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POTASSIUM DEFICIENCY AS A CAUSE OF RHEUMATOID ARTHRITIS (RA)

 

POTASSIUM DEFICIENCY AS A CAUSE OF RHEUMATOID ARTHRITIS (RA)

by Charles Weber, MS

http://members.tripod.com/~charles_W/potassium.html

 

This discussion of potassium is presented in the hope that one of

its readers will consider performing an experiment establishing the

effect of potassium on rheumatoid arthritis (RA). There is no report

in the literature going back to 1914 of such an experiment. Every

essential nutrient should have been explored before this. In view of

the way hormones which are regulated by or regulate potassium, such

as cortisol and DOC are involved with rheumatoid arthritis (RA), the

low whole body potassium content in rheumatoid arthritis (RA), and

the way potassium rich diets relieve arthritis, potassium especially

should have been investigated before now.

 

INTRODUCTION

 

 

Since the most serious aspect of the diarrheas is wasting potassium,

cortisol has acquired the attribute of conserving potassium by

moving it into the cells when cortisol declines. Cortisol (but not

corticosterone) is reduced during a potassium deficiency, and this

reduction accounts for many of the symptoms of RA.

Cortisol shuts down most of the copper enzymes when it declines so

that excretion of copper is increased and Lysyl oxidase inhibited.

These last two attributes are proposed to account for most of the

mortality from aneurysms and infections during rheumatoid arthritis

(RA). Thus the urgent necessity to survive during virulent diarrhea

has set people up in the course of evolution for some of the worst

symptoms of rheumatoid arthritis.

 

For a more elaborate discussion of potassium physiology and

nutrition see Arthritis as a Chronic Potassium Deficiencyand its

subsequent chapters, and for copper see this site.

 

DISCUSSION

 

 

Judging by the drastic decline of mortality in babies suffering from

a virulent strain of diarrhea by potassium supplements [1],

potassium loss in those diseases which force cyclic AMP to excrete

water into the intestines [2] must be the most serious effect of the

diarrheas. I suggest that this is the reason why cortisol has

acquired the attribute of moving potassium out of cells [3] and

therefore into the cells upon declining. It is also undoubtedly the

reason why the adrenal's cortisol secretion is inhibited by low

serum potassium in vitro (in the test tube) but not corticosterone

[4]. The body thus has a way of signaling for a decrease in cortisol

secretion during a serious intestinal disease independently of ACTH.

Thus the body inversely mobilizes its defenses against diarrhea

through cortisol. Endotoxin bacterial diseases force the body to

secrete cortisol by increasing ACTH [5] and this is probably an

adaptation by the bacteria to force the body to inhibit the immune

system. Glucosteroid response modifying factor (GRMF) secreted by T-

cells then prevents the cortisol from having full effect on white

cells other than suppresser cells [6] and thus raises the set point,

as does interleukin-I [6]. Interleukin-I also stimulates cortisol

secretion [7], as does cachectin (tumor necrosis factor) [8]. I

suspect that this is an adaptation to provide some cortisol

maintenance [9] when normal ACTH production is later cut off during

endotoxin attack [10]. In other words, the immune system takes over

its own regulation but at a higher set point. The role of GRMF has

not yet been demonstrated for physiological processes. GRMF will

probably prove to inhibit cortisol for most of those processes as

well as the immune cells, surely at least for cortisol's various

affects on potassium.

One of the most important of the cortisol controlled immune defenses

is the mobilization of the availability of copper to the white

cells, an attribute which probably arose because copper is crucial

to an adequate immune defense [11]. The primary way cortisol does

this is by, inversely to its concentration, shutting down production

of copper-containing enzymes such as Lysyl oxidase and superoxide

dismutase [12]. Lysyl oxidase catalyzes the formation of cross links

in all connecting tissue including elastin [13]. Since elastin makes

up the main strength of normal blood vessels [12] and has a rapid

turnover, this is the most serious problem in arthritis. Ruptured

aneurysms along with poor resistance to infection and heart disease

are the chief terminal events in arthritis [14].

