Help

[Guest guest]

Dear Chris(and AP group), I had an ASO titer done and it was negative. My

family doc did the minocin for me about 6 month ago but I could only take it

one or two times a week!(100mg) due to such bad reflux and esophagus motility

problems. I have done well keeping away from sugar and take acidopholus once

a day.I take stool softeners,magnesium and fiber tablets for constipation and

also take 20mg prilosec twice a day and reglan 3 to 4 times a day to help

with the reflux.also synthroid for a low thyroid. All my symptoms started

about 6 yrs ago but would come and go.Now it seems they are here to stay.

Since starting the reglan(which is not without side effects). I have been

able to tolerate the minocin 3x a week for the past month. Maybe I am in a

herx as I have a lot more shoulder and hand aching,especially at night over

the past few days. How do you know a herx from a flare? As of yet I have no

outward tightening of my skin. Mainly digestive problems and joint and muscle

pain.

I don't know if my family doc would do the IV's. He gave me the minocin at my

request(actually started with doxy but switched after a few weeks due to

stomach problems).I live in Michigan anyone you know doing the IV " s for SD in

Michigan?

One other question. I subscribed to the AP mailing list and there was a lot

of talk about zithromax. I took it for sinus infection about 3 months ago and

felt better with my SD symptoms. Is it ever used successfully with SD?

Thanks so much,

[Guest guest]

Be sure that " negative " means 0 (not <120)!! It needs to be 0 according the

Road Back Foundation.

-Mike-

rheumatic Re: help

From: ArtatMidla@...

Dear Chris(and AP group), I had an ASO titer done and it was negative. My

family doc did the minocin for me about 6 month ago but I could only take it

one or two times a week!(100mg) due to such bad reflux and esophagus

motility

problems. I have done well keeping away from sugar and take acidopholus once

a day.I take stool softeners,magnesium and fiber tablets for constipation

and

also take 20mg prilosec twice a day and reglan 3 to 4 times a day to help

with the reflux.also synthroid for a low thyroid. All my symptoms started

about 6 yrs ago but would come and go.Now it seems they are here to stay.

Since starting the reglan(which is not without side effects). I have been

able to tolerate the minocin 3x a week for the past month. Maybe I am in a

herx as I have a lot more shoulder and hand aching,especially at night over

the past few days. How do you know a herx from a flare? As of yet I have no

outward tightening of my skin. Mainly digestive problems and joint and

muscle

pain.

I don't know if my family doc would do the IV's. He gave me the minocin at

my

request(actually started with doxy but switched after a few weeks due to

stomach problems).I live in Michigan anyone you know doing the IV " s for SD

in

Michigan?

One other question. I subscribed to the AP mailing list and there was a lot

of talk about zithromax. I took it for sinus infection about 3 months ago

and

felt better with my SD symptoms. Is it ever used successfully with SD?

Thanks so much,

---------------------------

[Guest guest]

Dear ,

> Since starting the reglan(which is not without side effects). I have been

> able to tolerate the minocin 3x a week for the past month. Maybe I am in a

> herx as I have a lot more shoulder and hand aching,especially at night over

> the past few days. How do you know a herx from a flare? As of yet I have no

A herx is a artificial flare directly related to taking the antibiotic. Do you

see any pattern in your good and bad days related to when you take the Minocin?

> I don't know if my family doc would do the IV's. He gave me the minocin at my

> request

I find that many doctors are more willing to intra-muscular injections rather

than intravenous. If your doctor is willing to do IM injections, then the

maximum dose is 600mg, rather than 900mg as with IV. Let me know if you need

help with this option.

Otherwise he may be willing to prescribe oral clindamycin. Try 1200mg in a

single dose, once a week. It usually gives a good punch to the therapy and you

may get more herxing.

> One other question. I subscribed to the AP mailing list and there was a lot

> of talk about zithromax. I took it for sinus infection about 3 months ago and

> felt better with my SD symptoms. Is it ever used successfully with SD?

I hear Dr. Franco is prescribing minocycline/doxycycline with Zithromax for his

RA patients, but prefers the clindamycin for SD patients. However, we're all

different. If you felt better on Zithromax, then for sure discuss with your

doctor the addition of either clindamycin or Zithromax to the Minocin.

Chris.

[Guest guest]

Dear Bruno,

Welcome to our group We have people from many countries in the group, which

has over 400 people in it currently. I'm not sure if there are any other members

from Italy.

What antibiotic did you take before? The therapy described on our web site is

usually minocycline or doxycycline and other antibiotics can also be used. Do

you have rheumatoid arthritis or another rheumatic disease?

While I don't have any doctors listed for Italy, you might like to print off

the material from our web page and take it to a caring local doctor and request

the therapy. We can help you with any details about the therapy or give you

the contacts for an experienced doctor who would help via email or telephone.

These two doctors are likely to help you if you take the protocol from

rheumatic.org/protocol.htm

and also to look for any other problems that might need attention:

Dr. Michele Ballo, MD, D/C

Via Ruggero Settimo, 55

Palermo, 90139, ITALY

Phone: 39-91-580301 Fax: 39-91-6114380

Dr. Sandro Mandolesi, MD, D/C

Via Firenze 47

Rome, , ITALY

Phone: 39-6-4873984 Fax: 39-6-85301038

Let us know what information you need and how we can help.

Chris.

>From: isottabella@...

>

>Hello, my name is Bruno Fusaroli and I'm a new enter in your group.

>I'm writing from Italy and I need of your help.

>I would like to know if there are novelity about antibiotic therapy.

>I have take something on your web site on February 1998 and I would

>like to know if there is something different about your therapy.

>I would like also if there are in Italy some doctor that use the

>antibiotic therapy. I would also know if there are in this site some

>italian people that used the antibiotic therapy.

>Thanks for your help and I hope to recive notice early.

>Bruno

>

>

>------------------------------------------------------------------------

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>0.0% Intro or 9.9% Fixed APR and no hidden fees.

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>------------------------------------------------------------------------

>

>

>

[Guest guest]

i have been taking the shots now for about 3 months. It has made an

incredible difference in my mobility and pain. Almost normal. Giving yourself

shots isn't for the faint of heart, but it really doesn't hurt physically and

much as pains you mentally while getting hyped up to do it.

___FYI: below is what I sent to the group last month. Good Luck!_____

I haven't heard of anyone discussing the new drug Enbrel. I have been on it

for 2 months now, and it is the only thing that has touched the arthritis. I

fought the doctor on so many levels about taking drugs (i.e. methotrexate,

plaqunil, etc.), but I was fast losing the battle. I had been on Minocin for

almost 3 years, and after the Herxing, it did improve my stiffness, etc.

However, I seem to have plateaued on it, and because of the stress in my job

(I own a printing business) and personal life (I'm planning a wedding) and a

new business venture (creating a cyber cafe), I was getting much worse in the

last 6 months. I compromised with my Dr. that if I tried the Enbrel, I could

eliminate all the other damn pills that I have to take. So I started the

shots (2x's a week, self injected) and felt 200% better by the third week.

Also saw a homeopathic Dr. in Sacramento, who put me on the " Eat 4 Your

Blood Type " diet. It has helped alot. I can still have my coffee, and a glass

of red wine every night, but for my A blood, no wheat, nightshades, meats,

etc. To quote the Dr.... " The road to your good heath is paved with bean

curd! " Trying to adjust to that.

I understand that alot of people can't afford the $1,200 a month price on

the Enbrel, if I didn't have insurance that dropped it to $120 I couldn't

either – but by dropping all the other minocin, sulfa, Celebrex and yeast

combatting drugs, I think I actually pay less. Plus I don't have to be tied

to

a schedule of what drug goes with which suppliment. And I understand that it

is a new, untried for side effects drug. However, I am typing this to you

without ANY stiffness or pain in my fingers right now and have returned to my

gardening with a passion. As my roommate says, " Bushes tremble when you walk

by " –I'm a notoriously close pruner. I agreed to be on the drug for at least

six months, then to take a " vacation " . The return to the quality of life has

been worth the risks for me.

Also - my RA Dr. also believes in the Minocin helping with the RA. But I for

one was sick of the yeast infections, and worrying what it was doing to my

immune system. I needed a break.

Enbrel isn't for everyone, and I hope in the very near future the price

drops to something everyone can afford, if they choose to try it. I haven't

had any side effects from it, but like everything that combats this disease,

I'm sure they're out there. Meanwhile, I'm going to go like heck while the

going's good.

Deb from California

[Guest guest]

Problem is Enbrel is temporary, seems like its good for 1-2 years at best

before it quits. Also it effects your immune system in unknown ways, as i

have heard it effects to tumor narcosis factor which could leave you wide

open for cancer. On the other hand a pain free year doesnt sound too bad.

Re: rheumatic HELP

i have been taking the shots now for about 3 months. It has made an

incredible difference in my mobility and pain. Almost normal. Giving

yourself

shots isn't for the faint of heart, but it really doesn't hurt physically

and

much as pains you mentally while getting hyped up to do it.

___FYI: below is what I sent to the group last month. Good Luck!_____

I haven't heard of anyone discussing the new drug Enbrel. I have been on it

for 2 months now, and it is the only thing that has touched the arthritis.

I

fought the doctor on so many levels about taking drugs (i.e. methotrexate,

plaqunil, etc.), but I was fast losing the battle. I had been on Minocin

for

almost 3 years, and after the Herxing, it did improve my stiffness, etc.

However, I seem to have plateaued on it, and because of the stress in my

job

(I own a printing business) and personal life (I'm planning a wedding) and

a

new business venture (creating a cyber cafe), I was getting much worse in

the

last 6 months. I compromised with my Dr. that if I tried the Enbrel, I

could

eliminate all the other damn pills that I have to take. So I started the

shots (2x's a week, self injected) and felt 200% better by the third week.

Also saw a homeopathic Dr. in Sacramento, who put me on the " Eat 4 Your

Blood Type " diet. It has helped alot. I can still have my coffee, and a

glass

of red wine every night, but for my A blood, no wheat, nightshades, meats,

etc. To quote the Dr.... " The road to your good heath is paved with bean

curd! " Trying to adjust to that.

I understand that alot of people can't afford the $1,200 a month price

on

the Enbrel, if I didn't have insurance that dropped it to $120 I couldn't

either - but by dropping all the other minocin, sulfa, Celebrex and yeast

combatting drugs, I think I actually pay less. Plus I don't have to be tied

to

a schedule of what drug goes with which suppliment. And I understand that

it

is a new, untried for side effects drug. However, I am typing this to you

without ANY stiffness or pain in my fingers right now and have returned to

my

gardening with a passion. As my roommate says, " Bushes tremble when you

walk

by " -I'm a notoriously close pruner. I agreed to be on the drug for at

least

six months, then to take a " vacation " . The return to the quality of life

has

been worth the risks for me.

Also - my RA Dr. also believes in the Minocin helping with the RA. But I

for

one was sick of the yeast infections, and worrying what it was doing to my

immune system. I needed a break.

Enbrel isn't for everyone, and I hope in the very near future the price

drops to something everyone can afford, if they choose to try it. I haven't

had any side effects from it, but like everything that combats this

disease,

I'm sure they're out there. Meanwhile, I'm going to go like heck while the

going's good.

Deb from California

To unsubscribe, email: rheumatic-unsubscribeegroups

[Guest guest]

Deb,

I also had the dramatic instant results from Enbrel when I started it in

December of 1998. It recently has seemed to stop working for me, and that

is why I've started on the AB's. For many it seems that these drugs work

for awhile and then stop. I wish you luck and am happy to hear of your

success with Enbrel.

a

Sent: Monday, August 14, 2000 10:20 PM

Subject: Re: rheumatic HELP

i have been taking the shots now for about 3 months. It has made an

incredible difference in my mobility and pain. Almost normal. Giving

yourself

shots isn't for the faint of heart, but it really doesn't hurt physically

and

much as pains you mentally while getting hyped up to do it.

___FYI: below is what I sent to the group last month. Good Luck!_____

I haven't heard of anyone discussing the new drug Enbrel. I have been on it

for 2 months now, and it is the only thing that has touched the arthritis. I

fought the doctor on so many levels about taking drugs (i.e. methotrexate,

plaqunil, etc.), but I was fast losing the battle. I had been on Minocin for

almost 3 years, and after the Herxing, it did improve my stiffness, etc.

However, I seem to have plateaued on it, and because of the stress in my job

(I own a printing business) and personal life (I'm planning a wedding) and a

new business venture (creating a cyber cafe), I was getting much worse in

the

last 6 months. I compromised with my Dr. that if I tried the Enbrel, I could

eliminate all the other damn pills that I have to take. So I started the

shots (2x's a week, self injected) and felt 200% better by the third week.

Also saw a homeopathic Dr. in Sacramento, who put me on the " Eat 4 Your

Blood Type " diet. It has helped alot. I can still have my coffee, and a

glass

of red wine every night, but for my A blood, no wheat, nightshades, meats,

etc. To quote the Dr.... " The road to your good heath is paved with bean

curd! " Trying to adjust to that.

I understand that alot of people can't afford the $1,200 a month price

on

the Enbrel, if I didn't have insurance that dropped it to $120 I couldn't

either - but by dropping all the other minocin, sulfa, Celebrex and yeast

combatting drugs, I think I actually pay less. Plus I don't have to be tied

to

a schedule of what drug goes with which suppliment. And I understand that it

is a new, untried for side effects drug. However, I am typing this to you

without ANY stiffness or pain in my fingers right now and have returned to

my

gardening with a passion. As my roommate says, " Bushes tremble when you walk

by " -I'm a notoriously close pruner. I agreed to be on the drug for at least

six months, then to take a " vacation " . The return to the quality of life

has

been worth the risks for me.

Also - my RA Dr. also believes in the Minocin helping with the RA. But I for

one was sick of the yeast infections, and worrying what it was doing to my

immune system. I needed a break.

Enbrel isn't for everyone, and I hope in the very near future the price

drops to something everyone can afford, if they choose to try it. I haven't

had any side effects from it, but like everything that combats this disease,

I'm sure they're out there. Meanwhile, I'm going to go like heck while the

going's good.

