. Therefore, low potassium should decrease cortisol secretion by the adrenals in vitro in dogs and people. At the same time, potassium has no effect on corticosterone secreted by the adrenal fasciculata. 24 Since the fasciculata accounts for 5/8 of the corticosterone secreted, the net effect is very little decline in corticosterone secretion. This is evidence that the body does not rely on corticosterone against diarrhea. Potassium chloride supplements do not affect cortisol or corticosterone plasma concentrations in humans in vivo when the cell content is adequate. 25 I know of no experiment which would establish the effect of potassium, cholera toxin or detection of intestinal pathogen microbes on ACTH. ACTH has its greatest effect on cortisol and 18hydroxy 11 deoxycorticosterone [18OH DOC] That last hormone affect is probably to acidify the blood during an infection.
SODIUM
Cortisol is used to stimulate sodium inward for fresh water fish and outward for salt-water fish. 26 The necessity of conserving potassium while still unloading electrolytes to maintain osmotic pressure may explain cortisol's inverse sodium losing power in the small intestine in mammals. 27 By using the intestine to excrete sodium, less water is needed for kidney processes, which is crucial during diarrhea. Sodium depletion does not affect cortisol, 28 so cortisol is not used to regulate serum sodium. It is known that the sodium retaining hormone, 18-hydroxy 11-deoxycorticosterone [18OH DOC] acting on the kidneys is strongly dependent on ACTH. When ACTH sinks to zero, 18OH DOC also does. 29 Therefore, it also is inversely involved in unloading sodium in what little water is excreted from the kidneys. The need for sodium chloride by diarrhea bacteria in order to grow rapidly30 may be the main reason why cholera enterotoxin is so successful for this bacterium and of course increased water undoubtedly assists it also. 18OH DOC is probably the hormone which stimulates hydrogen ion excretion, so loss of this excretion would assist acidifying the serum as mentioned above as well.
If my contention that 16-alpha 18-dihydroxy 11-deoxycorticosterone [DOH-DOC] is relied on to excrete excess sodium and to conserve potassium17 is valid, it should follow that ACTH and/or cortisol either have no effect on DOH-DOC or, possibly more usefully, to inversely stimulate it. It should also be desirable for DOH-DOC to exert its effect in the intestines because in nature it is almost always during diarrhea that the body experiences a potassium deficiency and sodium glut. I have no direct evidence for either phenomenon. However, it is known that DOH-DOC has very little affect on the kidneys.17, p.446 The malaise, headache, loss of appetite, insomnia, and muscle cramps created by DOC injections31 may be due to the loss of potassium and retention of sodium, resulting from increased DOC, causing DOH-DOC to rise, since none of these symptoms appear from a high sodium and potassium diet which stimulates DOC.17 Some of those attributes would be useful during diarrhea, but I have no evidence for DOH-DOC's role. 11-deoxycorticosterone [DOC] is the only steroid left of the four I proposed for electrolyte regulation.17 Sodium retention must never completely disappear. This may be why, as possibly the only renal sodium retainer left, DOC has acquired its auxiliary powers with respect to amino acids and copper to be discussed later and why a fall in leucocyte potassium of over 10% is observed from DOC32 and a decline in muscle potassium,33 thus joining cortisol in inversely conserving potassium. It also probably explains why it is mediated partly by ACTH since ACTH must surely largely be an immune hormone with stress as an adjunct.17,p.445
WATER
Cortisol also acts as a water diuretic hormone. Half the intestinal diuresis is so controlled.27 Kidney diuresis is also controlled by cortisol in dogs.34 The decline in water excretion upon decline of cortisol [dexamethasone] in dogs is probably due to inverse stimulation of antidiuretic hormone [ADH or arginine vasopressin] the inverse stimulation of which is not overridden by water loading.34 Humans also use this mechanism35 and other different animal mechanisms operate in the same direction.
Since loss of water is the circumstance which produces the worst adverse effects of diarrhea, it would seem to be logical to use dehydration as a signal to decrease cortisol. Cortisol has been found to vary directly with water intake 36a ACTH hormone production is inhibited by water deprivation at the pituitary level. Basel secretion of ACTH is not affected, but high plasma ACTH resulting from immobilization stress is almost cut in half. Base corticosterone is increased in plasma from dehydration, but the much higher corticosterone from immobilization stress is not affected by water status.36 The above is additional evidence that corticosterone is used by the body to fight serum disease and cortisol is used to fight intestinal disease.
GLUCOSE
Reinforcing the concept that cortisol is relied on more for intestinal disease control and corticosterone for serum disease is the circumstance that corticosterone at physiological levels shows a marked inhibition of insulin and enhancement of glucagon in vitro.37 Cortisol shows a small inhibition of glucagon which reverses in a short time and has no affect on insulin.38 Insulin is used to help prevent hyperkalemia [high serum potassium] by the body. As glucose moves into the cell, it takes potassium with it. This mechanism is only used at low potassium intakes. At an intake of 8 grams per day, insulin stays normal.39 This is logical since there is no need to conserve potassium at high intakes and aldosterone is relied on to lower serum potassium. Cortisone greatly inhibits insulin secretion.38 The cortisone-cortisol equilibrium may explain why in vivo experiments contradict the above.40 It is possible that this equilibrium may permit the body to change cortisol glucose responses for particular kinds of situations.
The inversed stimulation of insulin by corticosterone would lower serum glucose and thus deny glucose to pathogens. Such an aptitude in cortisol would be of little value if my thesis is correct, and could even endanger an animal from hypokalemia [low serum potassium] during diarrhea. A sudden withdrawal of glucose by insulin in a potassium deficiency can lower serum potassium enough to be lethal. However, apparently there is an advantage in locking up the potassium that does enter the cell in a more orderly manner with glycogen, because DOC inversely stimulates glycogen formation.41 Cortisol does inversely cause serum glucose to fall, but this is probably an indirect effect caused by inverse inhibition of amino acid degradation.
The intestinal brush border disaccharide enzymes are inversely inhibited by cortisone.42 If it is cortisol that is actually involved, this could be a mechanism to deny energy to bacteria incapable of using sucrose. However, present day cholera can ferment sucrose43, p.557 so it would have to be an attribute developed against diarrheas which evolved before cholera evolved. It is also possible that it helps prevent the hypokalemia above or make copper more available if those enzymes are copper catalyzed. The fact that sucrose and fructose make a copper deficiency much worse suggests that they are. [100]
AMINO ACIDS
Glucocorticoids have the attribute of inversely lowering amino acids in the serum.44, p.273 They do this by inversely stimulating collagen formation, increasing amino acid uptake by muscle, and stimulating protein synthesis.44, p.273 Cortisol also inversely inhibits protein degradation.45, p.207 Such an attribute would help deny amino acids to bacteria. An additional advantage is that collagen can be very useful in repair of infected tissue. An indication of this last is that loss of collagen from skin by cortisol is ten times greater than from all other tissue in the rat.45 Thus the skin can be a reasonably safe source of energy during stress and be rapidly repaired during damage preliminary to or caused by infection. Lowering serum amino acid or even tissue damage repair during intestinal disease should be not nearly so advantageous. An indication that it is not is that DOC acts in the opposite direction for collagen [mice]46 and thus tends to cancel cortisol's effect if the same thing happens in other animals.
It can be seen that denying amino acids to bacteria above could be very advantageous in a serum infection. However, the inverse generalized stimulation of protein synthesis44, p.273 [I'm not certain how generalized it is] could have additional survival rationale against digestive disease. 40% of the protein synthesis is in the intestines of the rat, much of it for synthesis of IgA.47 IgA acts as an inert, nonlethal coating on bacteria to prevent adhesion to intestinal walls47 and is the predominant immunoglobulin in the human intestine.43, p.597 Cortisol probably inversely stimulates IgA precursor cells in the intestines of calves [opticortinol].48 Cortisol also inversely stimulates IgA in serum, as it does IgM, but not IgE.49 I cannot account for the effects on IgM and IgE.
Cortisol has an opposite effect on liver than it has on muscle, but I cannot tie this for sure into the immune concept now. I suspect that it may be to provide a small amount of maintenance amino acids when the muscles are withdrawing them from the blood and possibly also to provide liver amino acids for IgA. That same inability of mine is true of its inverse activation of luteinizing hormone.
HYDROGEN ION
Sodium, potassium, and chloride make strong bases and acid so that any unilateral movement by any of them has considerable implications in hydrogen ion control. Cortisol inversely inhibits gastric acid secretion.50 Since hydrogen ion interferes with potassium excretion at the kidneys,51, p.215 this could be having a potassium conserving effect, especially since gastric secretion carries 0.6 grams of potassium per day into the stomach as well. Corticosterone has a much greater effect on gastric acid secretion than cortisol.50 I cannot explain why it should have any affect at all unless there is some advantage to keeping the serum at a lower pH during infection for enzyme enhancement a possibility already mentioned. Some leucocyte enzymes have a pH optimum lower than serum. If so, 18hydroxy 11 deoxycorticosterone, which reduces bicarbonate and stimulates hydrogen ion excretion at the kidneys,52 operates in the same direction, since it also declines with ACTH half again more than cortisol.53 Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to inversely inhibit excretion of ammonium ion by inactivation of renal glutaminase enzyme.54 Glutaminase splits ammonia off of the amino acid glutamic acid, and this provides ammonium ion to take the place of potassium for excretion. However, cortisol's presence is necessary for the other hydrogen ion excretion regulator to operate.54 There would have to be some restraint on hydrogen ion loss because when potassium is deficient, the kidneys fail to absorb chloride and the serum tends toward alkalosis.55 Perhaps cortisol's inverse inhibition of gastric secretion being lower than corticosterone's is a compromise made necessary by the advantage in keeping the stomach reasonably acid, below a pH of 6, in order to help prevent reinfection by cholera bacteria.43, p.556 The acidosis of serum that attends cholera43, p.601 may become too high, so this lower inhibition may also be a compromise to help solve such a situation. The net effect of glucocorticoids is to inversely acidify the serum.
CHLORIDE
Chloride is intimately involved with potassium loss because when the cell loses potassium to take the place of serum losses and sodium migrates in, chloride must also be excreted as the only ion which has a chance of maintaining serum pH. In a potassium deficiency chloride is lost.55 This is a serious circumstance in nature because chloride is not bound very well by soils. It is a seriously limiting element inland where vegetation is devoid of it as a rule. Some indication of its importance is that it is the only essential nutrient we can detect and be attracted to other than water [the salty taste].
Net chloride secretion in the intestines is inversely decreased by cortisol in vitro [methylprednisolone].56 Cholera toxin forces chloride secretion to reverse from flow inward to larger flow outward.57 Thus cortisol tends to inversely neutralize cholera's effect. There is no net movement of chloride by cholera toxin in vivo.58 It is possible that this attribute is related to keeping the serum pH low as mentioned above, that is to say, acidic. It is possible that movement of sodium and/or chloride into the intestines is the chief advantage that diarrhea bacteria attempts to gain from their water losing toxin.
COPPER
The immune system is very sensitive to copper availability. Spleen of copper deficient animals show little growth during infections.59, p.334 Even a mild deficiency causes spleen derived immune cells to be significantly less competent as stimulators in general and also to be stimulated by endotoxin, pokeweed, or concanavalin A.60 Resistance to infection is reduced somewhat by a deficiency.59, p.334 A reduction in neutrophils is the first symptom of a deficiency in children.59, p.336
It is therefore probable that increasing copper for immune purposes is the reason why many copper enzymes are inversely inhibited to an extent which is often 50% of their total potential by cortisol.59, p.337 This includes lysyl oxidase, an enzyme which is used to cross link collagen and elastin.59, p.334 DOC acts in the same direction as cortisol for lysyl oxidase.59, p.337 Particularly valuable for immunity is the inverse shutdown of superoxide dismutase by cortisol61 since this copper enzyme is almost certainly used by the body to inversely permit superoxide to poison bacteria. Superoxide is lethal to cholera.62 Indication that superoxide dismutase is involved in immunity is that phagocytic activity is reduced by free radical scavengers.63
The safest way to transport copper to the immune system would be by the transport protein,59, p.335 ceruloplasmin. This avoids copper toxicity when copper availability to the cells from the liver is increased, since ceruloplasmin copper is not in equilibrium with the serum.59, p.335 The concept that ceruloplasmin is used by the immune cells as a source of copper is supported by the fact that ceruloplasmin quadruples in replete chickens during infection64 and several antigens raise plasma ceruloplasmin in mammals64, p.557 by an unknown hormone, which has been tentatively proposed to be leucocyte endogenous mediator, at low ACTH levels.65, p.557 Cortisol is not used to inversely stimulate ceruloplasmin. I suspect the reason why cortisol is not used is that stress requires extra copper, also, and at high ACTH levels epinephrine is used for this purpose.65, p.556 Transporting copper as the ion is not so important for denying copper to pathogens during digestive disease, which is probably why DOC inversely loses copper from the liver and inhibits liver uptake somewhat thus providing the immune cells with free copper to supplement the ceruloplasmin source.66 Some might argue that it is not likely that the immune cells depend on ceruloplasmin since people with Wilson's disease, in whom ceruloplasmin cannot be synthesized, are not prone to infection. However, such people cannot transport copper to the bile excretory proteins either, so their cells are already loaded and even overloaded with copper.
Cortisol causes an inverse four or five fold decrease of metallothionein,67 a copper storage protein. This may be to furnish more copper for ceruloplasmin synthesis. Cortisol has an opposite effect on alpha aminoisobuteric acid than on the other amino acids.68 If alpha aminoisobuteric acid is used to transport copper through the cell wall, this anomaly would possibly be explained.
MISCELLANEOUS
A large number of other molecules and processes are affected by glucocorticoids which I cannot tie into the immune system definitively at this time. A cursory examination has revealed none to me which is at variance with this thesis. They include smell sensitivity, fear, taste of chloride, pain, appetite, fever, immune cell activity, prostaglandins through arachidonic acid availability, fibronectins, capillary permeability, calcium absorption, intestinal permeability, phosphate, depression, oxidation of chloride, free oxygen formation, blood platelet activating factor, T-cell growth factor sensitivity, and lysosome membrane. Some of these are thought to be controlled by a second message protein, lipocortin, via its effect on phospholipases.69
ENDOTOXIN
Many gram negative bacteria have evolved a very potent way of subverting the cortisol control of immunity. They have a lipopolysacharride called endotoxin on their cell wall. Some endotoxin erodes off the wall and more is released into the blood stream when polymorpholeucocytes eject debris from bacteria which they have engulfed.70 The lipid A part of the molecule stimulates the hypothalamus to secrete large amounts of CRF (corticotrophin releasing factor). An amount of endotoxin which causes no other symptoms than a mild fever causes a six fold rise in ACTH, undoubtedly from CRF stimulation.71 When this way of bypassing ACTH immunity control first arose, it must have been catastrophic for vertebrate life.
A way of detecting endotoxin has apparently evolved and, also, a way of using it to activate a number of responses, some of which are reminiscent of glucocorticoids' inverse effects. Some responses are fever, creation of interferon by spleen cells as well as division of spleen cells, synthesis of IL-6, activation of complement by three mechanisms, creation of hypotension (low blood pressure), stimulation of adherence and oxidative processes of neutrophiles, activation of a burst of activity in macrophages in extremely small amounts, proliferation and maturation of B-cells, suppression of cholera toxin, low serum glucose, metabolic acidosis, and numerous other functions.73 Mice which lack these capabilities are susceptible to gram negative disease.73 Most of these responses are mediated by the peptide hormone cachectin, also called cachexin, or tumor necrosing factor (TNF) secreted by macrophages and they last only the first couple of hours.74 That the detection and cathectin system evolved after the endotoxin assault on ACTH evolved is indicated by the much different appearance of the response curve for endotoxin as opposed to cachectin .99 If both cachectin and gamma interferon are removed by antibodies, bacteria proliferate very rapidly to the host's death. Lipid A fraction of endotoxin enhances local IgA response to mucosally applied antigen [cholera toxin], at least when lipid A and antigen are associated on a liposome carrier.75 GRMFs' secretions are stimulated by endotoxin.76 Antidiuretic hormone quickly rises twenty fold in only 15 minutes.77 Endotoxin must therefore be acting directly on the source off this hormone through cachectin, in my view by a secondary evolutionary response of the hosts. Thus, the body forces endotoxin to mount a preliminary quick response even before the antigens can activate a response, and then quickly turns it off again assisted by a cachectin half life of only six minutes.78
The release of endotoxin by phagocytosis mentioned above is probably the reason why glucocorticoids inhibit digestion but not uptake of bacteria by macrophages.79 This mechanism probably gives the body time to mount its cachectin, GRMF, antibody to endotoxin, and other defenses before the endotoxin containing cell walls are released into the serum.
It would be advantageous if ACTH production could be cut off when under attack. Possibly two proteins detoxify endotoxin.80 Apparently, a mechanism has evolved to cause endotoxin to lose its ability to force ACTH secretion in a few hours.81 This loss may be difficult to control because lymphocytes have developed the ability to secrete a protein, interleukin 1 [IL-1], which has a function of stimulating cortisol secretion5, which it does indirectly by stimulating corticotropin releasing factor (CRF)97, as does IL-6 (the mode of IL-6 action is unknown to me). In other words, the immune system takes over its own regulation. Such a system would be necessary if the ACTH decline were severe because even the immune system cells require maintenance amounts of glucocorticoids. Those glucocorticoid hormones cause the immune cells to rise to a peak of activity at low concentrations and then decline again at increasing concentrations.82 The IL-1 system has an excellent negative feedback.83 IL-1 still retains at least part of the fight or flight override, because it is synergistic with CRF in its long term effects. Cachectin also stimulates ACTH production somewhat by a direct effect on the pituitary,84 possibly an advantage the first few hours, especially if the shutdown of ACTH is rapid.
It would seem desirable if the excess cortisol could be destroyed and, indeed, the half life of cortisol becomes markedly reduced.83 What really makes the IL-1 system practical, however, is the development of a glycoprotein produced by T-cells called glucocorticoid response modifying factor (GRMFs, also GAF) which along with IL-1 has the power to inhibit the response of immune cells to cortisol.6 In other words, the set point of cortisol is raised. Thus, the now multiple sources of ACTH stimulation can be accommodated.
The GRMF system has taken on an advantage not enjoyed by the previous cortisol only control. Since GRMFs do not inhibit cortisol's effect on the immune suppressor cells,6 as previously mentioned, the other immune cells must be stepped up to an even greater frenzy. I suspect a primary pressure forcing the evolution of this system was the advent of endotoxin. The pressure must have been intense because some very virulent diseases are endotoxin involved. They include cholera, typhoid, pneumonia, salmonella, campylobacter, and meningitis. Non-gram negative malaria may also synthesize endotoxin85 perhaps, but if so, probably by some ancient recombinant gene event. Evidence has not been obtained yet that GRMFs affect most of the physiological processes affected by cortisol other than immune cell activity. However GRMF does block phosphoenolpyruvate and fails to block Dibutyryl cyclic AMP induced enzyme synthesis and tyrosine aminotransferase.86, 87 I am not familiar enough with these systems to be able to comment on the significance of these phenomena to the immune system.
If glucocorticoids are truly immunocorticoids as suggested, it should be possible to use existing information to devise strategies for dealing with infection. It would seem likely that keeping the patient free of stressful thoughts and actions, warm,88 on a low food intake [except for virus], and on a high copper intake (prior to infection) would be advantageous. Also, heat lamps creating an artificial very high fever89, 98 directly on the infected part (except for fungae [personal observation] ), probably are very effective. It is possible that refraining from coffee, tea, soft drinks or cocoa would prove slightly advantageous also because of an effect on cortisol by caffeine.90 If the patient cannot be guarded from stress, then vitamin C (ascorbic acid) supplements would probably be useful, for they are said to have the effect of blocking a rise in corticosterone resulting from stress91. There is a discussion of diseases for which vitamin C would be advantageous, for some, very advantageous. The advantage may disappear at other times because corticosterone is said to rise some, normally.91 Making sure the patient has ample water during serum disease is probably advantageous because of the effect water status has on corticosterone as mentioned under "Water." Fasting at the noon meal may prove to be a good strategy since cortisol shows a surge then if one eats, but not at the evening meal.92 The efficacys of these strategies should be established as soon as possible with controlled experiments on primates and made known to the public early on. Such experiments would prove to be very cost effective indeed compared to hospitalization. To rely on hunches based on knowledge of similar chemistry, old wives' tales, and alterations of symptoms by chemicals, such as even the medical profession does currently, is sad and inane. Few will alter their life styles unless they are convinced that the matter is established. It is highly desirable that the theory behind any parameter be understood because even small variations in the patient's environment can sometimes make an otherwise desirable strategy backfire. Nutrition intake and ingestion of poisons and medicines vary wildly in our society, so that treatments based solely on empirical studies such as is the usual case at present in the medical profession can be more than mildly disadvantageous in particular instances. It simply is not possible to take anything for granted in the absence of an experiment. I strongly suspect that the current attitude of the medical profession that potassium can never be deficient, or that rheumatoid arthritis can not possibly be a chronic potassium deficiency even though no experiment has ever been performed, will prove to be tragically wrong, for instance.
In addition, there seems to me to be implied possibilities for clinical intervention against virulent diseases. A recombinantly produced antibody against ACTH or CRF could conceivably have considerable value early in diseases which force their secretion. Perhaps even more valuable and safer would be an antibody against endotoxin. Infection is like a waste paper basket fire. It should be snuffed early before it becomes a raging inferno. Recombinant GRMFs might also prove valuable early in almost any disease. Where GRMFs might prove invaluable at all stages could be in those diseases which compromise the T-cells, such as AIDS, and thus hopefully solve the possible relative excess of glucocorticoids in AIDS.93 Of course, the frequency of injections for peptides must take into account the half life of the peptide to be effective. Massive daily doses would be ineffective and possibly dangerous in many cases. Ceruloplasmin injections would probably be in order for people known to be in a copper deficiency.
It seems conceivable that if a strain of cholera bacteria could be developed which could not synthesize c-AMP toxin or any other toxin, encapsulated in enteric tablets in order to bypass the stomach acids, and swallowed in large amounts, it could act as a preventative to cholera during an epidemic by furnishing overwhelming competition to virulent cholera in the intestines. It might even be effective after an infection.
In any case, it seems to me to be very foolish to administer cortisol to any class of people whose immune system is known to be weak, such as arthritics. If it is desired to raise cortisol's affect in the body, why not use something safe like potassium supplements, or better and safer yet, leafy unboiled vegetables?17,p.447 At the same time, it would solve the problem of the other affects of low whole body potassium content which consistently afflicts arthritics. Arthritics have been shown to improve with a vegetable diet.94 Arthritics have normal cortisol,95 so the lower number of glucocorticosteroid receptors,95 or possibly an abnormal GRMF secretion, must be involved, perhaps triggered by the potassium deficiency itself or some poison. Attempting to solve the problem by injecting cortisol for more than a short time strikes me as dangerous. One author summed it up thus "It is amazing how effective cortisol is in getting a seemingly hopeless patient on his feet again. Sometimes it is so effective that he can walk all the way to the autopsy table". Cortisol is not a medicine, it is a hormone, a hormone whose effects ramify through multiple functions in most of the cell groups in the body. An indication of how fundamental it is, is that the liver's RNA synthesis in adrenalectomized rats is simulated 2-3 fold by cortisol.96 It is urgent that the effects of every known essential nutrient and poison known to be currently ingested be tested against arthritis, especially potassium, which last has never been tested.
The immune system is extremely important to us, so current exploration of immunity should continue on by all known means. However, as you explore, please differentiate between cortisol and corticosterone, use the natural versions, use physiological quantities for at least part of the experiment, use animals other than rodents, and translate jargon. As to this last, immunity is important and extremely complicated. Few theorists are expert in all phases of it and all vocabulary.
Under no circumstances should recombinant experiments be performed which give to any microbe the ability to synthesize cortisol, ACTH, CRF, or any hormone molecule which declines in concentration or effect during infection. No experiment of any kind should be performed on any microbe which synthesizes endotoxin, such as Escheriischia coli. There are thousands of other species.
REFERENCES for CHAPTER VI in; http://members.tripod.com/~charles_W/cortisol.html
Chapter VII ---
The body must continually take in potassium throughout life, for there is no way to prevent loss in the urine and there is no storage in the cells or any organ, other than potassium associated with glycogen (animal starch). Glycogen is really a means of storing glucose sugar. If potassium were to be cut off completely, most mammals would probably be dead in less than two months. Humans would probably not last much longer. The general strategy that the body adopts is to take in more potassium than it needs in food, to absorb most of it from the intestines, and then to adjust the concentration in the blood serum by excreting just exactly the right amount from the kidneys, and to some extent into the lower large intestines.
Before the kidneys have a chance to excrete the excess, the potassium diffuses into any deficient body cells. The cell is essentially a tiny bag of potassium salts. Since the blood serum in which these cells bathe is made up mostly of sodium with only about 187 milligrams of potassium per liter, it is necessary for the cell to have some mechanism for keeping out the sodium. As we have seen the sodium either diffuses in or is pumped in along with the potassium. The current evidence seems to indicate that both a pump or pumps and diffusion are involved, and that the diffusion goes through an enzymatic gate. After they get in, there is a net pumping out of the sodium through the sodium pump on the cell wall. There is evidence that possibly the outward pumping of three sodium ions is coupled with an inward pumping of two potassium ions. If so this coupling would greatly increase the energy efficiency of the pump. I need to examine the literature to establish current thinking more certainly. However the exact configuration of these pumps and gates would not change the matter from seeming to be a true Donnan equilibrium.
The sodium pump operates every hour of the day and night throughout life, powered by 10% of the body's resting energy [Potts p274-275]. Only certain poisons [Post] or cold in the vicinity of freezing [Hendricks] can stop it . If it were to stop in vital cells, death is certain in a short time, perhaps as little as 15 minutes. In the brain the situation is even more serious. If the brain is merely deprived of the oxygen necessary to power this pump for as little as 5 minutes, irreparable damage is likely.
Since the most immediately urgent role of potassium in the body is to act as a counter flow for sodium's role in nerve transmission, the body must put a high priority on regulating the potassium of the blood serum. If the animal is to survive, its nervous system must be in peak performing ability all the time. Too little potassium is normally not a problem, because the cell fluid contains enormous amounts of potassium compared to the plasma. This potassium can be made available merely by allowing sodium to displace 2/3 of that which leaves the cell [Rubini] and the rest moves out with some of the negatively charged ions [Gardner]. Too much potassium is a perennial problem, however. A minor mechanism can be used to help the body cope with an acute emergency. For instance when sugar is stored in the liver as glycogen it always takes one ion of potassium with every molecule of glycogen [Hungerland]. So in an emergency merely by secreting more insulin, the body can unload a fair amount of potassium from the blood [Hiatt]. It may also secrete more glucagon at the same time in order that the blood not be depleted of glucose [Hiatt]. The insulin mechanism is only used at high intakes.