 

The body uses ceruloplasmin to carry copper to the immune system

during infection [12]. Probably the main reason for this development

is that the copper in ceruloplasmin is not in equilibrium with the

serum and so is not available to pathogens. However, ceruloplasmin

is also used to carry copper to the bile for excretion [15].

Therefore I submit that the rise in serum ceruloplasmin in RA [16]

causes an increased excretion in members of a society who, even

before this, were receiving less than the minimum daily requirement.

 

CONCLUSIONS

 

 

Evidence can be provided for this proposal in several ways.

Arthritic people should have a lower whole body potassium content

than normal people. This has been proved [17]. Red blood cells have

a higher potassium content than normal during RA [18]. This should

not be taken as counter evidence because I suspect that this is an

adaptation to help avoid circulatory collapse when dehydration

reduces the blood volume during diarrhea.

There should be a lower concentration of potassium in blood plasma

during RA. The National Health and Nutrition Survey-III has

determined that of 39,695 people selected, there were 840 who said

they had been diagnosed with rheumatoid arthritis. Of these, 691 had

their serum tested for potassium. Of that number 7.8% had less than

3.6 milliequivalents per liter, 34.7% between 3.6 and 4.0, 40.7%

between 4.0 and 4.4, and 18.1% above 4.4. Only 18% appeared to be in

the normal range. The samples were refrigerated and sent out to

outside contract laboratories [48]. Refrigerating blood increases

the apparent amount when it is serum that is analyzed, especially if

there is a delay in the analysis. In addition to that, arthritics

lose potassium from the platelets [47]. If some were misdiagnosed,

had a remission since being diagnosed, or there was a longer than

usual delay in analysis, it could account for the 18% seemingly

normal. So this survey showed, at least, most arthritics low in

potassium. Many others in the survey were low in potassium also. So,

unless arthritis is caused by something besides a potassium

deficiency and low potassium is a symptom or accentuates RA, those

other survey people would have to have had arthritis as well. I

believe many people die of a potassium 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.

 

That first part of the above statement is plausible because

antibiotics ((tetracyclines, especially minocycline)) specific

against an odd bacterium species devoid of cell walls which can

enter the cells like viruses called " Mycoplasma " or mycobacteria has

been said to be shown to cure many arthritics [50]. However the

antibiotic is said to be only maximally affective if the patients

stop eating sugars, fats, and grains. This would greatly increase

potassium intake. In regard to resisting diseases, especially

bacterial, there is probably another reason for keeping cell

potassium normal with adequate nutrition. It seems that the white

cell vacuole requires an alkaline medium in order to both kill and

digest microbes. To achieve this it must pump potassium into the

vacuole using a calcium activated (Bkca) pump. This is known

because, when a chemical blocks this pump channel, microbes are not

killed in spite of normal phagocytosis (engulfing of microbes) and

oxidase activity [51]. So it seems plausible to me that, when the

pump is operating normally, a low cell potassium would make it more

difficult to achieve the enhanced alkalinity. This may be the reason

why potassium deficient kidneys are susceptible to infection [*]. It

is conceivable that this is a problem with mycobacteria also and

help explain why potassium supplements are so effective against

arthritis. (See this site for a discussion of mycoplasma physiology)

Mycobacteria as a factor in joint pain is plausible because those

bacteria may well be increasing secretion of glucosteroid response

modifying factors, although I have no evidence. A different spelling

for the bacteria calling them mycoplasmin has also been implicated

in arthritis according to this site. and this reference [49]. 50% of

rheumatoid arthritis patients have had mycoplasmal bacterial

infections [52].

 

There should be a lower incidence of RA among people on potassium

supplementation or who eat Morton's Lite Salt or Stirling's

Half and Half . I know of no epidemiological study showing this.