Deb from California

To unsubscribe, email: rheumatic-unsubscribeegroups

[Guest guest]

I dont know exactly what the difference is, but i use ascorbic acid powder.

rheumatic help

>

> I am confused :-)

> Is there a difference between ascorbic acid powder and citric acid powder

> and vitamin C powder?

> I need to order but I am not sure what to get.

> Thanks,

> Gloria

>

>

> To unsubscribe, email: rheumatic-unsubscribeegroups

>

>

>

[Guest guest]

Ana, I kind of went the same route and am still there. But my general practitioner has perscribed pain meds that help me to deal with the pain when it gets to bad for over the counter meds. It does get better and then it gets worse, but each cycle seems to be better than the one before it. Remember 3 steps ahead and 2 back.

Hang in there,

Skip

rheumatic HELP

Hi group,

I've been posting on and off (more off than on) for the past year and a half, and I've got an urgent question.

I've been on AP for 16 months, and at first I noticed a noticeable improvement in my fatigue levels and sore hands.

I've been on Cleocin IV's since October of last year, at first 600mgs once a week for 2 weeks, then it was upped to 900mgs for 4 weeks, then 1200mgs for 3 more weeks every other week....I'm now on 1500mgs once a month.....I noticed that after I started on the IV's my shoulders became very, very sore. They start sore and stiff in the morning, and by nighttime, I'm hardly able to lift my arms past shoulder height without pain......I'm having a lot of trouble keeping myself focused on the fact that I'm improving, I'm getting pretty depressed at the thought that this is not working.....I guess what I need is some reassurance that it is working and that what I'm going through is one heck of a herx......So, if there is anyone out there who has gone through this and has come out of it, please, please, let me know.

Thank you all and God bless.

Ana in Alaska

To unsubscribe, email: rheumatic-unsubscribeegroups

[Guest guest]

What I would do if I were you and I've been on IV's for a long time.....is.....have the doctor drop the IV back down to say 600 or 900mg and see if there is a reduction in pain in the shoulders. That would tell me that they are related. Do you have any other side effects?? Any differences that you notice with the IV's, rash, shortness of breath etc.

Also, go into a drug site and look it up and see what the adverse reactions are.

Are you also on Minocin and how much??

Any other meds??

Does the pain get less as the week progresses away from the initial infusion. Look for a pattern to unwrap the mystery.

And while you are doing this, don't worry, you are doing well. The improvements are real and this is just an interesting symptom that needs to be examined.

You may even just switch from cleocin to another similar med and see if something in the drug makes a difference. Maybe an allergy is popping up??

Sorry, not many answers are there? Just more questions.

ps: I'd sure like to take a cruise up there from Vancouver.

DonnaOttawa, CanadaScleroderma, Jan.95, AP Oct.97(Ottawa Support) http://www3.sympatico.ca/mousepotatoes/rbf.html

rheumatic HELP

Hi group,

I've been posting on and off (more off than on) for the past year and a half, and I've got an urgent question.

I've been on AP for 16 months, and at first I noticed a noticeable improvement in my fatigue levels and sore hands.

I've been on Cleocin IV's since October of last year, at first 600mgs once a week for 2 weeks, then it was upped to 900mgs for 4 weeks, then 1200mgs for 3 more weeks every other week....I'm now on 1500mgs once a month.....I noticed that after I started on the IV's my shoulders became very, very sore. They start sore and stiff in the morning, and by nighttime, I'm hardly able to lift my arms past shoulder height without pain......I'm having a lot of trouble keeping myself focused on the fact that I'm improving, I'm getting pretty depressed at the thought that this is not working.....I guess what I need is some reassurance that it is working and that what I'm going through is one heck of a herx......So, if there is anyone out there who has gone through this and has come out of it, please, please, let me know.

Thank you all and God bless.

Ana in Alaska

To unsubscribe, email: rheumatic-unsubscribeegroups

[Guest guest]

Hi Fran! Geoff Crenshaw here.

> Date: Wed, 28 Mar 2001 09:52:03 -0000

> From: fross@...

> Subject: HELP

(snip)

> couple of weeks. Her month course finishes in two days. She drinks

> every evening and I wonder if this causes a reaction with her meds

> and is holding her back. She feels the alcahol helps her get through -

> I understand to some degree, but only see her get worse with it. She

> says her liver function tests are normal. Can anybody give some

Alcohol worsens her condition, creates destructive issues with most

meds, depresses her central nervous system and adds to her depression -

said depression already being a well-documented presentation of

rheumatic diseases in general.

Simple steps:

1. CEASE ALL ALCOHOL

2. DRINK A BAZILLION TONS OF WATER (well not that much, but

you get the idea)

3. FORGET the 'Cetyl Myristoleate.' According to those in

this group that have tried it (a lot) it does not work.

4. SLEEP

5. WATCH the diet - avoid the suspects listed at

www.rheumatic.org

6. AVOIDING the steroids is good - there are other ways,

such as the RA Spes as long as it is still around.

HTH

Regards, -----------------------

Geoff ** Usual Disclaimers **

-----------------------

How can you have hope?

Get under the blood of the Passover Lamb.

EXO 12:7-3 / MAR 14:24 / REV 12:11

http://www.healingyou.org/ Nonprofit: Herbs, Homeopathics & supp's.

http://www.800-800-cruise.com/index-aff.html Make money & travel!

http://www.800-800-cruise.com/ Over a MILLION travel deals!

[Guest guest]

I suggest trying the flagyl protocal (use tinidazole instead of flagyl if

possible 14mg/10lbs) twice a week and perhaps amoxicillin on the off days or

olive leaf herb in place of the amox. the protocal follows. also no

alcohol especially with flagyl because it neutralizes it. start and half

dose of the flagyl or tinidazole and work up slowly. REgarding the cmo I

like the cmo... I also like msm and chlorella and I grow and blend barley

grass smoothies for extra nutrients. try this regime arthritis trust

protocal for 4 months and see if there is improvement or change. kathy

(your a good sister to care and help her. hang in there.)

Medical data is for informational purposes only. You should always consult

your family physician, or one of our referral physicians prior to

treatment " -

The Arthritis Trust of America.

This article provided by:

The Arthritis Trust of America

Free-Living Amoeba

Historical Note

A letter from Professor Wyburn-Mason (Formerly published in The

Journal of the Rheumatoid Disease Foundation, Volume 1, Number 1) The

Wyburn-Mason and Jack M. Blount Foundation for the Eradication of Rheumatoid

Disease

AKA The Arthritis Trust of America, , 7111 Sweetgum Road, Suite A, Fairview,

TN 37062-9384

Copyright 1986

Rheumatoid Disease is a generalized condition, not just one of joints and

muscle spasm. The occurrence of rheumatoid granulomatous nodules

subcutaneously, at the sites of pressure or even on the meninges or sclera

or of rheumatoid lung, heart, liver, and kidney lesions or of involvement of

the parotid and lacrimal glands and skin lesions can only be found in a

systemic pathology.

The autonomic neurogenic cause of the disease was exploded many years ago by

the fact that complete sympathectomy was repeatedly found to have no effect

on the disease. This is not a " one-of " finding, but has been repeatedly

confirmed. The nervous system may be involved in producing the inflammatory

changes in rheumatoid disease.

Years ago I showed that inflammation in a tissue is dependent on the

integrity of the unmyelinated C fibers of the posterior nerve roots and

mixed peripheral nerves. If these are destroyed, as in gun-shot wounds,

leprosy, tabes or syringomyelia then injury to the part normally supplied by

these nerve fibers results not in inflammation but in necrosis. While in the

condition of causalagia resulting from injury to the median or sciatic

nerves, mild trauma in the painful area may result in an exaggerated

inflammatory response as compared with that in normal tissues of the

patient. Inflammation depends on antidromic impulses passing down from the

spinal cord to the inflamed area through these special nerve fibers, in the

case of rheumatoid arthritis, to the region of the joints.

Such cases as the following:

All were fit middle-aged men, plowing the dry fields on windy days - one in

the Middle West of USA, one in Ontario and one in ia. During the

ploughing, there was a great deal of dust being blown about from the dry

surface soil and this was inhaled by the subjects. During the next night,

all three were wakened by drenching night sweats, general malaise and next

morning were found to have temperatures of 105ø F. Every joint in the body

was painful, swollen and immobilized even including the cryoarytenoids and

temporo-mandibular. They had a cough, sputum, severe headache and muscular

aching. All were admitted to the hospital and eventually found to be

suffering from acute rheumatoid disease. In spite of intensive treatment,

their symptoms only very gradually diminished over the next 3-4 months, but

they were left at this time with severe pain and swelling of the joints

which did not respond to any treatment over the next year or more. These

cases are typical of severe infection and NOT of a disturbance of the

autonomic nervous system. The origin of their infection would seem to lie in

something inhaled from the copious surface soil dust (which contains free

living amoeba).

I isolated free-living amoebae from all the body tissues in cases of active

rheumatoid disease, cultured them from the laboratory, found that

antiamoebic substances killed them and then treated cases of active

rheumatoid disease with various antiamoebic substances.

Incidentally, the eminent protozoologists Kofoid and Swezy, working in their

laboratory at the University of California (LA) in 1922 found the same

organism in the bone marrow of cases of rheumatoid arthritis and suggested

its aetiological relationship to the disease some 40 years before my work.

They reported this in a zoological journal which never reached the medical

profession.

Furthermore, any substance which in vitro kills the organism when given to

active cases of rheumatoid arthritis often produces a transient Herxheimer

reaction, that is an exaggeration of the inflammatory changes of rheumatoid

arthritis and often the appearance of lesions in previously unaffected

tissues, just like mercury exaggerated the symptoms of syphilis. When given

to healthy subjects, these antiamoebic drugs have no such effect, and

Herxheimer reactions do not occur when antibiotics or antiviral substances

are used against sufferers from bacterial or virus diseases. This

observation alone shows the presence in rheumatoid arthritic lesions of an

organism more complex than a bacterium, namely an amoeba. This is the

complete proof of the amoebic causation of rheumatoid arthritis. [subsequent

studies were unable to confirm this amoeba theory, but strongly suggested

that the treatment worked to normalize or stop auto-immune activity of

macrophages which happened to resemble amoeba. Ed. S.C.]

Local anesthetics have two effects - they are anti-protozoal and also

paralyze the unmyelinated C fibers, the discharge of which is responsible

for inflammation. Both these effects could explain some of the benefits from

procaine therapy in rheumatoid disease.

Free-Living Amoeba

The Cause of Rheumatoid and Autoimmune Diseases?

by ROGER WYBURN-MASON

Christ's College, Cambridge, England

[Reprinted by permission of Arthritis News Today, Yorba , CA August

1981; from a paper presented at the 15th International Congress of

Rheumatology in Paris this June]

Numerous species of the universally-found free-living amoeba are known. Most

fall into two genera - Acanthamoeba and Naegleria - and some are pathogenic

to man and animals. In inimical conditions, they form hollow spherical

cysts, which are present in the air in most parts of the world and can

readily be found on agar plates exposed to air. Free-living amoeba prefer

warm surroundings and tend to migrate to an environment at body temperature

(thermotropism).

All living beings are surrounded by many species of these free-living amoeba

which pass into mammalian respiratory passages as cysts or trophozoites.

These must also be present as trophozoites in the gastrointestinal tract of

many animals, including man, since they are found in their feces. These

organisms are motile and, once they enter an orifice, they migrate under

thermotropic influences into body tissues.20

Recently it has been shown3 that the blood contains antibodies against

Acanthamoebae and Naegleria, indicating universal infection of man and the

newborn with these organisms. Textbooks on protozoology state that

unspecified types of amoebae have been isolated from every tissue in the

body6; there is hardly an organ in the body from which somebody has not

obtained amoebae.2 Lesions due to species of such organisms have been

described in a few cases of plants and man, namely amoebic

meningo-encephalitis.1,16

In 1922, the eminent protozoologists, Kofoid and Swezy, reported the

presence of free-living amoeba in the bone marrow of rheumatoid arthritis

patients without dysentery or E. histolytica in the feces. These organisms

were distinguished from human cells by mitotic processes and contained only

6 chromosomes rather than the normal 46 of human cells. They showed a single

blunted pseudopodium and numerous vaculous, suggesting a causal relationship

between infection and the arthritic process.5,9-14

Anti-amoebic Substances

Recently I have shown19,21-23 that free-living pathogenic or non-pathogenic

amoebae can be made to migrate out of human tissue, including those of the

newborn and fetus, by using the property of thermotropism. Large numbers are

found in the affected tissues of all patients with rheumatoid disease, in

extra-articular tissues affected by autoimmune disease, in normal feces, in

uncooked butcher's meat, and in surface soil. Smaller numbers may be

recovered from some tissues of apparently healthy humans, when they are

presumably of non-pathogenic nature; they appear identical with those found

by Kofoid and Swezy. These findings have been confirmed in laboratories in

various parts of the world.

In the laboratory, these organisms can be cultured in " amoeba saline, " into

which a culture of E. coli has been introduced. Various antiamoebic

substances found effective in killing the organisms when added to the

cultured cells include bile salts (1% solution), 4-aminoquinolines, copper

sulfate (very dilute solutions), metallic copper, gold salts, emetine,

dehydroemetine, pentamidine, and levamisole (which contains an imidazole

group). Particularly effective are the 5-nitroimidazole group of drugs -

including metronidazole, tinidazole, ornidazole and nimorazole - which

possess a wide spectrum of antiprotozoal as well as antiamoebic activity.

Since the organisms are not numerous and look like macrophages or

lymphocytes, they can be recovered in spite of the fact that they are not

usually observed in affected tissues stained by ordinary methods. This is a

feature repeatedly observed in laboratory animals experimentally infected

with free-living amoebae and recalls the situation with syphilitic lesions

before stains for Treponema pallidum were discovered. The organisms in

rheumatoid arthritis, however, can be demonstrated in tissue sections by

immunofluorescent staining using sera containing appropriate antibodies to

the organisms and by studying their mitosis and chromosome content in marrow

biopsy material.