The main regulator, and the organ on which the body places most of its hopes to keep potassium normal, is the kidney. Aldosterone and deoxycorticosterone (DOC) stimulate the kidneys to excrete potassium. Most of the emergency unloading takes place in the distal and collecting tubules where potassium can be actively excreted in amounts as high as 26 grams per day for persons adapted to a high intake [Peterson 1972 p107,114, or 151]. A healthy young adult male can excrete about 2 grams per day in the urine and still maintain his optimum potassium level [Consolazio 1967]. Since this is the main stream of potassium excretion, it follows that the minimum daily requirement is a little over 2.0 grams per day for normal young adults who are not perspiring, not subject to fear or anxiety, and do not have diarrhea or vomiting
The potassium can not be completely absorbed by the intestines from the food. Very little is left in the absence of diarrhea, however, of the order of 1/6 gram per day [Consolazio 1963]. Therefore this amount has to be added to the 2 grams above to get the minimum daily requirement. Potassium is primarily absorbed in the large intestine. Under aldosterone stimulation the last part of the large intestine can reverse the normal direction of potassium movement [Edmonds] or at least prevent its reabsorption. The intestines thus assist the kidneys in preventing surges of potassium in the blood serum.
The frequent saunas or steam baths which the people of Finland take, may be helping to give them one of the highest rates of arthritis in the world [Kellgren] because of the attendant perspiration.
Block believes that whole towns died out in Holland because the sea rose slightly and covered salt evaporating pans during the middle ages [Block]. An armed insurrection in India almost happened when the British merely taxed salt and was averted only by a miracle and the personality of Mahatma Gandhi.
Such ripples from the past must seem bizarre and dreamlike to you who read this and are wrestling with the opposite problem. Huge front end loaders, enormous pumps, and excellent transportation have made salt so cheap that it is used in snow melting salt, water softeners, pickling fluids, and is sprinkled liberally on almost every processed food sold.
Rats on low sodium excrete more potassium than controls from all causes, including increasing the sodium intake above normal [Peterson][Wormersley]. It would seem that a very low or a very high sodium intake would increase the potassium requirement from the 2.2 plus or so minimum established so far. This could be as much as 1/2 gram (but I have no excellent information) to bring it to as much as 3 grams per day or so. Please keep in mind that this is a bare minimum and makes no allowance for disease, perspiration, emotional storms, mild genetic defects, poisons, odd intakes of other nutrients and old age. Going below such a minimum would not severely degrade health normally, but it would probably make the most optimum performance degraded somewhat. I currently suspect that one to two grams per day is the desired amount of sodium that would give an approximately equal number of atoms. This amount should keep the body reasonably well conditioned against the heat stroke of profuse perspiration (although 1/2 gram would be more efficient) and protecting against other circumstances, circumstances which I can not discuss with precision at this time. I am reasonably certain that the four grams (9 grams of salt) or so that Americans consume at present is too high. There are recommendations of 1/2 gram in the literature [Meneely]. This low a figure would be difficult to obtain but it is a figure some hypertensives should attempt [Abernethy]. It should be kept in mind that it may be the chloride in the salt which is part of the problem since potassium as the chloride raises blood pressure instead of lowering it. Sodium must be combined with chloride to raise blood pressure. Sodium alone, as the bicarbonate or probably as citrate also, lowers blood pressure [McCarty]. High ratios of potassium to sodium should not cause a major problem for people who have intact kidneys. Primitive tribes receive twenty to one ratios without apparent risk. It is possible that people descended from tribes with a long history of eating primarily meat may need a little more sodium than others. In people who are nourished by unprocessed food, not assaulted by poisons in tobacco and alcoholic drinks, and living a reasonable life, the regulatory systems should be able to tolerate a fairly wide range of sodium acute intakes. It is possible that chronic high intakes can eventually produce an intractable high blood pressure in some people, however, which conceivably could be arising from the chloride usually associated with sodium supplements as well. However, potassium as the chloride has the same affect as potassium from food coupled with hydrochloric acid supplements. There are times when this might be disadvantageous. High blood pressure may be one time. 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]. Chloride has not had much research into long term affects, but short term it increases blood pressure.
Magnesium is deeply involved in the body's energy metabolism (Krispin Sullivan, clinical dietitian has written an excellent article on magnesium deficiency as well as as practical ways to get more potassium from food) . Also see this site about magnesium deficiency. A magnesium deficiency can cause the body to lose potassium [Peterson 1963][MacIntyre][Manitius], possibly because of a poorly understood effect of magnesium on the efficiency of energy supply to the sodium pump [Fischer]. Conversely a potassium deficiency causes magnesium to accumulate [Southon]. I do not know whether this causes any adverse health problems. The nature of a magnesium deficiency on potassium [Grace] suggests to me that the effect should show up most strongly when the magnesium is supplied again. The symptoms of a magnesium deficiency are convulsions, gross muscular tremor, atheloid movements, muscular weakness, virtigo, auditory hyperacusis, aggressiveness, excessive irritability, hallucinations, confusion, and semicomma [Bajusz]. It consistently affects the kidneys, usually by calcification at the corticomedullary junction. Potassium content of the cortex does not change, but medulla content of potassium is diminished [Bajusz p 40]. Retinopathy (an eye disease) is associated with magnesium deficiency [Dorlach]. In monkeys the electrocardiogram in magnesium deficiency resembles that of high serum potassium (hyperkalemia) in spite of low serum potassium (hypokalemia) [Manitius p39]. So it is possible that lower cell potassium requires lower serum potassium for adequate nerve transmission, but the serum potassium does not drop [Manitius p38]. There is a fairly extensive review of magnesium nutrition along with foods high and low in magnesium [Seelig]. I suspect that people eating unprocessed food get enough magnesium. If so magnesium should have little affect on potassium requirements for such people. An exception might be people who do not get enough vitamin D which is said to be necessary for magnesium reabsorption or people not synthesizing enough parathyroid hormone (PTH) . If a magnesium deficiency does develope, half a year of supplements can be required for complete normalization of magnesium and potassium - sodium pumps [Anonymous].
I have already mentioned that the sodium pump dies down near the freezing point of water. I suspect that this is probably the reason for the pain we feel in cold fingers on a freezing day, since excess potassium causes local pain [Ghosh]. Calcium inhibits pain from damaged cells [Benjamin]. This release of potassium from cold tissue cells into the blood stream must surely be causing potassium excretion to rise some, thus raising the minimum requirement somewhat in winter. I have no proof of this concept from the medical literature, but it must be happening this way. It is possible that the greater misery which some arthritics claim to feel on cold days may be partly related to this circumstance. Gubner suggests that cold can lower heart potassium, although his own data does not confirm it [Gubner].
There are several disease states which cause higher excretion, and during which disease states a higher intake is desirable.
The most important and common of these is diarrhea. Certain peptide protein poisons given off by certain intestinal microorganisms prevent the large intestines from absorbing water and therefore also salts [Rowinski][Donowitz]. As a result not only the potassium in the food eaten, but also the 2.5 grams or more [[Potts p274][Perkins] of potassium in digestive fluids is lost. The body can become dangerously depleted in a short time. Most of the death rate from the more virulent diarrheas in children is from an acute potassium deficiency. The death rate was markedly reduced in one virulent strain using potassium supplements [Darrow][Govan]. The dead babies showed a loss of 40% of their muscle potassium. The dehydration which can take place in diarrhea can cause massive losses of potassium in urine in addition to the losses in the faeces. Every liter of water lost from the cells carries with it 6.5 grams of potassium [Weisburg p189]. His estimate is probably a little high, and in addition the net losses are lower because the blood plasma also loses water but those figures are probably not far off. Babies are especially vulnerable to this loss because they have no effective way of informing us of their thirst. Do not let any one in or out of a hospital talk you into drying the intestines to stop the loss of water by withholding water as hospitals used to do (and may still do some places). The microbes involved force the intestines to stop absorbing water regardless of intake probably in order to create a favorable environment for themselves. .It has been determined that guava fruit or leaves will inhibit the bacteria that cause diarrhea [Lozoya].
You must be careful with supplements because the dehydration causes very high blood plasma potassium contents, even though the cells are becoming deficient. At the same time the aldosterone which stimulates excretion goes away down. The way medical people get around this these days is to administer oral rehydration salts (ORT salts) which are a mixture of sodium and potassium chloride and sodium bicarbonate in water. See this site for a discussion of oral rehydration therapy (ORT salts).The antidotes for too high blood potassium contents will be discussed in the chapter on supplements but especially in the chapter XIII on high blood potassium (hyperkalemia).
Vomiting which persists can also deplete the body's potassium somewhat [Bartter]. Barter believes the loss of hydrochloric acid is as important as the potassium loss in reducing body potassium. This is because when acid is lost the kidneys excrete more potassium [Welt 1960 p215][Potts p262] thus countering the alkalinity implied in the loss of chloride. The stomach secretes over 1/2 gram of potassium per day.
The balance of evidence would indicate that hostile or fearful emotions can be a cause of excessive loss [Glaz][Davson]such as anxiety over exams [Venning]. Certainly the stress and pain which attends surgery is well established as a time of excessive losses [MacDonald]. Supplements during this condition were becoming increasingly standard procedure in clinical practice [Rubini].
There are several rare diseases which can cause potassium loss. Among these are aldosterone tumors or Conn's syndrome thought to be 5-15% of high blood pressure or hypertension (this site has diagnoses and treatments) with muscular weakness, paralysis, tetany, polyuria excessive urine, hypertension, hypokalemic alkalosis of the blood, parathesiae. Also involved are Cushing's syndrome (high cortisol), diabetic coma, and several types of kidney diseases [Wohl p832]. It said that hyperthyroid condition can cause such an acute low potassium that paralysis can occur. In these last cases a person would be under medical care so they are not really proper in a discussion of requirements for normal people.
There is a class of chemicals called diuretics which have the effect of forcing the body to excrete sodium. Since one loses water and therefore weight at the sane time, these chemicals have been used as a weight reducing technique. Unfortunately one loses potassium at the same time in most of them. No fat is lost in this procedure; only water. Trying to lose weight with these chemicals would rank in logic with reducing the weight of a truck full of sand by draining the radiator. More valuable than advising you to increase your potassium intake while taking diuretics, would be to advise you not to attempt to lose weight with them at all. As for their other uses; I doubt if they are very often in order in healthy well fed people. Often they are used to help a patient suffering from edema (expansion of body fluid) who are reluctant to restrict salt. Potassium itself can act as a diuretic [Liddle] to some extent. One must use care about supplements when using potassium sparing diuretics.
There are two other medical procedures which can cause increased losses. These are enemas [Dunning] (enemas lose more potassium when prolonged) and laxatives [Schwartz, ]. They are not procedures which should be indulged in routinely. Licorice is also strongly suspected of increasing losses [Gennari][Kolata]. Licorice (but not the licorice candy which is said to be anise seed extract) contains a chemical called glycyrrhizic acid which hydrolyzes in the intestines to form glycyrretic acid [Stormer] or glycerretinic.acid which interferes with degradation of aldosterone and cortisol. 50 grams of licorice sweets are enough to produce hypertension and low serum potassium in some people [Stormer]. Flavenoids in grapefruit are thought to have a similar affect on that enzyme [Lee].
There is evidence that negative ions in the air can increase potassium loss [Olivereau]. If this is proved true it would follow that people living in homes heated by ionizing type of electrical heaters or ionizing generators should have somewhat greater needs.
Sometimes cortisone or other steroids are prescribed for arthritis. One side effect of this therapy is the loss of potassium This is hardly a problem anyone would have who has already cured the arthritis by diet.
Surgery and injury cause increased losses [Randall][Selye p197-198]. This is probably because of secretion of steroids. [Elman]. Release of potassium into the blood from metabolic shock resulting from burns or injury is the chief cause of mortality in those states [Fox]. The release of potassium into the blood can be massive, and the corresponding losses as the kidneys attempt to clear this dangerous excess can be large.
There is a medicine called bitter root (wild ipecac, spreading dogbane, rheumatism weed) which is said to increase potassium excretion. If all the above increases in losses were to operate simultaneously it would place one in grave danger of heart failure, a disease to be discussed later.
Considering all the ways in which loses of a healthy person can be increased, it must be obvious that a preferred requirement must be higher than the bare minimum of 2.2 grams per day or so contributed by the kidneys and colon on a mild day mentioned earlier. I do not see how the actual minimum average could be much below 3 grams. Lane, et al, believe that over 3 grams per day is necessary for athletes on a hot day to prevent negative balance [Lane]. However for a recommended amount I would suggest more than 4 grams even on mild days. Hopefully this would provide most people with a reasonable margin of error. Almost no one has a way of monitoring his body's status and excretion. So if you seek optimum performance (not just freedom from arthritis symptoms) it would be best to err on the side of high. A high potassium intake is not possible if kidney function has been destroyed though.The amount should not be predicated on losses on balmy days spent with congenial friends. It is losses during summer heat and winter cold, the stress of battle and stormy emotions, and disease that should be determining since these conditions can never be predicted. Of course when recovering from a deficiency the amounts would ideally be higher yet, but not while dehydrated, at least not without plenty of water and sodium chloride salt.
There is another reason to set it on the high side. When the intake is high the kidneys gradually undergo modifications which make them much more efficient at excreting potassium [Wright]. It is thought that the distal tubules are involved normally and the collecting tubules when there is sodium deprivation [Silva].There is also a reduction in number of pumping sites on the muscle cell membrane in a deficiency [Nogaard]. Thus the muscle cells would presumably be less able to reabsorb potassium during metabolic shock as they do before the cells become saturated [Miller]. Thus a high intake should help guard one against a future low intake and, paradoxically, a future high plasma level as well.
Another reason for eating generous amounts of essential nutrients in general is that there is considerable variation in individual peoples’ requirements and very little ability to determine the variations.
Reaching this high intake using supplements may not be the best way because potassium interferes with magnesium absorption in some animals [Sheehan]. There is nothing like food. It tastes good too. There is extremely wide variation in the amounts of potassium per calorie each kind of food supplies so there are plenty of options. Chapter VIII , “POTASSIUM in FOODS”, will discuss this variation. It gives a link to a food content table expressing potassium as milligrams per Calorie at; http://members.tripod.com/~charles_W/table3.html. There is a site which gives food nutrient content tables for many nutrients at: http://www.ag.uiuc.edu/~food-lab/nat/mainnat.html but from which one must compute the weight of potassium per Calorie. The very extensive USDA Handbook #8 may be seen at; http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl. 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.
It should be possible to lift oneself out of even a severe deficiency in only a month or two using food alone with proper selection. Using potassium chloride supplements it could be as short as several weeks if magnesium, and perhaps inositol and vitamin D are adequate There is danger of imbalances with respect to other nutrients using such supplements only, to be discussed later. However, there should be little chance of danger in people with reasonably healthy kidneys if a gram or two per day of potassium is used in conjunction with an unprocessed diet high in leafy vegetables for a few weeks.
REFERENCES for CHAPTER VII in; http://members.tripod.com/~charles_W/arthritis8.html
Chapter VIII ---
Someone who has rheumatoid arthritis and therefore has a bad deficiency in potassium [LaCelle] should be able to acquire the as much as the missing fifty or sixty thousand or so milligrams missing from the one hundred thirty to two hundred thousand normally present (depending on the weight of non fat tissue, which is usually almost 2000 milligrams per kilogram of weight [Flink ] to 2,650 or so again in only a few months or less and largely heal or cure any reversible damage (such as possibly the fundamental changes in ion channels of arthritics [Trujillo] ) in only a few more weeks using food alone. This should be possible even though arthritics tend to have a higher amount of the potassium excreting hormone, aldosterone, than normal people [Khetagurova] do. It is only necessary to select the right food and prepare it correctly. Large amounts of potassium are possible from food alone as some South American Indians receive over 8 thousand milligrams per day from their food [Oliver]. Potassium can be increased more quickly with potassium chloride supplements also, but unprocessed food is the safest way, and can rarely cause imbalances or dangerous surges where the kidneys are in reasonable health. When they are not, you should be under the care of a doctor. An additional reason is that potassium can not be absorbed efficiently in the presence of a magnesium deficiency and magnesium tends to be correlated with potassium intake. Total body magnesium does not predict a deficiency, but blood serum must be low for that. If blood magnesium is 25% low, the enzymes depending on magnesium fail to operate adequately, including those responsible for its own absorption. [from a dead URL] Inositol may be similar to magnesium in its affect [Bian] [Allard] also (see this site for a discussion of nutrients which affect the potassium pumps, including inositol, especially as pertaining to pain during diabetes) and further information about inositol at this site.. Furthermore there is evidence from rats that excess chloride can increase high blood pressure (hypertension).
When attempting to increase our potassium intake to treat or cure rheumatoid arthritis, it is desirable to know which foods are high in potassium. It is not sufficient to know the amount of potassium in a given weight of food. What determines how much food we eat is largely determined by the number of calories contained in it. We eat until our appetite is sated by a sufficient intake of food energy, and then we lose our appetite. Therefore information on potassium in foods is much more useful if it is expressed as weight of potassium per calorie [Weber].
The justification for using Calories contributed by fat or oil in the potassium in foods table depends on the assumption that fat and oil contribute as much to appetite suppression as do carbohydrates. This is not the case short term [Blundell]. However this approach is still justified because trained muscles burn fat as well as carbohydrates [Saltin] and everyone except chronic fatigue syndrome (CFS) victims should get as much exercise as possible. While moderate to heavy exercise has been shown to be beneficial to fibromyalgia (probably a CFS variant) [Hadhazy], exercise in a pool has been shown to give improvement in pain, anxiety, depression, and number of good feeling days were more evident than land exercise [Jentoft]. I suspect that many short sessions of mild exercise across the day would be the best way, probably for arthritis also. Furthermore the foods which I recommend are low in fat and under such circumstances a high proportion of the fat is either burned or stored in the body's fat cells [Westertape] anyway. Therefore ultimately most of the fat and oil in a healthy diet contributes to appetite suppression long term and therefore no useful purpose would be obtained by attempting to compute a weighted factor against the fat contribution. A diet high in fat is disadvantageous for other reasons, so no net problem should arise including fat calories.
It is customary to designate potassium in milligrams. If potassium content is expressed as milligrams per Calorie (mg/Cal), most foods lie between 0 and 10, and none are higher than 20. These are convenient numbers, easy to read, and make a good comparison for foods when assessing their relative potassium contents. Such a designation is much more useful in attempting to decide which foods to eat than a "per serving" designation which gives very little hint as to relative value and is actually misleading for dry foods.
For a food content table for potassium in such a format, see http://members.tripod.com/~charles_W/table3.html A table like that is unobtainable elsewhere in that format. This same table may be viewed in descending potassium concentration at http://members.tripod.com/~charles_W/table2.html.The Table from which these values were computed 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 all the amino acids. It is available in a PDF printable form for potassium only also. with links to PDF caloric contents and other nutrients. You may also see a site which shows nutrients in food as is the case in this site.However, you must do the math here also to get weight per Calorie. 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.
1. Meat, fish, and dairy products, which we depend on for high quality protein (especially methionine and lysine), sodium, chloride, iodide and vitamin B-12. Vitamin B12 is said to be also present in spirulina, or blue green algae, but is thought to be an analogue of B-12 which may make a deficiency worse.
2. Vegetables, which we depend on for vitamin A, vitamin C, and potassium. They are also good sources of all the other vitamins and minerals except those listed under meat above, and vitamin D, which is not really a vitamin, but a hormone. To the extent that it is de facto a vitamin for those working and studying inside, it is present in liver, sardines, irradiated milk, cod liver oil, and tablets. For recommended amounts see the last of this site. It is necessary in the body to guard against tuberculosis [Wilkinson], to gain calcium for avoiding bone loss, and to retain magnesium. It has been proposed that vitamin D has an affect dampening the immune system. [Cantorna] and thus dampening inflammation during arthritis, although apparently this concept has not been followed up on. . It is more likely that the affect on magnesium is involved, and thus indirectly powers the potassium pumps [Grace]. The optimal values in the blood are proposed as 45-50 ng/ml or 115-128 nmol/liter of vitamin D. Fermenting vegetables will not provide adequate vitamin B-12 [Rauma 1995 with comments in 1997].
3. Grains and fruit, which are primarily cheap or tasty sources of calories. Grain price is made even lower since 90% of subsidy payments are made to farmers of corn, wheat, oil seeds, rice, and cotton [Doyle]. Grains also provide a fair amount of Vitamin E and B vitamins (other than B-12). Fruits are usually fair sources of potassium and vitamin C
Foods that contain 1 milligram per Calorie or better of potassium, as do whole grains, would probably meet the minimum daily requirement for most young people. This assumes a man in good health who burns 2,500 Calories per day, which would yield the 2,500 milligrams per day or so mentioned in Chapter VIII. It also assumes no drains on potassium from stress, disease (such as diarrhea), perspiration or other losses.
Lean meat low in fat has fairly consistent amounts of potassium, usually about 2 mg/Cal. It can range from 1 to 3 mg/Cal. Since fats or oils have no or little water to dissolve potassium, and since they are high in calories, they are very low in potassium, approaching zero. Therefore meat with much fat in it will be lower in potassium per calorie than lean meat. Milk compares to meat as a source of potassium, and has the same dependence on fat content. The lactose in milk is difficult to digest for adults outside of the Caucasian and Semitic races and causes digestive upsets. That problem can probably be solved by adding the proper enzyme to the milk. Also, milk is very low in copper.
Eggs, like meat, are an excellent source of protein, and for normal people should make a good adjunct to the diet. You should bear in mind, however, if you are in the throes of recovering from a deficiency, that they are low in potassium. This would be expected, since the developing chick is trapped inside the egg. It has no way of excreting potassium and must end up with the correct amount, after burning some energy and making some feathers. Eggs have been given some bad press because of the cholesterol hypothesis. However there are tribes, which eat large amounts of eggs in Africa, that have a much lower heart disease rate than we do. The Masai tribe members have low cholesterol [Brown p8-9] even though heart disease is a problem. Low cholesterol diet has little affect on cholesterol (or this site), since the high blood cholesterol is probably due to impaired conversion of cholesterol to bile acid [Mann p647] and an egg a day has no affect on cholesterol .[Slater] and Cholesterol lowering drugs give a higher death rate [Mann p646], and the cholesterol level is normal in the average heart attack victim. In fact, too little cholesterol in the body can cause health problems. It has been shown in some English children that cholesterol intake has no affect on blood cholesterol, but that saturated fat in boys and energy intake in girls increase cholesterol. For some possible causes and cures, see this pdf site. High sodium chloride (table salt) intake for 1-4 years has been found to frequently cause high blood cholesterol [Dahl].
There have been effective treatments rejected in the past solely because they did not conform to mistaken accepted hypotheses [Goodwin]. So eggs should make a reasonable source of protein for everyone. It is probable that most of the problem with cholesterol these days is from a pervasive copper deficiency. It is said that prolonged salt intake can also raise cholesterol, as mentioned above.
Most of the potassium is concentrated in the white of the egg. Egg whites are comparable to meat in content, and are in fact higher than most meat. One way to make a slight gain in potassium intake, if you are the only one deficient in your family, is to have your portion of the egg high in the whites.
Glucosamine has become popular as helpful in osteoarthritis. If it proves to have an equivalent affect on rheumatoid arthritis, I suspect the interference with potassium excretion by the ammonia generated will prove to be a considerable part of its efficacy.
Vegetables low in starch are the best sources of potassium. They rarely go below 5 mg/Cal., and range up to 20 mg/Cal. or more. The seaweeds are poor sources of potassium. The situation may be more favorable than this, since some of the Calories measured by the USDA may be indigestible to us. They are excellent sources of iodide which may be of interest to those who live in the interior of continents and do not use iodized salt. Perhaps they would be good as occasional salad dressing in summer. I can not recommend them as a substantial replacement for vegetables, however, because of their high salt content and because I am unfamiliar with the status of their other nutrition or the possibility of iodide toxicity. . 0.9 milligrams per day is said to be toxic in some people [Rauma, 1994] (However, excess iodide has been recommended against breast cancer [from a dead link] ).
If you wish to increase the variety or taste of the vegetables which you eat by growing your own perennials there is a site which lists growth parameters of trees and shrubs. --or-- This site discusses wild vegetables which are edible, and some evolutionary aspects of vegetable eating. You may see a list of vegetables which will grow in partial shade at this site.
Grain (see evolution of seeds as food) is the lowest of the major categories, and will usually run about 1 mg/Cal. Nuts are similar to grain. The bean, peanut and legume seeds are a fairly good source, usually running about 3-4 mg/Cal. They along with chocolate and other nuts are high in arginine amino acid which apparently should not be eaten when suffering from a herpes viral infection such as chicken pox, shingles, genital herpes [McCune] (see further discussion below). When first recovering from arthritis and attempting to build up your body's potassium, it would be well to use whole wheat bread and cake sparingly (and no refined flour products at all). Substitute wheat germ and yeast for some of it and vegetables for the rest. People who are intolerant of gluten protein should eat no wheat at all. A very important consideration is to eat extremely sparingly of foods containing sugar, starch, or fat, regardless whether the sugar, starch, or fat was placed there naturally or by the hand of man. Refined flour is extremely low in potassium but is not part of this discussion since no one should ever be using that useless rubbish under any circumstances because of a number of other deficiencies. A diet high in protein has been touted as superior to carbohydrates and for people who have not lost kidney function it is probably acceptable. However, the main reason why carbohydrates have received a bad perception is probably because the criminally incompetent jerks in the processed food industry have evolved clever ways to remove or destroy essential nutrients in carbohydrates, sometimes 100% of them.