However, people who work in potash mines have a 25% lower incidence

of heart disease than the surrounding population [19] and heart

disease is prevalent in RA. There should be a healing of RA upon

starting potassium supplements. No controlled experiment has been

reported which would indicate this. However there is a case history

of a single arthritic brought up to 3,500 milligrams per day in

order to explore the effects of various steroid hormones on the

body's mineral balance [20]. A total of 3,500 milligrams is about

the amount an adult would obtain from unprocessed food. The subject

showed consistent improvement throughout the experiment even though

potassium was the only consistent change. His total body potassium

slowly but consistently rose. I know of five case histories that

removed RA pain by supplements. There should be a negative

correlation between high potassium-caused muscle spasms and RA, but

I have no supporting data. Neither do I know of a positive

correlation with eating licorice (but not licorice candy, which is

made of anise seeds) grapefruit, or potassium losing diuretics, each

of which increase potassium loss. There should be a negative

correlation between eating acids that have an indigestible anion and

RA since the hydrogen ion interferes with potassium excretion [21].

I know of no good experiment or epidemiological study. However, it

has been suggested from folk custom that eating vinegar [22] or

cherries is efficacious. The vinegar seems doubtful since it is my

understanding that acetate can be metabolized by the body [22a].

However, it is conceivable that people on a diet high in calories do

not utilize all the acetate or even much of it. In any case, RA

should not be present much in people who eat predominantly

vegetables instead of grains. An experiment has been performed in

which RA was healed in a group of people by switching to a vegetable

diet [23b]. Eating bananas would increase potassium somewhat, but it

is only a moderate source per calorie, about the same as potatoes.

 

I suspect that people with rheumatoid arthritis tend to have a

poorer ability to conserve or absorb potassium than other people

because of damage to their kidneys by a poison such as bromine gas

(as happened to me) or long term poisons in plant foods or by a mild

genetic defect or by poisons excreted by pathogenic bacteria. Some

bacterial infections do trigger RA. Screening some common poisons

currently in food might be enlightening, both for retarding and

increasing excretion. Since GRMF inhibits cortisol, it is possible

that a discordance in the immune response involving GRMF in some

people or some infection types (that last does happen) may

accentuate RA and thus even cause an auto immune response.

 

If animals are used for experiments, it is futile to use rats or

mice because they rely on corticosterone to regulate the immune

response, not cortisol. I suspect that this developed because they

have a factor in their intestinal fluid which counteracts cholera

toxin [23]. They also have the ability to absorb water under cyclic

AMP stimulation in part of their colon [24] instead of to excrete of

water, unlike other animals.

 

Since the disturbance in copper metabolism is proposed as the most

serious aspect of RA, evidence for copper's effect should be

possible. Supplementing with copper should remove some of the

symptoms of RA. I know of no such experiment. However, it is known

that Finnish men who work in copper mines have little arthritis or

susceptibility to infection. [25]. The high milk diet along with

frequent saunas may be two reasons why other Finns have one of the

highest rates of arthritis in the world [26], since milk is the

poorest source of copper[27, p.92] and perspiration loses potassium

[28]. Milk has been shown to have a high statistical correlation

with cardiovascular disease, said to be as great a risk as smoking

[29], which disease in turn is correlated with RA. Laplanders on a

meat diet have a lower rate of RA not much further north [26]. The

Masai of Africa have a higher rate of RA than the surrounding tribes

[30, p768]. The Masai also use a lot of milk as well as very few

vegetables, which vegetables would have increased potassium intake.

Men who work in copper mines must have stronger tissues than other

miners because the percentage of injuries which result in lost time

is significantly lower [31], even though injuries like eye damage

and burns which are not affected by strength are part of the data.

Eating a lot of shellfish or liver should reduce those symptoms

related to copper deficiency since they are the richest sources, but

I know of no study. The same should be true of drinking acid water

out of copper plumbing.