The Effect of Anti-amoebic Drugs on

Active Rheumatoid Disease

Rheumatoid disease is not limited to joints but may involve any tissue of

the body. The same histological changes in joint capsules are found in

extra-articular lesions and consist of lymphocytic infiltration, formation

of germinal follicles, and often plasmocytosis accompanied by arteritis,

arteriolitis, or endarteritis. Many of the extra-articular lesions

constitute so-called auto-immune diseases but also include Sjogren's

Syndrome, bone marrow infiltrations, thymic lesions, and granulomatous

nodules. Symptoms typical of an infection - fever up to 40ø C, sweating and

raised ESR - may be present. Any of the extra-articular or autoimmune

lesions may occur in any combination with or without arthropathy.

I have shown that any substance which kills the free-living amoebae in

vitro, when administered to cases of active rheumatoid disease, may cause a

rapid disappearance of the inflammatory changes around the joints and

elsewhere in the body. Complete cure is obtained in early cases. But more

commonly these drugs may induce a transient exaggeration of the inflammatory

changes around the joints and elsewhere; and often, inflammatory lesions in

a part of the body not previously affected will appear. This may be

accompanied by influenzal symptoms, sweating, pyrexia, lymphadenopathy rise

in ESR, and eosinophilia. This reaction is also seen in cases of active

rheumatoid disease treated with gold salts18 and levamisole.15 Various

countries - notably the U.K., United States, Holland, and New Zealand - have

confirmed this reaction in cases of active rheumatoid disease treated with

anti-protozoal substances.

The Herxheimer Reaction

This phenomenon, first described by Herxheimer8 in cases of syphilis treated

with mercury, also occurs in diseases due to organisms more complex than

bacteria when drugs that kill the causative organism in the tissues are

administered. This " Herxheimer reaction " is due to the liberation of

irritant and antigenic substances from the dying organisms and is not

observed in healthy persons or in rheumatoid patients given antibiotics. Its

occurrence in rheumatoid disease (including those of autoimmune lesions)

treated with various antiamoebic drugs proves that a causative pathogenic

amoeba is present in the affected tissues. [since anti-amoebic medication is

also known to kill friendly bacteria, increased accumulations of

acetaldehyde byproducts from population explosions of Candida albicans could

also account for what was thought to be a Herxheimer reaction. Ed. S.C.]

After administration of antiamoebic drugs (especially 5-nitroimidazoles),

evidence of rheumatoid disease activity usually completely disappears in

both joints and extra-articular tissues within 3 to 6 months. Therefore,

autoimmune lymphocytic and humoral reactions are not the primary disturbance

in rheumatoid and autoimmune diseases; they are the cellular-antibody

response to infection and its antigens and contribute to the tissue damage.

The whole syndrome resembles syphilis. Indeed, Waldenstrom and others17

state that " if the spirochaete had not been discovered, syphilis could be

taken to be the ideal model of an autoimmune disease. The variety of tissue

reaction antibodies, the widespread lymphocytic damage, and the vasculitis

are characteristic features. "

Rheumatoid disease also closely resembles the rheumatic manifestations in

leprosy.4 This disease may present with acute arthritis affecting one or a

number of joints, polymyositis, skin lesions, fever, raised ESR, and other

signs; there will also be an increase in circulating gammaglobulins and

positive serological tests for autoantibodies RF and ANF, as in rheumatoid

disease. This is an immune complex syndrome with antigens provided by

disintegrating M. Leprae. The reaction known as Lucio's phenomenon, which is

identical to the Herxheimer reaction, may be precipitated by antileprosy

drugs.

The syndrome confirms deductions made regarding rheumatoid disease, proving

that every tissue in the body may contain unsuspected free-living amoebae.

If pathogenic, they may cause tissue infiltration by lymphocytes with

germinal centers and often plasma cells in genetically susceptible subjects

(as governed by their tissue types). They are also the source of unknown

chronic antigenic stimulation previously postulated by Glynn7 as the cause

of rheumatoid disease.

References Cited:

1. , R.F. Amoebic meningo-encephalitis. Trans. Roy. Soc. Trop. Med.

Hyg. 66: 195-197; 1972.

2. Dobell, C. The Amoeba Living in Man. London: Bale, Sons and

sson; 1919.

3. (Editorial). Pathogenic free-living amoebae. Lancet 2: 165-166; 1977.

4. (Editorial). Rheumatic manifestations in leprosy. Lancet 1: 648-649;

1981.

5. Ely, L.W.; , A.C.; Wyckoff, H.A. The amoeba as the cause of the

second grade type of chronic type of chronic arthritis. Calif. State J. Med.

20:59; 1922.

6. Faust, E.C.; , P.T.; Jung, R.C., editors. Clinical Parasitology.

8th ed. Philadelphia: Lea and Fibiger; 1970.

7. Glynn, L.E. The chronicity of inflammation and its significance in

rheumatoid arthritis. Ann. Rehum. Dis. 17: 105-111; 1968.

8. Herxheimer, Krause. Euber eine Syphilitischen vorkomende

Quecksilberreaktion. Dtsch. Med. Wchsch. 28: 895-896; 1902.

9. Kofoid, C.A.; Swezy, O. Amebiasis of the bones. JAMA. 78: 1602-1604;

1922a.

10. ------- . Mitosis in endamoeba dysenteriae in the bone marrow in

arthritis deformans. Univ. Calif. Publ. Zool. 20: 301-307; 1922b.

11. -------. On the occurrence of endamoeba dysenteriae in the bone lesions

of arthritis deformans. Calif. State J. Med. 20: 59; 1922c.

12. Kofoid, C.A.; Boyers, L.M.; Swezy, O. Endamoeba dysenteriae in the lymph

glands of man in Hodgkin's disease. Univ. Calif. Publ. Zool. 20: 309-312;

1922a.

13. ------- . Occurrence of endamoeba dysenteriae in the lesions of

Hodgkin's disease. JAMA 78: 1602-1604; 1922.

14. Kofoid, C.A; Swezy, O.; Boyers, L.M. The coexistence of Hodgkin's

disease and amoebiasis. JAMA 78: 1602-1604; 1922.

15. Multicentre Study Group. Levamisole in rheumatoid arthritis. Lancet 2:

1007-1012; 1978.

16. Nagington, J.; , P.G.; Playfair, T.S.; et al. Amoebic infection of

the eye. Lancet 2: 1537-1538; 1974.

17. Waldenstrom et al. Serological overlap with thyroiditis, throtoxicosis,

and systemic lupus erythematosus. In Doniach, D.; Roitt, I.M.; , K.B.

Autoimmune phenomena in pernicious anemia. Brit. Med. J. 1: 1374-1379; 1963.

18. , H.D.; Lockwood, G.M.; , B.A. Inhibition of

reticuloendothelial function by gold and its relation to post-injection

reactions. Brit. Med. J. 2: 235-237; 1979.

19. Wyburn-Mason, R. A New Protozoan: Its Relation To Malignant and Other

Diseases. London: Kimpton; 1964.

20. ---------- . The Causation of Rheumatoid Disease and Many Human Cancers:

A New Concept in Medicine. Tokyo: Iji Publishing Co.; 1978.

21. ---------- . The free-living amoebic causation of rheumatoid and

autoimmune diseases. International Medicine 1: 20-25; 1979a.

22. ---------- . The naeglerial causation of rheumatoid disease and many

human cancers: a new concept in medicine. Medical Hypothesis 5: 1237-1249;

1979b.

23. ---------- . New views on the aetiology of rheumatoid arthritis. British

Medicine 21: 12-14; 1979c.

The Free-Living Amoebic Causation and Cure of

Activity in Rheumatoid Diseases

by Wyburn-Mason

(Formerly published in The Journal of the Rheumatoid Disease Foundation,

Volume 1, Number 2)

A reactive arthritis may occur with gastrointestinal infection with

bacteria, such as Campylobacter jejuni, Salmonella, Shigella and Yersinia,

in patients with HLA-B27 tissue types and disappear with successful

treatment of the infection (Kosanen et al. 1980). Between 1922 and 1952,

numerous publications described E. histolytica bowel infection with or

without dysentery as associated with a condition practically identical with

rheumatoid disease. Both conditions are cured by emetine without any

exaggeration of the joint symptoms. Yet it is not unusual for sufferers from

rheumatoid arthritis to show E. histolytica or its cysts in the feces and

never in the rheumatoid lesions.

All terrestrial animals and plants, and those inhabiting fresh water and the

sea, live in a world surrounded by many species of free-living amoebae.

These may pass mammalian respiratory passages as cysts or trophozoites and

may be present as trophozoites in the gastrointestinal tract of many

animals, including man since they are found in their feces. As the organisms

are motile, it would be reasonable to suppose that once they had entered the

orifices of man or other warm-blooded animals, they would migrate under

thermotropic influences into some body tissues. Since amoebae may be either

non-pathogenic or pathogenic to animals, the same may apply should the

organisms reach human tissues.1

In 1922, the eminent protozoologists, Kofoid and Swezy, in California,

reported the presence in the bone marrow in cases of rheumatoid arthritis,

without dysentery of E. histolytica in the feces, of a free-living amoeba

distinguished from human cells by its mitotic processes which contained only

6 chromosomes as compared with the normal 46 of human cells. It showed a

single blunted pseudopodium and numerous vacuoles. They suggested an

aetiological relationship between the infection and the arthritic process.

In numerous recent publications, the speaker14, 18 has shown that, using the

property of thermotropism, free-living amoebae pathogenic or non-pathogenic,

can be made to migrate in varying numbers out of human tissues, including

those of the newborn and fetus (Figs. 1, 2). They are also found especially

in the affected tissues of patients with rheumatoid disease, in malignant

tumors, in normal feces, in uncooked butcher's meat, and in surface soil.

They may be recovered in small numbers from some tissues of apparently

healthy humans, where they are presumably of non-pathogenic nature. They

appear identical with those found by Kofoid and Swezy. These findings have

been confirmed in various parts of the world, including Vanderbuilt

University, U.S.A., the Oncological Research Institute, Bratislva,

Czechoslovakia, Waikato Hospital, New Zealand, the Hospital for Special

Surgery, and St. 's Hospital, New York and in England.1

These organisms can be cultured in the laboratory in " amoeba saline " into

which a culture of E. coli has been introduced. The effect of various

antiamoebic substances in killing the organisms can then be studied by

adding them to the cultured cells. Those which do so include one percent

solutions of bile salts, 4-aminoquinolines, very dilute solutions of copper

sulfate, metallic copper, gold salts, emetine, dehydroemetine, pentamidine,

levamisole (which contains an imidazole group), and in particular the

5-nitroimidazole group of drugs, including metronidazole, clotrimazole,

tinidazole, ornidazole and nimorazole. All of these possess a wide spectrum

of antiprotozoal, including some antiamoebic activity.

The organisms have been recovered with great difficulty because they are not

observed in affected tissues stained by ordinary methods. They are not

numerous and look like macrophages or lymphocytes. This is a feature

repeatedly observed in experimental infections with free-living amoebae in

laboratory animals. (This recalls the situation in syphilitic lesions until

stains for the treponema pallidum were discovered). The organisms in

rheumatoid arthritis can, however, be demonstrated in tissue sections by

immuno-fluorescent staining using sera containing appropriate antibodies to

the organisms and by studying their mitosis and chromosome content in marrow

biopsy material.

Rheumatoid Arthritis, a Generalized Disease

Rheumatoid Arthritis is not solely one of joints but may involve any tissue

of the body. The same histological changes in the joint capsules may be

found in extra-articular lesions and consist of inflammatory lymphocytic

infiltration, formation of germinal follicles and often plasmocytosis

accompanied by arteritis, arteriolitis, or endarteritis. Many of the

extra-articular lesions constitute so-called " auto-immune diseases, " but

also include Sjogren's syndrome, bone marrow infiltrations, and thymic

lesions with or without myasthenia, fever up to 40ø C, sweating and raised

ESR, typical of an infection. Any of the extra-articular of AI lesions may

occur in any combination with or without arthropathy.

From a study of the world literature, it seems that some of the

extra-articular lesions may involve:

1. Exocrine glands often producing enlargement and dilatation of the ducts.

It may involve the lacrimal and salivary glands (Sjogren's syndrome, R.A. in

miniature), breast (cystic mastitis), pancreas (lymphocytic pancreatitis,

which may exhibit calcification), liver (active chronic hepatitis, primary

biliary cirrhosis), gall bladder and bile ducts (chronic cholecystitis and

stenosing cholangitis), and kidneys (chronic nephritis, pyelitis).

2. Endocrine glands, including the thyroid (lymphocytic or Hashimoto's

thyroiditis), adrenals, parathyroids, thymus (with or without myasthenia)

and pituitary.

3. Polymyositis, myasthenia, bursitis, tenosinovitis, or rheumatoid nodules

in any tissue.

4. Mucosal inflammation followed by atrophy, which may involve the

gastro-intestinal tract producing atrophic stomatitis, pharyngitis,

esophagitis, gastritis, or coeliac disease and ulcerative colitis, or in the

respiratory tract leading to atrophic rhinitis, Eustachian salpingitis,

laryngitis, or bronchitis.

5. Fibrosing alveolitis, pulmonary nodules, lung fibrosis, or pleuritis.

6. Peri-, myo-, or endo-carditis.

7. Bone marrow infiltrations with various disturbances of blood formation.

8. Paget's disease of bone, spondylitis.

9. Lymphadenopathy or splenomegaly with reactive lymphoid hyperplasia.

10. Choroiditis, uevitis, retinitis, scleritis.

11. Various skin lesions, including icthyosis, dermatitis, leukoderma, and

melanoderma.

The serum may or may not contain RF, various auto-antibodies, ANF, increase

in gammaglobulins and usually a raised ESR.

The Effect of Antiamoebic Drugs on Active

Rheumatoid Disease

The author has shown that when any substance which kills the free-living

amoebae in vitro is administered to cases of active rheumatoid disease or

its extra-articular manifestations, it may cause a rapid disappearance of

the inflammatory symptoms around the joints and elsewhere in the body.1 This

includes coeliac disease, ulcerative colitis, cystic mastitis, lymphocytic

thyroiditis, etc. Myasthenia gradually disappears and in early cases11,

complete cures may be obtained. These drugs often induce an Herxheimer

reaction that is a transitory exaggeration of the inflammatory changes

around the joints and elsewhere. This may be accompanied by influenzal

symptoms, sweating, pyrexia, lymphadenopathy, rise in ESR, and eosinophilia.