When people speak of a balanced diet, they usually mean that you should get a fair share of each category of food each day. By so doing you make it unlikely that there will be too little or too much of any essential nutrients. If you get about equal calories from each of the three categories, you should have a reasonably balanced diet as defined by the crude definition at the beginning of this paragraph and most people will be reasonably healthy. However grain and fruit are not essential. You can see a table which shows all nutrients for many fruits at this site. You can probably get all your nourishment from meat and vegetables, and it is undoubtedly a superior way to eat [LaVecchia et al]. [Van Duyn]. This is a case history in which using vegetable juice and vegetables healed a woman of arthritis There was also a study which used a so called vegan diet with vegetables and legumes to cure diabetes, but no refined food, meat, or milk which showed substantial improvement including much less loss of protein from the kidneys. There also has been a study which showed a strong negative correlation for arthritis with a usual diet versus with cooked vegetables in Greece [Linos]. A similar diet, the so called mediterranean diet, showed marked improvement in Sweden [Skoldstam] and in Finland [Hanninen]. In addition, there is a suspicion that some unessential compounds in vegetables can have desirable affects such as the significantly much lower cancer rate in people who eat garlic.
It is desirable to have variety in the vegetables since almost every plant has a different mild poison or another and variety prevents difficulty from any one of them. For instance parsnip root and diseased celery have a phototoxic poison [Ivie]. Each plant family is usually different from the others. Therefore, it is important to vary your menu. If you concentrate on one particular plant, you may find yourself in the embarrassing position of the man who turned orange from eating too many tomatoes and carrots, or have a vital food element tied up in the digestive tract as the oxalic acid in spinach and rhubarb is alleged to do to calcium, or much worse to be badly sickened by alkaloids as the poor people in India are sometimes when they eat only a local wild pea during a famine. Most of these toxic substances are only mildly toxic and present in small amounts in cultivated plants so variety should solve the problem satisfactorily for edible plants for most people. You can see which foods belong to which families in order to rotate and maximize the advantage at; http://www.mall-net.com/mcs/rotate.html . One way to achieve variety is to find recipes for good tasting mixtures of food. You may see a link to a trail mix recipe in this site.
There are no toxic meats in commerce, so that variety in meat is probably not essential to take care of the above circumstance about poisons. It has been proposed that red meat is unhealthy, but this is an invalid myth, and people with adequate kidneys can eat large amounts of meat safely. Liver is an exception. Eating only liver can produce vitamin A and vitamin D toxicity. Another exception is fish. Fish contain unacceptable amounts of mercury (see this site for mercury analyses) and tropical fish contain ciguatera toxin. This ciguatera is a poison of many carbon rings generated by algae, which toxin can not be degraded by heat and which is thought to bind to sodium cell wall pumps. It remains in the body for a long time. It gives symptoms similar to chronic fatigue syndrome You may see an extensive discussion of this toxin along with a proposal of a vitamin B-12 antidote hereand here. Mannitol has been proposed as a treatment [Karlin]. Since fish migrate and in addition are transported all over the world, eating oceanic fish (especially large reef fish) or pigs or chickens (it is said that chickens receive only 2% fishmeal) fed such fish may not be worth (Tyson Inc. claims no use of fish) the risk even for healthy people. I suspect that cod-liver oil is safe since it is a northern fish.. A recurrence of neurological symptoms may be brought on by consumption of alcohol (probably not the alcohol itself, but poisons associated with it) or certain foods such as other fish, fish-flavored food products, meat such as chicken and pork , and peanut butter or nut oils. An address of a lab which analyzes this toxin is here.The cost of an analysis is $100. It is said that the amino acid cysteine and phytic acid in bran act as chelators (removal agent) of heavy metal.
It is also said to be important to receive at least a small amount of meat or dairy products at every meal since these are quality proteins. Many nutritionists believe that you should eat more than the 50 grams of protein in a 2000 Calorie diet, which the US government recommends, as much as double that amount or more. [from a dead URL]. I can not help with advice on this for sure, but I suspect the governments recommendation is a minimum. Much of the usefulness of quality protein (protein high in lysine and methionine amino acids) is said to be lost if it is eaten even as little as two hours after the main meal [I have lost the reference]. Lysine can have some additional importance because arginine amino acid accentuates the symptoms of an attack of the herpes type of virus [McCune]. Thus an attack of shingles, which disease is a resurgence of chicken pox virus from the pain nerves near the spine where they have been dormant, will be accentuated and perhaps even triggered by foods high in arginine. These foods are said to include peanuts (peanuts are 50% higher than cashews, but which last are substantial nevertheless), other nuts and non grass seeds, and chocolate (see here for a table which gives lysine and arginine values by weight of food and lysine\arginine ratios). Lysine helps to mute the effects of the virus, significantly reducing the occurrence (when taken routinely during the disease), severity, and healing time of herpes simplex virus [Griffith]. You can recognize shingles by large patches of a painful rash which appears on one side of the body in people under emotional stress [Irwin], older people, or people whose immune system has been compromised. It is said that injections of adenosine monophosphate and interferon gamma will also help heal herpes infections [Nikkels].
Since whatever long lasting infection (70 to 80 % retrovirus signs [DeFreitas] ) or/and poison [Bell 1998][Racciati] or/and small adrenal glands [Scott & Dinan] or/and disruption of the brain-pituitary axis [Scott & Svec & Dinan] (but beyond any reasonable doubt not hypochondria or mass hysteria from reading newspapers) is causing chronic fatigue syndrome (CFS, postinfectious neuromyasthenia, chronic virus infection, myalgic encephalomyelitis, chronic fatigue immune dysfunction syndrome, CFIDS, fibromyalgia, FM, ME, PVFS) seems to make people more susceptible to herpes virus with 77% of CFS patients containing antibodies to HHV-6 EA as IgM and IgG [Patnaik] it may be prudent for these CFS people also to eat sparingly of high arginine foods continuously after CFS or maybe until tests determine that the immune peptide hormones [Patarca] are all normal again. For a more elaborate discussion of chronic fatigue syndrome, see chapter XIV.
Potassium has a wider margin of error in timing when eaten than the above two amino acids may have, but you should avoid any deficiency or starvation which lasts more than 2 or 3 days if at all possible when you are replete in order to remain in top notch shape, and you should make a considerable effort to avoid any deficiency in food at all when you have a deficiency in potassium or have arthritis. There is an excellent article on practical ways to get more potassium from food. It is possible that eating smaller amounts at five or more meals each day would enable you to retain a larger fraction of the total potassium since surges would be avoided. There seem to be advantages with weight control and other problems from such a procedure.
Of course, even when you are receiving a "balanced diet" (as defined by the food pyramid), you should still give some reasonable attention to each of the other essential nutrients. Magnesium is directly related since the body can not absorb potassium easily during a magnesium deficiency. Magnesium supplements can take up to six months to normalize the magnesium, potassium, and sodium pumps. It may not happen at all if vitamin D is deficient since the kidneys depend on vitamin D to reabsorb magnesium [Ritchie]. Krispin Sullivan, clinical dietitian, has written an excellent article on magnesium deficiency. Agar seaweed is a very rich source of magnesium since a hundred grams dry weight contains 770 milligrams. It is also very rich in copper. It does not pay to go overboard on anything and it is possible that huge amounts of it could cause iodide toxicity, although I have no evidence. Magnesium appears to be especially important when suffering from chronic fatigue syndrome, fibromyalgia, or some asthmas. Also see a proposal to increase magnesium in drinking water for heart disease, asthma, migraine headaches, etc. Magnesium activates some of the dozen or so electrolyte pumps, is said to inhibit the potassium chloride cotransport pump, blocks some pumps, and is said to increase the potassium pore permeability [Bara]. To imagine that the housewife (or house husband if he prepares the food) can get on top of all that in addition to bizarre large additions of nutrients such as chloride and phosphate placed there by the criminally incompetent junk food processors on her way out to the food store and adjust the food destruction with pills is dream like. The top researchers and dietitians of the world can not. So her only real chance is to acquire a wide array of unprocessed food and hope her family has no serious genetic defects. Medications are not a satisfactory substitute for food, indeed are usually harmful. The following is a statement in a long term research into effect of arthritis medicines; "It was in 1988 that Pincus suggested that short-term studies may give rise to false expectations, and that radiological and laboratory values are overemphasized at the expense of long-term outcomes of functional status and death," Dr. Gibson and colleagues comment. "Perhaps our study serves to reinforce this message." [Gibson]
Extra copper may be necessary when recovering from arthritis. It is reasonable to suspect that healing would be more effective if all the other nourishment is adequate. Arthritics are deficient in pyridoxine, zinc, and magnesium versus the recommended daily allowance and copper and folate versus the typical American diet [Kremer 1997] (which itself is not sensational). They also have inadequate calcium, vitamin E and selenium [Stone]. You should pay particular attention to vitamin A on a series of bright sunny days, vitamin B-1 if you eat foods made with sulfur dioxide (which destroys B-1 in the intestines [Fitzhugh][Amerine p487] ) such as wine, vinegar, and some dried fruit and a vitamin B-1 deficiency is especially dangerous to the heart and kidneys when potassium is becomes replete [Folis], vitamin C if you have been cooking most of your food or have been eating stale food or have a viral infection, possibly vitamin E to protect the heart, maybe linoleic (omega 6) and linolenic (omega-3 fatty) acid if you have been eating hydrogenated foods, (which is definitely not recommended). The ratio of omega 6 to omega 3 oils should be one, but modern diets are much higher [Simopoulos]. Fish oils are high in omega 3, which is said to mute arthritis symptoms. However it is probably not a good idea to add excessive amounts of these oils to your diet because they have been associated with breast cancer and omega 6 could possibly inhibit the immune system [Grimm 2002], although white cell (T and B cells) functions are apparently not affected [Kelley]. so perhaps neither one should be supplemented to excess. You may see a graph showing ratios of these essential oils in some foods here. A compound related to omega 3 and omega 6 oils is cetyl meristoleate and is said to improve arthritis [Kremer 2000] but I know of no supportive theory other than that prostaglandin hormones may be increased and dampen immunity in some way. You may see a site which rates its effectiveness here. ). You should give some thought to calcium if you have been subject to cramps, spasms (spasms are more likely on a high potassium intake in the absence of calcium), probably tuberculosis [Wilkinson], or tooth decay. Vitamin D is necessary in conjunction with the calcium and is probably important for magnesium absorption also. Equally important is to keep the teeth sound with adequate intakes of calcium, phosphate, and vitamin D. The last is especially important for people who must be inside away from sunlight. Vieth argues that the 200 international units (IU) RDR is too low. He maintains that 200 IU merely prevents osteoporosis after a fashion. He recommends 800 to 1,000 IU total per day. Apparently he claims that epidemiological studies and circumstantial evidence show lower rates of multiple sclerosis, hypertension, osteoarthritis, and colorectal, prostate, breast, and ovarian cancer from increased vitamin D. Since naked Africans receive 10,000 IU, he suggests that concerns of toxicity are inappropriate [Vieth].. However, It has been proposed that vitamin D accentuates the symptoms of sarcoidosis (thought to be a bacterial infection), and supplements or sunlight probably should not be used then. For complete safety iodide must be supplemented in the absence of seafood and table salt. Vitamin B-6 (pyridoxine) deficiency has been found to increase tumor necrosis factor (TNF) in arthritis [Roubenoff]. TNF stimulates parts of the immune system which have to do with inflammation, among other things. There is a suspicion that vitamin B-6 can permit reabsorption of rheumatoid nodules [McCarty]. Vitamins B-6, B-1, and B-12 were found by Vetter et al to lower pain somewhat more when combined with a painkiller [Vetter].
Fruits are not a good source of nourishment. They generally contribute little besides vitamin C and potassium as you can verify by looking at the USDA Handbook #8 from the US Govt. Printing Office, and are not even sensational in these as a rule. The plants which have formed the fruits have endowed them with lovely attractive color pigments, seductive aromas, and titillating flavors. These attractants are a snare and a delusion designed to persuade animals to eat them and then scatter the bitter, hard, even poisonous seeds far and wide. They tend to be high in sugars such as fructose and sucrose, which are attractive to our sweet tooth but which interfere with copper absorption. When it comes to anything with nutritional value, the plant puts as little in as possible and still form the fruit since vitamins and minerals are tasteless. The only exceptions are vitamin C and potassium with which they are moderately endowed (although acerola berries, jujube dates {Chinese dates}, tropical guava, and kiwi fruit are outstandingly high in C). See this site for a discussion of fruit. The usefulness that I see for fruit is as a clever technique for making less palatable food more attractive, such as raisins for bran or carrots, apples for salad, or juice for oatmeal for instance.
A wide spread fallacy is that bananas are a rich source of potassium. As you can clearly see from the table, they are only a moderate source, about the same as potatoes. I have a feeling this is a classic case of the success plants have had in fooling the primates or possibly also the success of advertising campaigns. Today there are monolithic stands of banana trees as far as the eye can see probably because of banana oils (but no doubt with considerable assistance from fruit company ads). Even so, bananas are a 3 or 4 times better source of calories than most whole grain, for arthritics at least.
Somewhere I have seen a hypothesis that plants containing pectins such as apples cause a favorable intestinal flora to grow and so may be worth eating for that reason. Also an experiment has disclosed that copper is absorbed enough more efficiently if apples are eaten with the meal to cause a considerable net increase of copper absorbed, much more than enough to compensate for the apple's lower copper content [Sable-Amplis]. This could be the reason that apples seem to lower cholesterol. I have heard that cherries have a favorable affect on arthritis [Blau]. It could be that they have a poison which retards potassium excretion or that they have an acid which is absorbed but which can not be metabolized. If interference with potassium is the mechanism, it is likely that increasing potassium would be a superior strategy than use of cherries. A recent study gives kiwi fruit a high nutritional rating, including magnesium and potassium. However, in any case, I will stay with my contention that fruits in general are of marginal value until someone comes up with crisp evidence to the contrary. We tend to put considerable weight on instincts and emotional feelings of pleasure when evaluating food, so that fruit will continue to be eaten in large amounts regardless of what I say, and people in good health should be able to do so with little problem. However you should be aware of fruit's true nutritional content. In fact you should be aware of the true nutritional value of all the food which you eat, almost as much aware as you are aware of the quality of oil that you put in your car.
If every one had an average intake of potassium equal to his fair share of the as grown potassium, they would receive about 3,500 milligrams per day [Economic Research Service]. After processing losses and uneaten food is subtracted from the total [Adelson], my best guess is that the average daily intake is about 2,000 milligrams per day. Keep in mind that half the people are eating less than the average. Old people have an intake less than the average [Dall & Gardner]. [Dall, et al], which is no doubt at least partly due to a lower caloric intake. Black people in Georgia average 1,500 milligrams per day, while their white neighbors average 2,000 milligrams [Grim 1970,1980]. I say the above is an unacceptably high loss. Anyone taking a pay cut like that would be very, very unhappy.
Low potassium intake is also somewhat implicated in high blood pressure, stroke,[Khaw] and kidney stones. Potassium has been endorsed for use against stroke and high blood pressure by the FDA, although potassium ingested as the chloride can actually raise blood pressure (hypertension).
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 You may see elaborate discussions of magnesium with regard to potassium, diabetes, high blood pressure, headaches, and fibromyalgia. At; http://magnesiumresearchlab.salu.net/ The “magnesium and potassium in lone atrial fibrillation” link is especially informative. REFERENCES for CHAPTER VIII in; http://members.tripod.com/~charles_W/arthritis9.html
Chapter IX ---
Since cell potassium is always low in rheumatoid arthritis, it is important to know how to avoid losses during processing. This chapter discussion shows how.
For millions of years humans have been omnivorous, that is they ate both plants and animals for food. Such a diet gives plenty of potassium from the plants, and sodium chloride, and iodide from the animals. For land animals remote from the sea, getting enough chloride is probably usually the single most serious nutritional problem, with sodium and iodide close behind. There is little significant binding action in the soil for iodide and chloride, and rather little for sodium in mature tropical soils. Plants do not concentrate these elements. As a result, almost the whole pool of sodium, chloride, and iodide is probably in the fluid of higher animals in many areas. This poses a fairly serious problem for animals which eat only plants. Some species will undergo great exertion to reach a salt lick if one is available. Their hormone system is geared to drastic conservation of these elements. Animals’ attraction to salt is probably centered around detection of the chloride ion, the only essential nutrient which can be tasted, by humans at least.
So far as we humans are concerned, we had the considerable advantage of an omnivorous diet. It was probably largely adequate in spite of considerable reliance on fruits, partly because of a slow growth rate. At least it was until recently. Within the last few thousand years and especially the last few hundred years, a series of agricultural practices, food processing procedures and industries have evolved which have altered our nutritional status dramatically. While some of these alterations have given us considerable advantages in stabilizing variations in our food supply, destroyed some potent poisons, and others have rid us of some terrible food borne diseases such as trichinosis, nutritionally they are almost all destructive to one or more nutritional molecules. Some are so destructive that they leave no essential value in the food at all.
Almost every nutrient is affected by one process or another. Potassium is often severely affected, and is lost in most of the processes. I will largely confine the discussion to the affect that these processing losses have on potassium and sodium. It must be realized though, that even when your potassium intake is adequate, processed foods should never be selected over unprocessed foods when you have a choice, for every nutrient is affected. I will discuss the processes more or less in the order in which they came into use historically.
Cheeses
Making cheese amongst those races of men who herd cattle or goats must go far back in time. It was and still is a rather good way to preserve milk for use on the trail, or for storage when the milk flow is too great for consumption. In the course of making cheese, the whey, which has a disproportionate share of the potassium, is discarded to feed animals at present. The only cheeses which retain the same potassium as whole milk are the yogurts and buttermilk. Cottage cheese is in an intermediate position with moderate losses. Milk is less costly than cheese per unit of protein, tastes good, and with modern refrigeration is fairly easy to store. It can be easily curdled with enzymes. There is little reason for eating cheese, then, in North America, and I do not recommend it for most people. I am not familiar with the affect on lactose of making cheese. If cheese is more digestible to people who can not tolerate lactose, this recommendation may have to be modified for them.
Refined Flour
Grain has been milled for a long time. It is possible that even cave men pounded seeds on rocks. As long as mortar and pestle was used. the so called "stone ground" technique, it was virtually impossible to lose any nutrients out of the flour by milling. However as time went by clever ways were developed to separate the bran and germ from the rest of the grain. Most of the nourishment is in these two parts. At first this was fairly laborious, and only the rich could afford the fine white flour that resulted, and was held in high esteem as luxurious. The poor envied the noble people who ate this food, but Marie Antoinette's advice to eat cake notwithstanding, they could not afford to do so. As cheap power came to be harnessed to the milling procedure, white flour came to be increasingly available to those who envied it, as a prestige symbol. Since they depended on grains for a considerable part of their food supply, millions of people lost their lives to the "wet" heart disease of beriberi and other B vitamin diseases. At the same time as the vitamins which prevented these diseases were lost, potassium was cut 75% in flour to a 25% remainder. They were probably protected to some extent from the "wet" heart disease of beriberi by the potassium loss. However vitamin B-1 is now added to most white grains so this protection, if it obtains, no longer is pertinent. I suspect that most of the heart disease currently is probably influenced by this potassium. Since these losses are the cases, white flour is completely off the list of foods, which should be eaten by anybody, but especially by arthritics. This obtains even if the flour has been fortified. Grains and nuts in general should be used sparingly by arthritics until they fully recover.
Sugar
The use of honey as a sweetening agent goes far back in history. It is not surprising that the bees supply a food low in potassium for the winter since they have no urinary system, and not only do not need it as mammals do, but probably would be hurt by too much. Honey did not, as a rule, make up a large part of people's diet because of the difficulty of obtaining it.
Starting in Roman times, sugar cane became available, and began to spread around the world. It reached Spain in the eighth century, the rest of Europe in the thirteenth, and was carried to America by Columbus [Abrams]. More and more efficient ships transported it to the far corners of the world. At the present time, not only does it make up a large part of the diet of the affluent people of the world, but it is usually in the form which has been recrystalized for purification so many times that it has no essential nutrients of any kind left. Its potassium loss is total. This "food" should never be eaten at all by anyone. If sweetening food is a psychological must for you, then at least use Barbados molasses or fruits. Molasses that has been extracted several times is especially high in potassium. It is called "black strap" molasses. It has moderate amounts of some other vitamins and minerals also.
Fats and Oils
Fats and oils contain little water and therefore little potassium. At the same time they are very high in calories. Therefore when this part of the food is extracted, and the remainder fed to the animals, the animals may benefit (if they get enough essential oil elsewhere) but people do not. In addition, Hunter believes that those oils which are extracted by solvents always contain traces of the solvents used [Hunter] Since these solvents are usually chlorinated molecules, a residual of poison is left behind.
Animal fats are even worse because they have very little of the oil soluble essential vitamins in them in addition to being low in potassium (except butter which at least has vitamin A). One of the frustrating circumstances is that their increase in our diet is even codified into law. Meats, for instance, are by federal statutes not to be defined as high quality unless they have flecks of fat. People should be free to eat as much fat as they wish, but to put a federal stamp of approval on such a senseless custom has got to be almost in same class as insisting that only high quality heroin be sold. The rigid codification around milk is just as bad. A simple labeling requirement for dairy products and meat is all that should be required.
Hydrogenated oils are almost in the same class as animal fat since the linoleic and linolenic acid vitamins (the omega oils) are destroyed. I suspect that this is contributing to swollen prostrate tissue at least. There should be enough oil in the vegetables eaten to take care of those two vitamins as well as vitamin E. If not, hydrogenation undoubtedly makes the matter worse by tending to wash the oil soluble vitamins out.
At any rate there is no law that says you must eat fats and oils, so they should be used by arthritics as sparingly as possible. Those that are used should be not hydrogenated and preferably not extracted by solvents, but mechanically pressed out.
Salt
Salt used to be a commodity of great value, comparable to gold. Wars were fought over its trade [Kaunitz]. Towns in England and Germany ending in "wich" and "Halle" where salt was traded bear mute witness to this ancient trade. When efficient mining techniques made salt inexpensive, it became practical to use salt to preserve food by raising the osmotic pressure of the fluid that the food was carried in or the food itself. Fish, meat, cucumbers and other vegetables were preserved this way. These foods became so popular because of our attraction to the chloride ion, that even in summer time when preserved foods were unnecessary, they became part of many meals and picnics.
This means of preserving has two major drawbacks in regard to potassium. First, the sodium displaces potassium in the food cells, and the potassium is discarded with the liquor in those cases where the food is immersed or loses liquid. A glance at the food tables where salt treated frozen or canned goods are shown will confirm this. This can cause fairly considerable loss of potassium.
The second problem is that an increase in sodium above its optimum intake causes a greater excretion of potassium as was discussed in Chapter VII, "NUTRITIONAL REQUIREMENTS". It is a significant increase and fairly well documented [Koch]. Of course too little sodium causes a much greater potassium loss than too much [Peterson]. I suspect that the adverse affect on health from sodium (or chloride?) is not so much from reduced cell potassium as it is from the hormone imbalance that one or both create in hormones. Ultimately each mineral must be independent of the others and attaining this independence for odd intakes may be damaging over a long time. Hypertension and heart disease are what seem to be primarily involved. So far as I know no one has defined every detail of this [Kolata]. There are at least two hypertension syndromes and potassium plays a central role in at least one half the cases [Meneely 1958]. Hypertension can often be reversed by sodium restriction alone. However hypertension from sodium chloride can also be irreversible [Meneely & Battarbee 1976]. Keep in mind that when sodium is restricted, chloride is also, and chloride is said to account for 80% of the hypertension of salt [Whitescarver].
It is my opinion that the body is organized around a drastic sodium retention, and that the sodium in meat is adequate and may even be optimum for normal human needs [Oliver]. A total of about 1.5 grams of sodium per day (equivalent to about 3.8 grams of salt) should be close to the above amount. This amount of sodium has the same number of atoms as about 2.5 grams of potassium. It is an amount that should be easily obtained from the average unprocessed diet. It is considerably less than that which the average American receives [Grim 1970]. The above amount is a rough estimate and is not based on a precise estimate or survey of American intake.
It is possible that a little more may be desirable on hot days. Such supplementation is probably not usually critical, because apparently the bones store up to 45% of the body's sodium [Grim 1980].
Sodium acquired by mother's milk is instructive. It furnishes 0.2 milligrams per Calorie on the average. If an adult were to receive his sodium from this source, he would then receive about 0.5 grams of sodium per day. It may be that the sodium evolved low in mother’s milk partly as a compromise to protect the mother, and partly to prepare the child for a life on the African Savannah. Until the optimum amount is determined for sure, it might be better to organize one's thinking and strategy around a moderate amount, rather than use salt and processed food.
There are two procedures which have come into vogue largely within the last century or so. These are the canning and freezing of food. Freezing of vegetables would be especially valuable if it were done correctly. The way it is actually done is to boil the vegetables to kill the enzymes, called blanching, and then moving the vegetables around the plant in water filled troughs or flumes to the subsequent processing and packaging steps. By the time they arrive at a store, they have lost anywhere from 20 to 50% of their potassium and some much more if the liquid is drained off [Bills], and other water-soluble vitamins are similarly affected. My best guess as to an average loss would be one third. Since these are our richest source of potassium, these losses are serious. It may be a considerable part of the degenerative diseases which have arisen in our society in recent years [Snively][USDA]. There is no way for the shopper to know which if any vegetables are unaffected, so that it is important that arthritics use as few vegetables as possible from this source. It might be possible to make a crude estimation after the purchase by how washed out the taste is, but it is dubious.
It may be that vegetables cooked right in the package will prove to be an exception. Also foods which have high migrations of sugar out while immersed may have minimum reductions. Brussels sprouts may be an example as can be noted from the table.
The safest habit to get into until processors start listing procedures and losses on the label is to use only vegetables straight out of the fields. It makes eating a little more difficult in the winter, but not especially so for vegetables are trucked up from the south all winter, and their cost per nutritive value is comparable to preserved food. REFERENCES for CHAPTER IX in; http://members.tripod.com/~charles_W/arthritis10.html
Chapter X
At least one of the industrial processes is possible in the kitchen, and is a characteristic way of cooking vegetables in America. Whichever vegetables are boiled suffer losses equivalent to processing losses if fresh, or often suffer further losses if they have already been processed. Unless salt is present in the boil water or canning liquids, there is a limit to how much potassium can be lost. This is probably because large negatively charged molecules can not diffuse out of the heat damaged cell wall, and the charges inside the cell must remain balanced. This limit appears to be over 50% for most vegetables. The losses tend to be greater with larger amounts of water and longer boiling times, but apparently not always. The losses are unnecessary. There are numerous ways of cooking vegetables so that there are no losses at all, and several where the losses are small.