 

I believe that it is unwise to give cortisol to any class of people

whose immune system is weak, such as arthritic people. If it is felt

that cortisol should be raised in the body, why not use something

relatively safe, like potassium supplements? If potassium

supplements are used, be certain that vitamin B- 1 is adequate

because the " wet " heart disease of beri-beri can not materialize

when potassium is deficient. [32] Obviously the reverse is also true

for vitamin B-1 supplementation. For this reason, If the patient has

heart trouble, it is very important to determine whether it is

caused or accentuated by vitamin B-1 or potassium.

 

If potassium chloride is dissolved in fruit juice it tastes good and

avoids the danger to the intestines that even slow release enteric

tablets may present. The chloride is the most easily retained form

[33]. It would be better and safer yet to provide potassium from

food high in potassium such as celery or bamboo shoots as Effinger

proposed [34]. Unboiled, unfrozen, uncanned vegetables low in starch

are the richest sources [35]. However, removing a deficiency will be

slower since the potassium is not associated with chloride and would

take a few weeks or months longer.

 

A deficiency can arise from diarrhea, eating processed food,

reliance on grain or fatty foods [35], psychic stress stimulation of

aldosterone [36] (which is the main regulator of potassium) [37],

stress stimulation of cortisol (as in an operation, for instance

[38]), diuretics, licorice [39] as well as probably grapefruit

[39a], profuse perspiration [28], excessive vomiting [40], eating

sodium bicarbonate [41], hyperventilating [42], laxatives [43],

enemas [44] (especially if prolonged), shock from burns or injury

[45], hostile or fearful emotions [36], and very high or very low

sodium intake [46], All of these increase excretion or decrease

intake of potassium and many at once would be very dangerous. and

probably even lethal if prolonged.

 

A chronic potassium deficiency must surely cause a degenerative

disease. I believe it materializes in some people as RA, or at least

accentuates RA. If not, then what is the name of the degenerative

disease which attends a potassium deficiency ? It is not

hypokalemia. This is only a word which describes low serum

potassium, a marker or symptom. It is about time we found such a

name.

 

There is a principle which is a bar against all information, which

is proof against all argument, and which cannot fail to keep man in

everlasting ignorance. That principle is condemnation without

investigation " (from Herbert Spencer). From the time that cod liver

oil was suggested as a treatment for rickets one hundred and fifty

years went by during which 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.

 

 

REFERENCES are below

Some links related to health

 

 

CONTENTS of other chapters about potassium

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

cortisolVIII. Potassium Nutritional Requirements --- IX. Potassium

in Foods --- X. Potassium Processing Losses --- X,cont. Losses in

the kitchen --- XI. Potassium Supplementation --- Potassium Side

Effects and Heart DiseaseHigh Blood Potassium --- Helpful strategies

against CFS and fibromyalgia

Potassium Content of Food, a table: Potassium expressed in

milligrams per Calorie.

Copper Response in Rheumatoid Arthritis: Nutrition and physiology of

copper, especially relating to hemorrhoids, aneurysm, herniated

discs, anemia, emphysema, and gray hair..

The Purpose of Cortisol: Cortisol is presented as an immune hormone

used inversely to defend against diarrhea

Cashew Nuts to Cure Tooth Abscess: Anacardic acids in raw cashew

nuts may cure tooth abscesses and possibly gram positive diseases

such as acne and leprosy.

Observations on Diabetes: Diabetes may be caused by a poison in food.

The Eve Controversy: A proposal as to why the human species seems to

be derived from a single couple.

 

 

You may find useful for definitions and easy to use a search for

abstracts of journal references, " Gateway " . You must click on "

MEDLINE/PubMed " or for definitions click on " find terms " . or a list

of medical search engines and also a site with several links to

potassium nutrition articles and another site that has many links to

nutrition sites around the world.

 

There are numerous links to a site which has numerous links to

arthritis. There is a site with numerous links to arthritis

amelioration, which stress a healthy life style.

 

 

There is a site that lists hospitals worldwide here.

 

 

SOME LINKS RELATED TO ANCIENT ECOLOGY

 

Did the Wood Roach Cause the Permian - Triassic Coal Hiatus? The

ability to digest cellulose may have sparked Permian aridity and the

conifer rise.