This reaction has been reported by others in cases of active rheumatoid

disease treated with gold salts18 and levamisole19, (which kill free-living

amoebae). Such a phenomenon, first described by Herxheimer20 in 1902, when

cases of syphilis were treated with mercury, also occurs in syphilis treated

with penicillin and in other diseases due to organisms more complex than

bacteria when drugs which kill the causative organism in the tissues are

administered. This reaction is due to liberation of irritant and antigenic

substances from the dying and dead organisms. The Herxheimer reaction in

cases of active rheumatoid disease treated with antiprotozoal substances has

been confirmed in various countries, notably in U.K., U.S.A., Holland, and

New Zealand.1 It is not observed in healthy persons so treated or in

rheumatoid diseases given anti-biotics. It's occurrence in rheumatoid

disease, including " autoimmune " lesions during treatment with various

antiamoebic drugs proves the presence in the affected tissues of a causative

pathogenic organism.

By administration of antiamoebic drugs, especially 5-nitromimidazoles, to

cases of rheumatoid disease for 3-6 months, the evidences of disease

activity usually completely disappear in joints and extra-articular tissues.

" Autoimmune " lymphocytic and humoral reactions are thus not the primary

disturbance in rheumatoid and " autoimmune " diseases, but are the

cellular-antibody response to the infection and its antigens and contribute

to the tissue damage.

Practical Details of Treatment of Rheumatoid and Related Diseases

A simple method of treatment of rheumatoid disease is to administer 2 grams

on 2 successive nights of one of the 5-nitroimidazoles for a 70 Kg patient.

In some cases, the organism , as judged by the severity of the Herxheimer

reaction, may prove to be susceptible to one or another of the

5-nitroimidazoles.

In order to prevent any severe Herxheimer reaction, the patient may be given

an anti-inflammatory drug. The drug may remain at an effective level in the

blood for four or more weeks while the inflammatory reaction is dying down.

If it is necessary for a further dosage of the antiamoebic drug to be given,

wait until three months after the original doses to give the induced

inflammatory response [time] to die down. Often only a single treatment is

necessary and improvement may continue over the course of a year or more

with return of a normal ESR and disappearance of all signs of disease

activity.

References

1. Wyburn-Mason, R. The causation of rheumatoid disease and many human

cancers. A new concept in medicine. Tokyo, Iji Publishing Co., Japan; 1978.

2. Editorial. Pathogenic free-living amoeba. Lancet ii: 165-6; 1977.

3. Craig and Faust. Clinical parasitology. Ed. by Faust, E.C., ,

P.T., Jung, R.C. 8th Edition, Lea and Fibiger, London; 1970.

4. Dobell, C. The amoebae living in man. Bale, Sons and son,

London; 1919.

5. , R.F. Amoebic meningo-encephalitis. Transactions of Royal Society

of Tropical Medicine Hygiene. 66: 195-7; 1972.

6. Nagington, J., , P.G., Playfair, T.S., et al. Amoebic infection of

the eye. Lancet ii: 1537-8; 1974.

7. Kofoid, C.A., Swezy, O. Mitosis in Endamoeba dysenteriae in the bone

marrow in arthritis deformans. Univ. Calif. Publ. Zool. 20: 301-307; 1922.

8. Ely, L.W., , A.C., Wyckoff, H.A. The amoeba as the cause of the

second grade type of chronic arthritis. Calif. State J. Med. 20:59; 1922.

9. Kofoid, C.A., Swezy O. On the occurrence of Endamoeba dysenteriae in the

bone lesions of arthritis deformans. Calif. State J. Med. 20: 59; 1922.

10. Kofoid, C.A., Swezy, O. Amebiasis of the bones. JAMA 78: 1602-4; 1922.

11. Kofoid, C.A., Boyers, L.M., Swezy, O. Endamoeba dysenteriae in the lymph

glands of man in Hodgkin's disease. Univ. Calif. Publ. Zool. 20: 309-12;

1922.

12. Kofoid, C.A., Swezy, O., Boyers, L.M. The coexistence of Hodgkin's

disease and amoebiasis. JAMA 78: 1602-4; 1922.

13. Kofoid, C.A., Boyers, L.M., Swezy, O. Occurrence of Endamoeba

dysenteriae in the lesions of Hodgkin's disease. JAMA 78: 1604-7; 1922.

14. Wyburn-Mason, R. A new protozoon, its relation to malignant and other

diseases. Kimpton, London; 1964.

Criteria and Treatment Methods

Using Anti-Protozoal Drugs

Selection of Patients

There must be verification of some form of ACTIVE Rheumatoid Disease.

The patient should have four out of nine of these indications.

1. History of a rheumatoid disease syndrome.

2. Physical findings diagnostic of the condition.

3. Positive serology.

4. Elevated sedimentation rate.

5. 2% or more eosinophilia.

6. Secondary anemia.

7. Two or more inflamed joints.

8. Atropic joints by x-ray.

9. Morning pain and stiffness.

Drugs of Choice (May be Limited by Local Availability)

This dosage based on 70 Kg. (150 lb.) man:

Flagyl. (Metronidazole) 2 Gm./day for 2 days a week, for six weeks.

Or 2 Gm./day for 10 days. Then, for 3 days a month for 3 months. Then,

repeat laboratory tests before continuing treatment. A change of drugs may

be indicated if substantial improvement or a remission has not been

obtained.

Lomotrin. (Clotrimazole) 1.0 mg. per 10 Kg. body weight per day for 8 weeks.

Then, repeat lab. etc.

Diodoquin. Yodoxin. (Di-lodohydroxiquin) 650 mg. three times a day with

meals for 10 days. Then, for 3 days a month for 3 months. Recheck lab. work.

Fasigyn. Tinidex. (Tinidazole) 500 mg. in a single dose for the first week,

increasing to twice a week for 10 weeks.

Pentamidine 200 mg. day by injection 3 days a week for three weeks. Then,

recheck laboratory findings.

The total course of treatment may be from 3 to 6 months in the average

patient. Those previously treated with drugs affecting the immune systems,

such as gold, penicillamine and the cortico-steroids, are more resistant to

anti-protozoal drugs.

A nutritional diet, adequate vitamin and mineral supplementation, exercise

with appropriate rest periods and avoidance of stress are necessary factors

in care of the rheumatoid disease patient.

This is a personal protocol: ROBERT BINGHAM, M.D.

Rheumatoid Disease - Discoveries of

Wyburn-Mason, M.D., Ph.D.

Originally published in The Journal of the Academy of Rheumatoid Diseases,

c1987

by A. Chapdelaine, Sr.

Wyburn-Mason was a research physician and protozoologist. During his

life-time, he received the highest possible academic grades in every degree

undertaken. He was involved with the testing of sulfa dugs; was the first to

identify a viral form of cancer; had two nerve diseases named after him; was

a specialist on nerves and also did research on cancer; and he wrote a

number of definitive medical books1 and numerous articles.1 This eminently

acceptable medical physician and researcher became the genius who first

developed and effective theory and treatment for Rheumatoid Diseases.

Over a life-time of brilliant work, he concluded that a certain kind of

commensal organism, an amoeba (limax amoeba: a one celled, free-living

animal organism which he named Amoeba chromatosa), creates conditions inside

the body that result in damage, and this damage presents itself in many

different forms depending upon which tissues are infected.

If one has a genetic susceptibility toward the products of this presumed

amoeba, or its toxins, or resulting proteins from the dead amoeba, then,

over a time-period, one can and usually does have one or more symptoms:

Rheumatoid Arthritis, Bursitis, Ankylosis, Spondylitis, Psoriasis, Lupus,

Rheumatic Heart, Carpal Tunnel Syndrome - in all about 100 different

symptoms not previously recognized as stemming from the same source.

What He Did

Professor Wyburn-Mason claimed to have isolated out a limax amoeba

from human tissue and sera by taking advantage of the fact that the organism

is attracted to heat. He cooled one side of a collection of specially

prepared tissue and heated the other side. The amoeba migrated to the warm

side, also passing through a very fine filter. The collection of amoebae was

then grown in the laboratory. He claimed that some were placed back in

animal tissue, where exactly the same cellular lesions were observed as

found in Rheumatoid Disease patients. He concluded that the protozoan had

escaped attention because they looked under the microscope very much like

human macrophages.

He studied a number of medicines and found several that would stop the

progress of Rheumatoid Disease. He announced these findings in 1964 at a

scientific conference,27where he received a standing ovation. No one

followed up on his discoveries until Bingham, M.D., reported the

findings in a magazine24; and Jack M. Blount, Jr., M.D., tried metronidazole

(chemically related to then unavailable clotrimazole) on himself.24

Whether or not the amoeba is ever verified to be the cause, we are certain

of this: his treatment works!

If You Are a Rheumatoid Disease Victim -

How Does the Presumed Amoeba Affect You?

According to Wyburn-Mason's theory2: To those of us who are

genetically susceptible to the amoeba and its products, the organism is

dangerous and very damaging.

The amoeba is found freely floating in the air, in water we drink, in ponds,

swimming pools, health spas, and in some foods. It is almost impossible to

stay away from the amoeba, although there are some things that can be done

to minimize risk of exposure.

When the amoeba is killed inside the human body with an antiamoebic, the

body responds by creating " flu-like symptoms. " These symptoms can include:

Itching, ringing in the ears, bronchitis symptoms, coughing, nocturnal

muscle spasms, bone pain, bitter or metallic taste, temporary memory loss,

sleepiness, depression, palpitations, frequent urination, burning sensation

during urination (clotrimazole does this, sans Herxheimer), pain in joints

and flu-like symptoms, no appetite, flushing of skin and reddish patches,

general malaise, fever, vomiting, nausea, diarrhea, headache, heavy

perspiration especially at night.

A patient will not have all of these symptoms, but only those where the

amoebae has been quietly working - and such symptoms are clear evidence of a

genetic susceptibility to the amoeba and its products.

The above symptoms are titled the " Jarisch Herxheimer reactions, " and they

are also found when killing other organisms, as in the treatment of

Tuberculosis, Syphilis, Leishmaniasis, Leprosy (Lucio's phenomenon). From

anecdotal reports,3 it apparently can also happen under appropriate

nutritional regimes.

Jarisch Herxheimer theory and interpretation states that the above symptoms

may be found whenever an organism more complex than a simple bacteria is

killed inside the human body.4 Whether or not the presence of an inimical

organism, and its death, is both a necessary and sufficient condition is not

known.

When you've gone through the Jarisch Herxheimer (which may be very mild or

very heavy), you should be well - except for damage already done - until

you've gotten reinfected with the organism.

Related Treatments

A physician may decide to simply give a patient antiamoebics or to give the

medicines at the same time he is treating other problems. Nutrition,

physical exercise, and allied treatments (such as Candidiasis8) that

supplement overall well-being are very important. Why? Because they are

designed to improve the immunological system - the ability to fight the

presumed amoeba in a natural way. It is assumed that the " stronger " an RD

victim's immunological system, usually the longer they can go before

receiving more antiamoebics.

The RD victim may also receive a second treatment, called " intra-neural

injections, " 5 which is very effective in controlling the pain of Rheumatoid

Disease as well as the pain of Osteoarthritis.

How Many People Get Results?

Our experience in open studies6 shows that results are obtained from 78% to

95% of the patients treated for Rheumatoid Disease using our treatment

protocol.7

These results differ greatly because different physicians select patients

differently, and they may also include in their clinical study some patients

that are not affected by the presumed amoeba, but in fact may be affected by

other organisms, such as Candida albicans8 that can present similar

symptoms.

If there were a placebo effect (belief) factor involved, our results would

not be greater than about 30%, the same results that trained Rheumatologists

get with various " accepted " but often dangerous treatments.9

The Rheumatoid Disease Foundation [now The Arthritis Fund] prays that all

patients will be among those who respond.

The Movement is Growing

I founded and chartered the Rheumatoid Disease Foundation [now The Arthritis

Fund] as a non-profit, charitable, IRS tax-exempt organization on October

13, 1982 with a number of lay people (notably treasurer Frederick Binford

and vice-treasurer Vansant and others now resigned) and five

physicians on the Board of Directors: Bingham, M.D., Jack M. Blount,

M.D., Gus J. Prosch, M.D., Dr. K. Pybus, Eugene S. Wolcott, M.D., and

Professor Wyburn-Mason, M.D. ( Wyburn-Mason died, and two

resigned: Gus J. Prosch, M.D., and Bingham, M.D.)

Eugene S. Wolcott, M.D., stayed on to become Senior Vice-Chairman. Dr.

K. Pybus became the Foundation's Chief Medical Advisor - he had worked with

Wyburn-Mason as 's house physician many years earlier, and holds

a deep respect for Wyburn-Mason's skill and knowledge. Jack M. Blount, M.D.,

became the Rheumatoid Disease Foundation's Chairman until succeeded by

Baron, D.O., recently. Jack Blount is now Chairman Emeritus, after serving

nearly four years. Interestingly, Eugene S. Wolcott, M.D., was my family

physician for twenty years, having treated my wife, myself and ten children.

Like many other physicians, he joined the Board only after having tried our

treatment on patients and having observed the results on me and others.

Since then hundreds of physicians20 located in many different countries (but

chiefly the U.S.) have skeptically tried our treatment and have been quite

impressed with results.

We are now funding double-blind studies on the use of one antiamoebic

(clotrimazole) at Bowman Gray School of Medicine and have funded or are

funding other scientific studies at the Medical College of Virginia and

Vanderbilt University. Dr. Kwang Jeon, protozoologist, University of

Tennessee, has done some work without pay, as has Dr. K. Pybus and

pathologist A. H. Davies, Ph.D., (South Africa) and medical student, Tony

Chapdelaine, assisted by protozoologist J. Neff, Ph.D.

Tens of thousands of concerned citizens have joined with this Foundation, in

spreading the word, and by sending in their contributions.

