Potassium physiology as involved in osmotic pressure, acid and base regulation, nerve transmission, and collagen or elastin formation, especially as related to rheumatoid arthritis.
CONTENTS of other chapters Back to INTRODUCTION chapter -- II. Arthritis Research -- III. Arthritis and Potassium -- IV. Roles of Potassium in the Body -- V. Electrolyte regulation (sodium and potassium) -- VI. Purpose of cortisol -- VII. Copper nutrition and physiology -- VIII. Nutritional Requirements -- IX. Potassium in Foods -- X. Processing Losses -- X,cont. Losses in the kitchen -- XI. Supplementation -- XII Side Effects and Heart Disease -- XIVPotassium and thiamin in heart disease -- Strategies for CFS and fibromyalgia
When Blood Potassium is too High
Potassium makes up 70% of the positive ions in the cells [Harper (with graphs)]. The cell is essentially a little bag of potassium salts. The remaining positive ions are sodium, magnesium, calcium, argenine and other miscellaneous ions, primarily charges on the amino acids of the proteins. A lean 70 kg man will have a total potassium content of about 175,000 milligrams when replete [Shohl] (there is some disagreement in the literature as to the exact amount, and a man high in fat would have a lower amount than others per weight). About 2,500 milligrams are in the blood serum. Virtually all the potassium is disassociated [Lev]. This last implies very little storage of potassium beyond its concentration tolerance.
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]. Thiamin [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 in. 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 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.
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.
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, used to retain water by humans), 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.4>
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 (probably including those that destroy infection microbes engulfed by white cells), this drift toward acidity could easily be the reason why people usually can not get over arthritis and may be responsible for some of the symptoms from a potassium deficiency such as heart disease.
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 (This site discusses many herbal remedies) [Blau].
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 potassium supplements (especially after dehydration), 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 that can happen to a person. It is undoubtedly an important reason why the medical profession is apprehensive about potassium and why pills have been limited to a paltry 100 milligrams. Some of the implications of this will be elaborated further in a supplements chapter.
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 that 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).
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 [Alper]. Healthy bone, which is essentially an ossified connective tissue, has a strength which approaches that of cast iron [Summerfeldt]. 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 current losses in nutrition of this much or more (100% from sugar).
Chapter VIII, COMPUTATION of DAILY POTASSIUM REQUIREMENTS
POTASSIUM CONTENT in FOOD TYPES, with links to tables.
REFERENCES are BELOW
EPILOGUE
Dr. Reza Rastmanesh from Iran has recently performed a large controlled clinical trial testing potassium supplements against rheumatoid arthritis with dramatic decreases in pain in all subjects and increases of cortisol [Rastmanesh]. He would now like to continue his clinical research testing potassium in conjunction with other nutrients, especially magnesium, in an English speaking country. His credentials are impressive. If you know of any rheumatology department able to employ him, please contact him with the email address = r.rastmanesh at nnftri.ac.ir - or me with isoptera at att.net , and one of us will send you a copy of the article he has submitted to a journal.
The author, Charles Weber, has a degree in chemistry and a masters degree in soil science. He has researched potassium for 45 years, primarily a library research. He has cured his own early onset arthritis (33 years old). He has published articles on allied subjects in; The Journal of Theoretical Biology (1970, 1983), The Journal of Applied Nutrition (1974), Clinical and Experimental Rheumatology (1983), and Medical Hypotheses (1984, 1999).
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 site which archives such experiences.
All printed rights to this article are reserved. Electronic rights are waived.
SOME LINKS TO HEALTH ARTICLES
The pioneering efforts about potassium for arthritis by Charles de Coti-Marsh enabled him to form a foundation currently active in England that promotes the use of potassium and has helped 3500 people. There is a site that contains reviews of natural remedies for many diseases .
Fluoride in city water will cause fluorosis discoloration of teeth, weakened bones, damage to the kidneys an immune system, and, worst of all, damage to the nerves resembling Alzheimer’s disease.
See this site for some links to health articles.
Olive leaf extract has shown clinical evidence of effectiveness against a wide range of viruses, including AIDS [Bihari], herpes, and cold viruses. It sometimes produces a Herxheimer or pathogen die off symptoms (from effectiveness against bacteria?). There is evidence that it is synergistic (reinforce each other) with Naltrexone. There have been a few case histories of improvement in what were probably arthritis patients and CFIDS patients. The active ingredient is said to be oleuropein or enolate. There has been very little follow up research done on it.
Also it has been found that curcumin in turmeric or curry powder will inhibit several forms of cancer, including melanoma. People who live in India where these spices are eaten, have one tenth the cancer elsewhere.
Here is an article with anecdotal evidence for pressurized oxygen, zinc, vitamin B6, and vitamin C after head injuries. They also claim a fair percentage of prison inmates from psychiatric disorders after head injuries.