Permian Atmospheric Carbon Dioxide and Prototermite Migration A huge

comet strike may have caused extinctions and spread of proto

termites around the world.

Permian Phosphorus Amphibians such as dragonflies may have caused

the Permian marine phosphorites and armored fish.

Termites Affect on Phosphorus in the Jurassic Sheet erosion by soil

borne termites starting in late Jurassic may have caused fertile

oceans and a decline of vertebrate bones and teeth on savannas from

a phosphorus famine.

Paleocene and Modern Termites Evolution of termites may have

contributed to the small size of vertebrates in early Paleocene.

Angiosperm Evolution Broad leafed plants may have evolved on the

Ontong - Java plateau in the Permian.

Deciduous Forests from Glaze Ice It is proposed that the temperate

deciduous forest zone is caused by glaze ice storms.

 

FOR YOUR COMPUTER

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.

 

If you have Iexplore, there is a tool bar by Google that enables you

to search the internet from the page viewed, mark desired words,

search the site, give page rank, etc.

 

There is a free program available which tells on your site what web

site accessed your site, which search engine, statistics about which

country, statistics of search engine access, keywords used and their

frequency. It can be very useful

There is a news system that scours the Internet once a day for

arthritis (RA and osteo) resarch and treatment related news stories

from thousands of state, national and international publishers,

including all of the major media outlets. The articles discuss

medications primarily and is provided by InjuryBoard.com.

 

 

REFERENCES

 

1. Darrow, D.C. 1946 " Retention of Electrolyte during recovery from

severe dehydration due to diarrhea, " Journal of Pediat. 28; 515.

 

 

2. Mekalanos, J.J.; Swartz, D.J.; Pearson, GDN.; Harford, N.;

Groyne, F.; Wilde, M. 1983. " Cholera Toxin Genes: Nucleotide

Sequence, Deletion Analysis and Vaccine Developement, " Nature 306;

551.

 

 

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

Press.

 

 

4. Mikosha, A.S.; Pushkarov, I.S.; Chelnakova, I.S.; Remennikov,

G.Ya. 1991 " Potassium Aided Regulation of Hormone Biosynthesis in

Adrenals of Guinea Pigs under Action of Dihydropyridines: Possible

Mechanisms of Changes in Steroidogenesis Induced by 1,4-

Dihydropyridines in Dispersed Adrenocorticytes. " Fiziol. ZH (Kiev)

37:60.

 

 

5. Melby J.C.; Egdahl, R.H.; Spink, W.W. 1960 " Secretion and

Metabolism of Cortisol after Injection of Endotoxin. " Journal of

Lab. Clin. Med. 56;50.

 

 

6. Fairchild, S.S.; Shannon, K.; Kwan, E.; Mishell, R.I. 1984 " T-

cell Derived Glucocorticosteroid Response Modifying Factor (GRMFt):

A Unique Lymphokine Made by Normal T Lymphocytes and a T-cell

Hybridoma. " Journal of Immunology 132; 821.

 

 

7. Besedovsky, H.O.; Del Rey, A.; Sorkin, E. 1984 " Integration of

Activated Immune Cell Products in Immune Endocrine Feedback

Circuits. " p. 200, Leukocytes and Host Defense Vol. 5 (Oppenheim,

J.J.; Jacobs, D.M., eds). Alan R. Liss, NY.

 

 

8. Milenkovic, L.; Rettori, V.; Snyder, G.D.; Beutler, B.; McCann,

S.M. 1989 " Cachectin Alters Anterior Pituitary Hormone Release by a

Direct Action in Vitro. " Nat. Acad. Sci. 86; 2418.

 

 

9. Finlay, G.J.; Booth, R.J.; Marbrook, J. 1979 " Antibody Responses

of Human Lymphocytes in Vitro; Enhancing Effects of Hydrocortisone. "

Austr. Journal of Exp. Biol Med. Sci. 57; 597.