We are represented in more than 9 different foreign countries, and there

will be Chapters to serve localities with free-treatment for the indigent

one day, hopefully soon.

So What Have We Learned

First and foremost, we believe (but cannot prove) that we have learned that

Wyburn-Mason, M.D., like Semmelweis, had the wrong theory but the

correct solution. Many will remember that Semmelweis preceded Pasteur's germ

theory by his theory of the " odor of death " and thus brought child-bed fever

deaths down drastically. For this wrong theory, right treatment - and the

savings of lives that embarrassed others in the medical profession who had a

higher death rate - he was cast out of his medical association.

Science, you may remember, grows by development of theories which, when they

work, are accepted whether or not they make sense. Later, with refinements,

they may be changed, so long as the changed theories also work and usually

work better. Please keep in mind W. 's statement which defines

proper scientific method as thus: A theory need not be correct, it need only

work!20

When Wyburn-Mason worked with Admiral Stamm, protozoologist, according to

his now deceased wife, Joan Wyburn-Mason11,27 himself could not accept

the protozoan theory of the causation of RD. After many nights of work with

Stamm, back in the fifties, he was finally convinced by Stamm that a

protozoan was the culprit. Stamm, remember, was an eminent and

well-published protozoologist.

When invented his thermotropic separating device, he sterilized his

samples by the use of penicillin and streptomycin to ensure that no foreign

bacteria would go through the minced samples into their collection jar. By

so using these antibiotics, he ensured the creation of what has come to be

known as Cell Wall Deficient (CWD) organisms.12

To be aware of the fact that he had created Cell Wall Deficient organism,

Wyburn-Mason would have had to know about them, and the scientific field had

not clearly defined them until 1974 by Domingue, Schlegel, and Woody.13

Note, further, that without access to electron microscopy - unavailable to

either Wyburn-Mason or Stamm - had they known about Cell Wall Deficient

organisms, they could not have studied them, nor observed the cell-wall

striping effects of antibiotics on common bacteria that they thought to kill

by use of antibiotics to prevent experimental contamination in the amoebae

thermotropic separation device.

A further note of strong interest: well-trained protozoologists of today

will often observe Cell Wall Deficient organisms, or colonies of them, under

ordinary microscopes, and conclude that they are viewing amoebae!12

And-

Even today, 1987, there are virtually no clinical laboratories that have the

expertise and training to isolate Cell Wall Deficient organisms from human

tissues and to study them, nor can anyone determine the implications of the

existence of such organisms inside the immunologically deficient patient,

nor can anyone determine whether or not such organisms contribute to

immunological deficiency.23

The study of Cell Wall Deficient organisms is not an unknown field, but

simply an esoteric specialty that has yet to be integrated into the routine

of physician knowledge and practice.

Be it further noted that Neff, Ph.D., through separate studies using

knee effusions and other techniques, concluded that Wyburn-Mason and

protozoologist Stamm had used faulty filtering equipment and insufficiently

differentiating microscopic equipment, so that they were unable to

differentiate microscopically between host cells and amoebae, and that more

likely he observed blood cells that persisted but did not grow or divide,

further, that it seems probable that the structures he called cysts were

damaged and clumped host cell nuclei.30

Kwang Jeon, Ph.D., concluded that no amoeba were present in knee effusion

samples submitted from our referral physicians.31

Dr. K. Pybus and A.H. Davies, Ph.D., at first thought they were viewing

amoebae, but later concluded they viewed macrophages.32

Susskind, Ph.D., also concluded through use of both synovium and other

tumor samples, that only macrophages were present, not amoebae.13

It is easy to understand, then, how it was that Wyburn-Mason and

Stamm - after repeatedly " viewing " protozoans in their cultures, after

pursuing world literature on protozoan2 and seeing therein much that

corroborated and explained, and especially after developing an

" anti-amoebic " treatment that worked spectacularly for the first time in

world history on 80% of those Rheumatoid Disease victims treated, that they

felt their case was closed, that protozoans were proved.

What Do We Know For Sure?

Thanks to many funded and unfunded researchers (and chiefly to the synthesis

of Dr. K. Pybus,11 our chief medical advisor) from what we seem to know

through our research to date, we can guess at the following facts:

1. Our treatment works 48% to 65% better than present rheumatology

practices; i.e. it works 78% to 95% of the time, depending on patient group

and physician practices.6,9

2. If a placebo effect were involved, this percentage would not be greater

than 30%.9

3. Clotrimazole inhibits formation of phospholipase (PLA2), in a calcium

dependent manner. PLA2 precursors the arachidonic cascade. Further, note

that an under/over concentration of Ca or Fe ion determines the quantitative

nature of the dependency, thus explaining to some extent the nutritional

relationship of Ca/Mg et al. to RD.14

EDTA also inhibits PLA2,14 thus explaining to some extent why EDTA therapy

gives temporary relief (not to mention the presumed cleaning up of " free

radicals " generated during the inflammatory process.15 -We would guess that

DMSO, properly used, also temporarily cleans up presumed free-radicals, but

also contributes to the change in ratio of HDL to LDL28,35).

4. Clotrimazole kills a very wide spectrum of protozoans in the test tube,

as opposed to metronidazole and tinidazole.16 Tinidazole and clotrimazole

can be metabolized by either human enzymes or intestinal micro-flora;

metabolization of metronidazole relies solely on intestinal micro-flora.17

This may explain why the first treatment of metronidazole may be effective,

but not the second: during the process of being metabolized by intestinal

micro-flora, it also kills off the " good-guys. " When micro-flora is

replaced, or taken with metronidazole, the treatment often becomes effective

again.18 (We presume " good guys " micro-flora includes Lactobacillus

acidophilus, Lactobacillus bifidus, and Streptococcus faecium, but more

research needs to be performed to be certain, or more information needs to

be gathered.)

5. Clotrimazole kills Candida albicans.8,19

6. Clotrimazole stimulates cortisol.14,35 (Perhaps a means of getting

marginally deficient patients weaned away from external cortisone?)

7. Metronidazole kills over-active macrophages according to work by K.

Pybus and A.H. Davies (1st reported), and seems to be corroborated by Kwang

Jeon, Ph.D. reports.)21

8. Clotrimazole does not kill over-active macrophages.11

9. Various nutritional substances affect the disease state and the progress

of wellness. (Copper, Boron, selected fats, sugars, various other vitamins

and minerals, various diets that work or harm, et al.)22

10. Candida albicans often spreads with the presumed Amoeba chromatosa under

the same rules related to " weakening " of immunological system, and probably

ought to be treated simultaneously, if suspect.8

11. There is a relationship between allergenic responses from various

antigens and RD symptoms.22 (See various treatments based on " allergenically

clean " clinics, pure water fasts, bio-detoxification programs developed by

L. Ron Hubbard, now implemented by Zane Gard, M.D., San Diego, CA, et al.)

12. Our treatment protocol includes different " anti-amoebics " which affect

amoebae differently, according to environment, concentration and other

factors, according to in vitro chemosensitivity studies.34 This has been

presumed to explain varying effects in vivo as due to varying body chemistry

and varying genus, species and strains of amoebae. Varying organisms may

still be involved and so may varying body-chemistries.

So, What is Our Direction of Search Now?

1. The Bowman Gray Medical School Rheumatoid Arthritis Study on use of

clotrimazole in double-blind trials goes onward. Whether or not

Wyburn-Mason's theory is correct, the treatment works, and we must establish

through double-blind means that it is both safe and effective (FDA

criterion).

2. At the suggestion of many (Pybus, Neff, Franson, Susskind, Jeon, others,

and because of negative results in reproducing the Stamm/Wyburn-Mason

protozoan, we should concentrate primarily on the bio-chemical connections

involving principally clotrimazole and metronidazole. For example, at

Bowman Gray has taken randomized knee effusions which have been supplied to

Franson35 at Medical College of Virginia. Franson and Susskind are

cooperating in developing further Franson's breakthroughs related to

clotrimazole, and Susskind's further findings. Experimental results will be

eminently useful and publishable.

3. J. Neff, Ph.D.,30 and Kwang Jeon, Ph.D.,31 both have interesting

suggestions potentially fruitful for further research that should decidedly

be followed up.

Kwang Jeon would " test the hypotheses that infective amoebae are directly or

indirectly involved in the manifestation of arthritic symptoms and that

anti-amoebae drugs such as Imidazole compounds cause the remission of

reducing the secondary effects of amoebae on other cells such as synovial

cells. For example, Imidazole compounds may act on altered synovial cells in

the joints of rheumatoid arthritis patients to prevent the production of

rheumatoid factors, thus reducing chronic inflammation in arthritic

patients. " He would further " examine synovial fluid samples from arthritis

patients for the presence of possible infective agents such as amoebae,

study the effect of Imidazole compounds on cultured synovial cells, with

special emphasis on the viability of synovial cells in vitro and subsequent

production of immune complexes, and compare growth behavior of synovial

cells from patients treated with drugs, and use animal models such as

susceptible rats to examine the in vivo effect of Imidazole on synovial

cells. " 31

Neff, Ph.D., would suggest determining " the concentration of amoebae

antibodies in both the synovial fluid and serum of RA patients. The

enrichment of the antibody might be determined by comparing the antibody

concentration with the concentration of a non-immune constituent such as

human serum albumen; determine if amoebae antibody complexes with antigen

and C fragments are present in the phagosomes of leukocytes of a series of

both RF plus and RF minus RA patients. If present, determine if the

antibodies are enriched in the phagosome aggregates as compared to other

antibodies or other proteins found in the same synovial fluid; determine if

neutrophils, present in both synovial fluid and peripheral blood, are

already activated to attack amoebae and if the attack is mediated by amoebae

antibodies; determine the complement pathway/s present in synovial fluid in

serum. " 30

4. Susskind, Ph.D., suggests: " Therefore clotrimazole, levamisole,

tinidazole, and metronidazole may yet be found to subserve similar

immuno-modulatory mechanisms [as cyclosporin and levamisole] in rheumatoid

arthritis. Further studies are necessary to determine if clotrimazole exerts

modification of the inflammatory response at one or more specific sites, and

if it acts as a general immuno-suppressant or as an immuno-potentiator under

selective conditions. Hence, the paramount importance of correlating in

vitro data with an experimental in vivo system in order to determine which

effects are relevant to the drug's therapeutic activity. Complete

understanding of the clotrimazole's immuno-modulating activities will also

lead to the design of more effective protocols. " 33

5. C. Franson, Ph.D., states that " We have demonstrated clearly that

clotrimazole inhibits the human synovial fluid PLA2 (as well as other

neutral-active and calcium ion dependent PLA2s) in a calcium ion-dependent

fashion. That is, the lower and more physiologic levels of calcium ion ...

clotrimazole produced dose-dependent inhibition. Because membrane

phospholipids contain the bulk of arachidonate (the precursor for

prostanoids and leukotrienes) in the SN-2 position of the molecule, the

ability of this molecule to act as an anti-inflammatory agent was proposed.

Tinidazole and histamine had little or no effect on enzyme activity; similar

results were obtained [with] metronidazole ... . The mode of action appears

to bind clotrimazole to the phospholipid substrate since centrifugation

studies of drug plus substrate E. coli resulted in cosedimentation of both

components leaving no inhibiting activity in the supernatant fraction. ...

" ...we are continuing the search for endogenous regulators of what we

believe is a proinflammatory PLA2 in SF [synovial fluid]. It is clear from

these studies that both inhibitory lipids and proteins are present in

synovial fluid that moderate the expression of PLA2. We believe that

clotrimazole is an additional modulator and that the very interesting

studies that Dr. Susskind now pursues with respect to the drug's effect on

monocytes may be membrane-lipid mediated and thus be directly related to our

basic observation of phospholipase inhibition.35

6. Lida Mattman, Ph.D., of Wayne University suggests relating, if possible,

knowledge of Cell Wall Deficient organisms to Rheumatoid Disease.23

Reason: If you will look on pages 38 and 39 of Rheumatoid Diseases Cured at

Last (Third Ed.),24 you'll read mention of work performed by Marmor and

Warren. They isolated a heat resistant RNA molecule from active Rheumatoid

Disease synovium. On injections in mice and chickens, active RD was created.

Isolates taken from these were again passed through other mice and chickens

and these produced active RD.

On first reporting this satisfaction of Koch's Postulates, attempts to

reproduce their study failed. According to Lida Mattman, when Warren and

Marmor pointed out that it required synovium from " active " RD victims, the

study was indeed replicated as reported. Yet no one seems to have followed

up on this lead.

Dr. Lida Mattman, herself, has taken Cell Wall Deficient propiono bacteria

(common on skin) and on injecting it into chicken eggs, has created chickens

with Rheumatoid Disease.12

Dr. Lida Mattman speculates that: A heat resistant RNA molecule may ride

piggy-back on the Cell Wall Deficient organism and, on entering human

tissue, sets up the " genetic sensitivity " to the Cell Wall Deficient

organism.12

Thus, it is clear that either an RNA molecule or a Cell Wall Deficient

bacteria, or some combination of both can cause Rheumatoid Disease in

certain animals.

This would also suggest a correlation nicely with Brown's,26 M.D.,

(Arthritis Clinic of Northern Virginia, P.C.) thesis that a mycoplasmic

bacteria is involved with gorillas, and presumably humans (Cell Wall

Deficient bacteria are often protozoan in appearance, just as they may be

mycoplasmic in appearance).

And the effects of Cell Wall Deficient bacteria inside the human body would

begin to explain peculiarities of the immunological envelope as well as

disease states.29

7. And while it may be an insignificant point - no stone should be left

unturned. During my recent visit to Hoekstra, III, and Lida Mattman,

Ph.D., Hoekstra, using a darkfield microscope, showed in my own blood both

the existence of a Cell Wall Deficient Candida albicans and a strange

appearing leukocyte. He made a photo of the leukocyte, stating that he had

noted a strong correlation on viewing this kind of abnormal leukocyte in all

RD victims. The photo will be made available to our physicians and

scientists for further possible correlations.