Baked or broiled vegetables retain everything except a fairly large loss of vitamin C and lesser losses of some of the B vitamins [Pearson][Krehl]. Usually only potatoes and stuffed peppers are baked, but in theory all foods could be baked or microwaved. One way to cook food which would lose so much moisture if baked so that they would not taste good, would be to place them in a casserole or closed pot along with a small amount of water. Meat which is broiled sometimes actually increases in potassium content if fats are rendered out of them. Pumpkins and squash can be baked right in the shell if they are punctured to avoid exploding. It is easy to make pudding after baking them. If a young pumpkin or squash is used it is possible to eat it seeds and all. I have no analysis of the seeds.
In order to gain the greater speed that using the top of the stove implies you could fry the vegetables. This is already often done with onions, potatoes, mushrooms, eggplant, peppers, squash, and tomatoes. Many vegetables which are difficult to fry can be fried by placing them in the pan with vegetables which are easy to fry. Oil is often used to prevent sticking to the pan. A small amount of oil for frying is much preferable to boiling and discarding the boil water. It is even conceivable that a small amount of unhydrogenated vegetable oil may be a nutritional plus. If a Teflon coated pan is used with careful control of heat, no oil at all needs to be used.
Actually it is not the boiling itself which is bad, but the subsequent discard of the water, If the cook were to retain the water as when making soup or for use when boiling future vegetables the situation is solved, for if they are not allowed to boil dry, there are no losses at all. The boil water can also be used as a beverage. It is especially tasty when derived from mixed vegetables (to my taste buds). This would be a way of augmenting your potassium intake if your family would be willing to grant you more than your fair share of the liquid when pulling out of a deficiency.
If small amounts of water are used in closed pots, known as steaming, the losses should be minimized. I have no analysis available for this procedure, but my knowledge of the physical chemistry involved makes me suspect that the losses are small. If the liquid at the bottom of the pot is used, there are no losses at all. Pressure cooking is a form of steam cooking. It is much faster and less likely to run dry. I do not have information of its affect on heat sensitive vitamins.
Microwaving should lose no potassium but I have no analysis.
Gravies and drippings consisting of watery material are usually rich in potassium. You should always make an effort to sop up, spoon up, or drink up the watery liquids on the bottom of your plate or in the pan while attempting to leave the fats behind. If it is impossible to separate them, it is often possible to skim the solid off the top after a sojourn in the refrigerator. Decanting fat off of a tall glass is another possibility.
Table Scraps
Another loss, although not strictly a processing loss, is the tendency to leave food on the plate when not very hungry. The foods which are most likely to be left by most people are precisely those foods which are highest in potassium, the vegetables [Young][Adelson]. One way to avoid this type of loss would be to eat the most nourishing food first. So far as cooking is concerned, the cook should make a considerable effort to make the vegetables appetizing. Like Popeye the sailor, concentrate on the vegetables. There are numerous combinations with milk, meat, spices, fruits, and other popular foods which can make vegetables anywhere from palatable to irresistible. Just combining several miscellaneous vegetables can be a considerable improvement.
The following table lists some food combinations which I have found to be better tasting than either alone, or at least better than the first on the list. Some of those on the left side of the list are almost intolerable alone.
asparagus-------------------milk
If every one had an average intake of potassium equal to his fair share of the as grown potassium, they would receive about 3,500 milligrams per day [Economic Research Service]. After processing losses and uneaten food is subtracted from the total [Adelson], my best guess is that the average daily intake is about 2,000 milligrams per day. Keep in mind that half the people are eating less than the average. Old people have an intake less than the average [Dall & Gardner].[Dall, et al]. Black people in Georgia average 1,500 milligrams per day, while their white neighbors average 2,000 milligrams [Grim]. I say the above is an unacceptably high loss. Anyone taking a pay cut like that would be very, very unhappy.
You hardly have to wait for the best estimate of an ideal intake. The human race has been living with virtually these same foods for millions of years. We must be adapted to the concentrations in food as grown by this time. So the as grown amount should be a minimum to aim for, and I therefore propose it as a recommended daily requirement or RDR (or RDA), that is, required for optimum health as opposed to minimum daily requirement or MDR, a requirement for bare survival by young healthy adults under no stress. South American Indians receive about seven thousand milligrams per day.
Poisons
You should bear in mind that almost all plant products have mildly toxic materials in them. Each plant family is usually different from the others. Therefore, it is important to vary your menu. If you concentrate on one particular plant, you may find yourself in the embarrassing position of the man who turned orange from eating too many tomatoes and carrots, or have a vital food element tied up in the digestive tract as the oxalic acid in spinach and rhubarb is alleged to do to calcium, or much worse to be badly sickened by alkaloids as the poor people in India are sometimes when they eat only a local wild pea during a famine. These toxic substances are only mildly toxic and present in small amounts in cultivated plants so variety should solve the problem satisfactorily for edible plants. You can
see which foods belong to which families in order to rotate and maximize the advantage at; http://www.mall-net.com/mcs/rotate.html
There are no toxic meats in commerce, so that variety in meat is probably not essential to take care of the above circumstance. Liver is an exception. Eating only liver can produce vitamin A and vitamin D toxicity. It is important that seafood seaweed be eaten from time to time if you discontinue eating iodized salt or receive no iodide in some kind of supplement. Some seafood has fairly high concentrations of cadmium, mercury, and other poisonous atoms.
Most fruits and grains are probably largely devoid of poisons or disadvantageous substances. The custom of many cultures to concentrate on one grain, such as wheat, for instance, is probably not harmful from the circumstance of poison although wheat has a substance that interferes with copper. This lack of poisons is probably the usual case for unstored grain in developed countries. In undeveloped countries,
aflatoxins on moldy seeds have been shown to cause liver cancer in animals.
One exception to variety being sufficiently protective for a few people may be the solenaceous food of the nightshade family, tomatoes, potatoes, peppers, and eggplants as was discussed in chapter II, HISTORY of ARTHRITIS RESEARCH. It may prove to be a good idea to delete these vegetables until clear of arthritis symptoms until there is good evidence to the contrary. If they are eaten, be sure to eat only red, ripe, vine ripened tomatoes and baked unsprouted potatoes. It has been demonstrated that baking destroys at least some of the poisons. If green potatoes are eaten raw it is possible to be poisoned badly enough to die.
In summary I suggest that you take Hunter's advice and select your food only from the outside edges of the supermarkets where the unprocessed vegetables, meats and dairy products are displayed [Hunter BT in an address] until such time as the processed food industry gets its act together and stops destroying nutritional value and putting poisons in the food and lose nothing yourself by boiling it.
If for some reason beyond your control it is impossible to receive adequate nourishment from the food which you are able to obtain it will be necessary to use the supplementation route. The next chapter, chapter XI, SUPPLEMENTS, will show you how to do this with reasonable safety for potassium. REFERENCES for CHAPTER X in; http://members.tripod.com/~charles_W/arthritis10b.html
Chapter XI --- This is a discussion of when and how to take potassium supplements, especially for diarrhea and heart disease.
Potassium is the most dangerous of the essential nutrients. While mild chronic overdoses are probably not damaging, because of the efficiency of the kidneys in clearing excesses, a very large acute overdose can be extremely dangerous if not cleared in time. As little as 8 to 10 thousand milligrams of potassium taken suddenly can give nausea. A teaspoonful of potassium salt contains about 3300 milligrams of potassium. As little as 14000 milligrams of potassium can cause death in some replete people, especially those who normally have a low intake at other times. Therefore, one may not use supplements without regard to any caution. However the reason I do not recommend supplements because normally it is quite possible to receive all the potassium you need from food, and this source is inherently safe, inexpensive, and with reasonable wisdom, balanced with respect to other nutrients. My recommendation against supplements is based primarily on concern of an imbalance with other nutrients rather than any likely chance of an acute overdose. The status of magnesium is especially important because potassium can not be absorbed efficiently if magnesium is deficient [Petersen][MacIntyre][Manitius]. The imbalance that I know of which is probably most dangerous is the imbalance with thiamin (vitamin B-1) if animal experiments are an indication. If potassium supplements are given during the wet heart disease of beriberi (thiamin deficiency) the heart disease is made much worse [Mineno][Gould]. Wet heart disease is impossible if potassium is also deficient [Follis]. Instead a muscular atrophy similar to that from vitamin E deficiency appears [Hove][Blahd]. During a vitamin B-1 deficiency the heart loses potassium [Mineno]. This may be why heart damage in beriberi resembles that in a potassium deficiency. Hove and Herndon suspect that muscular dystrophy is a potassium deficiency since body potassium is low during muscular dystrophy [Hove]. Why the heart should be protected by a deficiency of both potassium and vitamin B-1 is strange, and I know no explanation for it. It could be the sulfur dioxide left in wine might be part of what statistically protects people from the more prevalent potassium deficient heart disease by destroying vitamin B-1 in the intestines. It is obvious that if potassium supplements are given, it is very important that the vitamin B-! intake must be adequate at the same time. The reverse is also the case. Vitamin B-1 supplements should be dangerous for people with rheumatoid arthritis. This may be the reason why people with rheumatoid arthritis (but not osteoarthritis) have a much higher heart disease rate than others. This information should be especially pertinent for those who drink much alcoholic beverages or vinegar fermented with sulfur dioxide with their meals or fruit dried with sulfur dioxide since this destroys vitamin B-1 in the intestines. Arthritics are deficient in pyridoxine, zinc, and magnesium versus the recommended daily allowance and copper and folate versus the typical American diet [Kremer] (which itself is not sensational). They also have inadequate calcium, vitamin E and selenium [Stone]. So it is quite possible that other imbalances besides the one above are possible. The recent discovery that something in vegetables, especially onions, prevents bones from losing density [Muhlbauer & Li] is just one more hint that we can not use supplements instead of food with complete assurance that there is no other advantage from good food. I am also concerned about liability were I to recommend supplements and someone were to have real or imagined difficulties. However there are a few times when supplements would be desirable, sometimes even life saving. Severe diarrhea is one such a time. Cholera is an especially lethal diarrhea and oral rehydration therapy (ORT salts) is in order. It has been suggested that supplementation with potassium would be in order for cirrhosis of the liver also [Conn]. Potassium bicarbonate has been used to correct the acidic serum associated with diabetes [Soler]. It has been found to increase the density of bone [Sebastian]. Severe emotional stress and stress of surgery might be two other occasions when supplementation would be in order.
Rarely acute hypokalemic paralysis afflicts people and can be life threatening. The symptoms are weakness, low plasma potassium, progressing to paralysis. Most cases are due to familial hypokalemic paralysis; however, a few cases are associated with diverse underlying causes including thyrotoxic periodic paralysis from hyper active thyroid, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. Immediate potassium replacement is in order coupled with an aggressive search for the underlying cause [Stedwell]. Also see this site for treatment.
SODIUM FREE TABLE SALT Sodium free table salt is the means usually used for supplementation of heart disease patients. The original justification for this was to provide for the psychic dependence on a salty taste without providing sodium. So medical men said in effect, since people will satisfy their craving for salty flavor whether we warn them against it or not, we will give them the salty flavor without the sodium. Since the chloride provides the salty taste this was easy. Just substitute another positively charged atom for sodium. This philosophy carried to its logical conclusion led them even to use lithium as a substitute atom. It was then that lithium's pronounced properties as a tranquilizer became evident [Maletzky].
Potassium was considered inert, or largely so. In addition to potassium, ammonium and choline molecules were also used. These molecules may not be useless. Choline is a biologically active material similar to vitamins but made by the body. Its long-term effects as a supplement are unknown to me. Ammonium, at least, may interfere with potassium excretion if it is absorbed in the intestines and has been used to protect the kidneys [Selye 1945]. So far as I know the substitutes above are reasonably harmless for healthy people who have normal blood pressure. . Ammonium is even synthesized by the kidneys during a potassium deficiency from glutamine, and this is probably a strategy, the purpose of which, is to prevent potassium loss. Sulfate is an excretory product, so the sulfate as the anion with potassium should be, at the least, useless. I suspect that potassium as the sulfate should have the same effect on high blood pressure as the chloride, but I know of no evidence. Adding potassium sulfate to a processed food diet should have the same effect as adding sulfuric acid to a normal diet, whatever that is. GLUCOSAMINE This synthesis of ammonia just mentioned may be part of the reason that glucosamine has shown evidence of being useful for arthritics, especially osteoarthritis, since this is a combination of glutamine and glucose. The rationale usually given is that this provides a molecule which is incorporated in connecting tissue. Glucosamine is a combination of glucose sugar and glutamic amino acid. Glutamic acid breaks down forming ammonium ion in the body, so I suspect that it is getting part of its beneficial results by virtue of providing ammonium ion in the kidneys, which interferes with potassium excretion. If so, glucosamine could be considered a potassium supplement of sorts, also. Glutamine or glutamic acid is a major transporter of nitrogen, transporting one third of nitrogen [Labow p1503]. Labow claims that the less than 10 grams per day usually eaten should be increased to 20 to 40 grams for those under stress and considerably increases survival of hospital patients and should in addition be part of intravenous feeding [labow p 1503,1510]. Conserving potassium may be part of its efficacy. It is apparently used to help excrete acid since glutaminase and glutamine consumption are both increased by acidosis [Labow p1504]. Glutaminedipeptide is more soluble and has a longer shelf life than glutamine [Labow p1509].
You can tell which materials are present in a product by the list of ingredients. The materials of highest concentration are supposed to be placed at the beginning of the list. Select the substitute, which has potassium nearest the beginning of the list in order to avoid the small chance of side effects of the other ingredients should you decide to use supplements unless the other supplement you are sure you need also. Ingredients of some clinical supplements are given in a book by Friedberg [Friedberg p348]. VEGETABLE LIQUORS Green coconut milk has been proposed as a potassium supplement for cholera patients [Carpenter]. I assume that celery or bamboo shoot juice would have a similar value. If used for diarrhea it is important that salt and perhaps bicarbonate of soda be eaten at the same time in amounts approximating ORT salts. Such a juice strategy would probably be not quite as effective as potassium chloride or ORT salts, but might be all that is available at times. TABLETS and LIQUIDS
There is a liquid supplement in which the bitter taste of potassium is masked by cherry extract. It is conceivable that a child could get a fatal overdose in this form. Non of the above concoctions are substantially more dangerous than other household items like aspirin, for instance. I would recommend against storing potassium in an easy to eat form, however. Liquids containing more than 390 milligrams of potassium must have a prescription in order to be sold in the USA. I believe 100 milligrams is the limit for tablets.
Enteric tablets are also available. These are tablets that will not dissolve until they reach the intestines. Since there are no pain nerves in the intestines as in the stomach, you are not distracted by the commotion that ensues when they suddenly create a saturated potassium chloride solution near the intestine wall, as you would be if they dissolved in the stomach which has pain nerves. Gastric release tablets give a bad stomachache on an empty stomach. There have been cases [Baker} reported of enteric tablets becoming caught in the fold of the intestines and causing ulcers, some even fatal, when the enteric coating dissolved. You can eat these tablets with safety so far as ulcers are concerned by chewing them while drinking a glass of juice. The bitter taste is largely eliminated also. Of course tablets are an expensive way to increase potassium.
A new enteric tablet has been developed which is prescribed by 99% of the doctors today. It is called "slo-release". It is designed to release its potassium slowly so that no portion of the digestive tract is overwhelmed with a concentrated solution. It is probably as reasonably safe as anything is in this dangerous world [Palva][Block]. The safest of all would be to also chew these tablets with juice. Sakoutakis, et al believe that slo release tablets are safe [Sakoutakis]. The American law prevents more than 100 milligrams of potassium in each one, so that seven or more must be taken with each meal to double the potassium intake of a junk food diet. There is also a liquid that contains tiny enteric particles containing potassium chloride. This is only available by prescription. It should be similar to Slo release enteric tablets and should be inherently safe against ulceration, but not overdose.
Potassium gluconate comes in a tablet that can be chewed with juice also. Since gluconate is metabolized in the body, this form should be similar in effect to potassium from plants or from the bicarbonate (bicarbonate to be discussed later with sodium free baking powder). Potassium has been prescribed as the aspartate usually with magnesium for heart disease. I do not know what the rationale for using the aspartate anion is. However both magnesium and potassium are absorbed more effectively as the chloride than as the aspartate [Classen]. However the magnesium is in order to power the ATPase [Hamil-Ruth] because potassium can not be absorbed effectively during a magnesium deficit [Kohvakka]. It takes six months for the sodium/potassium pumps to return toward normal after a magnesium deficiency is corrected [Anonymous]. JUICE
There is a safety advantage in keeping your taste in touch with potassium supplement. Potassium chloride dissolved in fruit juice gives it a fine, rich flavor in reasonable amounts. When too much is put in, the flavor becomes nauseating and bitter. Thus you have a built in safeguard. Another inherent safeguard is the presence of adequate water. Potassium supplementation is especially dangerous during dehydration, as was mentioned in Regulation of Electrolytes because of a drastic decline of aldosterone. The use of juice reduces danger during dehydration somewhat. Even so, supplements should not be taken until at least an hour after dehydration has been largely corrected to give aldosterone a chance to be resecreted. An additional advantage of juice in conjunction with potassium is that it can be more readily taken between meals. Potassium can be more readily absorbed then because it does not tend to form an overload combined with potassium in food. That also makes it less dangerous for people with weak hearts or kidneys. People with very weak kidneys should be under a doctor’s care and should not take potassium supplements. In addition, between meals probably provides minimum interference with other nutrient absorption, such as that of magnesium. For a similar reason it is probably advantageous to divide meals into more than three per day when recovering from a deficiency [Fabry]. SODIUM FREE BAKING POWDER
Sodium free baking powder is a supplement also, including those times when used for baking. It is potassium as the bicarbonate or tartrate. Dissolved in fruit juice, the bicarbonate gives it a delightful tang like soda pop soft drinks. The bicarbonate has been shown to be not as effective as the chloride in relieving a deficiency both as to reducing cell sodium content and raising plasma levels of potassium [Giebisch][DeLand]. However, potassium as the chloride has the same affect as potassium from unprocessed food coupled with hydrochloric acid supplements. There are times when this might be disadvantageous. High blood pressure may be one time , 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 because sodium chloride was already high in their diet. Both sodium and chloride is 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.
The phosphate is probably similar to the bicarbonate in regard to being absorbed. Phosphate is probably very dangerous for those with heart disease. Excess phosphate has caused 100 per cent mortality [Selye 1958]. I have taken potassium as the bicarbonate for several weeks when I was young without any obvious great difficulty. I did have the strong feeling during that time that I was more susceptible to muscle cramps. However this was probably a function of too little calcium or vitamin D at the same time since potassium as the bicarbonate should not be substantially different from potassium in food. If the bicarbonate should prove to be not, on balance, be a desirable route, then it follows that it may be desirable to go back to the use of yeast for leavening bread. The bicarbonate should be equivalent to potassium acquired from food, though. Sodium bicarbonate is very undesirable for leavening because it is basic. Potassium is extremely sensitive to hydrogen ion, and sodium bicarbonate can triple excretion, as discussed in Chapter IV. Even hyperventilating (breathing too hard) will have an equivalent effect. The effect of potassium tartrate in baking powder would probably depend on whether the tartrate is metabolized or not and this I do not know.
The bicarbonate may be indicated in renal tubular acidosis {Morgan]. It is also said to be desirable to have either part of the sodium as the bicarbonate in ORT salts during diarrhea and dehydration or an equivalent amount with the potassium. COMBINATION TABLE SALTS
For some time now the main table salt suppliers have placed on the market a table salt that contains both potassium and sodium. Two brands which I am familiar with are Morton's "LITE" salt and Sterling's "LO-SALT". There is also "HALF SALT" from Canadian Salt Co., a sister company to Morton Salt Co. If you must have the salty taste of the chloride these brands would be a fairly reasonable way to go. In the case of diarrhea they would, I suspect, be the best way next to the ORT salts mentioned above. In many areas of the undeveloped countries they may be the only way. They have not caught on much in the developed countries, I suppose because the diarrheas are not often fatal in the temperate regions. They are more intrinsically safe from an overdose than pure potassium salts. On balance, though, the possible long term effect of the sodium chloride on hypertension would be sufficiently disadvantageous to make their routine use undesirable except in moderate amounts for there is evidence from rat experiments that excess chloride can increase high blood pressure. . Also I have a suspicion based on personal experience that potassium chloride can accentuate pain from some other cause (but I have no proof). It may be eventually shown that the best way would be a salt that contains many essential minerals, including magnesium, calcium, potassium and trace elements and other anions, including bicarbonate, in addition to chloride. Currently I am aware of no supporting theory nor of anything in supermarkets or health food stores similar to this last, although Cardia contains magnesium and lysine. The above combination salts contain about one atom of potassium to two of sodium.
SEA SALT
Sea salt is not a source of potassium. Even if the salt is obtained by evaporating seawater to dryness, it will still only contain about 4% of potassium salts. Sea salt is really only a sodium table salt no matter how it is made. In addition it has the potential of retaining all the mercury and other poisons contained in seawater which could be a slight disadvantage. FERTILIZER
Potassium is sold for fertilizer under the designation "muriate of potash". I have no reason to suspect that it contains any bad poisons. Ultimately it came from the same original source as sea salt, but was the last to evaporate in ancient inland seas. It is without a doubt the least expensive source of potassium. I have used it both before and after decanting the sediments it contains for several weeks with no obvious bad effects. It may be a reasonable way to go for people too poor to acquire ORT salts if it were decanted. Decanting may be necessary because its red sediments may be high in iron, which is poisonous in large amounts. DE COTI MARSH’S SALTS
In 1957 De Coti Marsh of England wrote a book advocating various potassium salts as a treatment for arthritis. He proposed a veritable pot-pouri of negative ions to be associated with the potassium, some, like arsenate, actually poisonous. He was the first to definitively propose potassium as an arthritis remedy. His discussion used a chemical jargon which would have even embarrassed the alchemists and with strong overtones of mysticism. ATHLETIC DRINKS
There are several artificial drinks on the market catering to athletes who exercise in the hot weather. They are in effect, supplements. All but one of those known to me are really sodium chloride supplements. "Brake-Time" put out by Johnson and Johnson is a sodium supplement, but it also has small amounts of potassium, about equal to the potassium in blood fluids, in addition to vitamin C, phosphate, chloride, and a somewhat lower sugar content than the other athletic fluids. The reason given for lower sugar is to decrease the retention time in the stomach [from Johnson and Johnson brochures].
These drinks are designed to prevent four types of disorders that are associated with heat, as follows: 1. Heat cramps are caused by large sodium chloride losses in sweat. The symptoms are headache, dizziness, fatigue, nausea vomiting, muscle cramps and circulatory failure in late stages. It can occur from any sweating, even shoveling snow. Muscle cramps are thought to be possible even when cell potassium is low, and may even be more likely then.
You would think that the athletic drinks fill a real need, at least those containing reasonable amounts of potassium. For the general population they may. I address myself to healthy people who presumably are eating a diet that is moderate in sodium and at least adequate in potassium, and reasonably adequate in other nutrients. Such people should rarely be affected by the disorders above if they behave with reasonable common sense. Given that we are discussing such people, water or dilute fruit juice imbibed often in moderate increments should be sufficient and possibly preferable. Vegetable juice is really a food and would probably be inappropriate during strenuous exercise in the absence of a break in the activity.
Paradoxically, low sodium intake probably protects people from sodium losses on a hot day. I have no documentation, but I strongly suspect that the time it takes a one gram per day person is much shorter to become acclimatized than the week or so it is known to takes a four gram per day person. The time may be instantaneous or virtually so. I strongly suspect that the high sodium intake of our society is a fair part of the regulatory difficulties of the summer time. A well-fed normal person should be a tough, adaptable person well able to tolerate even unreasonable assaults of temperature and exertion.
In addition to dietary protection against environmental distress, it should be usually possible to solve some of these assaults by planning your activities, by wearing shorts to make use of the considerable heat dissipating area of the legs, using shaded areas, using wide, loose fitting hats, and most effective, dousing with water. Wet clothes would be preferable to damage to your body and brain, and perspiration would probably make you wet anyway. It is possible that moderate perspiration would be advantageous to people whose kidneys have reduced function provided adequate water is available.
Therefore I tentatively recommend against drinks high in sodium. It is conceivable that you could get an inadequate sodium intake if you were to happen to select only vegetables low in sodium or only garden vegetables in a low sodium area and at the same time ate no or small amounts of meat. Such a situation could conceivably introduce dangers. So watch what you eat and consider the possibility of salt supplements, but not necessarily athletic drinks. Salt is much more useful to enhance food flavor than as athletic drinks. . For an additional discussion of potassium supplements including many prescription trade names see; http://www.rxlist.com/cgi/generic/kclsr.htm REFERENCES for CHAPTER XI in; http://members.tripod.com/~charles_W/arthritis11.html
. Chapter XII ---
I recommend that you design your diet to receive large amounts of potassium, at least up to the as grown amounts in vegetables. As already mentioned, I believe that this strategy will tend to protect you against future excess potassium shock as well as short term losses. However, you should keep in mind that too much potassium can have some undesirable side effects. It is fairly well accepted that potassium can create a situation in which muscle spasms or cramps are more likely. While the relation is not established beyond any doubt, the statistical evidence is reasonably convincing . The spasms are actually from too low a calcium coupled with too high a potassium [Engel][Gunn][Elkington]. For triggering diseases, EKG changes, and treatment of high blood potassium see Recheigl [Recheigl]. In as much as calcium entry into the body is involved, it would seem logical to keep vitamin D adequate. Vitamin D is really a hormone which depends on ultra violet light in sunshine for synthesis. However, people who work indoors, or wear a lot of clothing, and almost everyone in winter time in frigid areas would have to treat it as if it were a vitamin. Since it is present only sporadically in foods, such people would have to supplement to get realistic amounts. Liver, sardines, and irradiated milk are the only food sources that I know of, and even milk is usually inadequate alone. Vitamin D is especially important for people who must be inside away from sunlight. Vieth argues that the 200 international units (IU) is too low. He maintains that 200 IU merely prevents osteoporosis after a fashion. He recommends 800 to 1,000 IU total per day. Apparently epidemiological studies and circumstantial evidence show lower rates of multiple scelerosis, hypertension, osteoarthritis, and colorectal, prostate, breast, and ovarian cancer. Since naked Africans receive 10,000 IU, he suggests that concerns of toxicity are inappropriate [Vieth].You can not expect any magical relief from vitamin D and calcium. Any affect on spasms would be exerted in a statistical way over several days or more. It would also seem prudent to reduce your potassium intake temporarily if the spasms were from this cause, and certainly discontinue supplements. Sodium chloride (salt) supplements might also be in order, and bicarbonate of soda may be an antidote of sorts. But do not rely solely on this discussion of nutrients, but seek other medical consultation if you are sick .