 

 

10. Jones, R.S.; Howell, E.V.; Eik-Nesk. 1959 " Inactivation by

Plasma of ACTH Releasing Property of C-14 Labeled Bacterial

Polysacharride. " Proc. Soc. of Exper. Biol. Med. 100; 328.

 

 

11. Prohaska, J.R.; Lukaseqycz, O.A. 1981 " Copper Deficiency

Suppresses the Immune Response in Mice. " Science 213; 559.

 

 

12. Weber, C.E. 1984 " Copper Response to Rheumatoid Arthritis. "

Medical Hypotheses 15; 333.

 

 

13. Harris, E.D.; Rayton, J.K.; Baltriop, J.E.; Di Silvestro, R.A.;

Garcia de Quevedo. " Copper in the Synthesis of Elastin and

Collagen, " p. 163, Biological Roles of Copper, Ciba Foundation

Symposium No 79, Exerpta Medica NY.

 

 

14. Matsuoka, Y.; Obana, M.; Mita, S.; Kohno, M.; Irimajiri, S.;

Fujimori, I.; Fukuda, J. " Studies of Death in Autopsied Cases with

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( Shiokawa, Y.; Abe, T.; Yamauchi, Y., eds.) Excerpta Medica

Internat. Cong. Series #535.

 

 

15. Frieden, E. 1981 " Ceruloplasmin: A Multifunctional

Metalloprotein of Vertebrate Plasma. " Metal Ions and Biological

Systems, Vol. 13, p. 117 (Sigel, H.; Sigel, B., eds.) Marcel Dekker,

NY & Basel.

 

 

16. Aiginger, P.; Kolarz, G.; Wilvonseder, R. 1978 " Copper in

Ankylosing Spondylitis and Rheumatoid Arthritis. " Scand. Journal of

Rheumatol. 7; 75.

 

 

17. LaCelle, P.L., et al. 1964 " An Investigation of Total Body

Potassium in Patients with Rheumatoid Arthritis. " Proc. Ann. Meeting

of the Am. Rheumatism Assoc. Arth. Rheum. 7; 321.

 

 

18. Knudsen, E.T.; Thomas, M.J. 1957 " Erythrocyte Potassium Level in

Rheumatoid Arthritis. " Lancet 272; 251.

 

 

19. Waxweiler, R.J., et al. 1973 " Mortality of Potash Workers. " J.

Occup. Med. 15; 486.

 

 

20. Clark, W.S, et al. 1956 " The Relationship of Alterations in

Mineral and Nitrogen Metabolism to Disease Activity in a Patient

with Rheumatoid Arthritis. " Acta Rheum. Scand. 2; 193.

 

 

21. Berliner, R.W, et al. 1951 " Relationship between Acidification

of the Urine and Potassium Metabolism. " Amer. Journal Med. 11; 274.

 

21a. Mills, J.H.; Stanbury, S.W. 1954 " A Riciprocal Relationship

between K+ and H+ Excretion in the Diurnal Excretory Rhythm in Man. "

Clin. Sci. 13; 177.

 

 

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

London.

 

 

22a. Winegrad AT Reynold AE 1958 Effects of insulin on the

metabolism of glucose, pyruvate, and acetate. Journal of Biol. Chem.

233; 267.

 

 

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

 

 

22d Ifudu O Markell MS Friedman EA 1992 Unrecognized

pseudohyperkalemia as a cause of elevated potassium in patients with

renal disease. American Journal of Nephrology 12; 102-104.

 

 

23. Donowitz, M.; Binder, H.J. 1976 " Effect of Enterotoxins of

Vibrio Cholerae, Escherichi coli, & Shigelladienteriae Type 1 on

Fluid and Electrolyte Transport in Colon. " Journal of Infect. Dis.

134; 135.

 

 

24. Hornyck, A.; Meyer, P.; Milliez, P. 1973 " Angiotensin,

Vasopressin, and Cyclic AMP: Effects of Sodium & Water Fluxes in Rat

Colon. " Am Journal of Physiol. 224; 1223.