Therefore, as can be seen, The Rheumatoid Disease Foundation [now the

Arthritis Fund] started with a hypothesis that works very well but - by

keeping an open mind toward all possibilities - has made much progress in

understanding the reasons for the treatment's successes and, like any good

research orientation, can now point to areas of research that are likely to

conclude our understanding of Rheumatoid Disease [to] the benefit of all.

The Rheumatoid Disease Foundation [The Arthritis Fund] has done more good

for those afflicted with Rheumatoid Disease, and it has made more progress

in conquering Rheumatoid Disease - with less money - than any other

organization in history, starting with Wyburn-Mason's apparently

faulty hypothesis that led him to the world's first correct treatment.

It is believed that we are on the virtual threshold of understanding all,

and had we not gotten ourselves involved with an unethical fund-raiser, our

financial plight would not have suffered, as our understanding has grown.

Others Helped

If you are a patient taking antiamoebics, or are about to be treated with

them, or if you are a physician about to treat patients with our protocol,

you got where you are because others shared their knowledge and resources to

let you know there was a cure, or at least control and probable remission.

If others had not benefited, you would not be reading this today, or

administering our treatment to others today.

Can You Help Others?

There are literally millions of good, decent folks of all ages - young and

old - who need to be treated for crippling Rheumatoid Disease. They need to

know that there is help, that others are well, that the disease can now be

conquered and the terrible scourge brought to an end.

You Can Help

If you are a Rheumatoid Disease victim, you can help by getting yourself

well, telling others about your recovery, working with newly founded local

Chapters to raise funds to help others get well, writing to influential

people, contributing funds to support our research, buying and distributing

literature and books and by your thoughtful suggestions.

If you are a physician, you can help by many of the same activities

described above, but also by telling other physicians about us and letting

your patients know about us - especially through solicitation materials

available through our office that you can give to those you treat, using our

treatment protocol.

It's Up to You

How fast do you want the disease to disappear from the Earth's face?

It's up to you!

Tell folks about us - get them well - support our research and/or a local

chapter - everything and anything, no matter how small, will get us there!

What If You Have Further Questions or Wish to Donate?

If you wish to donate or desire more information, write to our National

Office, at The Arthritis Fund, 5106 Old Harding Road, lin, TN 37064,

Fax/phone the same: start sending before you hear our signal (615) 646-1030.

References

1. Wyburn-Mason, . The Causation of Rheumatoid Disease and Many Human

Cancers - A New Concept in Medicine, A Pr‚cis and Addenda, The Arthritis

Trust of America, 7111 Sweetgum Dr. SW, Fairview, TN 37062-9384.

2. Wyburn-Mason, . The Causation of Rheumatoid Disease and Many Human

Cancers - A New Concept in Medicine, Iji Publishing Co., Tokyo, Japan, 1978.

3. Numerous personal letters.

4. Pybus, K. Intraneural Injections for Rheumatoid Arthritis and

Osteoarthritis and The Control of Pain in Arthritis of the Knee. The

Arthritis Trust of America, 7111 Sweetgum Dr. SW, Fairview, TN 37062-9384.

Also see Haraldur Gudjonsson. " The Jarisch-Herxheimer Reaction, " Stockholm,

1972.

5. Pybus, K. ( Notrik, pseudonymously) The Control of Pain in

Arthritis of the Knee, [based on Wyburn-Mason's neural theory of 30 years

earlier] The Arthritis Trust of America, 7111 Sweetgum Dr. SW, Fairview, TN

37062-9384, 1984.

6. See Bingham, M.D., Prosch, M.D., Dr. Pybus, Simons, Ph.D. " Imidazole

Compounds for the Treatment of Rheumatoid Disease, " presented at American

Academy of Medical Preventics, November 16, 1985. Also see Renforth,

M.D. " Metronidazole Cures Rheumatoid Arthritis, " Historical Documents in

Search of the Cure for Rheumatoid Disease, both published by The Arthritis

Trust of America, 7111 Sweetgum Dr. SW, Fairview, TN 37062-9384, 1985.

7. Renforth, M.D., should be credited with independent research

using metronidazole in the treatment of Rheumatoid Disease. See item 6

above.

8. Crook, , M.D., The Yeast Connection, Professional Books, PO Box

3494, , TN 26508, 38301, 1986. C. Orian Truss, M.D. The Missing

Diagnosis, The Missing Diagnosis, PO Box 26508, Birmingham, AL 35226, 1982.

9. Klippel, H., M.D., Decker, L., M.D., Eds. Clinics in Rheumatic

Diseases Vol. 9/No.3, W.B. Saunders Company Ltd., December 1983.

10. See The Arthritis Fund's Physician and Referral listing.

11. Personal Communication from K. Pybus.

12. Personal conversation with Lida Mattman, Ph.D., Wayne University,

Detroit, MI, and Hoekstra, III, Ph.D., Thermascan, Inc., 21519

Harper, St. Clair Shores, Detroit, MI 48080.

13. Dominigue, Gerald J. " Naked Bacteria in Human Blood, " Microbia, Tome 2,

No. 2, 1976.

14. Franson, ; Moseley. " Relation between Calcium Requirement,

Substrate Charge, and Rabbit Polymorphonuclear Leukocyte Phospholipase A2

Activity, Biochemistry, American Chemical Society, 17: 4029; 1978. Franson,

R., Dobrow, R., Weiss, J., Elsbach, P., Weglicki, W.B. " Isolation and

Characterization of a phospholipase A2 from an inflammatory exudate, " The

Journal of Lipid Research, Vo. 19, No. 1, Jan. 1978. Franson, C.,

Eisen, D., , R., Lanni, C. " Inhibition of Highly Purified Mammalian

Phospholipases A2 by Non-Steroidal Anti-Inflammatory Agents, " Biochem. J.

186: 633-636; 1980. Franson, R., Weiss, R.J., , L., Spitznagel, J.K,

Elsbach, P. " Phospholipase A Activity Associated with Membranes of Human

Polymorphonuclear Leukocytes, " Biochem. J. 167: 839-841; 1977. Franson,

C. " Intracellular metabolism of ingested phospholipids, "

North-Holland Biomedical Press, Knight (Ed) Liposomes: From Physical

Structure to Therapeutic Applications, Chap. 12: 349-380; 1981. And many

other related papers with Franson.

15. Cranton, E. Bypassing Bypass, Stein and Day, 1984; also see Morton and

The Chelation Answer, Morton and , publisher unknown to author

but available at most stores.

16. Chapdelaine, Tony. Unpublished Vanderbilt University research paper,

available through The Arthritis Trust of America, 1985.

17. Personal Communication with Vanderbilt University Research

Pharmacologist.

18. Personal Communications with various Rheumatoid Disease Victims.

19. Personal Communication from Dr. K. Pybus. Also see Physician's Desk

Reference.

20. Chapdelaine, A., Sr., Hay, ; Chapdelaine, Tony. The W.

Letters, AC Projects, Inc., 1985.

21. Personal Communications: Dr. K. Pybus & Kwang Jeon, Ph.D.,

University of Tennessee, Dept. Protozoology.

22. Randolph, Theron G., Moss. Ralph W, Ph.D. An Alternative Approach to

Allergies, Bantam Books; 1982. Also, for nutritional components, read most

everybody, everywhere.

23. Mattman, Lida. Cell Wall Deficient Organisms, Chemical Rubber Company,

1976.

24. de Fabio, . Rheumatoid Diseases Cured at Last, The Arthritis

Trust of America, 7111 Sweetgum Dr. SW, Fairview, TN 37062-9384, 3rd ed.,

pp. 38-39; 1985.

25. Personal Communication with Tony Chapdelaine.

26. Brown, , M.D. " The Cure and the Controversy, " The Washington Post,

Sunday, April 22, 1984.

27. Wyburn-Mason, Joan. Dedication, Love and Humour, The Arthritis Trust of

America, 7111 Sweetgum Dr. SW, Fairview, TN 37062-9384.

28. Personal trials and lab tests.

29. Personal Communications, Tony Chapdelaine.

30. Neff, J., Asbell-Gillespie, Deborah; Chapdelaine, Tony.

" Isolation and cultivation of soil amoebae from fluids and tissues of

patients with rheumatoid disease, " Unpublished final report on a research

grant from The Arthritis Fund, November 8, 1986.

31. Jeon, Kwang, Ph.D. " Effect of antiamoebae drugs on synovial cells of

arthritic joints, " Unpublished research proposal, March 5, 1985, together

with personal conversations and letters.

32. Davies, Dr. A.H.; Pybus, K. Unpublished paper (untitled) together

with personal letters and conversations, 1985-86.

33. Susskind, , Ph.D. Unpublished final report on a research grant from

The Arthritis Trust of America and research proposal, letter, November 6,

1986.

34. Neff, J.; Chapdelaine, Tony. " Preliminary report on drug research

involving Acanthamoeba and Naegleria, " Unpublished final report on a

research grant from The Arthritis Trust of America, July 14, 1984.

35. Franson, C., Ph.D. Progress Report: Rheumatoid Disease

Foundation, unpublished, The Arthritis Trust of America, November 1986.

The Free-living Amoebic Causation and Cure of

Activity in Rheumatoid and Auto-Immune Diseases

by ROGER WYBURN-MASON

Editor's Note: This is from the last manuscript by Doctor

Wyburn-Mason. While it repeats information previously published, it also

includes material inserted shortly before his death and an updated

bibliography to 1979. As a basis for the research work at three schools of

medicine and the clinical practice of over 250 physicians throughout the

world and the formation and function of the Rheumatoid Disease Foundation

[now The Arthritis Fund], it has historical as well as medical value.

However, numerous species of free-living amoebae are known. Most fall into

two genera, Acanthamoeba and Naegleria and some are pathogenic to man and

animals; they are found on the surface soil preferring warm, moist

conditions and proliferate in warm stagnant pools and at the bottom of

rivers and lakes, particularly around the entry sites of warm effluents.

They have been found in the domestic water supply, in human feces and in

unpasteurized milk. Pathogenic free-living amoebae are readily isolated from

chlorinated swimming pools, potable water, sewage and human nasal and throat

cavities. They often contaminate tissue cultures. In inimical conditions,

they form hollow spherical cysts which are present in the air in most parts

of the world and can easily be found on agar plates exposed to air.

Free-living amoebae prefer warm surroundings, and they tend to migrate from

cool environments to body temperature, a property known as thermotropism.1

All terrestrial animals and plants and those inhabiting fresh water and also

probably the sea, live in a world surround by many species of free-living

amoebae, which certainly pass into the mammalian respiratory passages as

cysts or trophozoites in the gastrointestinal tract of many animals,

including man, since they are found in their feces. As the organisms are

motile, it would be unreasonable to suppose that, once they had entered the

orifices of man or other warm-blooded animals, they would not migrate under

the thermotropic influences into the body tissues. Since the amoebae may

prove to be either non-pathogenic to animals, the same must also apply

should the organisms reach human tissues.1

Recently it has been shown10 that the sera of all humans, including that of

the cord blood, contain antibodies to either Acanthamoeba or Naegleria,

indicating universal present or past infection of man and the newborn with

these organisms. Textbooks on protozoology state that " unspecified types of

amoebae have been isolated at times from every tissue in the body, " 3 or

" there is hardly an organ in the body from which somebody has not obtained

amoebae. " 4 Thus, all human bodies appear to contain free-living amoebae

somewhere in the tissues. A few cases of lesions due to species of such

organisms have been described in plants and man, in particular amoebic

meningo-encephalitis.5,6

The whole syndrome resembles syphilis. Waldenstrom and others, indeed, state

that " if the spirochaete had not been discovered, syphilis could be taken to

be the ideal model of an autoimmune disease. The variety of tissue reaction

antibodies, the wide-spread lymphocytic tissue damage and the vasculitis are

characteristic features. " 21 Rheumatoid disease closely resembles the

rheumatic manifestations in leprosy22 which may present with an acute

arthritis affecting one or a number of joints, polymyositis, skin lesions,

fever raised ESR, etc., with increase in circulating gammaglobulins and

positive serological tests for autoantibodies, RF and ANF, as in rheumatoid

disease. This is an immune complex syndrome with antigen provided by

disintegrating M. leprae. The reaction may be precipitated by antileprosy

drugs, a reaction known as Lucio's phenomenon, which is identical in nature

with the Herxheimer reaction. The syndrome confirms the deductions made

regarding rheumatoid disease. Such observations prove that every tissue in

the body may contain unsuspected free-living amoebae, which, if pathogenic,

may cause tissue infiltration by lymphocytes with germinal centers and often

plasma cells in genetically susceptible subjects as governed by their tissue

types. They are the source of Glynn's previously postulated unknown chronic

antigenic stimulation,23 as the cause of rheumatoid disease.

References

15. Wyburn-Mason, R. The free-living amoebic causation of rheumatoid and

autoimmune diseases. International Medicine 1: 20-25; 1979.

16. Wyburn-Mason, R. New views on the aetiology of rheumatoid arthritis.

British Medicine 12-14; August 21, 1979.

17. Wyburn-Mason, R. The Naeglerial causation of rheumatoid disease and many

human cancers. A new concept in medicine. Medical Hypotheses 5: 1237-49;

1979.

18. , H.D., Lockwood, G.M., , B.A. Inhibition of

reticuloendotheial function by gold and its relation to post-injection

reactions. Brit. Med. J. 2: 235-7; 1979.

19. Levamisole in rheumatoid arthritis. Multicentre Study Group, Lancet ii:

1007-12; 1978.

20. Herxheimer, K. Ueber eine Syphilitischen vorkommende

Quecksilberreaktion. Dtsch. Med. Wchsch. 28: 895-6; 1902.

21. Quoted in Doniach, D., Roitt, I.M., , K.B. Autoimmune phenomena in

pernicious anaemia. Serological overlap with thyroiditis, thyrotoxicosis and

systemic lupus erythematosus. Brit. Med. J. i: 1374-9; 1963.