A site is available which shows foods which are high in one nutrient and low in another (including calories). This last site should be especially useful for a quick list of foods to consider first, or for those who must restrict another nutrient because of a genetic difficulty with absorption or utilization
The very extensive USDA Handbook #8 may be seen here. To access the information you must press "enter" to search, and then divide Kcal into milligrams of potassium. This last table is very comprehensive, is used in search mode, and even lists the amino acids. There are also links in it to PDF types of printouts from the table for individual nutrients available here Just click on the “A” or “W” button for the nutrient you desire. A table that has already done the potassium calculation is here in descending concentration or in alphabetical order.
There is a free browser called
Firefox, which is said to be less susceptible to viruses or crashes, has many interesting features, imports information from Iexplore while leaving Iexplore intact. You can also install their emailer. A feature that lists all the URLs on a viewed site can be useful when working on your own site. There is a tool bar by Google that enables you to search the internet from the page viewed, mark desired words, search the site, give page rank, etc. It has a link to a literature search. There is a free program available which tells on your site what web site accessed you, which search engine, statistics about which country, statistics of search engine access, keywords used and their frequency. It can be very useful.
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Alper J 2002 Protein structure: stretching the limits. Science 297; 329-331.
Baker PF 1966 The nerve axon. Scientific American 214; 74
Bennett CM et al 1968 Micropuncture study of nephron function in the rhesus monkey. Journal of Clinical Investigation 47; 203
Berliner RW et al`1951 Relationship between acidification of the urine and potassium metabolism. American Journal Med. 11;274.
Bihari B 1995 Efficacy of low dose Naltrexone as an immune stabilizing agent for treatment of HIV/AIDS [letter] AIDS Patient Care 9; 3.
Blau LW. Cherry diet control for gout and arthritis. Tex Rep Biol Med 1950;8:309-11.
Charalampous FC 1971 Metabolic functions of myoinositol: VIIII - Role of inositol in Na+-K+ transport and in Na+ and K+ activated adenosine triphosphate of KB cells. Journal of Biol. Chem> 246; 455 & 461
Davis BB Jr. Knox FG 1970 Current concepts of the regulation of urinary sodium excretion - a review. Amer. J Med. 259; 373;
Davis WH 1970 Does potassium deficiency hold a clue to metabolic disorders associated with liability to coronary heart disease? South African Medical Journal 44; 1297
Dean RB 1941 Theories of electrolyte equilibrium in muscle. Biol. Symp 3; 331-348
Eckel RE et al 1954 Lysine as a muscle cation in potassium deficiency. Arch. Biochem. Biophys. 52; 293
Fourman P 1952 The ability of the normal kidney to conserve potassium. Lancet 262; 1042
Fuhrman FA 1967 Tetrodotoxin. Scientific American 217; 60-71
Halla JT & Ball GV 1982 Seminars Arth. Rheum. _ Saturnine Gout: A review of 42 patients - 11, #3
Hendricks SB 1964 Salt transport across cell membranes. American Scientist. 52; 318
Harper HA 1957 Review of Physiological Chemistry, 6th ed, Lange Med. Pub., Los Allos, California
Holliday MA 1955 Acute metabolic alkalosis: its effect on potassium and acid excretion. Journal of Clinical Investigation 34; 428
Kernan RP 1965 Cell K. Butterworth, Baltimore
Kilburn KH 1966 Movements of potassium during acute respiratory acidosus and recovery. Journal of Applied Physiology 21; 679.
Lamont-Havers RW 1963 Nutrition and the rheumatic diseases - part II, Collagen Diseases, Review of Nutrition Research, Bordons 24; 15-27
Lans HS et al 1952 The relation of serum potassium to erythrocyte potassium in normal subjects and patients with potassium deficiency. American Journal Med. Sci 223; 65-74
Lev AA 1968 Determination of activity and activity coefficients of potassium and sodium ions in frog muscle fibres. Nature, London 201; 1132
Meneely GR Ball COT 1958 American Journal of Medicine 25; 713-725.
Mills JH & Stanbury SW 1954 A reciprocal relationship between K+ and H+ excretion in the diurnal excretory rhythm in man. Cinical Sci. 13; 172.
Orent-Keiles E & McCollum EV 1941 Potassium in animal nutrition. Journal Biol. Chen. 140; 337
Post RL et al 1960 Membrane adenosine triphosphatase as a participant in the active transport of sodiu and potassium in the human erythrocyte. Journal of Biological Chemistry 235; 1796-1802
Potts WTW & Parry G 1969 Osmotic and Ionic Regulation in Animals. MacMillan Co., New York
Rastmanesh R 2008 A pilot study of potassium supplementation in treatment of hypokalemic patients with rheumatoid arthritis: a randomized, double-blinded, placebo controlled trial. The Journal of Pain 9; 722.
Rector FC Jr. et al 1955 The mechanism of ammonia excretion during ammonium chloride acidosis Journal of Clinical Investigation 34; 20
Robinson JD 1968 Regulating ion pumps to control cell volume. Journal of Theoretical Biology 19; 90
Rubini ME & Chojnacki RE 1972 Principals of parenteral therapy. American Journal of Clinical Nutrition 25; 96-113
Schoner W 1971 Active transport of Na+ K+ through animal cell membranes. Angew. Chem. (Eng) 10; 882-889
Sharp GUG & Leaf A 1966 Mechanism of action of aldosterone. Phys. Rev. 46; 593
Shohl AT 1939 Mineral Metabolism. Reinhold Pub. Co., New York
Solomon AK 1962 Pumps in the living cell. Scientific American 207; 100-108
Suelter CH 1970 Enzymes activated by monovalent cations. Science 168; 789-795
Summerfeldt D Rubin C 2001 Biology of bone and how it orchestrates the form and function of the skeleton. 10; supplement 2.