Symptoms of an acute toxicity are listlessness, mental confusion, numbness, tingling of limbs, a sense of weakness, a cold gray pallor, low blood pressure, and a slow heart beat [Darrow][Recheigl]. The EKG at 7 meq per liter gives prolonged conduction time, sharp and high T waves, and finally heart blocks at 10 meq per liter [American Medical Association p455]. One of the most likely triggering diseases in most peoples lives not on medication would be shock, including surgical shock (the time to bring potassium up to normal would be prior to the surgery), burns, and injury [Fox]. High serum potassium is the chief difficulty of physiological shock and is the chief cause of death in shock from injury or burns [Millican]. In surgery the release of cortisone and other steroids into the blood stream causes a release of potassium into the plasma too rapid for the kidneys to clear. one eighth the potassium is required to kill a mouse in shock as to kill a normal mouse [Weil]. It is a dangerous life threatening situation , and rates immediate medical attention. If there is breathing difficulty, irregular heart beat or black, bloody, or tarry excreta seek emergency treatment, and if there is confusion, nausea, difficulty breathing, vomiting, weakness, or tingling or numbness in hands or feet [from a dead site], call a doctor.
If death occurs, it will be because of inability of vital organs such as the heart or lung muscles to fire and contract. If the blood pressure drops, the situation can deteriorate even further, because the kidneys depend on blood pressure to force plasma through the kidney's glomerulus filtering mechanism. It is not a situation to be complacent over. Use of potassium supplements at such a time could prove fatal. If anyone is taking medication, potassium supplements should be under a doctor's advisement. This is especially the case for potassium sparing diuretics, angiotensin converting inhibitors, diabetic acidosis (acidosis can put low cell potassium in the normal serum range), adrenal insufficiency, kidney failure (for using diet and other strategies for helping to mitigate high chronic blood potassium, see this URL) , or severe burns.
If medical attention is not available, some procedures which could be helpful would be to keep warm, drink dilute salt water containing bicarbonate of soda (to interfere with hydrogen ion excretion at the potassium site), keep quiet and lie down, and eat some sugar, preferably glucose (say honey) for rapid absorption. The reason for the glucose is that this increases insulin which in turn moves potassium into the cells to associate with glycogen (animal starch). Increased urine flow increases potassium loss, so part of the effect of the salt solution may be from this phenomenon [Giebisch]. While sodium is a good antidote for high serum potassium, kidneys which have been conditioned by a prior low sodium intake can excrete an additionally larger amount of potassium from the collecting ducts than kidneys which have had a prior large intake. It is possible that a prior low potassium intake may reduce the muscle cell's ability to re absorb potassium in an emergency, since the sodium-potassium pumping sites on the membrane are apparently decreased in number, thus making a person more at risk during shock, if the shock comes when cells become full again [Nogaard][Miller]. A baby was saved from hyperkalemia or high serum potassium by 15 cc of calcium gluconate (smith's) and 150 cc of 17% glucose. The hyperkalemia was caused by supplements plus low aldosterone during dehydration from recurrence of diarrhea [Miller].
Aldosterone is excellent for increasing survival in shock, but amounts must be kept between 0.2 and 0.4 milligrams per kilogram of body weight in rats [Schumer ]. Licorice has been proposed as a safe way to counter the hyporeninemic hypoaldosteronism (low renin, low aldosterone) that produces hyperkalemia (high serum potassium) in diabetes mellitus by virtue of licorice's inhibition of the enzyme which degrades aldosterone and cortisol [Murakami]. It is possible that that procedure would be advantageous for metabolic shock also, although the fact that cortisol is increased by that enzyme's decline also [Stormer] makes it uncertain, especially routinely. Licorice has a chemical, glycyrrhetinic acid, in it which interferes with degradation of aldosterone so licorice (but not the licorice candy which is said to be anise seed extract [from a dead site] ) should be a reasonably safe temporary palliative. I do not know if long term use is desirable or not. The same may be true of the flavenoids in grape fruit also. Hyperventilating (breathing hard) may be helpful in an emergency. Plenty of water is desirable because aldosterone declines precipitously during dehydration.
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 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]. There is kidney tubule damage thought to be present in 30% of rheumatoid arthritis [Mikkelsen]. It is conceivable that relief of the cause arthritis symptoms may actually create some danger when the body becomes replete. Kidney abnormalities are thought to be largely from toxic medication, amyloidosis, or Sjogren's syndrome, but nephropathy (kidney disease) may arise from rheumatism [Mikkelsen].
Potassium supplements are most dangerous in ,a
A. Hyperkalemia, unless severe, is usually asymptomatic. The effect of
hyperkalemia on the heart becomes significant above 6 mEq/L. As levels
increase, the initial EKG change is tall peaked T waves. The QT interval
is normal or diminished.
B. As K levels rise further, the PR interval becomes prolonged, then the
P wave amplitude decreases. The QRS complex widens into a sine wave
pattern. Later P wave disappears, QRS becomes irregular and merges with T waves. This is followed by ventricular fibrillation and ultimately cardiac arrest [Bajusz p 222].
C. At serum K levels of >7 mEq/L, muscle weakness may lead to a flaccid
paralysis that spares cranial nerve function. Sensory abnormalities,
impaired speech, and respiratory arrest may follow.
However you should not be unduly alarmed about the possibility of high blood potassium or hyperkalemia. In a study of hyperkalemia induction caused by supplementation of hospital patients using potassium, the following statistics were obtained: out of 16,000 general patients, 4,900 received potassium chloride (86% to prevent low serum potassium, the rest to treat it) and 176 got hyperkalemia. Of these only 7 died and 21 were threatened with death [Kassirer]. This represents a mortality of only 0.14% among sick people. If diuretics were not being used it is possible that it would be lower yet. Among healthy active people on an adequate diet it must surely be virtually zero. Contrast this with the large death rate in the past from potassium deficiency especially in cholera and with heart disease. Without supplements or ORT salts many, many more would have died. A tribe of South American indians routinely eat 8 grams (8 thousand milligrams) or more per day of potassium without any obvious signs of ill effects [Oliver]. Healthy kidneys in people used to a large intake are said to be able to unload 26,000 mg in a day if necessary [Peterson]. In my opinion the plasma potassium must rise 1.0 meq/liter or so before one would start to use the word alarm. The electrocardiogram changes at 6.5 meq [Seekles]. I believe the dangerous symptoms of metabolic shock start to materialize after about 7.0 meq. I believe death is possible in the vicinity of 8.0 meq at which point the first clinical symptoms of heart failure appear [Seekles] and that life is impossible beyond 10.0 meq or so. Periodic paralysis is another circumstance, the cause of which is unknown to me, which requires potassium supplements. The lower limbs become paralyzed by too little serum potassium. However there are two forms, one of which is from too much potassium. It is important to know which is involved and so it is desirable to be under the care of a doctor. If a doctor is unavailable, and the attack was triggered by a meal heavy in carbohydrates, the chances are it is the low potassium version [Dajer]. Even so, it would probably be safest to use very small increments of supplements, certainly at first. Heart disease
Heart disease is another life threatening situation with which potassium is involved. Potassium has been used in heart disease therapy since 1930 [Sampson]. If the heart disease is the "wet" heart disease as associated with beri-beri (vitamin B-1 deficiency) , potassium supplements will probably aggravate the situation [McQuarrie][Mineno][Gould]. People who drink much wine, lemon juice, or vinegar fermented with sulfur dioxide with their meals are at risk for beri-beri and the diet can vary widely as to vitamin B-1 [Dept. of Health]. Even in the more likely circumstance that the heart disease is largely a potassium deficiency, potassium should be used with great caution shortly after an attack. Even though the cellular content is low, and some heart cells are actually dying for lack of potassium, the plasma content can be high.[Flear][Hurley][White] and so supplements can be dangerous. Raab, in a comprehensive review, suggests that dying cells may not be able to reabsorb potassium during the acute phases and thus cause death from this and the adjacent hyperkalemia. He suggests adopting the words "disionic cardiopathy" in order to avoid the semantic confusion and invalidity inherent in such words as "coronary heart disease" [Raab]. The way some doctors in the world get around the impasse is to administer the potassium in conjunction with glucose sugar and insulin [Sodi-Pollares][Iosava][Landman][Hjermann][LaMarche]. Thus much of the potassium enters the cell to be tied up with glycogen (animal starch). This is called a "polarizing solution" or "GIK". It is fairly effective although it must not be used during the "wet" heart disease of beri-beri (vitamin B-1 deficiency). The insulin may be also speeding movement across the cell wall because of its effect on a glucose - potassium pump [Lundman]. The insulin response is similar in both normal and potassium deficient animals. They therefore conclude that potassium deficient animals secrete less insulin [Mondon]. This procedure was originally proposed by Laborit and Huguenard [Laborit & Huguenard]] in France and Sodi-Pollares in Mexico in 1962 [Rackley]. This therapy benefits some patients but is unpredictable [Thadani][Fletcher] probably because the “wet” heart disease of beri-beri is sometimes involved. This procedure has fallen into disfavor but is now being restudied. It has been suggested as a way of suppressing the tumor necrosis factor (TNF) of arthritis recently [Das]. The unpredictability for heart disease may be also partly because some of the disease is caused or accentuated by copper or magnesium or vitamin C deficiencies . It has been proposed to add magnesium to GIK and calling the therapy MAGIK [Whang and Flink]. Also see this site about magnesium deficiency. (see [Kohvacca] for an experiment involving low serum potassium, in which potassium could not be increased in the body with one gram of potassium supplement without magnesium), because of the dependence of the sodium/potassium pump on inositol [Charalampous] [Greene](a B complex vitamin or myoinositol), or because of unpredictable huge sodium, chloride, or phosphate (from soft drinks) excess. There is 100% mortality in heart attack during potassium deficiency in the presence of excess phosphate [Selye] for instance. It has been suggested that diabetics should not be treated with polarizing solution [Rackley]. However, a recent experiment has indicated improved results post operatively for GIK for coronary operations [Szabo]. If whatever nutritional imbalance is not corrected correctly the prognosis is poor for heart disease patients. Potassium is prescribed for 40% of heart disease patients. This percentage should probably be much higher, but not so high as to include patients with beri-beri (vitamin B-1 deficiency). Only 50% of one group survived after 5 years [from a dead site]. Anyone suffering from a vitamin B-1 deficiency would be especially at severe risk if animal experiments are an indication [Follis]. Anxiety often attends a potassium deficiency [Davis], probably because of low aldosterone, so this may serve as a clue as to which kind of heart disease is involved and would bear investigation. The only sure way is with a whole body scintillation counter, although plasma potassium below about 4.0 meq/L would be an indication. The risk of heart disease does not change significantly when the mean serum potassium content of patient groups changes between 4.1 milliequivalents per liter (meq) and 5.3 meq [Walsh], so while it is no doubt desirable to attain the normal 4.8 milligrams per liter, the situation does not seem to be desperately dangerous above 4.0. There is also a new procedure using neutron bombardment of cells that may yet show promise. In any case there is no good substitute for whole foods with lots of vegetables either alone or with supplements to prevent heart disease in the first place.
Serum potassium of 3.5 mEq or less increases problems in heart surgery and doubles arrhythmias. Below 3.3 mEq doubles the necessity of resuscitation [from a discontinued URL]. These figures maybe should be higher for people with rheumatoid arthritis because such people often get anomalously high readings, especially of serum rather than plasma.
Judging by the statistics associated with heart disease therapy , potassium and magnesium [Bajusz p 168] must be playing dominant roles in a majority of current cases, because potassium whether in polarizing solutions, GIK (glucose-insulin-potassium), as potassium chloride, or as potassium and magnesium aspartate [Laborit, et al][Classen] causes a considerable reduction in mortality in the USA and especially abroad. Kadaner found that 3 to 4,000 milligrams of potassium chloride for 3-4 weeks prevented or considerably alleviated vascular crises. Most showed a decrease in blood pressure of 30-40 mm of mercury when taken with reserpine, hydrochlorothiazide, and some other drugs, which by themselves did not give such an effect [Kadaner]. Also people working in potash mines have a lower heart disease rate than others [Waxweiler]. Elderly heart disease patients given potassium supplements usually show an increase in whole body potassium [Potter]. It is impossible to cause heart disease experimentally by any known poison unless the potassium intake is also restricted or the kidneys destroyed [Prioreschi]. The total body potassium parallels the severity of the disease [Pierson]. Heart disease as caused by blockage of blood vessels by cholesterol has been attributed to cholesterol in the diet. While excessive intakes may contribute to this blockage somewhat, a disruption of normal cholesterol synthesis in the body must be the primary cause and in any case adequate potassium has a protective affect [Young]. Considerable evidence indicates that this is indeed the case. Cholesterol in the diet has only risen from 683 milligrams to 734 in 1961 since the start of the century and Masai tribesmen have low blood cholesterol in spite of high unsaturated fat in the diet [Brown, et al]. Copper deficiency is a much more plausible explanation for high cholesterol and maybe a vitamin C deficiency. For other possible causes and cures, see this pdf site.
Because the clearance of blood through the liver is reduced in heart disease, partly because of lack of exercise, aldosterone builds up [Cope]. Aldosterone is normally constantly destroyed by liver enzymes as fast as it is produced [Messerli]. As a result it is difficult to restore the body's potassium with food alone [Howard][White][Liddle][Randall]. If supplements are prescribed, probably the safest way to take them would be between meals, in small doses, and dissolved in juice. It should be possible to largely restore the body's potassium with potassium chloride supplements in two weeks or so [Conway]. Using potassium chloride may not be a good idea after repletion for those susceptible to high blood pressure for there is evidence from rats that excess chloride can increase high blood pressure..Also it would be wise to receive as much as possible from food. In addition it is probably advantageous not to supplement one's diet with sodium and chloride from salt, phosphate from soft drinks, or vitamin B1.(thiamin). Death of heart cells from a potassium deficiency is prevented by a thiamin deficiency [Follis 1942], so supplementing vitamin B-1 prematurely could be dangerous unless the heart disease was the "wet" heart disease of beri beri. When both are deficient lesions of the muscles occur instead similar to muscular dystrophy (potassium is low in muscular dystrophy [Blahd] ). The danger might be especially present if you have been imbibing wine fermented with sulfur dioxide or eating fruit dried with sulfur dioxide because sulfur dioxide rapidly destroys vitamin B-1 at the pH of the intestines [Amerine p487] [Fitzhugh].
Naturally, the most effective lifetime strategy would be to get all the potassium and other nutrients which was originally in the food, no huge excesses, and to eat, drink or smoke no poisons in the first place Then you will not likely to be forced into a bind in which you must make such dangerous, expensive, and time consuming compromises and unnecessarily tie up medical facilities.
The wide spread of nutritional contents of foods should make it possible for a knowledgeable person to meet all his needs by wise selection and preparation. Celery, for instance, has twenty times the potassium content of wheat per calorie, and eighty times of refined wheat. Bamboo shoots and green coconut water are also said to be very high. Such foods as celery have, in effect, many of the characteristics of a supplement, but with some built in safety. The potassium content can probably be increased still further for most vegetables by extracting the liquid and drinking it as a juice or as a broth. The best sources are sufficiently high that they should be treated with some of the respect accorded supplements in the event of illnesses which can cause high blood potassium or which immobilize you. REFERENCES for CHAPTER XII in; http://members.tripod.com/~charles_W/arthritis12.html
Chapter XIII --- Some people are afflicted with high potassium in their blood (hyperkalemia). Even a fairly small consistent rise in serum or plasma potassium of 0.5 milliequivalents (meq) or so over the norm, which is 4.8 [Scribner], is cause for some concern, because a healthy body is capable of a rather precise regulation of potassium, and a considerable portion of the kidney (renal) function must be gone before symptoms start to show. In my opinion the potassium must rise 1.0 meq/liter or so before one would start to use the word alarm. The electrocardiogram changes at 6.5 meq [Seekles]. I believe the dangerous symptoms of metabolic shock start to materialize after about 7.0 meq. I believe death is possible in the vicinity of 8.0 meq at which point the first clinical symptoms of heart failure appear [Seekles] and that life is impossible beyond 10.0 meq or so. Very high potassium which gives very noticeable symptoms is a medical emergency and a hospital should be sought. Only 2 or 3 decades ago potassium was not even listed in the index of books devoted to discussing metabolic shock, even though metabolic shock IS high blood potassium. It was another manifestation of the cavalier attitude of most medical professionals toward potassium then and to a considerable extent now. Potassium supplements were referred to by such euphemisms as "pharmaceuticals", "salt substitutes", "polarizing solutions", "GIK", and "ORT salts". It is so even today to some extent. Before assuming that your potassium is too high be sure that the analysis of blood is of plasma and not of serum since serum can give inaccurately high readings. Analysis of serum within one half hour would prevent the disparity [Bellevue]. This inaccuracy results when blood stands at low temperatures and potassium can leak from the cells and also there can be cell losses if the blood is handled roughly. Even without poor technique serum potassium will be higher than plasma by 0.2 meq/liter in normal subjects [Ifudu]. ]. Even with careful determination plasma potassium can be anonymously high because of potassium losses from platelets during rheumatoid arthritis [Ifudu]. If there is an inappropriate high reading there can be a degrading of health from the treatment itself as well as sometimes high, unnecessary expense. A difference of 0.4 mEq/liter can occur when platelets release potassium. This can occur in rheumatoid arthritis [Ifudu]. Electrocardiogram readings (ECG) can act as a check on serum analysis in the case of readings above 5.5 or so and affects on the heart are the most important manifestations anyway. As levels increase, the first ECG change is tall peaked T waves. The QT interval is normal or diminished. As potassium levels continue to rise, the PR interval becomes prolonged, then the P wave amplitude decreases. The QRS complex widens into a sine wave pattern, with subsequent cardiac arrest. There are things one can do to ameliorate high blood potassium temporarily at home, and I will propose some possible strategies. However, high blood potassium is a symptom of a rather serious underlying problem and you should contact a medical professional and make a great effort to find out what the problem is and correct it if at all possible. You may see mention of the symptoms of too high a blood potassium [Recheigl] in Chapter XI, on supplements, and Chapter XII, on side effects, which also has many of the references for statements in this article. Some symptoms are said to be irregular or fast heartbeat, paralysis of limbs, drop in blood pressure, convulsions, coma, cardiac arrest, black or bloody stool, diarrhea, confusion, breathing difficulty, vomiting, extreme fatigue, irregular heart beat, nausea, numbness, tingling hands and feet, and breathing difficult. The two most likely causes of a chronic situation are damaged kidneys or a hormone disruption. People tend to get despondent at such times, and not completely without reason. However, if the underlying cause is removed, and you then eat, drink, or breathe (translate; smoke) no poison and receive all the nutrients originally in your food including most of a small amount of protein from high quality sources such as meat, eggs, and milk and no overwhelming amounts of any (say sodium, chloride, zinc or phosphate of soft drinks) and get plenty of exercise (one contraindication to the value of excessive exercise is probably chronic fatigue syndrome or CFS), it is my belief that there is a good chance that adequate healing will usually take place if the damage has not been overwhelming. The body has considerable power to repair itself for most tissue, although I am not certain of the kidney's ability to do so. If there has been extensive damage to the kidneys it probably will not be possible to return completely back to normal especially in people past 15 years of age or so, but this need not be cause for despair because a healthy pair of kidneys has much more capacity than they need to just maintain normal life. They are said to be able to unload 26,000 mg of potassium in a day if necessary [Peterson]. So losing some capacity is not necessarily ruinous. I could be mistaken in this, but if it were me, I would not give up trying, even if I was on a dialysis machine. Keep in mind that people beyond 50 or 60 usually heal up slowly though, and much more than a year may be necessary. In the rare cases when a genetic defect is involved the underlying problem may be intractable. However some reasonable changes in lifestyle may nevertheless ameliorate the situation. It is instructive to know what the possible causes of high blood potassium are. Most of them are probably renal (kidney) failure. Diabetes causes over 30% of kidney failure for unknown reasons. In kidney failure during diabetes, potassium elevates after eating 100 grams of glucose, unlike normal people who show a slight decline [Knochel p447]. About 30% are related to hypertension, which itself is at least several syndromes. Black people have 18 times more hypertensive kidney failure than white people which Tobian believes is due to a much lower potassium intake [Tobian]. As many as 15% of cases are thought to result from atherosclerotic renovascular disease from plaque build up on the kidney arteries which in turn along with glomerular derangement may often be from a copper deficiency combined with a high salt intake [Moore]. Osteoarthritis itself probably does not cause kidney damage, but too much acetaminophen (Tylenol, Anacin-3, Liquiprin, Panadol. and Tempra) taken for it probably will. Since pain-killing drugs usually do not cure a disease, it is usually better to tolerate the pain. An additional reason is that painkillers have been implicated as a risk factor in acquiring chronic fatigue syndrome (CFS). I do not know which ones are implicated yet. One exception to adverse affects of pain medicines may be Methylsulfonylmethane ( MSM). It is said to be fairly effective and virtually free of side affects. You may see the results of numerous case histories at this site. Pain can cause increased losses but I do not know if it can cause increased retention. I suspect not. People at risk, such as diabetics, should have regular urine and blood tests so that if small changes show up from the baseline they can be alerted to a much more serious underlying problem since kidney capacity is normally much more than we need and obvious problems are late in showing up. 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]. Other causes of hyperkalemia are crush injury, severe burns, hemolysis (red blood cell destruction), hyperkalemic periodic paralysis (during paralysis episodes), acute tumor destruction after chemotherapy, transfusion of hemolyzed (aged) blood, Addison's disease (rare), hypoaldosteronism (very rare), severe dehydration, and respiratory acidosis. The last is a failure of the lungs to remove carbon dioxide leaving behind carbonic acid. Since acid (hydrogen ion) interferes with potassium excretion, potassium can build up. Respiratory acidosis can result from failure of the lung to remove carbon dioxide because of bronchitis, asthma or airway obstruction. . In this case, the hyperkalemia can be mild or severe. People who have weak kidneys probably should sleep at night with the window open. In my opinion excessive dreaming is an indication of high carbon dioxide in the air. It is also conceivable that there is such a thing as a 16alpha,18dihydroxydeoxycorticosterone tumor analogous to aldosterone tumors rarely. It would presumably cause potassium to be retained. If such a tumor exists, I have not heard of it being reported. There are several poisons which can cause high blood potassium (hyperkalemia) for a short time after actual use. Angiotensin-converting enzyme (ACE) inhibitors {Captopril, Enalapril, Fosinopril}, non-steroid anti-inflammatory drugs (NSAIDs)
{Indomethacin, Ibuprofen, Ketorolac}, and potassium sparing diuretics {spironolactone, triamterene, amiloride} prevent excretion. The combined use of nonsteroidal anti-inflammatory drugs (NSAIDs) and beta-adrenergic blockers may increase the risk of life-threatening hyperkalemia through their suppressive effect on the renin-aldosterone system, whereas the simultaneous administration of Lobenzaret (CCA) with NSAIDs through impairment of the renal tubular function [Ichinohe]. Angiotensin receptor blockers {Losartan, Valsartan, Irbesartan, Candesartan} and antiinfective agents {Trimethoprim-sulfamethoxazole, pentamidine} are said to be involved by a mechanism unknown to me. Digitalis glycosides, digoxin, and oleander (nerium oleander) inhibits the sodium/potassium cell wall pumps. Arginine (nuts and chocolate are very high in arginine), hypertonic solutions, and fluoride salts cause cell leakage. This last would seem to cast some doubt on use of fluorinated water for those with hyperkalemia or old people (and maybe everybody) especially since fluoride has been proposed to damage the kidneys and inhibit the thyroid. Tea is said to be especially high in fluoride. It has also been proposed to act synergistically with aluminum to produce Alzheimer's disease. Richmond says that fluoride strengthens the bones but reduces resorption [Richmond p131]. That last may imply an occasional increased problem with muscle spasms from hyperkalemia if calcium should be low. He says that fluorinating water has no perceptible affect on kidneys in children, but that fluoride in water for dialysis should be controlled [Richmond p133, 134]. For old people who are forced to drink a lot of water (or imagine they are) fluorination seems a dubious strategy to me though. The anticoagulant Heparin, alpha-adrenoreceptor stimulants, succinylcholine, and beta-adrenergic nerve blocking agents also produce high blood potassium. The kidneys are said to be a critical target organ for cadmium and this is especially ominous because the half-life of cadmium in the body is 17 years [World Health Organization p64]. I do not know if the damage affects potassium. In my opinion cadmium should not be used for plating screws or cathodic protection. Poisoning rarely causes severe high blood potassium directly unless the kidneys have been damaged or muscles destroyed as well. I believe that damage to the kidneys is the most common chronic problem. Ironically the kidneys can be damaged by a potassium deficiency [Epstein] especially if high blood pressure is also involved [Tobian]. A deficiency state is very common in our society. Rubini believes that even a modest deficiency can cause irreversible kidney lesions [Rubini] in the collecting tubules, which is where the potassium is excreted. Some people with end stage kidney disease can have a total body deficit even though plasma potassium is normal [Knochel p450]. This is because when the cell potassium is low the body attempts to make the plasma potassium low also. Excess calcium can also damage the distal tubules of the kidneys [Epstein]. It is said that excessive magnesium can damage the kidneys, especially for those who have poor kidney function to begin with [from a dead site]. I do not know if any of those damages can directly cause damage of such a nature that potassium can not be excreted properly. However I would be greatly surprised if it did not at least contribute to making poison or other damage somewhat more severe since the effect of a potassium deficiency is very generalized and any decrease in the effective size of the kidneys makes the situation more difficult as well. Besides, in chronic kidney failure aldosterone secretion is often high and more potassium is excreted per unit of decreased glomerular filtration [Knochel p446]. Persistent high blood pressure can damage the glomerulus, which is where the fluids are initially filtered into the kidney tubules. The most common glomerulous degeneration in the world is called Immunoglobulin A (IgA) nephropathy (IgAN) [Donadio]. Its progress can be muted by increasing ingestion of omega 3 oil in food [Donadio] You may see a graph showing ratios of omega 3 to omega 6 oils at this site. The ratio of omega 6 to omega 3 should be one, but it is usually much higher in our society [Simopoulos].