22. Glynn, L.E. The chronicity of inflammation and its significance in

rheumatoid arthritis. Ann. Rheum. Dis. 27: 105-11; 1968.

rheumatic HELP

>Hi there

>

>I have written to some of you as individuals before on behalf of my

>sister Joan. I have to apologise for not getting back to you. I have

>my own medical problems with dysautonomia. Joan has had RA for about

>4 years now and is really really bad. She has been taking Mynocin for

>over 2 years now but apart from 6 months inbetween has got steadily

>worse. She has no access to the internet and can't even make it from

>her house to mine and we live 2 doors apart. I am really really

>worried about her. She is on her own with a five year old son. It has

>got to the stage where I have to do her housework, search for things

>in drawers, cook for her etc. I don't mind helping her but I'm not

>that well myself and the more I help her the less I do for my own

>family and house. She has a home help that comes for an hour each day

>but creates more mess eg. washes the dishes but leaves them dirty,

>empties the ashes from the fire and leaves scatters on the carpet

>which ruin the carpet. She enjoys this womans company - she is really

>lonely - but is scared to mention anything to her. I don't know what

>else I can do to help her. I think she needs more than I can give

>her - also the fact she is so dependent on me is depressing her.

>

>She is really depressed and is considering going into hospital but is

>afraid to leave her son who she has never been parted from. He is

>quite clingy. She has also been taking MSM for the last couple of

>months and splashed out on the 'miricle cure' of Cetyl Myristoleate.

>She has taken these for just over three weeks. If anything she has

>got worse since taking them - although the literature I've read says

>there is no side effects and should show signs of working after a

>couple of weeks. Her month course finishes in two days. She drinks

>every evening and I wonder if this causes a reaction with her meds

>and is holding her back. She feels the alcahol helps her get through -

> I understand to some degree, but only see her get worse with it. She

>says her liver function tests are normal. Can anybody give some

>feedback on her drug therapy - why it may not be working for her?

>What else she could try before she goes down the road of steroids -

>which she has been vehemently opposed to.

>

>Thanks in advance for anything or letters of support that I can print

>off for her.

>

>Fran

>

>

>

>To unsubscribe, email: rheumatic-unsubscribeegroups

>

>

>

[Guest guest]

I'm sorry I grabbed the wrong file. The ARthritis trust protocal follows

this article. kathy

Chapter IV

The " MIRACLE " Treatment

Recommended Treatments

To your family doctor, we say: Antiamoebics have never been considered for

use against rheumatoid diseases because the various arthritis associations

have not yet

investigated Professor Wyburn-Mason's brilliant scientific work,

published now since 1964.

You must decide if the prescriptions that follow are harmful to your

patient. If not, is the cost involved worth a trial, considering the

hopeless and insidious nature of the diseases?

Many cooperating physicians are using the protocol that follows:

The Wyburn-Mason & Jack M. Blount Foundation

for Eradication of Rheumatoid Disease

7111 Sweetgum Drive SW, Suite A

Fairview, Tn 37062-9384; (615) 799-1002

The Rheumatoid Disease Foundation, now The Arthritis Trust of America

A non-profit, charitable, tax-exempt organization

The Rheumatoid Disease Foundation through its cooperating physicians in a

committee chaired by , M.D. (ton, SC) has established

the following standards of practice when treating rheumatoid disease. These

are suggested standards. Many physicians will exceed these basic standards.

What follows is an outline developed through research and experience of

cooperating physicians. A SIMPLE AND INEXPENSIVE CURE/REMISSION FOR

RHEUMATOID DISEASES IS SET OUT IN WHAT FOLLOWS. DRAW YOUR DOCTOR'S ATTENTION

TO THE MEDICATIONS THAT OTHER PHYSICIANS ARE ALREADY USING EFFECTIVELY. IF

YOU DO NOT HAVE A FAMILY DOCTOR, WRITE FOR OUR LIST OF COOPERATING

PHYSICIANS.

Your family physician should know that there are at least two genus of limax

amoebae (one-celled animal life) that cause Rheumatoid Disease if you are

genetically susceptible to it, or its products: Acanthamoeba and/or

Naegleria.

Within these two genus, are many species, and strains within species, and

they vary considerably in their ability to adapt to various antiprotozoal

agents. Where one antiamoebic will kill one organism inside they body,

another will not, and which organism affects you can only be learned by

trial and error. Success rates from the first application of the treatment

program listed below varies from 78% to 95% depending on which physician and

which group of patients is being treated. The success rate is higher

whenever further applications of the appropriate antiamoebic is used.

If the first treatment does not bring about a Herxheimer reaction, the

physician is advised to move to another antiamoebic, and in any case, both

this Foundation as well as any of the cooperating physicians will be more

than happy to share their experiences.

The Foundation cannot, of course, be responsible for mal-application,

mis-application, or inappropriate treatment of any kind, and again suggests

that all treatment, if possible, be through your family physician.

Rheumatoid Disease Protocol

The central theme of treatment is based on the preliminary work of Professor

Wyburn-Mason and Jack M. Blount, M.D., and later findings or

Bingham, M.D.; it also seeks to introduce physicians to alternative or

extended courses of treatment that have been found to be useful by other

physicians in the organization, the goals being to: (1) arrest rheumatoid

disease, (2) repair damage caused by rheumatoid disease, (3) further the

maintenance for wellness.

This protocol is intended as an outline, and cannot serve as a " course in

treatment " for rheumatoid disease. It is necessary for each physician to

pursue his/her own intricacies of modalities mentioned.

I. Diagnosis: Shall be made on the basis of

A. Patient History - to include

1. Time of onset

2. Degree of disability

3. Family history

4. Remissions and exacerbations

5. Contributing factors

6. Previous treatment modalities and results thereof

7. Activity pattern

8. Medications being taken

B. Physical Examination

1. General appearance

2. Weight and height

3. Blood pressure and pulse

4. Head and neck

5. Cardio-vascular system

6. Abdomen

7. Musculo-skeletal system (to include evaluation of joints)

C. Laboratory testing

1. Urinalysis

2. SMAC -24

3. Rheumatoid pane (to include sedimentation rate and CPR)

4. Analysis of synovial fluid (when present)

5. Other (as indicated)

6. Electrocardiogram

7. X-rays of affected joints (if indicated)

8. Any of the above that have been performed by another physician within the

past 60 days may be utilized at the discretion of the treating physician.

II. Treatment: (several treatment regimens are available)

A. Oral Medications

1. Nitroimidazoles

(a). Metronidiazole

(. Tinidazole

©. Clotrimazole

Whichever nitroimidazole is used, the dosage (modified by weight) is the

same: 2 grams for two (2) days each week X6 weeks. (Children 250mg/25 pounds

body weight).

2. Furazolidone (Furoxone) 100 mg q.i.d. X1 week

3. Iodoquinol 650 mg t.i.d. X3 weeks

4. POTABA 2 grams 6 times daily X2 weeks

5. Allopurinol 300 mg t.i.d. X1 week (this in conjunction with one of the

above 5 antiamoebics - 1.(a), 1.(, 1.©,2,3. --used together acts as

broad spectrum antiamoebic).

6. Rifampin or Rimactane 600 mg daily X1 month (If reactions are severe,

stop treatment immediately).

B. Injections

1. Intraneural Injections (technique of Dr. K. Pybus, Dr. I.H.J.

Bourne)

2. Cleveland Clinic treatment (method of Jack M. Blount, M.D.: Lumbar

subarachnoid injection of 2.5 cc of 0.3% procaine with 20mg Depo-Medrol)

C. Nutrition (to include vitamin and mineral supplements as well as

counseling relative to diet. [updated guidelines are now available through

The Arthritis Trust of America for this nutritional support. Ed. S.C.]).

D. Steroids -- the use of Prednisone 20 mg daily X5 days or Depo-Medrol 40

mg injection X1 will reduce considerably the Jarisch-Herxheimer reaction

often seen when initiating therapy (See General Information).

E. Ancillary treatment modalities (as used by various advisory committee mem

bers).

1. Mega vitamin dosage (Prosch, Reich, Bingham)

2. Chelation therapy (American Academy of Medical Preventics -- AAMPS)

3. Hot mineral baths (Bingham)

F. Return visits

1. Return visits should probably be in 1 week, 3 weeks, 6 weeks, then every

3 months thereafter.

2. Preventive maintenance: It usually helps to prevent the recurrence of

rheumatoid disease if he patient is given a round of treatment with

Allopurinol at 6 months post-original treatment and every 6 months

thereafter. If symptoms are present, the entire original treatment regimen

should be repeated. Allopurinol can cause a very severe reaction on the

second round of treatment -- Wyburn-Mason).

G. General Information

1. Most patients will need counseling about diet and nutrition.

2. Explanation of the Jarisch-Herxheimer reaction often will prevent patient

drop-out in many cases.

3. Since Metronidazole is the only nitroimidazole currently available in the

United States, it is probably the drug of choice for beginning treatment.

4. Utilization of the " Cleveland Clinic " injection and intraneural

injections should probably be reserved until the individual physician has

had the opportunity to learn the technique from a physician already using

it.

5. Most of the foregoing treatment is directed toward rheumatoid disease.

Osteoarthritis has been found to respond much less dramatically, although it

does often show some degree of improvement. (Best results seem to be

achieved with intraneural injections.)

6. Rationale for treatment with antiamoebics: Based on Dr.

Wyburn-Mason's work which demonstrated free-living limax amoebae to be the

causative agent in rheumatoid disease, amoebicidal drugs have been

postulated as a treatment of choice. When these drugs kill the organism, the

release of foreign proteins usually results in a Jarisch-Herxheimer reaction

(similar to the old arsenic treatment for syphilis). This results in a

temporary generalized increase of rheumatoid symptoms with the

administration of an antirheumatic drug.

7. Drug reactions

(a). Rifampicin -- violent Herxheimer. In this event, discontinue treatment

with rifampicin at once.

(. Allopurinol -- leg pain, temperature spike, chills, sweating, rash on

body and face.

This protocol is subject to revisions (additions, deletions, changes) as The

Rheumatoid Disease Foundation, now The Arthritis Trust of America completes

relevant research.

A. Chapdelaine, Sr.

Executive Director/Secretary

Revised 1985: Physicians & Scientists Committee

Since alcohol in presence of antiamoebic (metronidazole, Allopurinol) (or

antibiotics) makes some people sick, it may be best not to take any alcohol

during period of treatment of six weeks. (The medicine will stay in the body

during the first four weeks. Also sometimes alcohol destroys certain

chemical compounds and, in the case of several antiamoebics, alcohol is

definitely not a good idea.

Note: The following table was prepared in 1982]

Chemical

Generic Name Compound Group Brand Name Manufacturer

allopurinol pyrimidine Zyloprimr Burroughs-Wellcome

Clotrimazole* imidazole Mycelexr Dome

clotrimazole imidazole Lotriminr Delbay

diiodohydro-oxyquinon oxyquinoline Yodoxinr Vitarine

furazolidone nitrofuran Furoxoner Eaton

metronidazole nitroimidazole Flagylr Searle

nimorazole nitroimidazole Emtrylr Salsbury

nimorazole nitroimidazole Naxoginr Erba

ornidazole nitroimidazole Tiberalr Roche

prednisone*** glucocorticoids Deltasoner Upjohn

rifampin rifamycin B Rifadinr Dow

rifampicin rifamycin B Rimactaner Ciba

tinidazole nitroimidazole Fasigynr Pfizer

potassium para amino

benzoate vitamin B POTABAr Glenwood

*Available in USA only as vaginal tablets and cream.

** Not yet released by FDA for use in USA. (Tinidazole, for example, is

available in Australia as Fasigynr 500; but known as Tinidexr in Mexico

without prescription; Most nitroimidazoles can be obtained through a

compounding pharmacy in the United States)

Davies, A.H. " Metronidazole in Human Infections with Syphilis. " Brit. J.

Vener. Dis. 43:197-199; 1967. We submitted a paper to the New England

Journal today. Here is the press release for local papers.

Thanks to everyone for their input.

****************************************************************************

***

Dr. Atkinson-Barr CPhys PhD (Calabasas, CA) and Dr. Vernon Padgett MD

(Calabasas, CA) together with Dr. Horowitz MD (Hyde Park, NY) are

pleased to announce the discovery of a new treatment for Lyme Disease using

the antimicrobial metronidazole (Flagyl).

Metronidazole was introduced 40 years ago for the treatment of

trichomonas vaginalis and has previously been used for gingivitis, giardia

and anaerobic bacterial infections. Though metronidazole is less widely used

than it once was it is routinely available on prescription.

Lyme disease, named for the town of Lyme, Connecticut, is caused by the

spirochetal bacterium Borrelia burgdorferi and is normally contracted from

the bite of an infected deer tick Untreated or inadequately treated Lyme

disease progresses to a severely debilitating condition called chronic or

late-stage Lyme disease in which the spirochete affects the brain, organs

and joints of the patient resulting in almost complete disability.

Neurological effects include loss of cognitive function, slurred speech,

violent rages and memory loss.

Normal antibiotics, whether administered orally or by the intravenous route,

have been only partially successful in treating late-stage Lyme disease

leading some physicians to conclude that late-stage symptoms may persist

even after the infection had been cured.

Using metronidazole the authors have successfully treated late-stage Lyme

patients where conventional therapies have not been beneficial. In

particular severe neurological symptoms were eliminated leading to the

conclusion that Lyme symptoms are a consequence of an ongoing infection and

usual therapies are inadequate to treat the disease.

The authors have submitted a report of their discovery to the

prestigious New England Journal of Medicine for publication. Following the

initial work Dr. Horowitz confirmed the results in over 100 of his most

severely affected patients and will report those results at the Lyme

Federation Conference in New York, April 9-10th.

Lyme disease affects as many as 300,000 persons throughout the United States

and cases have been reported in all of the states with the exception of

Alaska and Hawaii. Lyme disease was recently confirmed to be carried by

ticks in Southern California. The current cost of

treatment and disability is estimated to be many billions of dollars and

areas with a high incidence of the disease, particularly Pennsylvania, Rhode

Island, Connecticut and New York, suffer from impacts on tourism and real

estate values.

Metronidazole is a simple and inexpensive treatment, costing $10 per month,

using tablets taken by mouth. The required duration of the treatment is

currently a matter of investigation though it is known that improvement in

patients continues even after 4 months of metronidazole therapy. It is

anticipated that metronidazole will be useful in the early stages of Lyme

disease and possibly as a topical cream for the prevention of Lyme disease

immediately following a tick bite.