 

 

25. Sorrenson, JRJ;. Hangarter, W. 1977 " Treatment of Rheumatoid and

Degenerative Diseases with Copper Complexes. " Inflammation 2; 217.

 

 

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

 

 

27. Underwood, E.J. 1972 " Trace Elements in Human and Animal

Nutrition. " Academic Press NY.

 

 

28. Consolazio, C.F., et al. 1963 " Excretion of Sodium, Potassium,

Magnesium, and Iron in Human Sweat and the Relation of Each to

Balance and Requirements. " Journal of Nutr. 79; 407.

 

 

29. Seely, S. 1981 " Diet and Coronary Disease: A Survey of Mortality

Rates and Food Consumption Statistics of 24 Countries. " Med.

Hypotheses. 7; 907.

 

 

30. Best, C.H.; Taylor, N.B. 1950 The Physiological Basis of Medical

Practice, 5th ed. Williams and Wilkins Co., Baltimore (p. 768).

 

 

31. U.S. Dept. of Labor, Mine Safety and Health Administration.

1981 " Injury Experience in Metallic Mineral Mining, " IR 1142 Table #

6. pp. 24 & 58.

 

 

32. Folis, R.H. 1942 " Myocardial Necrosis in Rats on a Potassium Low

Diet Prevented by Thiamine Deficiency. " Bull. Johns-Hopkins Hospital

71; 235.

 

 

33. DeLand, E.C., et al. 1979 " A Theoretical and Experimental Study

of Ionic Shifts Induced by K Depletion and Replacement. " Journal of

Theor. Biol. 76; 31.

 

 

34. Eppinger, H. 1939 " Einiges Uber Dietetische Therapie. " Ztschr.

F. Artzl. Fortbild. 36; 672 & 709.

 

 

35. Weber, C.E. 1974 " Potassium in the Etiology of Rheumatoid

Arthritis and Heart Infarction. " Journal of Applied Nutrition. 26;

41 (Bibliography published separately).

 

 

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

209).

 

 

37. Weber, C.E 1983 " Corticosteroid Regulation of Electrolytes. "

Journal of Theor. Biol. 104; 443.

 

 

38. Elman, R., et al. 1952 " Intracellular and Extracellular

Potassium Deficits in Surgical Patients. " Ann. Surgery 136; 111.

 

 

39. Stormer, FC, Reistad, R, Alexander, J 1993 Glycyrrizic acid in

licorice - evaluation of health hazard. Food Chem. Toxicol 31; 303-

312.

 

 

39a. Lee YS, Lorenzo, BJ, Koufis, T, Reidenberg, MN 1996 Grapefruit

juice and its flavenoids inhibit 11 beta - hydroxy steroid

dehydrogenase. Clin. Pharmacol. Ther. 59; 62-71.

 

 

40. Barter, F.C. 1980 " Clinical Problems of Potassium Metabolism,

Contributions to Nephrology. " p. 21, Disturbances of Water and

Electrolyte Metabolism. Bahlmann, J.; Brod, J., eds. S. Karger,

Basel.

 

 

41. Berliner, R.W, et al. 1951 " Relationship between Acidification

of the Urine and Potassium Metabolism. " Amer. Journal of Med. 11;

274.

 

 

42. Kilburn, K.H. 1966 " Movements of Potassium during Acute

Respiratory Acidosus and Recovery. " Journal of Applied Physiol. 21;

679.

 

 

43. Schwartz, W.B.; Relman, M.B. 1953 " Metabolic and Renal Studies

in Chronic Potassium Depletion Resulting from Overuse of Laxatives. "

Journal of Clin. Invest. 32; 58.

 

 

44. Dunning, M.F.; Plum, F. 1956 " Potassium Depletion by Enemas. "

Amer. Journal of Med. 20; 789.

 

 

45. Fox, C.L.; Baer, H. 1947 " Redistribution of Potassium, Sodium,

and Water in Burns and Trauma and Its Relation to Phenomena of

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