I am not certain of what that kind of damage does to the potassium equilibrium. Probably it is not an important part of it by itself. Albumins in the urine are an indication of such damage. Early problems can only be detected by routine special tests on microalbinuria. People with insulin dependent diabetes should have such tests. There are medications which can damage the kidney tubules. Among the prescription and over the counter medications that predispose patients to such damage are acetaminophen (Tylenol, Anacin-3, Liquiprin, Panadol, and Tempra) but not aspirin [Perneger] (There is a link to aspirin [Fored] but predisposing conditions could not be ruled out), the following antiinfective medicines; pentamidine (NebuPent, Pentam), cephalosporins, and amphotericin B or Fungizone (80% affected by this drug), foscarnet, cidovir, vancomycin (Vancocin) , and the aminoglycosides, [Schwartz] which include gentamicin or Garamycin (20% of patients on gentamicin develop renal insufficiency), amikacin (Amikin), tobramycin (TOBI, Nebcin), neomycin (Mycifradin), and aminoglycoside gentamycin (Garamycin). Cox-2 inhibitors are suspected to cause kidney damage. It has been proposed that acetaminophen damages the liver by degrading the detoxifier, glutathione peptide so it is possible that that is the mechanism for the kidneys also. If so anyone who must take that drug should possibly increase cysteine (perhaps by means of whey), glutamate, and glycine in the diet, since those amino acids make up glutathione, and take as little as possible of the drug.
Immune stimulation by cytokine treatment (mainly interferon-alpha) involves several kinds of autoimmune renal diseases like acute interstitial nephritis or glomerulonephritis as well as interstitial and vascular rejection of renal transplants. [Schwarz] Aristolochic acid found in certain plants and botanicals is toxic to the kidneys and is a potential carcinogen. This chemical can cause serious kidney damage and the use of products that contain aristolochic acid has been associated with several occurrences of kidney failure. The use of aristolochic acid-containing product has also been linked to increased risk of kidney cancer in people who have consumed it. Bluelight, Inc., Ithaca, N.Y. has initiated a recall of these products sold under the "Treasures of the East" label with "MFG #200008" (2000=year, 08=month) and earlier production dates. Products with "MFG # 200009" and later production dates are not affected. The American Food and Drug Administration has a program called MEDWATCH for people to report adverse reactions to untested substances, such as herbal remedies and vitamins call 800-332-1088. Never permit a radiological (x-ray) dye into your blood stream out of mere curiosity, but only if it is desperately important. A high percentage of people have kidney damage from such drugs, especially people with mild to moderate kidney impairment [Black] and over half of diabetics [Thompson]. In my opinion it is highly probable that healthy people have some hidden damage also, even in the absence of symptoms, from all the above substances. It is therefore not a good idea to use these drugs for trivial problems like pain or discomfort, or for problems which can be solved in time with nutritious unpoisoned foods and healthy living or emotional support. I do not know if diuretics can damage the kidneys. Howeever there is a study which indicates that patients with kidney failure who are on diuretics had a higher death rate but also a higher rate of subsequent chronic kidney failure requiring dialysis. The death rate was especially high in patients who failed to quickly respond to the diuretics with an increased flow of urine [from a dead URL]. Other toxic agents that can damage kidneys include heavy metals like lead, arsenic (arsenic is given to chickens for worm control and gives young poultry meat 0.39 parts per million [Laskey], and mercury, carbon tetrachloride (used in the dry cleaning industry), pesticides, and fungicides. Hydrocarbons are said to cause damage to the kidneys [Ravnskov]. I do not know which of these last poisons causes damage which prevents excretion and which prevents retention. Lead probably prevents retention [in my opinion] and is the main cause of gout [Batuman]. 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]. Ethylenediaminetetraacetic acid
chelator of lead has sucessfully increased uric acid excretion [Lin 2001]. Other poisons may move one a little closer to gout also, such as timalol [Blocadran] combined with hydrochlorothiazide and amiloride (Moduretic) [Laren]. I have no information in the medical literature on any direct link between gout and a potassium deficiency. I have a strong suspicion that there is a link however. 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. William Ellis 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][Halla] so there is a circumstantial connection. Urate kidney stones form during gout in a fifth of the cases. Making the urine less acid with potassium citrate or sodium bicarbonate is a current treatment for urate stones [Shekarriz]. I suspect that potassium bicarbonate would be preferable to sodium bicarbonate, but I have no evidence. The initiating factor is probably usually lead poisoning though [Wright]. Personal experience leads me to believe that toluene in automobile enamel reducers is also a poison which can trigger gout. There is an association in peoples minds between gout and rich foods and lifestyle, probably because people with gout have trouble excreting nitrogen, which is high in meat, in a soluble form and perhaps also because wine bottles and plumbing used to contain lead. Until such time as the matter is elucidated it would be a good idea to stop eating lead, eat less proteins, and not allow any potassium to be lost from one's food. There is a discussion of current treatment for gout online. 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.
If there is a partial blockage of the urinary tract it can interfere with excreting potassium. For a discussion of causes of urinary blockage click here. or here for diagnosis. Blockage would be most common in men because of the problem of swelling of the prostate tissue being common. I suspect that this prostate swelling is most often caused by a deficiency of the vitamins linoleic or linolenic acids (omega 6 and omega 3 oils) produced by the foolish custom of hydrogenating vegetable oils. I also suspect that it is sometimes caused by a zinc deficiency which in turn can be created by excessive intake of copper. Anyone having trouble with potassium should have a urologist rule out prostate blockage as a source or contributor to the problem early on. It is also possible to check the matter oneself by inserting a catheter after urinating. If a significant amount of urine continues to come out there is an obstruction beyond the bladder from the kidneys. You have to be very careful and use good sterilization of both the catheter and as much of the organ as possible or bacteria can be introduced into the bladder and may be anyway. Bladder infections are difficult to get rid of although they are not usually dangerous. If there is an obstruction from swollen prostate it can usually be corrected without the necessity of an abdominal incision. There are also hormone therapies which are said to be fairly effective for lesser prostate swellings. Blockage is presumably possible from kidney stones. I do not know what affect this has on potassium. I do have some information on some of the causes. If calcium intake is normal but phosphorus is too low calcium citrate stones can form [Sager]. On the other hand if phosphorus is much too high, say from drinking soft drinks, calcium phosphate stones should form [I have no reference for this and am not sure it happens from soft drinks]. Stones are said to have an incidence as follows; calcium oxalate (65% - 75%), calcium phosphate (5%), uric acid (7%), cystine (2%), and ammonium phosphate (2%) stones [from a dead site]. Uric acid stones are less probable when potassium was adequate in the diet in healthy people. Medications which can cause too high a blood potassium are cyclosporine, lithium, heparin, enalapril, triampterene, amiloride, spironolactone, and trimethoprim. They imply other malfunctions to make the increase possible. Indomethecin by inhibiting prostaglandin stimulation of renin and captopril by prevention of angiotensin II can also produce hyperkalemia [Kaufman]. There has also been proposed a rare, unknown genetic malfunction as a cause of hyperkalemia [Stewart] There are some procedures available in a hospital which can provide some short term relief from a dangerous surge in blood potassium. Intravenous calcium, intravenous glucose and insulin will work for an hour or so. Intravenous aldosterone will help the kidneys get rid of excess potassium. Both in a hospital and at home, sodium bicarbonate will help considerably short term if there is any kidney function left, especially if the hyperkalemia is caused by acidosis (low blood alkalinity or pH), but is said to be dangerous if used for prolonged periods. See this article for an extensive technical discussion of blood acidosis and urine acidity. Drinking salt (sodium chloride) water as a vehicle for the bicarbonate is helpful. Increased urine flow increases potassium loss, so part of the effect of the salt solution may be from this phenomenon [Giebisch]. While sodium is a good antidote for high serum potassium, kidneys which have been conditioned by a prior low sodium intake can excrete an additionally larger amount of potassium from the collecting ducts than kidneys which have had a prior large intake. Furthermore, a low sodium intake causes higher potassium losses than an excessive sodium intake [Peterson 1977]. So it seems to me that a very low sodium intake normally would be the best way to go to avoid hyperkalemia. However I am not certain of this. Drinking extra water should be helpful, and indeed essential if dehydrated. However, drinking huge amounts of water (say a gallon) if severely dehydrated without sodium chloride is very dangerous and can kill you from hypernatremia (low sodium). Such dehydrated states should be relieved slowly and combined with some sodium chloride salt, as well as some potassium chloride in the case of normal people (ORT salts). You may see a discussion of drugs to correct hyperkalemia (but not aldosterone) along with doses, contraindications, symptoms, tests, and ECG charts at this site. Also fludrocortisone acetate; FCA, has been found to increase potassium excretion without much other changes [Furuya]. If drinking extra water is prescribed and you gag on pure water, adding extra water to your soup and using two thirds of fruit juice as water (although I do not recommend fruit juice routinely during kidney failure because of a high potassium content relative to its other nutrition) should help. You would immediately think that reducing the amount of potassium which you eat was in order long term and this is, indeed, usually prescribed. The main problem is that potassium tends to be correlated with other essential nutrients. However an immediate gain can be achieved by cutting out foods unusually high in potassium per calorie such as celery. It would seem to be in order to cut out foods moderate in potassium per calorie which are rather low in other nutrients such as apple juice. Increasing intake of foods unusually high in other nutrients such as wheat germ and liver (liver if uric acid is normal) would no doubt solve part of the above problem. You may see a table which expresses potassium as weight per calorie at; this site. A table like that is unobtainable elsewhere in that format. This same table may be viewed in descending potassium concentration at http://members.tripod.com/~charles_W/table2.html.You may see the table from which the previous two tables are computed in the USDA handbook #8 site. It is an unusually good site and even gives amino acids. You must press "enter" to search and then divide a value of any nutrient obtained by the kCal number. It is available in a PDF printable form for potassium only also. with links to PDF caloric contents and other nutrients. A site is available which shows foods which are high in one nutrient and low in another nutrient (including calories). This last site should be especially convenient for people with high blood potassium. It would be extremely valuable for someone with high blood potassium who suffers from a genetically caused deficiency or extra need of a nutrient. It is entirely possible that it would be necessary to take vitamin and mineral supplements as well. If so, be sure they are complete and balanced. Dangerous imbalances are possible otherwise. In particular, unless you get copper at about one-seventh the amount of zinc, you could suffer from a severe copper deficiency with hemorrhoids, slipped or herniated discs, and aneurysms (strokes) some of the most dangerous symptoms. The reverse is also true for copper's affect on zinc with other adverse symptoms although they are somewhat less immediately dangerous symptoms. People on dialysis have low copper and zinc in their serum as well as too much retinol (from vitamin A) [Komindr]. It could be that ceruloplasmin injections would solve that problem for copper. You should keep in mind that no vitamin capsules have adequate amounts of the macro nutrients such as calcium, magnesium, sodium, chloride, phosphate, and amino acids, so imbalances are possible. If animal experiments are an indication, vitamin B-1 (thiamin) is a potentially dangerous imbalance with respect to potassium. If vitamin B-1 is deficient when potassium is adequate, the wet heart disease of beriberi is possible [Folis]. Presumably cell potassium IS adequate when blood potassium is high (although not necessarily always) so presumably this would usually not apply in high blood potassium. Even if you are eating foods adequate in vitamin B-1 you could still have a problem in the other direction if you are also eating foods which have sulfites in them such as wine, vinegar, beer, and some dried fruits, since sulfites degrade vitamin B-1 in the intestines [Amerine] [Fitzhugh]. Wine can be obtained without sulfites but since it also has a poison in it which interferes with potassium excretion [McDonald], wine probably should not be used during high blood potassium in any case. I have no information as to whether this poison has been identified and ethanol is said to increase excretion [McDonald]. However by all means cut out wine and alcoholic beverages fermented with sulfur dioxide whether potassium is high or not and cut them out with or without sulfur dioxide during high blood potassium. I do not know how potent the affect is, but there is no point testing the matter on yourself. Wine has been proposed as good for the heart in normal people, but if the mechanism for this goodness is retardation of potassium excretion, I suggest that getting adequate potassium is a superior strategy for kidney intact people. When the protein in meat, eggs, and milk is burned for energy the nitrogen in it degrades to ammonium, uric acid, and urea. Damaged kidneys can have trouble excreting these wastes also. For this reason people with damaged kidneys are often urged not to eat excessive amounts of high protein foods. A trial suggests that 0.6 gram of protein per kilogram of body weight slows down progression of kidney disease [D'Amico]. This would be roughly less than 50 grams for a lean 150-pound person. There may be an additional reason so far as potassium is concerned. When the body suffers from a potassium deficiency the kidneys activate an enzyme which degrades glutamic acid. This seems to me to be an adaptation to conserve potassium by interfering with excretion at the excretion site. It may be that extra ammonium in the body may interfere somewhat as well, not something desirable when suffering from an excess of potassium. It is probable also that the ammonium can act as if it were potassium so far as nerve conduction is concerned because it has the same size and charge which would make the situation even worse than the potassium value itself would seem to indicate. I know of no experimental evidence which would cast light on ammonium in the blood though. In any case it is fairly important in the long run not to remove meat, milk and eggs from the diet completely since these foods provide amino acids lysine and methionine which plants are low in. I suspect that the equivalent of the weight of an egg at each meal would be adequate. They also provide vitamin B-12 although that is easy to provide with pills. An additional argument is often advanced against using meat, liver, and eggs because of the anti cholesterol fad. It is very unlikely that dietary cholesterol is an important part of the problem (or this site) but rather excessive synthesis within the body. Cholesterol has only gone up in the diet from 683 to 734 milligrams between 1909 and 1961 and the Masai tribe have low cholesterol [Brown p8]. If the problem is most often caused by low copper [Carr] as I suspect, warning against eating shellfish or liver is exaggerating the problem, not helping. So be sure to get a small amount of high quality protein at every meal, or at least within 2 hours of a meal. If your cholesterol is high, make sure it is not milk, which is low in copper. Glucosamine is currently being touted as advantageous for some of the arthritis diseases. I have a suspicion that part of its efficacy may be due to it furnishing glutamine for ammonium synthesis in the kidneys for ammonia production goes up and potassium excretion goes down when ingesting glutamine [Tannen p458]. If so, I suspect that taking this material should be counter productive and therefore contraindicated during high blood potassium. Acids which can be absorbed but not burned (metabolized) will interfere with potassium excretion since hydrogen ion competes with potassium at the excretion site. Unfortunately I do not know which foods are involved. However, I do suspect vinegar (acetic acid) since vinegar has been suggested as being advantageous for rheumatoid arthritis which I am convinced is a potassium deficiency. Acetic acid can be metabolized [Winegrad] but it could be that much of it is excreted before entering the cells or that well-fed people do not burn it all. Cherries and cranberries fall into this same suspicion also (however researchers have proposed antioxidants responsible for the affect of cherries on arthritis and gout), cranberries because I have heard they increase urine acidity (but no hard evidence). I am almost certain that the citric acid in citrus fruit is burnt in the body since citric acid is part of the Kreb's cycle so I assume that citrus fruits are safe. It would be a good idea for researchers to perform experiments to determine this for sure or to make the information well known if it has already been done since a little fruit like citrus should be reasonable if a patient's potassium overage is mild and the low nutrition value of fruit would not be a major problem in that case. Of course potassium supplements, salt substitutes, ORT salts, some athletic drinks, and potassium-based baking powders must not be used at all except possibly during virulent diarrhea. Since aldosterone suffers a drastic decline during dehydration it is important that you drink more water than just barely enough to satisfy thirst. Extra water probably makes it easier for the kidneys to unload potassium in addition. Perspiration should help considerably to remove excess potassium also, but only if it is not allowed to dehydrate the body. Enemas also cause large potassium losses [Dunning]. Leaving water in contact with the mucous membranes for a long time increases the losses. I do not know whether this is a desirable strategy routinely or not, but I should think it would be helpful in an emergency. Licorice has a chemical, glycyrrhetinic acid, in it which interferes with degradation of aldosterone, so licorice (but not the licorice candy which is said to be anise seed extract) should be a reasonably safe temporary palliative. I do not know if long term use is desirable or not. The fact that it also increases cortisol indicates that it probably is not. The same degradation is said to be true of grapefruit. I do not know what the status of other citrus fruits is. Aldosterone injection is excellent for increasing survival in metabolic shock, but amounts must be kept between 0.2 and 0.4 milligrams per kilogram of body weight in rats [Schumer]. This last would only be available in a hospital of course. It may be that deoxycorticosterone (DOC) would be better for people eating too much salt. Since acid interferes with potassium excretion, it should not be surprising that bicarbonate of soda (baking powder) causes large potassium loss. This also should be a reasonably safe temporary palliative. Whether it is safe as a routine strategy or not, I do not know. Sodium bicarbonate is often used as baking powder, but this is not necessarily a good idea. It has recently been questioned as to being of any help in life threatening high blood potassium, but I find this hard to believe except in almost complete loss of kidney function. Hyperventilating (breathing rapidly) gets rid of carbon dioxide (carbonic acid) to an abnormal extent. This should be an advantageous procedure to know if you are in a taxicab on the way to a hospital to treat metabolic potassium shock. I have no knowledge of it being tried, but I would have thought it should help temporarily to avoid a lethal ending. I do not know for sure what value potassium must attain before drastic remedial action should be taken. I suspect that over 6.0 meq per liter is necessary to start to threaten actual death. However attempting to alleviate the problem nutritionally until the underlying problem is discovered should be inherently fairly safe and without a doubt almost always a desirable additional strategy at least. It is good sense to forego processed food, alcohol, and tobacco in order to stay as healthy as possible even when that garbage is not the direct cause of the disease you are trying to avoid. What little phony pleasure, financial advantage, or excitement that garbage gives you is much more than counter balanced by the pain and misery that garbage ultimately brings in my opinion. It would be better to attempt to attain camaraderie or good jokes. REFERENCES for CHAPTER XIII in; http://members.tripod.com/~charles_W/blood.html
Chapter XIV ---
“Chronic fatigue syndrome” (CFS or CFIDS) or “myalgic encephalomyelitis" (ME) is a disease characterized by several of the symptoms of impaired sleep, muscle twitching at night, extreme long lasting fatigue which gets much worse with exercise (the fatigue has been suggested to be from creation of proteins which interfere with and/or destroy thyroid hormone receptors by interferon [Englebienne] ), loss of memory [Marcel], disruption of the circadian rhythm [Tomoda], sore throat, muscle and joint aches, headache (see abstracts of research into magnesium related to migraines or also for an article relating magnesium deficiency to migraine headache), cough, photophobia, night sweats [Evengard] depression that has much lower ACTH and cortisol secretion than typical depression [Demitrack], also a much lower secretion of growth hormone which Cheney believes can be used to repair some of the damage to the hypothalamus of the brain (but growth hormone is degraded when eaten so can not be used by patients) and which failure is thought to be from over secretion of somatostatin in the hypothalamus [Paiva], a failure for a 383 amino acid cortisol binding protein to decline under stress as it usually does when not ill, lower secretion of DHEA (Dehydroepiandrosterone ) [Kuratsune] which is the most abundant circulating steroid [No authors], there is a less rise of DHEA under ACTH stimulation compared to cortisol than normal [Scott 2000] (You may see how some people rated DHEA treatments at this site) and ( claims for use of several catabolic hormones), dramatically lower blood volume (hypovolemia), lymph node pain low blood pressure upon standing (othostatic intolerance), eye pain and fibromyalgia (muscle pain) [Bell DS] as well as white spots on MRI brain scans [Buchwald 1992] and single-photon emission computed tomography (SPECT) scans [Schwartz], brain scans using 18Fluorine-deoxygluxose (18FDG) positron emission tomography (PET) CFS patients showed a significant hypometabolism in right medium frontal cortex (p = 0.010) and brain stem (p = 0.013)
reduced blood
flow to the part of the brain which controls the stomach muscles, loss of fingerprints in a third of the patients [Johnson H p345], changes in the body's hormones, increased sensitivity to glucocorticoid hormones [Zisser], alterations in some of the immune hormones (also see a review of immune hormone interaction) evidence of disruption to calcium ion transport in the muscle of ME/CFS patients (but not in fibromyalgia) possibly from modification of the sarcoplasmic reticulum membrane [Fullea] and a chronic low level activation of the immune system [Cannon] which last may be accounting for many of the non neurological symptoms, but most very variable, perhaps because different parts of the brain are attacked, perhaps because there is more than one species of virus involved, and perhaps because of strong affects from the large variety of secondary infections which have been identified or even all three [Richardson]. The most consistent laboratory abnormality in patients with CFS is an extremely low erythrocyte sedimentation rate (ESR), which approaches zero. Typically, patients with CFS have an ESR of 0-3 mm/h. If the ESR is elevated or even in the high-normal range, another diagnosis is suggested. Many physiological parameters are altered. Another consistent abnormality is an increased excretion of citrate in the urine. It has been suggested that this binds with and causes an increased excretion of magnesium. It is conceivable that this is a mechanism for conserving chloride in order to keep the serum acid in order to make immune enzymes more effective. This would seem to suggest that use of citrus food should be investigated and maybe other acid foods like vinegar as well. Women are much more often affected than men no doubt a tiny bit because they complain more often than men and are more likely to be afflicted with emotional trauma which is a triggering circumstance (but see endometriosis below). Women who have CFS have a significantly higher level of isopregnanolone (a metabolite of pregnanolone). Oddly it is inversely correlated with depession, which would seem to indicate that depression does not cause CFS [Murphy]. There is also the circumstance that women who have fibromyalgia generally do not inhibit undistracted pain, unlike men, especially normal men, who inhibit both types [Staud]. Some research indicates that pain in women is said to activate emotional centers while men tend to have cognitive centers activated. Doctors are more likely to treat women with less sympathy than men because of this perception of complaint. Perhaps it would be a good idea for women to use lady doctors. One or two percent of the population are affected or more likely one third of a percent of women for the more severe form of CFS, which is about one third the breast cancers. There have been other names for the syndrome proposed. Chronic fatigue immune dysfunction syndrome (CFIDS) was proposed because the immune system was distorted and it was hoped that this name would gain the victims some support and research funds. After all, the magic letters "ID" had gained massive support for AIDS. It would be too bad if the early cavalier attitude toward CFS resulted in adopting such a cumbersome name. It may be necessary though, because the contempt and loathing by patients for this name is intense, for it has resulted in some dangerous and expensive behavior by doctors. Recently the U.S. Department of Health and Human Services CFS Coordinating Committee proposed the name neuroendocrineimmune dysfunction syndrome, or NDS. This name is hopelessly cumbersome. Yuppie flu was proposed because at first only higher income people had enough money saved to hire doctors or lobby officials. High income has been ruled out as a risk factor for fibromyalgia [White] and also CFS [*] (actually less than 16 years of education is a risk factor [Clark], perhaps because better educated people tend to know more about good nutrition). The name "myalgic encephalomyelitis" (ME) was assigned to a similar disease by medical researchers in the British Commonwealth. The last two have also been combined into the acronym CFS/ME, an acronym preferred by patients. Post viral fatigue syndrome (PVFS) and post-infectious neuromyasthenia were also used. The majority of patients are said to prefer “ME” as a name, so in view of this , if so, maybe the medical profession should adopt this acronym. I prefer CFS because such an extensive literature already exists for this acronym, thus facilitating future searches, but only if all doctors can be educated to its horror. Another acronym that has come into existence is “PWC”, which means “people with CFS”. Fibromyalgia, which is widespread muscular pain, was proposed as a variant of CFS (80% 0f fibromyalgia victims have CFS) and probably is [Buchwald 1994] However cell wall electrolyte pumps appear to be fundamentally different between the two syndromes [Fulea].(see this site for a personalized discussion of fibromyalgia symptoms). Low molecular weight R Nase L increased activity correlates well with severity of CFS symptoms but is normal in fibromyalgia, rheumatoid arthritis, lupus erythmatosis, HIV, and depression [Levine - Copies of the complete article are available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address:mailto:getinfo@haworthpressinc.com.]. 74% of fibromyalgia patients had antibodies against serotonin and gangliosides, which are absent in rheumatoid arthritis and polymyalgia rheumatica [Klein]. 65% of patients with systemic lupus erythematosis have fibromyalgia symptoms [Neumann].
Some of the more striking abnormalities are those found in the 2-5 Synthetase/RNase L anti-viral pathway. These are not specific to CFS/ME though, and abnormalities can occur in other viral illnesses. This pathway works as follows: viruses activate the 2-5- synthetase enzyme. This in turn converts ATP into 2-5 oligoadenylate and activates the RNase L enzyme, which degrades viral and single stranded RNA. Various Protein kinase enzymes also becomes activated and elevated, which again inhibits both viral replication and protein synthesis. It has been suggested that environmental toxins in the presence of heat shock proteins can also activate this pathway.