Borrelia burgdorferi is one of a family of slow growing, spiral shaped

bacteria which have been implicated in several difficult diseases. If

metronidazole can be shown to be effective therapy against other similar

bacteria it may open new approaches to the treatment of other conditions

where there is evidence of a spirochetal cause including multiple sclerosis

and Alzheimer’s disease.

The authors believe that this is one of the first medical discoveries to be

made through the use of the Internet. Internet communication with patients

on the newsgroup sci.med.diseases.lyme allowed anecdotal reports to be

collected and Lyme patients to report their experiences. One characteristic

of Lyme treatment is that patient’s condition initially deteriorates as the

bacterium is killed. Using this

information Lyme patients were canvassed for any adverse reactions they had

experienced when taking metronidazole for unrelated conditions and some 30

patients confirmed worsening symptoms under such circumstances.

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rheumatic HELP

>Hi there

>

>I have written to some of you as individuals before on behalf of my

>sister Joan. I have to apologise for not getting back to you. I have

>my own medical problems with dysautonomia. Joan has had RA for about

>4 years now and is really really bad. She has been taking Mynocin for

>over 2 years now but apart from 6 months inbetween has got steadily

>worse. She has no access to the internet and can't even make it from

>her house to mine and we live 2 doors apart. I am really really

>worried about her. She is on her own with a five year old son. It has

>got to the stage where I have to do her housework, search for things

>in drawers, cook for her etc. I don't mind helping her but I'm not

>that well myself and the more I help her the less I do for my own

>family and house. She has a home help that comes for an hour each day

>but creates more mess eg. washes the dishes but leaves them dirty,

>empties the ashes from the fire and leaves scatters on the carpet

>which ruin the carpet. She enjoys this womans company - she is really

>lonely - but is scared to mention anything to her. I don't know what

>else I can do to help her. I think she needs more than I can give

>her - also the fact she is so dependent on me is depressing her.

>

>She is really depressed and is considering going into hospital but is

>afraid to leave her son who she has never been parted from. He is

>quite clingy. She has also been taking MSM for the last couple of

>months and splashed out on the 'miricle cure' of Cetyl Myristoleate.

>She has taken these for just over three weeks. If anything she has

>got worse since taking them - although the literature I've read says

>there is no side effects and should show signs of working after a

>couple of weeks. Her month course finishes in two days. She drinks

>every evening and I wonder if this causes a reaction with her meds

>and is holding her back. She feels the alcahol helps her get through -

> I understand to some degree, but only see her get worse with it. She

>says her liver function tests are normal. Can anybody give some

>feedback on her drug therapy - why it may not be working for her?

>What else she could try before she goes down the road of steroids -

>which she has been vehemently opposed to.

>

>Thanks in advance for anything or letters of support that I can print

>off for her.

>

>Fran

>

>

>

>To unsubscribe, email: rheumatic-unsubscribeegroups

>

>

>

[Guest guest]

This is just a thought in the dark - have you had your water tested for sodium content?

I cannot think of any other ideas.

Carol/Piney

rheumatic help

Hi group, I am still having an extreme salty taste in my mouth and have now for a couple of months. It is not like phlegm. It is though you put salt in my mouth all of the time. It ruins the taste of foods and water and it is real frustrating. At times it is a lot worse. You can even taste it on your lips. I posted this once before but was not receiving any group mail at the time for what ever reason? So I am not sure whether anybody has had this themselves. I am juicing daily eating no sugar, drinking lots of water in spite of the taste. I have cut back on the supplements thinking maybe they cause it. I am on colostrum, moducare, and a greens drink. I sure would appreciate any help on this. Thanks. Blessings. Judy/Florida To unsubscribe, email: rheumatic-unsubscribeegroups

[Guest guest]

Note: This is my attempt to translate the message of and Chas

Adlard to Portugese using SYSTRAN for fventura. It sort of half

way makes sense when translated back to English, so I am hoping it

makes at least that much sense in the Portugese.

-- Ron

P.S.

Nota: Fazer exame do antihistamine de Benedryl pode também ajudar

reduzir o alargamento de Herximer.

_______________________________________

Caro ,

Enquanto o antibiótico mata fora da infecção que causa o RA, os

toxins são liberados e viajam em torno do corpo. Estes toxins são o

que a causa a dor e a quantidade de toxins liberados depende do dose

do antibiótico.

Assim se você estiver em demasiada dor, você deve reduzir o dose do

antibiótico por um quando. O Dr. Marrom usou-se começar seus

pacientes no antibiótico como este:

Primeira semana minocycline segunda-feira e sexta-feira de 50

milligrams

Segunda semana minocycline segunda-feira quarta-feira e sexta-feira

de 50 milligrams

Terceiros semana milligrams segunda-feira da semana 100, 50

milligrams quarta-feira e sexta-feira

Adiante semana milligrams segunda-feira da semana 100, 100 milligrams

quarta-feira, 50 milligrams sexta-feira

Quintos semana milligrams segunda-feira quarta-feira e sexta-feira da

semana 100

Assim você poderia começar outra vez esta maneira e construir

gradualmente acima do dose e do você teria menos dor. Certifique-se

que você está bebendo ao menos oito vidros da água um o dia para

nivelar para fora de seu corpo, e está comendo a abundância de

vegetais frescos, quase nenhum açúcar. Um suplemento bom a

vitamin/mineral é também bom.

Eu espero que Lucy possa traduzir todo o este e isso nós possamos lhe

ajudar. Deixe-nos saber você começa sobre e espera se ouvir para

trás muito logo de você.

Chris.

[Guest guest]

In a message dated 8/30/01 8:51:34 AM Pacific Daylight Time,

moriam@... writes:

> I think you can also get capsules of somewhat lower strength

> from Kirkman's ?? Someone??

>

>

Kirkmans capsules are 25mg each.

Margaret

[Guest guest]

At 03:24 PM 8/30/2001 -0000, you wrote:

>can anyone help?

>i have been reading and reading all the posts but im still not clear

>on something. im only using ala for my 4 year old son. i started

>yesterday. i bought it at a health store and they said the capsules

>only come in 100 mg strength. they said to give my son i pill 3 times

>a day. after reading i see i should give him a dose every three hours.

>so i must be giving him too much of a dose then? he is 40 pounds. if

>im to give him less how do i do that with a powder capsule?

>rebecca

Hi ,

Glad to see you " made it here "

Andy's recommendation for amount is 1/8 to 1/2 mg per pound of

body weight per dose. For your son that works out to

5 mg to 20 mg per dose (please check my math, I'm not always

right!) every 3 hours.

You mix the 100 mg into carefully measured liquid then divide into

parts. I don't actually do this myself so I can't give the

greatest " tips " on how to do it. (I'm doing chelation on mySELF,

not a kid. I weigh about 170 and take 100 mg at a time, so it

is easier for me.)

I think you can also get capsules of somewhat lower strength

from Kirkman's ?? Someone??

best,

Moria

(I'm on round 16 today)

[Guest guest]

You can empty the capsule in a pre-measured (ex: 10

teaspoons) amount of liquid and empty the capsule in

the water. Shake thoroughly and make dosages (10 in

this case). You could also get 12.5mg of ALA from

Kirkman's. Vicky

--- rebecca <mytristy@...> wrote:

> can anyone help?

> i have been reading and reading all the posts but im

> still not clear

> on something. im only using ala for my 4 year old

> son. i started

> yesterday. i bought it at a health store and they

> said the capsules

> only come in 100 mg strength. they said to give my

> son i pill 3 times

> a day. after reading i see i should give him a dose

> every three hours.

> so i must be giving him too much of a dose then? he

> is 40 pounds. if

> im to give him less how do i do that with a powder

> capsule?

> rebecca

>

>

__________________________________________________

[Guest guest]

I am replying and introducing myself at the same time................ in

Scotland, here, who has son, , autistic, 4 and a half. This post has me

worried............

I just joined this list, and am reading up on chelation, although our doc is

against it and has put my husband off too.

Anyway, not for chelation, but for liver stress after fluconazole, a doctor

suggested take 100mg ALA per day, and he has been on it at that dose for

about a year.

Other docs we have seen have never queried this............

Why must it be given every 3 hours? Is this when also using DMSA?

Could it have done harm? Could it be the reason has had a problem

absoorbing magnesium and zinc? COULD IT PERHAPS HAVE BEEN CHELATING HIM FROM

TOXIC STUFF?

That would be great to hear, since the mercury thingg scares me but hubby is so

anti chelation, due to stories of regression.

Thanks in advance for all help.

Re: [ ] help

You can empty the capsule in a pre-measured (ex: 10

teaspoons) amount of liquid and empty the capsule in

the water. Shake thoroughly and make dosages (10 in

this case). You could also get 12.5mg of ALA from

Kirkman's. Vicky

--- rebecca <mytristy@...> wrote:

> can anyone help?

> i have been reading and reading all the posts but im

> still not clear

> on something. im only using ala for my 4 year old

> son. i started

> yesterday. i bought it at a health store and they

> said the capsules

> only come in 100 mg strength. they said to give my

> son i pill 3 times

> a day. after reading i see i should give him a dose

> every three hours.

> so i must be giving him too much of a dose then? he

> is 40 pounds. if

> im to give him less how do i do that with a powder

> capsule?

> rebecca

>

>

__________________________________________________

[Guest guest]

How has your son been doing? Is he progressing well? Have youseen him regress

or improve?

Re: [ ] help

You can empty the capsule in a pre-measured (ex: 10

teaspoons) amount of liquid and empty the capsule in

the water. Shake thoroughly and make dosages (10 in

this case). You could also get 12.5mg of ALA from

Kirkman's. Vicky

--- rebecca <mytristy@...> wrote:

> can anyone help?

> i have been reading and reading all the posts but im

> still not clear

> on something. im only using ala for my 4 year old

> son. i started

> yesterday. i bought it at a health store and they

> said the capsules

> only come in 100 mg strength. they said to give my

> son i pill 3 times

> a day. after reading i see i should give him a dose

> every three hours.

> so i must be giving him too much of a dose then? he

> is 40 pounds. if

> im to give him less how do i do that with a powder

> capsule?

> rebecca

>

>

__________________________________________________

[Guest guest]

you must be online same time as me! This has arrived only minutes after my

post!

At age 3 and a half, he had lost all speech after the diflucan,,,,,he hadd used

about 20 words fairly often from age 2 and a half to 3, after we started therapy

ands diet. Then it took some time for the speech and especially the

pronunciation to return, and then it also improved. A year ago, we did a DMSA

challenge test with Doctors Data lab. It showed high within ref for arsenic,

tin, lead, aluminium and nickel. Since then, he has had his ups and downs as

most kids have, and now uses phrases os up to 4 words spontaneously and

meaningfully. But while I have no doubts about his intelligence, or his being

able to gain speech, he still has real attention deficits at times, and still

has much stimmy babbling when I know he is lost in a world of disney characters,

despite most of the videos being locked away. From time to time my daughter gets

on on hire that he has not seen, however, and he loves books of disney stories.

His sleep is mostly good and stools are better now, but when he slipped up with

the gfcf one day in June, we all knew about it for 2-3 weeks................

Perhaps it is just that he is getting older and bigger, or older and maybe more

typical.............he has always been very gentle and compliant to now, but has

started to climb up on furniture, window ledges etc, and also become quite

headstrong at times. Tonight when husband went off back to work late, was

inconsolable for about half an hour, crying for daddy..................this is

not usual for him, and I wonder if he is getting worse in some ways, although

our doc would say this is actually an improvement. But then he has caught onto

the one sentence in the DAN protocol that talks of regression, and said he would

not be able to help us use chelation. I am however, definitely going to get my

amalgams out and chelate myself..................any tips on this? Or will

answers be in the FAQ? Have not read them yet, and just posted this first

question off in a bit of a panic after the letter about ALA.

i'LL BE ONLINE FOR AWHILE, AND LOOK FORWARD TO HEARING FROM YOU.

tHANKS...........jULIE.

Re: [ ] help

You can empty the capsule in a pre-measured (ex: 10

teaspoons) amount of liquid and empty the capsule in

the water. Shake thoroughly and make dosages (10 in

this case). You could also get 12.5mg of ALA from

Kirkman's. Vicky

--- rebecca <mytristy@...> wrote:

> can anyone help?

> i have been reading and reading all the posts but im

> still not clear

> on something. im only using ala for my 4 year old

> son. i started

> yesterday. i bought it at a health store and they

> said the capsules

> only come in 100 mg strength. they said to give my

> son i pill 3 times

> a day. after reading i see i should give him a dose

> every three hours.

> so i must be giving him too much of a dose then? he

> is 40 pounds. if

> im to give him less how do i do that with a powder

> capsule?

> rebecca

>

>

__________________________________________________

[Guest guest]

Only people on this list would understand what " stimmy babbling " is! I

can relate... I was about to start my son on Diflucan tomorrow and now

you have me worried about regression. Has anyone else had their children

regress after using Diflucan??

________________________________________________________________

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[Guest guest]

I have read lots now about fluconazole making things worse........i'd definitely

look into it again.

Off the top of my head, i've heard folks recommend nystatin plus enzymes, Yeast

Avenger, molybdenum, lactoferrin, specific carbs diet, colostrum, lamisil,

garlic..........mind you, I know of someone whose son recovered after the

fluconazole plus nystatin then anti-virals. But it was hard to see our son go

down and then do a repeat OAT only to find his arabibose had doubled to 986.

Hate to have to say this!

Re: [ ] help

Only people on this list would understand what " stimmy babbling " is! I

can relate... I was about to start my son on Diflucan tomorrow and now

you have me worried about regression. Has anyone else had their children

regress after using Diflucan??

________________________________________________________________

GET INTERNET ACCESS FROM JUNO!

Juno offers FREE or PREMIUM Internet access for less!

Join Juno today! For your FREE software, visit:

http://dl.www.juno.com/get/tagj.

[Guest guest]

I also need the websites to locate DAN doctors in my area, thank you.

[Guest guest]

Thanks Dana. Vicki