Tannen RL 1977 Relationships of renal ammonia production and potassium homeostasis. Kidney International 11; 453-465
Tarail R 1953 The role of the potassium depletion. Journal Lancet 73; 182-183
Ulrich F 1959 Ion transport by heart and skeletal muscle mitochondria. American Journal of Physiology 197; 997-1059
Yellen G 2002 The voltage gated potassium channels and their relatives. Nature 419; 35-42. Send email to – isoptera@att.com telephone – 1 828 692 5816 (USA)
For a procedure that discusses tetrathiomolybdate for removing copper and thus preventing further solid cancer growth and Hodgkin’s, see this site. This might buy some time until you can persuade a doctor to try tumor necrosis factor or interferon or an opioid antagonist drug called Naltrexone (Naltrexone in the large 50 mg size, originally manufactured by DuPont under the brand name ReVia, is now sold by Mallinckrodt as Depade and by Barr Laboratories under the generic name naltrexone) that blocks some endorphin receptors. Said blockage is thought to cause the body to temporarily secrete more endorphins, especially after midnight at night. These endorphins are thought to stimulate the immune system, and in particular to stimulate the TH-1 or type 1 antiviral response by decreased interleukin-4 and with increased gamma interferon and interleukin-2 and a simultaneous decrease of type 2 anti bacterial response [Sacerdote].
It appears to be especially effective for minimizing symptoms and retarding progression of multiple sclerosis (MS) There are drugs listed in this site that should not be taken with low dose Naltrexone, including cortisol. Advice how to proceed if you have been taking cortisol may be seen here. There are drugs listed in this site that should not be taken with low dose Naltrexone, including cortisol. There is information in this site for mitigating side effects, including starting with one milligram doses. Advice how to proceed if you have been taking cortisol may be seen here. (also see these sites; this site and this site and this site and a trial) . A few doctors have had
encouraging results in Crohn's Disease, and even to some extent in cancer. Low doses of Naltrexone (LDN), 1.5 to 4.5 milligrams, at bedtime is used (timing is important, and it is important not to buy slow release forms). It is said to have no known bad side effects at those doses other than insomnia the first week or two in some. There is also reports from an extensive survey in this site. and an extensive discussion at this site.
I think some clinical studies on Naltrexone are in order, and it should not be a prescription drug (I have a petition to make Naltrexone an over the counter drug with the Center for Drug Evaluation and Research
FDA Rockville MD 20857, Re; Docket No. 2006P-0508-CPI. Perhaps if enough people wrote supporting the petition it could be enacted). Though side effects appear unlikely, it is not proven over longer periods. If you try it (it is a prescription medicine in the USA), it seems likely that you should discontinue if you get a bacterial infection in view of its inhibition of antibacterial response. It is also being explored for AIDS by Dr. Bernard Bihari, 29 W 15th St. New York, NY 10011, 212) 929-4196 who is still prescribing Naltrexone for HIV/AIDS. (and currently Executive Director of the Community Research Initiative). Dr. Gale Guyer of Advanced Medical Center located in Zionsville, Indiana also is using it for cancer. Dr. Bihari has shown promising results for a large percentage of his cancer patients.
See this site for evidence of a correlation between magnesium deficiency and cancer. The taurate is proposed as the best magnesium supplement. Taurine or 2-aminoethanesulfonic acid is an acidic chemical substance sulfonated rather than carboxylated found in high abundance in the tissues of many animals (metazoa), especially sea animals. Taurine is also found in plants, fungi, and some bacterial species, but in far less abundance. It is an amine with a sulfonic acid functional group, but it is not an amino acid in the biological sense, not being one of the twenty protein-forming compounds encoded by the universal genetic code. Small polypeptides have been identified as containing taurine, but to date there has been no report of a transfer RNA that is specifically charged with taurine [from Wikipedia]. It is essential to babies.
It has been found that supplements of the amino acid, taurine, will restore the abnormal electrocardiogram present during a potassium deficiency by an unknown mechanism. This information has been used in several case histories by George Eby to control a long standing type of cardiac arrhythmia called pre atrial contractions (PACs), a benign but irritating and nerve racking heart problem, with 2.5 grams of taurine with each meal. Taurine is said to be low in the diets of vegetarians. The 2.5 grams recommended by the American Heart Association causes diarrhea in some people and should probably be reduced in those people. Taurine has been used
for high blood pressure, migraine headache (I have often removed a headache within an hour), high cholesterol, epilepsy, macular degeneration, Alzheimer’s disease, liver disorders, alcoholism, and cystic fibrosis, and depression. Keep in mind that some people may have a genetic defect that limits the amount of taurine tolerated and that adequate molybdenum may desirable.
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REFERENCES for "Roles of Potassium in the Body"
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