No one has been able to assign a definitive cause to CFS with certainty, although it has been proposed to be a hypochondria from misdiagnosis [Johnson H p 126] or mass hysteria from reading newspaper articles proposed by the Center for Disease Control in the USA [Johnson H p 135-138, 339, 342] (both extremely unlikely [White] ), an Epstein-Barr virus [Holmes] (because that virus antigen is often found in it as an opportunistic infection, but refuted [Buchwald 1988] ) or other herpes type viruses, poor nutrition compounded by lack of exercise [Johnson H p685] (probably a factor prior to onset but not after), a poison [Racciatti] , or a retrovirus (because fragments were detected in some of its victims similar to retrovirus) [DeFreitas]. The retrovirus work has ended because DeFreitas has become very sick and no one else has been competent to continue her work. Pozzetto detected genetic material (specifically RNA) from enteroviruses in 20 percent of muscle biopsies from patients with chronic inflammatory muscle diseases and 13 percent of patients with fibromyalgia/chronic fatigue syndrome, but not from healthy volunteers. This will become a very significant finding if other tissue harbors such a virus to bring the percentage up to near 100 per cent. The Center for Complex Communicable Disease has proposed that a new type of virus called a stealth virus is responsible for CFS and fibromyalgia and are currently doing research and testing. The stealth virus is thought to be capable of taking genetic sequences from bacteria and other hosts. That CFS is caused by a virus which damages the immune system is highly probable since it comes on suddenly with flu like symptoms and shows up in clusters associated with social groups [Buchwald 1992]. Several cases of chronic fatigue syndrome brought on by parvovirus B19 was cured by intravenous injection of 400 milligrams per kilogram of imunoglobin per day for 5 days were cured. Fragments of mycoplasma pathogen species have been found in CFS [Nicolson] and fibromyalgia but they are probably opportunistic infections because when multiple species are found in the same patient it correlates with the length of time CFS was present [Nasralla]. However a high percentage of veterans with Gulf War syndrome are infected with Mycoplasmin fermentans especially and quite a few of their family members also become infected with symptoms of autism in their children. There is said to be a benign treatment for mycoplasma and other intracellular pathogens using glutathione from whey (at the end of this site). Platelets are proposed to have an immune function [Yeaman] and it has been suggested that CFS is from a defect in the platelet’s immune function [Gallagher, Co-Cure communication]. Cheney has proposed that the immune system is divided into two mutually exclusive modes. He believes that CFS victims are stuck in the mode which fights serum bacteria and as a result can not kill viruses and inside the cell pathogens. Instead, the body secretes Rnase L peptide protein for the time being which prevents the viruses and mycoplasmin bacteria (bacteria that have no cell walls which resemble viruses) from replicating but does not kill them. If this is so, I would think that people with CFS should have a lower incidence of cancer than normal people. A form of RNase-L, the low molecular weight (37 kilo Dalton) RNase-L, has been found in CFIDS (CFS) patients. It can be six times as destructive as the typical RNase-L. If the virus-fighting system is working normally, the normal form of RNase-L prevents the virus from reproducing. The rest of the immune system goes to work and wipes out the virus, and then the entire immune system returns to normal levels, and the person recovers. In CFIDS, the RNase-L shifts to the more destructive form, and instead of de-activating, it stays active much longer, causing serious cellular metabolic dysfunction, which ultimately affects the liver. The cells can no longer produce essential enzymes, and without them, the liver can't do its job of detoxifying the body. This last link by Cheney is one of the best theoretical articles written on CFS I have seen. Glucocorticoids have a different affect on IL10 in CFS patients than in normal people while the affect on IL12 is the same. This may explain some of the reduction in antiviral activity [Visser, Grafferman]. Van Konynenburg has proposed that the shift to the above disrupted immune function has been enhanced by long term emotional stress and that a deficiency in glutathione and cysteine accentuates it [CoCure message]. Proposes that an important part of CFS is a chronic disruption of the coagulation system, a variant of Hughes syndrome or antiphospholipid syndrome (APS). It can be triggered by various infections such as epstein bar virus, chicken pox, lyme disease, leprosy, mycoplasma, tuberculosis, and ricketstia. but can be accentuated by some foods such as The hypothesis that CFS is a psychosomatic illness has resulted in millions of ruined and destitute lives. There probably has not been so ruinous a result from a failed hypothesis since governor Phips ended the Salem witchcraft trials. Even the blood letting of the 18th century was fairly minor. After all, how much harm can you do removing a few drops of blood? The hypothesis by medical doctors that it was not necessary to wash hands for childbirth caused many deaths, but at least these mothers were given a fairly quick end. The CFS victims could not collect insurance support or disability and descended into poverty. That hypothesis was probably an important part of the chief cause of death, which was suicide. It is not only in the USA that the physical nature of this disease was denied. A young girl in Australia was taken away from her mother until the age of 18 because the mother dared to disagree with a doctor that the girl was faking her symptoms. It is true that sometimes children do fake symptoms, but it is desperately dangerous to assume any such diagnosis just to avoid some unnecessary medical attention on those other rare occasions. This would be something like a fire department refusing to answer a fire alarm until proof of a fire was mailed to them in order to avoid rare false alarms. Parents were better than physicians at judging their children’s pain, but neither parents nor physicians adequately assessed the children’s pain severity [Singer]. The matter is further complicated with children because they are usually more resilient than adults, so sometimes something wrong is not detected. If anyone attempts to molest your child in this way, it is probably in order to migrate to a more humane country temporarily if at all possible. We should be demanding, that when people are evaluated for social disability benefits and are tested with endurance tests, they should be given follow up tests on following days because the malaise that results can go on for days. Indeed, this inane hypothesis seems to be pervasive worldwide. The psychosomatic hypothesis was probably the main reason why funds were diverted from a USA congressional mandate by the NIH. It is conceivable that lawsuits could arise from it in the future. To see a history, philosophy, and legality of ME (CFS) in the United Kingdom , see this site A poison can not be ruled out as at least a contributing factor [Bell IR 1998], and may have been involved, by virtue of protective chemicals, in the gulf war syndrome. Also the symptoms similar to the gulf war syndrome afflicted many Iraqi civilians, so these are a suspicious coincidence and hint at release of poison gas by bombardment of a depot. Supportive of this is that 45% of Kansas Gulf War veterans who were in forward positions came down with the syndrome compared to 12% in undeployed troops [Steele]. Anthrax vaccine has been proposed as triggering gulf war syndrome with some convincing statistical evidence. However, I believe there may have been other medical procedures at the same time. Also large amounts of aspartame laced soft drinks were provided. Close to two hundred thousand were sickened and over seven thousand have died, most probably from this disease. These brave men were denied support at first also, but CFS and fibromyalgia are now recognized for compensation. One reason the Pentagon denied that poison was involved was that they asked the soldiers who captured the arsenal rather than the soldiers who blew it up. Gulf war syndrome is still unrecognized in the United Kingdom. Ciguatera poisons picked up by oceanic fish in the tropics have been linked to CFS, especially in Japan. This is a poison of many carbon rings generated by algae, which toxin can not be degraded by heat and which is thought to bind to sodium cell wall pumps. It remains in the body for a long time. You may see an extensive discussion of this toxin along with a proposal of a vitamin B-12 antidote hereand here. Mannitol has been proposed as a treatment [Karlin]. Since fish migrate and in addition are transported all over the world, eating oceanic fish or pigs or chickens (it is said that chickens receive only 2% fishmeal) fed such fish may not be worth (Tyson Inc. claims no use of fish) the risk even for healthy people. I suspect that cod-liver oil is safe since it is a northern fish. While the link to CFS has been suggested as misdiagnosis [Ting], it seems obvious that ciguatera poisoning must surely accentuate CFS at least, and should be avoided by everyone. An address of a lab which analyzes this toxin is here.The cost of an analysis is $100. There is a discussion of a case history of a patient who believes that mercury poisoning caused a CFS like affliction. and a controlled experiment found corroboration to this concept [Sterzl]. Removal of mercury amalgam tooth fillings have resulted in significant improvement of CFS symptoms (numerous references in this URL). Mercury release is especially high if amalgams are touched by gold or stainless steel, Having this known poison removed would seem prudent to me. For information on protective measures when having mercury removed as well as other information see this site. and this one. But for a contrary opinion see this site. It is possible that coating the filling with epoxy resin would solve the problem. Fish contain unacceptable amounts of mercury So probably fish should not be eaten, perhaps even by healthy people. Fish oils may be safe, but I have no sure analyses.See this site for fish which have lowest amounts of mercury. or this site for a discussion of fish eating compromises.and this site for analyses,
Aluminum has been found to be significantly higher in CFS than in normal people [Van Rensburg]. Perhaps aluminum baking powder and pots and pans should be avoided. Aluminum in vaccines have been significantly linked to a CFS like disease [Gherardi].
Women who have taken the medicine Lupron for endometriosis, a fibrous growth of vagina liner growing outside the vagina which afflicts almost 10% of women before menopause, suspect that it makes fibromyalgia worse. It was found that almost 7% of women with endometriosis had chronic fatigue syndrome or fibromyalgia (CFS) and CFS was 100 times as common as in the female population and fibromyalgia was twice as common. Half of women with endometriosis had allergies and even a greater per cent of those with allergies also had CFS [from a dead URL]. Some of these ratios may have been affected by medications like Lupron they had taken and some due to some extent to much higher rates of low thyroid secretion than in other women. That there is an intimate connection and not due to any generalized decline in health seems likely because fibromyalgia and rheumatoid arthritis was correlated much less and diabetes not at all [Sinaii]. According to this study there must be a relation between CFS and multiple sclerosis, lupus erythematosis, or Sjogren’s syndrome as well. [Sinaii] A recent study has shown a correlation with dioxin from living near an incinerator or a diet high in fish and endometriosis [Rier]. Half of people who have fibromyalgia are sensitive to pollution/exhaust, cigarette smoke, gas/paint/solvent fumes, and perfumes [Bell IR 2001]. Poisons like DEET and permythrin when combined with stress or synergism with other poisons causes brain damage in animals [Abou-Donia]. This may be the reason why poisons seem to be causal. Chemical sensitivity may be operating through a
nitric oxide/peroxynitrite mechanism. [Pall 2002] [Pall & Satterlee]. Also see this site. and this one. It could be that viruses can trigger this problem. This may be acting through four known mechanisms, nitric oxide-mediated stimulation of neural transmitter release; peroxynitrite-mediated stimulation of post-synaptic NMDA sensitization; peroxynitrite-mediated blood brain barrier permeabilization and nitric oxide inhibition of cytochrome P450 metabolism, all of them acting synergistically to create an extreme sensitization and much misery. NMDA (N-methyl-D-aspartate) is (part of?) a neuroreceptor in the brain and spinal cord for the neurotransmitter glutamate (the most important excitatory transmitter in the brain) and is said to be involved in the toxic effects of excessive glutamate. NMDA is said to be not only a neuroreceptor but is also an ion channel and is involved in chronic pain [Pall, in a paper to be published soon]. This hypothesis does not immediately suggest to me a course of action (but see Konopin below). However there is one circumstance that does. Those with multiple chemical sensitivity are often reported to have low magnesium pools, and Pall says that magnesium is known to lower NMDA sensitivity (see further discussion of magnesium below
). Also cobalamin (vitamin B-12) has been proposed as a nitric oxide scavenger [Pall 2001]. Some people have enzymes missing capable of degrading poisons and insecticides are extremely susceptible to even minute amounts of poisons. As a result insecticide residues and many pharmaceuticals are ruinous for them. It has been proposed that aspartame, an artificial sweetener, will damage the hypothalamus, which part of the brain controls steroids and seems to be defective in CFS. Aspartame degrades to the very poisonous methyl alcohol (methanol), poisonous because it can become formaldehyde. Aspartame is suspected to cause blindness, systemic lupus, and cancer among other things, and mimics multiple sclerosis in some people. The following abstract was obtained from Gateway: Malcolm Randall Veterans Affairs Medical Center, Gainesville, FL, USA; “CASE SUMMARY: Four patients diagnosed with fibromyalgia syndrome for two to 17 years are described. All had undergone multiple treatment modalities with limited success. All had complete, or nearly complete, resolution of their symptoms within months after eliminating monosodium glutamate (MSG) or MSG plus aspartame from their diet. All patients were women with multiple comorbidities prior to elimination of MSG. All have had recurrence of symptoms whenever MSG is ingested. DISCUSSION: Excitotoxins are molecules, such as MSG and aspartate, which act as excitatory neurotransmitters, and can lead to toxicity of nerves when used in excess. We propose that these four patients may represent a subset of fibromyalgia syndrome that is induced or exacerbated by excitotoxins or, alternatively, may comprise an excitotoxin syndrome that is similar to fibromyalgia. We suggest that identification of similar patients and research with larger numbers of patients must be performed before definitive conclusions can be made. CONCLUSIONS: The elimination of MSG and other excitotoxins from the diets of patients with fibromyalgia offers a benign treatment option that has the potential for dramatic results in a subset of patients.” [Smith]. See http://www.lassesen.com/cfids/cheap_help.htm for some inexpensive, non prescription medicine protocols against CFIDS and a site at http://www.lowdosenaltrexone.org/ that describes a prescription medicine called naltrexone, which is said to increase endorphins in the body by temporarily blocking endorphin receptors without serious side affects.
You may see numerous links to discussions of aspartame at this site. . Nevertheless it seems to me that it would be good common sense to eat, drink, breathe or smoke no poisons if you are afflicted with CFS or fibromyalgia, or for that matter, anytime. Imidazolidinyl, a preservative in cosmetics, has been shown to cause a disequilibrium of potassium, sodium, and calcium channels in sea urchin eggs [Amouroux]. Until researchers figure out the affect of chemicals on CFS/ME it might be prudent to eat or apply no chemicals of any kind, even in small amounts. Sodium stearate soap is safe though, more than likely. There is some circumstantial evidence that strong electromagnetic fields can create some of the symptoms of chronic fatigue syndrome [Levallois]. It seems to me that it can not be true, but you should know of the suspicion just in case. DISCUSSION So the cause is suspected but unknown. This leaves us with the problem of what to do about the disease currently while we wait for researchers to find the cure. It has been proposed that poor nutrition and lack of exercise are contributing factors [Johnson H p 685]. It certainly is plausible that a poorly nourished body would be more at risk as is probably the case with most diseases. A vegetarian diet using lots of raw vegetables has significantly improved the symptoms of fibromyalgia with 19 out of 30 subjects reporting considerable improvement of all symptoms after a few weeks [Donaldson]. A Finnish study found raw vegetables devoid of meat, but with vitamin B-12 supplement, reduced the pain, slept better, reduced weight, and reduced cholesterol at the end of three months, but did not improve exercise ability by the end of three months. Despite its benefits, none of the patients chose to adhere to the diet beyond the study period. They did report, however, that their pain gradually returned as they drifted back to their previous omnivorous and probably junk food diet [from a dead URL]. The American Neutraceutical Association editorializes that the diet should be rich in vegetables to cure CFS, and suggests other dietary strategy. Instincts to eat what we were taught to eat when young and to eat sweet foods are overridden with great difficulty. It would be a good idea to find out what in raw vegetables was responsible, especially since it has been found that cooking some food increases the growth rate of animals, probably because interfering materials are destroyed in some of the vegetables by the cooking, something that would be especially important for children. It is possible that increased vitamin C implied in not cooking food may have had an affect, since a pervasive vitamin C deficiency probably exists in our society. and it has been shown that vitamin C cures viral infections. However I suspect that such a diet increased potassium and magnesium inadvertently and, if so, cooking without throwing away the boil water should work almost as well (vitamin C is easily supplemented). Donaldson's diet gave five to six thousand milligrams of potassium per day and 460 milligrams of magnesium. It has been discovered that magnesium injections mute the symptoms significantly [Takahasha][Cox] and in particular,
magnesium is probably central in depression (has numerous links). So magnesium supplements may be in order for CFS and fibromyalgia people who eat junk food and maybe for everyone with CFS and fibromyalgia.. See this site for some case histories of magnesium suplementation. It is said that excess magnesium can damage the kidneys [from a dead URL]. If so, this would be another argument for getting as much nourishment from food as possible and perhaps for not using excessive supplements interminably once body content is normal (see this site for how magnesium was rated by people taking it). This site shows how to increase magnesium in the diet. Also it has been said that the following medicines can help create a deficiency; benzthiazide, bumetanide, chlorothiazide, chlorotrianisene, chlortetracycline, cholestyramine resin, conjugated estrogens, corticosteroids, demeclocycline, diethylstilbestrol, digoxin, doxycycline, esterified estrogens, ethacrynic acid, furosemide, hydrochlorothiazide, hydroflumethiazide, indapamide, methyclothiazide, indapamide, methyclothiazide, metolazone, minocycline, oral contraceptives, oxytetracycline, penicillamine, polythiazide, quinethazone, tetracyclines, torsemide and trichlormethiazide. as well as diabetes, use of diuretics and digitalis, excessive stress, exercise, malabsorption, poor diet, alcoholism, and heavy metal poisoning [from a dead URL]. Magnesium is said to be excreted in greater amounts during respiratory acidosis, so it may be desirable to sleep with the windows open at night or to install a carbon dioxide absorber in the bedroom. This suspicion is reinforced by the fact that the steroid hormone which stimulates acid excretion, 18hydroxy deoxycorticosterone is secreted poorly during CFS, possibly a mechanism to allow an acid serum to activate immune enzymes. This last magnesium matter may be invalid because respiratory alkalosis is also said to increase magnesium excretion. However, the logical way to handle magnesium is to make sure it is adequate in the diet in the first place at least. Magnesium was found to be normal in the red cells in CFS patients [Hinds] and magnesium is normal in blood cells during a magnesium deficiency as well, so red cell content can not be used in diagnosis. For a discussion of several types of magnesium diagnostic tests, see a link in this site. There also has been developed 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. You may see an excellent article by Seelig which proposes magnesium as of central importance in CFS and fibromyalgia. and also see
this site for magnesium in fibromyalgia. In addition there is an article which discusses clinical aspects of magnesium with extensive references. Potassium can not be absorbed efficiently in the presence of a magnesium deficiency and magnesium tends to be correlated with potassium intake. Total body magnesium does not predict a deficiency, but blood serum must be low for prediction. If blood magnesium is 25% low, the enzymes depending on magnesium fail to operate adequately, including those responsible for its own absorption. and it is possible that inositol (vitamin B-8) [Charalampous] [Bian] is also. Inositol may be similar to magnesium in its affect [Bian] [Allard]. Also see this site for a discussion of nutrients which affect the potassium pumps, including inositol, especially as pertaining to pain during diabetes and this site for sources (a commercial site).. For a large number of articles presented to a recent symposium on magnesium, see this site. Chlorella pyrenoidos (an alga plant) supplements have also been found to improve fibromyalgia in a three month study [Merchant]. The amounts of chlorella per day were 10 grams of dry chlorella which furnished 83 mg of potassium and 33 mg of magnesium [Merchant, private communication]. This is not enough of these electrolytes to account for any affect. However people eating a vegan diet which included nori and chlorella algae had double the vitamin B-12 in their blood [Rauma]. Chlorella contains vitamin B-12 [Davis]. However there is a suspicion that this vitamin B-12 is only a useless (or worse), analog. Chlorella also contains inositol [Pratt] which is essential for some of the electrolyte pumps [Bian].
It is possible that the fact that Donaldson’s diet tripled the usual intake of potassium was a considerable advantage of the diet. (see this site for a case history of successful use of potassium supplements). (see this site for a case history of successful use of potassium supplements). A whole body (cell content) analysis of potassium has found that potassium averaged a little lower in CFS than the general population [Burnet] which general population is low in potassium in our society to start with. The CFS average was about two thirds of the highest values of healthy people. This is ominous because the highest of these values is the normalcy which the body attempts to attain, since there is no storage of potassium in the body other than the tolerable range of the small amount of soluble potassium in the cell fluid. The low cell potassium may be the reason why the resting energy output is somewhat greater in CFS than normal [Watson]. Chaudhuri, et al suggest that this rise in resting energy is due to abnormal ion channel function similar to that in syndrome X (sic) [Chaudhuri].However red blood cells are not the same as other cells, and show no correlation with plasma potassium [Ladefoged]. It could be that potassium supplements are in order [Lawson 1996], especially if the diet consists of processed food. Magnesium should be part of the experiment since potassium requires adequate magnesium in order to be absorbed effectively [Petersen][MacIntyre] and it is possible that inositol [Charalampous] [Bian] is necessary also (see this site for a discussion of nutrients which affect the potassium pumps, including inositol, especially as pertaining to pain during diabetes). While excessive salt intakes are detrimental to potassium retention, it is necessary to receive moderate amounts of sodium salt because extremely low intakes of sodium (or chloride?) also increase potassium excretion. Experiments must be performed with caution, however, because when a patient thought to be exhibiting symptoms of fibromyalgia was brought to 5.0 mEq/l in her blood (which is close to normal) she contracted paralysis [Gotze]. This may be because experiments have shown that people who have CFS with muscle pain have normal serum potassium [*] and so fibromyalgia must be a different variation of CFS. It is possible that the greater incidence of fibromyalgia among women who do not drink alcoholic beverages [Schochat] is related to the poison (in this case medicine?) in wine that interferes with potassium excretion [McDonald]. I have no information as to whether this poison has been identified and ethanol is said to increase excretion [McDonald]. In monkeys the electrocardiogram in magnesium deficiency resembles that of high serum potassium (hyperkalemia) in spite of low serum potassium (hypokalemia) [Manitius p39]. So it is possible that lower cell potassium requires lower serum potassium for adequate nerve transmission, but the serum potassium does not drop correspondingly [Manitius p38] during a magnesium deficiency. This may be part of the pain in fibromyalgia, analogous to the pain from cold fingers [Benjamin] probably arising from potassium [Ghosh] released from the cells by cold [Ulrich] below 4 degrees C [Hendricks]. Another possibility is that the low secretion of ACTH by the pituitary gland causes a lower secretion of 18 hydroxy deoxycorticosterone (18OH DOC) steroid. This in turn interferes with excretion of acid since the body probably uses that steroid to stimulate excretion of hydrogen ion. As a result aldosterone is decreased in order to prevent loss of potassium and the serum potassium rises. The cell fluid becomes more alkaline [Strobel] and the cell fluid pH (alkalinity) is the most reliable indicator of the intensity of muscle spasms [Krapf]. If muscle spasms are associated with chronic fatigue syndrome, it is possible that a low cell calcium in that disease even though serum calcium is normal [Magaldi] could be the reason. If a magnesium deficiency does develop, half a year of magnesium supplements can be required for complete normalization of magnesium and potassium - sodium pumps [Anonymous] [http://www.lef.org/prod_hp/abstracts/potassiumabs.html#26 ]. Not all the phenomena associated with a magnesium deficiency take so long. Magnesium supplements reduced leg cramps during a pregnancy in three weeks without any change in serum [Dahle]. Interleukin-1, interleuken-6, and tumor necrosis factor increase dramatically in the serum after 3 weeks of magnesium restriction in rats as well as the neuropeptide substance P [Weglicki 1992], which last causes histamine and PGE2 to rise [Weglicki 1994] in only 5 days, so it is possible that these would recede just as fast after repletion. It is obvious that the changes in the immune system (such as any change in IgE antigen [Wei] or rise in white blood cells [Gaudin-Harding] ), during CFS that might occur could easily be augmented by a magnesium deficiency. There is a suspicion that malic acid is helpful in the CFS diseases, so perhaps magnesium should enter as the malate (see this site for rating of malate by people taking it). Aspartate has been used with magnesium during heart disease therapy in the past, so the aspartate may prove advantageous as well. Agar seaweed is a rich source of magnesium and contains 770 milligrams per hundred grams of dry weight. Also the greater ease with which potassium enters the body as the chloride [Classen] suggests that perhaps this anion should be tried as well for magnesium. It is also possible that associating magnesium with the chloride might prove disadvantageous since 18 hydroxy deoxycorticosterone (18 OH DOC) may be low during CFS and that is probably the steroid the body uses to stimulate acid excretion. Using the chloride would have the same net affect as supplementing the diet with hydrochloric acid. If so, eating vinegar may be not a good idea either. Recent experience of mine with damage from toluene in automobile enamel reducer and pain it caused makes me suspect so since vinegar and potassium chloride supplements seemed to augment the pain. I do not know which steroids stimulate or inhibit chloride excretion and it may not be known. This then would be an additional reason for being cautious about chloride. An additional reason is that potassium as the chloride raises blood pressure (in rats) rather than lowering it. So presumably potassium chloride should not be used as supplements if your blood pressure is high (hypertension) or you are in pain. If you wish to try increasing potassium by diet you may see a table which gives the relative values of potassium as milligrams per calorie at http://members.tripod.com/~charles_W/table3.html or in descending order of concentration at this site http://members.tripod.com/~charles_W/table2.html. Considerable increases in potassium are possible without the necessity of eating food raw and there is less danger of imbalances with other nutrients using food rather than supplements. For instance the magnesium problem should be adequate that way, at least for maintenance amounts. For CFS patients magnesium injections may be necessary at first. Vitamin D is proposed as necessary for reabsorption of magnesium in the kidneys [Ritchie]. Half of fibromyalgia patients have vitamin D levels less than the amount which starts to stimulate parathyroid hormone [Huisman] and fibromyalgia patients are much more often showing low vitamin D in their blood than normal women [Al-Allaf]. It is likely that the affect on magnesium is involved, and thus indirectly powers the potassium pumps [Grace]. The optimal values in the blood are proposed as 45-50 ng/ml or 115-128 nmol/liter of vitamin D. It is possible that CFS victims may have net bone resorption. which would be an additional reason for keeping vitamin D more than adequate. People getting no sunlight should supplement with 1,000 IU of vitamin D, which is 5 times the usually recommended amount [Glerup]. A double blind experiment was performed testing the efficacy of a complete spectrum of nutrient supplements and no significant improvement was found. [Brouwers] However only 20 mg extra per day of magnesium was added which is hopelessly inadequate. Also there was only 750 mg extra of potassium which in most people would probably be only a maintenance amount added to the usual 1500 to 2000 most people receive these days. In addition, the potassium was probably as the chloride, which might not be the best form for these diseases. In any case, it would seem to be desirable to know what are the optimum ratios of the electrolytes in the diet to make their correct regulation the easiest. It would seem that the determination should be made differently for fibromyalgia than for CFS because the changes in cell pH (acidity) are similar to controls during CFS [Wong]. It may be that meals should be more than three times per day in smaller increments. I suggest this because secretions from the adrenal glands are important in handling nutrient disposition in the body, especially potassium. Since the adrenal glands in CFS patients average smaller than other people [Scott & Dinan 1999] and the patient's depression has much lower ACTH (and therefore cortisol and 18 hydroxy deoxycorticosterone secretion) [Demitrack] which lower cortisol may be partly from the smaller glands, it is possible that any disruption in secretion mediators would be making it more difficult to handle food surges. There is a good chance damage to the part of the brain which controls the pituitary is a more important part of that low cortisol than gland size, by virtue of disruption of the brain-pituitary axis [Scott, Svec & Dinan] and therefore ultimately of ACTH secretion, which ACTH stimulates cortisol secretion and is absolutely essential for 18 OH DOC. Determination of salivary cortisol upon awakening has been found to be a good noninvasive test for lack of normalcy [Roberts]. Some long-term negative feedback operating on the viability of the cells themselves could conceivably be accentuated by nutrient surges. Also smaller meals would help prevent surges of potassium too high for those with weakened kidneys to handle efficiently as well as possibly increasing the useful cell retention by virtue of preventing the correction of high plasma potassium which otherwise takes place by excretion in the urine and lower colon. Richard Burnet recommends small solid food meals. His rationale is that such a strategy helps prevent the bacterial overgrowth resulting from delayed emptying of the stomach. Since liquids have an even greater delay, he suggests drinking liquids 20 minutes later. I know of no additional experiments to further verify this explanation. However there is epidemiological evidence for the desirability of more small meals during the day. Choline dihydrogen citrate along with vitamin C has given considerable improvement in myalgic encephalomyelitis (ME, probably fibromyalgia). Vitamin C has been given very little attention in CFS research, but extra vitamin C creates less fatigue in healthy people. A trial with alanthamine hydrobromide which inhibits the enzyme which degrades choline gave dramatic improvement in sleep defects in CFS. Richardson believes that correcting the choline deficiency is better than the use of alanthamine hydrobromide [Richardson]. This author nature boy is inclined to agree but perhaps both would be helpful at first. Vitamin B12 and folic acid are said to be cofactors with choline [Richardson]. Melatonin is the hormone which is thought to be central in circadian sleep patterns and has been shown to be helpful [Smit] against depression caused by poor sleep habits. It should be fairly harmless. However its affects on birth defects is said to be not known yet and research has indicated little relief [Williams]. Most indicative of contraindication for melatonin is that it is dramatically elevated in juvenile CFIDS [Knook]. Because of very low vitamin B-12 in the brain large injections may be in order, which are only available by prescription or perhaps less expensively, by use of DMSO for skin absorption and this site. In any case, all this should be on top of a nutritious diet to start with. In particular it has been proposed that linoleic acid (omega 6) may be deficient in myalgic encephalomyelitis (ME) [Richardson] and very few people take magnesium or potassium in supplements. The ratio of omega 6 to omega 3 oils should be one, but modern diets are much higher [Simopoulos]. You may see a graph showing ratios of essential oils in some foods here. However it is probably not a good idea to add excessive amounts of these oils to your diet because they have been associated with breast cancer and omega 3 may could possibly inhibit the immune system [Grimm] in excess (but apparently not the white cell (T and B cells) functions [Kelley] ). For that matter excesses of anything are probably rarely advantageous. However, supplements of omega-3 may be in order if you are afflicted with depression since depression has been negatively correlated with amount of omega 3 oil eaten. Copper intake in America is about half of the RDA. Researchers fed 24 male subjects low copper diets and found a closely tied drop in the levels of enkephalins (the internally produced substances that provide us with pain relief and pleasure) that were produced in the brain. [Journal of the American Medical Assoc. 224: 1578 (1973) ][Bhathena]. Depression has been relieved with copper supplements [Hansen], so it is possible that the depression often associated with CFS could be reduced that way also. It has been found in the past that copper supplements reduced the inflammation of rheumatoid arthritis. The reason why copper seemed to impact arthritis may be because a copper deficiency increases mast cells half again as much in rats [Schuschke], which in turn increases inflammation caused by histamine released by those cells as stimulated by the immune peptide hormones. Therefore it may be that copper supplements should be tried for people with fibromyalgia, since there is often depression and sometimes some inflammation. There is the additional possibility that relieving the low copper intake characteristic of our society would be helpful in view of the known strong dependence of the immune system on adequate copper. To see how to increase copper in the diet read this site; mollusks and liver are the richest food sources. However shellfish in some areas have very large amounts of cadmium and are high in lead and arsenic also. I also have concern that shellfish from the tropics may contain ciguatera toxin, as has been mentioned above. Spirulina seaweed is said to be a very rich source of copper, six milligrams per hundred grams of dry weight. Cheney believes that extra copper is damaging, however. Extra copper during a zinc deficiency certainly can be. In any case you may see a table for copper and zinc in food expressed as milligrams per thousand Calories here. It has been found that there is a significant inverse relation between vitamin E and fatigue in CFS [Vecchiet].
