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POTASSIUM DEFICIENCY AS A CAUSE OF

RHEUMATOID ARTHRITIS

by Charles Weber --- weber@brinet.com

(A more complete discussion of the role of potassium in ar-

thritis may be found at Weber’s homepage http://

members.tripod.com/~charles_W/arthritis.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. 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 deoxycorticosterone (DOC) are in-

volved with rheumatoid arthritis (RA), and the low whole body

potassium content in Rheumatoid Arthritis (RA), potassium espe-

cially should have been investigated before now.

INTRODUCTION

Since the most serious aspect of the diarrheas is wasting po-

tassium, cortisol has acquired the attribute of conserving potas-

sium 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 de-

clines so that excretion of copper is increased and Lysil 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 diarrheas

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

symptoms of rheumatoid arthritis.

DISCUSSION

Judging by the drastic decline of mortality in babies suffering

from a virulent strain of diarrhea by potassium supplements,

1

po-

tassium 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 seri-

ous intestinal disease independently of ACTH. Thus the body in-

versely mobilizes defenses.

Endotoxin bacterial diseases force the body to secrete cortisol

by increasing ACTH

5

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-1.

6

Interleukin-

1 also stimulates cortisol secretion,

7

as does cachectin (tumor ne-

crosis 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 regula-

tion 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, 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 Lysil oxidase and superox-

ide dismutase.

12

Lysil 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 turn-

over, this is the most serious problem in arthritis. Ruptured aneu-

rysms 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 devel-

opment is that the copper 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 re-

ceiving 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 con-

tent 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 dehydra-

tion reduces the blood volume during diarrhea. There should be a

lower incidence of RA among people on potassium supplementa-

tion or who eat Morton's Lite Salt (TM) or Stirling's Half and Half

(TM). I know of no epidemiologic 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 3.5 grams per day in order to explore

the effects of various steroid hormones on the body's mineral bal-

ance.

20

A total of 3.5 grams is about the amount an adult would

obtain from unprocessed food. The subject showed consistent im-

provement throughout the experiment even though potassium was

the only consistent change. His total body potassium consistently

rose. There should be a negative correlation between potassium-

caused muscle spasms and RA, but I have no supporting data. Nei-

ther do I know of a positive correlation with eating licorice or po-

tassium losing diuretics, both of which increase potassium loss.

There should be a negative correlation between eating acids which

have an indigestible anion and RA since the hydrogen ion inter-

feres with potassium excretion.

21

I know of no good experiment or

epidemiologic 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.

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

not utilize all the acetate. RA should not be present in people who

eat predominantly vegetables instead of grains.

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