NADH (nicotinomide adenine dinucleotide) has helped in CFS, SAM (S-adenosylmethionein) has reduced pain and depression in fibromyalgia, and 5-HTP (5 hydroxytriptophan) is thought to increase the brain’s sleep and antidepression hormones [from a commercial site], but it is very expensive. It has been found that depression is relieved somewhat by inositol supplements. If so, it is conceivable that this may be related to increasing the power of the sodium and potassium cell wall pumps.
While individual nutrient supplements may prove to be in order for CFS, it is futile to think that any patient can get nourishment just right by eating processed food with varied nutrient losses and additions, and then exactly correcting with pills. This is so even if the macronutrients like potassium, calcium, phosphate, and magnesium are supplemented also and even for people who are expert dietitians. There is NO GOOD SUBSTITUTE for an undamaged diet. There have been encouraging improvements achieved in CFS victims with lifestyle changes including nutrition, alterations in intestinal bacterial flora, and removal of foods causing allergic reactions. Food elimination strategies have been said to produce significant clinical responses in 50-80% of patients with particular benefits seen in gastrointestinal complaints, migraine, arthralgias, recurrent upper respiratory tract infections including the sinuses and urinary tract infections. It is also thought that weight gain during CFS could be largely from food sensitivity [from a dead URL]. There is another elimination which was found to eliminate headache That was the elimination of monosodium glutamate [from a dead URL].I also suspect that acid foods such as vinegar or potassium chloride can augment headache. Adding potassium chloride to a junk food diet should have the same affect as adding hydrochloric acid to a normal diet. I also suspect that something in raw cashew nuts can also produce a headache in some people based on personal experience. There is a report of relief from intestinal bacterial overgrowth by means of enteric coated peppermint oil [Logan and Beaulne]. I would be hesitant about such a strategy if other means were available however. Natural medicines can be just as risky as artificial ones. Digitalis, ricin, ciguatera, and cyanide are all natural, for instance. It has been proposed, though, that lactic acid bacteria can have therapeutic value [Logan, Venket, and Irani]. If so, I would suspect that they would be most affective introduced encapsulated in enteric capsules and taken with milk. CFS RELIEF BY EXERCISE Exercise has also been found to be helpful in CFS by numerous experiments [Hakkinen][Mengshoel]. Both moderate and intense exercise has shown to be helpful [Hadhazy] (it is possible that his patients were misdiagnosed). However, over training can precipitate CFS [Shephard] and exercise brings on a severe fatigue which lasts for days [Johnson H p329-330, 491-492] so it seems to me that exercise should be very mild (such as slow walking [Coutts] ) or better yet swimming for both CFS and fibromyalgia. This is supported by an experiment which showed that exercise in a pool gave less pain, anxiety, depression, and more days of feeling good [Jentoft] than terrestrial exercise and the effects lasted more than six months [Mannerkopf]. Short, mild treadmill exercise caused no obvious problem [Clapp]. I suspect that many short periods of mild exercise across the day would be the preferred routine. I suspect "across the day" partly because clearance of blood through the liver in order to remove electrolyte hormones such as aldosterone [Messerli] (which removal decreases potassium losses and sodium retention) is probably an important part of the value of exercise. A rocking device has been found to increase nitric oxide similar to actual exercise, so this may prove to be a mild substitute for exercise and thus avoid the deleterious effects from rigorous exercise. Even robust exercise had beneficial results in some of the symptoms other than the symptoms mentioned above [Hadhazy] but it is conceivable that these patients had a different part of their brain affected by the disease and most researchers believe that if robust exercise made an improvement the situation was misdiagnosed. Lerner has a hypothesis that the poor tolerance to exercise in CFS is because the heart is infected with various herpes viruses and has considerable autopsy evidence. If so exercise that puts a strain on the heart would be dangerous. There have been a number of situations in Queensland, SA and NSW Australia where CFS children, mainly in a hospital setting, have been made quite ill by excessive exercise, and when parents intervened to halt the harm, were threatened with loss of the child if they do not allow the practices to continue. Athletic ability before becoming ill has nothing to do with post-illness exercise capacity, and often sedentary persons become less ill than those who were athletic. In some of the outbreaks, the bedridden hospital patients were the only ones to escape contracting the disease [Bruce].
Until researchers get it figured out it would be a very good idea to approach exercise cautiously and very moderately indeed. It is rare in life when moderation is harmful. It has been suggested that patients make a "NOT TO DO" list. It might be a good idea for healthy people too. It has been proposed that cytokine peptide protein hormones which regulate the immune system are responsible for much of the problem and that they can be reduced by vertical immersion in water at 85 degrees Fahrenheit several times a week. Of course this may not be a good idea if an infection is still being resisted. DEVICES There are many clever devices which have been invented for other degenerative diseases. There is no reason why these devices can not be made available if they can be financed by society. Societal support would be necessary for most because severe CFS is so debilitating that it is impossible for some of these people to support themselves. The most debilitating infirmity other than fatigue is loss of memory. CFS patients should carry maps with them showing the way home and notebooks with important information like phone numbers and grocery lists. This should help considerably. For those who have lost fingerprints [Johnson H p345] a good ID should always be on them and perhaps name and phone number imprinted on their arm with a dye. Another procedure, which should be effective, would be to set up a system whereby a CFS patient could carry a cell phone with a button which automatically dials a central office which has people on duty familiar with the important information in the patients life. That office should be skilled at giving emotional support in order to deal with the depression often present. For a dozen or so clever devices to use during the fibromyalgia type CFS see this site. POSSIBLE NATURAL MEDICATIONS AND OTHER NUTRIENTS It has been suggested that not eating or drinking caffeine before going to bed will aid in muting restless legs syndrome, which often also afflicts people with rheumatoid arthritis, diabetes, and some types of anemia [from a forbidden URL]. Coffee, tea, cocoa, and many soft drinks are sources of caffeine. Keep in mind also that caffeine is suspected of increasing potassium excretion. There is evidence of opportunistic herpes infection since 77% of CFS patients contain antibodies to HHV-6 EA as IgM and IgG [Patnaik]. It may therefore be prudent for these CFS people also to eat sparingly of foods high in arginine continuously after CFS or maybe until tests determine that the immune peptide hormones [Patarca] and natural killer cells [Caligiuri] are all normal again. This is because the amino acid, arginine, accentuates the symptoms of herpes [McCune] and maybe even trigger a resurgence of a dormant infection such as shingles (which disease is a resurgence of dormant chicken pox virus from nerves near the spine). Foods high in arginine are peanuts, cashews (peanuts are 50% higher than cashews but cashews are substantial), chocolate, and seeds other than the grass derived grain. See http://www.herpes.com/Nutrition.shtml here for a table which gives lysine and arginine values). You may see an excellent table of nutrients including amino acids ( Just divide the values by the Kcal figure to get valid comparisons. Gain access by typing in food desired and then using the enter or return key. There are also links to PDF types of printouts from the table for individual nutrients). Zinc has been proposed as being able to prevent and kill cold viruses and other viruses. This they are thought to do by making the cell membrane less permeable and by inhibiting viral replication. Zinc concentration in fluid outside the cell is normally 0.015 millimoles. Zinc at 0.1 t0 2.0 millimoles is as effective in controlling virus as the most effective interferon-beta concentration. Recommended topical application is 0.2 to 2.0 per cent or 9 to 90 millimoles. Zinc is most available as the acetate [Eby]. Of especial interest to CFS victims is that Eby mentions a single case history of a successful cure of Epstein Barr virus (mononucleosis). Sitosterol, a steroid present in plants, has evidence to indicate that it boosts the immune system [Bouic]. Wheat germ is said to be a rich source. This is another hint that whole foods are in order. Those who have CFS should not be afraid to experiment with nutrients. The human body is very resilient. As long as you do not use a poison or procedure known to be harmful, there is not much chance that irreversible harm will transpire. Experimenting has some risk but doing nothing is even riskier. You may see an article which gives a diet for fibromyalgia arrived at by experimenting at this site. If you do come across a nutrient, combination of nutrients, or procedure or other circumstance which produces perceptible positive or negative effects, perhaps you could see yourself clear to email the information into a site which is attempting to archive such experiences and/or the author of this article at; Charles Weber ------- isoptera@angelfire.com with CFS as the subject. The author will never use your name or email address for any purpose. Single case histories can sometimes be more effective in moving forward research than blind experiments averaged [Buchanen][Urowitz]. ALLERGIES As to NOT eating something in order to test the possibility of food allergy, which is often present, the chances of irreversible harm are vanishingly small. Some of the reactions to foods were pain, headache, and gastrointestinal distress in one study. The most common problem-causing foods or ingredients for the patients in this study were corn, wheat, dairy food, citrus and sugar [Edman]. I am inclined to doubt the citrus, although it could be acting in a non allergic way as mentioned above. It is very unlikely that sugar can produce an allergy. However sucrose and fructose can interfere considerably with copper metabolism so a different mechanism could be involved with sugars. Wheat is another matter. Some people are genetically unable to digest the gluten protein in wheat and as a result are afflicted with coeliac disease. This is probably not an allergy as allergy is usually defined. It is conceivable that the damage to the intestines that this causes may be interfering with absorption of potassium and other nutrients. See this site for food that do and do not contain gluten.You should consider the following from a CoCure post by Dr. Charles Shepherd; Of course your single case history for allergy or deficiencies is almost useless epidemiologically (the study of health statistics) by itself. However, perhaps it could become useful if you became a member of a group that keeps records and is willing to make the records public anonymously. Millions of people eat things about which no records are kept, such as hydrogenated oils and additives. If they are not studied by the people who sell them, the government agencies, or the universities, then it would be a good idea if the people who eat food did so. Keep in mind that adverse connections to food probably usually take twelve hours or more to materialize. Desirable connections to essential nutrients can take days or weeks, such as potassium for instance, and can often depend on synergistic affects. MEDICAL PROCEDURES There have been two case histories in which dramatic improvements were attained in which removal of pathogenic bacteria by doxycycline 2 was the principal medication. It is said that that medicine has anti-inflammatory affects also, so one can not draw certain conclusions yet. As already mentioned, doxycycline may cause greater magnesium excretion, so supplements might be necessary. A way of stimulating the immune system by use of a medicine called Ampligen (polyI-polyC12U, produced by Hemispherx Biopharma Co. or HEB) is said to show promise. There is a discussion of numerous medications for killing infectious diseases at this site. Just do not engage in any procedures out of the ordinary which go on interminably, especially medication or pain deadeners (analgesics) since pain deadeners have been proposed as a risk factor for CFS [Johnson H p574]. Also several pain deadeners have been found to damage the kidneys. Among the prescription and over the counter medications that predispose patients to such damage are acetaminophen (Tylenol, Anacin-3, Liquiprin, Panadol, and Tempra) but not aspirin [Schwarz]. Kidney damage is extremely serious. Also it is plausible that anything which can damage kidney cells could damage immune cells as well. The chance that a pain deadener will have any direct curative affect is extremely small, so it usually is better to tolerate the pain if at all possible. A 1998 medical report estimated that adverse reactions to prescription drugs kill about 106,000 Americans annually, roughly three times as many as are killed in automobile accidents. You may see side effects of medicines at this site. One exception to adverse affects of pain medicines may be Methylsulfonylmethane ( MSM). It is said to be fairly effective and virtually free of side affects. You may see the results of numerous case histories at this site. It may be that it warrants more investigation [Parcell]. However some people report an adverse reaction to it, which could conceivably be due to a bad batch. Another pain deadener which is said to work by inhibiting brain transmitters is the drug, Neurontin. I do not know if it has side effects or not. Cheney says that the medicine called Klonopin protects brain cells from over stimulation and cell death without dangerous side effects. Flechas uses essential plant oils to decrease pain. It is useful to know that smoking enhances pain but not fatigue [Yunnus]. Fibromyalgia seems often to be made worst in hypertensive patients who are treated with ACE (angiotensin conversion enzyme) inhibitors and ACE receptor blockers. A study of the side effects of these medications shows muscle pain as a potential side effect. Medications by name include accupril, altace, atacand, avapro, capoten cozaar, diovan, hyzaar, lotensin, mavik, micardis, monopril, univasc, vasotec, and zestril. Ask your doctor if your medications for high blood pressure are any of the above. See this site for other natural ways of lowering blood pressure. Attempting to correct the low cortisol in CFS with cortisol is useless because there are no significant good effects [Levine ( Copies of the complete article are available for a fee from The Haworth Document Delivery Service: 1-800-342-9678. E-mail address: getinfo@haworthpressinc.com ) ]. In any case cortisol or any other glucocorticoid should not be taken during any infection because of its known considerable dampening of the immune system. If cortisol is used, a single daily dose is probably not effective because cortisol is rapidly converted to an inactive form [Ulrich 1958].
There is an extensive discussion of drug and herbal medicine adverse interactions at this site. There is a suspicion that isotretinoin (brand name Roaccutane, for acne) can trigger an attack of chronic fatigue syndrome. The American Food and Drug Administration has a program called MEDWATCH for people to report adverse reactions to untested substances, such as herbal remedies and vitamins. Call 800-332-1088. There is a suspicion that isotretinoin (brand name Roaccutane, for acne) can trigger an attack of chronic fatigue syndrome. The American Food and Drug Administration has a program called MEDWATCH for people to report adverse reactions to untested substances, such as herbal remedies and vitamins. Call 800-332-1088. Infusions or injections intra muscularly of the immune hormone IgG, especially intramuscularly (probably this way because the IgG was not degraded too quickly by the blood enzymes), to pregnant mothers has shown to give very effective protection in preventing birth defects in the babies when the mothers showed titers to a Coxackie virus. 500 mg weekly provided the affect [Richardson]. The affect was probably from enhancement of the immune system. P>There is a report that Hypobaric treatment (increased oxygen pressure) will ameliorate the symptoms of fibromyalgia. . This would seem to indicate another reason for providing plenty of ventilation, especially while sleeping.
When surgery is necessary for CFS patients (including dental procedures) it is imperative that doctors become familiar with contraindications for medication because CFS patients are very susceptible to adverse reactions from some anesthetics and other medications and usually much smaller doses are indicated.
EMOTIONAL SUPPORT Depression often shows up in CFS. Therefore it is almost certainly desirable for those who love the sufferer to apply as much emotional support as possible. Emotional abuse has been found to be correlated with fibromyalgia [Walker]. Good jokes, camaraderie, and tactile approval (like hugs) will not cure the disease since psychological state has little affect on the disease itself (as opposed to the disease creating the psychological state [Tiersky] ), but there is a good chance they will mute or distract some of the symptoms and make an eventual defeat of whatever infection is involved or become involved opportunistically a little more likely (see this site for ways of coping with stress). There has been a study which indicates that women seek female companionship when stressed and that this soothes them. It is proposed to operate through the oxytocin hormone (see this site for treatment of fibromyalgia with oxytocin) with an assist from estrogen. Considerable health and lower mortality benefits are statistically obtained [Taylor]. Massage has been helpful for fibromyalgia [Field], massage being the most helpful of physical manipulations [Hong], but there is a good chance that this is also a placebo effect on the immune system. Massage of the neck is said to make the situation worse if there is a compression of the neck vertebrae. Emotional support for children is especially important since emotional abuse is said to be a risk factor for children who have been emotionally abused [Imbierowicz] and children who have had psychiatric problems in the prior year were much more affected by their CFS [Rangel]. Just be sure to make kissing or eating and drinking out of the same plate not part of the procedure because there is a suspicion that the last of the two is a risk factor for others and also increases the chance of opportunistic infections. Staying warm will also probably prove to be advantageous since it has been shown that staying warm enhances immunity [Hanson]. I have often cured a cold within a couple hours with an infrared heat lamp directed to my nose and I have heard of people who claimed to have eliminated CFIDS with infrared saunas. How to make or acquire a sauna is discussed here. I suspect that a few electric light infrared bulbs would be all that is required. Guarding the sufferer from fear and tapping spiritual resources and fear is well known to affect the immune hormones. Fear may be contributing to the lower potassium in CFS by increasing aldosterone as well and ways of coping with emotions, both good and bad ones, which last are said to worsen symptoms, at this site. There is a site that enables singles with CFIDS to contact each other. I have no experience with the site. Do not allow anyone convince you that the disease is hypochondria, or hysteria, or a spell from the wicked witch of the west. Everything is something, even if the something is unknown.
SOCIETY EFFORTS CFS and fibromyalgia are potentially extremely dangerous to society because of their severity and length of recovery time. The vector for this disease or these diseases is unknown at present but there is a good chance that pathogens are causal. 6.4% of patients in an unreported study were triggered by a blood transfusion [from an unreported study]. If a mosquito ever "learns" how to transmit it, the situation will be desperate for society. Therefore enormous research effort should be mobilized to not just ameliorate it, but like smallpox, to eradicate it.
If all the mitigating factors which have been discovered so far are all implemented, in my opinion there is a good chance that people with CFS and fibromyalgia will be able to lead reasonably satisfactory lives of higher quality .(also see this site for a multi treatment experiment). Be very cautious of medicines based on chemicals, however. In particular it is important to eat a nourishing diet. This means much more vegetables and ruling out almost all processed food and making sure that people do not leach or boil out any nutrients themselves. I warmly recommend this even for healthy people. It is by no means necessary that such a diet be unpalatable. If many vegetables are blended together in salads and soups they will taste much better than eaten separately in my opinion. Also there are many harmless foods with strong flavor such as lemon juice for instance, which can add “zing” to the food, as well as spices, many of which are probably reasonably harmless. If you use lemon juice or vinegar, be sure they contain no sulfites and keep in mind that these acids may yet prove to be disadvantageous. I am almost certain that vinegar gave me a headache during the days immediately after I was poisoned with toluene, for instance. It is possible that supplements may prove to be necessary, but if so, they should be on top of a good, UNPROCESSED nutritional platform and will almost certainly have to include adequate amounts of the macro nutrients, magnesium, potassium, calcium, and phosphate if the diet is not already adequate. Thyroid problems can cause fatigue. See - http://www.ithyroid.com/ - for thyroid. It is possible for people with CFS to have low thyroid secretion, but use of thyroid hormones (thyroxine) must be done with extreme care and be carefully monitored, because cortisol is usually low in CFS and thyroid hormone can have serious consequences with heart rhythm or especially to the adrenal glands. Endometriosis is said to be associated with low thyroid. See - http://www.nlm.nih.gov/medlineplus/ency/article/003468.htm - for explanations of standard blood tests. Click on the name of each test, and it will tell you what could cause that value to be high or low. You may see an elaborate discussion of magnesium with regard to potassium, diabetes, high blood pressure, headaches, and fibromyalgia at - http://magnesiumresearchlab.salu.net/ - .The “magnesium and potassium in lone atrial fibrillation” link is especially informative. See - http://members.tripod.com/~charles_W/tooth.html - for a discussion of raw cashew nuts for tooth abscess. A site is available which shows. foods that are high in one nutrient and low in another (including calories) at - http://www.nutritiondata.com/nutrient-search.html - 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. REFERENCES for CHAPTER XIV in; http://members.tripod.com/~charles_W/cfs.html
PROCESSING LOSSES of POTASSIUM from FOOD
Losses of Potassium in the Kitchen
bean seeds-----------------tomato
beans, green---------------milk
beans, lima----------------corn
beets------------------------milk and/or vinegar
bran-------------------------raisins and milk
cabbage---------------------buttermilk or yogurt
carrots, raw-----------------raisins
carrots, cooked-------------peas
celery------------------------lettuce and apple
chives------------------------cottage cheese
cress, water-----------------other salads
cucumbers------------------vinegar or sour cream
milk--------------------------carob powder
oatmeal----------------------apples, bananas
onions, fried------------ ----liver
parsley-----------------------potatoes
peppers, sweet--------------meat
peanuts----------------------dates
pumpkin, mashed---------eggs, milk, cinnamon
spinach, raw----------------other salads
spinach, cooked------------milk
wheat germ-----------------meat loaf
yeast--------------------------milk
yogurt------------------------strawberries Average Potassium Eaten
POTASSIUM SUPPLEMENTS as AFFECTING RHEUMATOID ARTHRITIS, DIARRHEA and HEART DISEASE
2. Water intoxication can occur if a body low in sodium is inundated with pure drinking water. The symptoms are cramps, fever and confusion. The symptoms are similar to alcohol intoxication. You should not suddenly drink enormous amounts of pure water with no salt when very thirsty. Taken too extreme it can even be fatal.
3. Heat exhaustion is caused by loss of body salts in general, but with strong overtones of potassium loss. Symptoms include muscle weakness, lassitude, nausea, vomiting, and fainting when the body's weight loss is 5% (10% of the water). Treatment can be accomplished with fluids containing sodium and potassium chloride, rest, and cooling. Lane, et al maintains that the minimum daily requirement for potassium on a hot day is over three grams [Lane]. I suspect that it should be considerably higher than that. If a potassium-depleted person who is dehydrated is suddenly supplied with large amounts of pure water, dangerous low blood serum potassium can develop causing respiratory distress [Ellison].
4. Heat stroke is the worst disability because of high death rates. It is a medical emergency and is the result of high body temperatures in the vicinity of 105-16 degrees F. The whole heat regulatory mechanism has broken down by this time due partly to damage to brain cells, which damage may be permanent if not corrected immediately. The symptoms are headache, weakness, vertigo (dizziness), and dry skin. Cooling by dousing with water, especially on the head, is imperative. The situation is sufficiently dangerous that medical help should be called immediately, because intravenous fluids may be necessary to prevent death. The body continues to generate heat so time is of the essence so far as cooling the affected person is concerned. Heat stroke is the extreme of heat exhaustion and is also thought to be largely a potassium deficit [Coburn]. Babies can suffer from heat stroke and is at least as serious to them. Too warm clothes or an overheated car can trigger it. Treatment is the same as adults except it is possible to remove clothing in addition. SUPPLEMENT’S SIDE EFFECTS and HEART DISEASE
WHEN BLOOD POTASSIUM is too HIGH (hyperkalemia}
INTRODUCTION
CORRECTIVE PROCEDURES
CHRONIC FATIGUE SYNDROME (CFIDS, CFS, ME) and FIBROMYALGIA, Some possible helps.
1 'Irritable bowel' symptoms are quite common in ME/CFS but it's worth screening for adult onset coeliac disease (AOCD), especially if the onset of ME/CFS is gradual.
2 Anemia is not caused by ME/CFS (a fairly common misconception). When anemia occurs, another explanation should always be sought.
3 Before experimenting with a gluten-free diet it's a good idea to be screened for AOCD, especially in people who have 'irritable bowel' type symptoms.
4 Some people who claim to have been 'cured' of ME/CFS by a gluten-free diet may not have had ME/CFS at all. The real explanation may have been AOCD - important because treatment of this condition isn't just a gluten-free diet. There are a number of other management issues (for instance increased risk of osteoporosis and small bowel adenocarcinoma) which need to be considered as well. Some physicians even recommend an annual lifelong review of their AOCD patients.
Gastroenterologists believe that we are currently only seeing the tip of the 'coeliac disease iceberg' with many people remaining undiagnosed or being misdiagnosed with irritable bowel syndrome, depression, ME/CFS etc.
EPILOGUE (some links)
To see patient evaluations of magnesium, whey protein, NADH (enada), DHEA (dehydroepiandrosterone), vitamin B-!2, and etc. see - http://remedyfind.com/hc-Chronic-Fatigue-Syndrome.asp - .If you should wish to research past articles involving CFS, see - http://www.me-net.dds.nl/meweb/library.html#bibliography - You may see abstracts of the 2nd World Congress on chronic fatigue syndrome and related disorders with 73 paragraphs on almost every current line of research at - http://www.co-cure.org/infocon1.htm. -
