Nan, you might want to consider this first

[Guest guest]

Patty and Nan ~

I have read that mycoplasma and mycotoxin and nano bacteria

are culprits with fibro and arthritic, and auto-immune and CFS, and

all that, and I am wondering if the Mycoplex and the other one that is the miracle mineral will help get rid of those things.

Along with taking B-12, and magnesium and mineral complex.

I believe that this kefir and magnesium is doing lots of good for me.

I believe that medical toxic tabs the pharmaceutical companies make

and sell us make us more toxic in the long run.....mask symptoms, and create new problems for us to deal with.

I was caught up in the whirlwind of Rheumatologist and Neurologists, and it was a very expensive stent of time both for my pocket book and my body's toxic load. Nan, you and I have alot in common with our implant disease.

Explant, then cap explant and many lymph node removal surgeries, and all the symptoms you are going thru, I have too. When I read your posts, it is written almost as I ha written it myself ! !

Silva Method of mind control is a wonderful tool. Meditation is wonderful. I am sorry you are going thru so much, and so much of it is so scarey. Bless your heart, you are in my prayers ! ! ! Love DedeSee what's new at AOL.com and Make AOL Your Homepage.

[Guest guest]

Rogene and Patty ~ Nan

I tell ya, steroids were miracles for me for a couple

years ! Ya, they were the ticket..........yep the

ticket to permanent pain and loufah sponge bones !

I cant believe that I traded pain for pain and sponge bones

Not a good trade.......now I also have steroid cushings

I fit the whole bill on that one, body morphed into the

exact pic of cushings, and of course, with this heart deal

I have had plenty of them IV........No doc has diagnosed

me with cushings, but they dont have to, and I dont need

to spend the money on it. I totally fit. My body looks

exactly as the cushings, buffalo hump, huge smushy lumps on

either side of my neck, puffy face, huge waist, and all of this practically

over night. I pray this goes away. When I look in the mirror

it is as if I am seeing someone else.

Steroids are sometimes needed, I guess, but they can

do so much damage to you. If at all possible try to stay

away from them......I am so sorry you are so ill right now.

Your body has had so much crap IV this past year from

all the surgeries, that right now it is going thru a huge

herx and makeing you really ill. Just know, this will get better.

It took 9 months off the drugs for my kidneys to calm down some.

So, please have lots and lots of patients.......do what you can to

divert your mind away from the pain.

Love DedeSee what's new at AOL.com and Make AOL Your Homepage.

[Guest guest]

Nan,

I hate the thought of you starting to doctor hop again. Pain seems

to be one issue that our sickest women deal with. I've known many

women dealing with unending pain, and I am not sure what the cause

is. But I know that they do suffer. Some have successfully gotten

off all pain medications. Others met their deaths due to overdosing

on pain medication. I just want you to get better.

I know this is hard to read, but you may want to check it out. It

covers fibromyalgia, and rheumatic diseases. I have not done this,

but I know of other women who have. Research it and see if you think

it would be a worthwhile endeavor. You may have to search for a

doctor willing to work with you on it.

I highly doubt that other doctors such as neurologists and rheumy's

who deal only in drugs and surgery are going to have anything healing

to offer--maybe something to help you feel better, but leave you sick

on the long run. I have never found a woman who has gotten better by

seeing a rheumy or neurologist with breast implant illness. NEVER.

They just do not offer the right kind of help. Lynda, do you know of

anyone who has been helped this way? Rogene, do you? I'd like to know.

But this low dose antibiotic therapy may be worth investigating. I

trust Dr. Mercola's opinion because his focus in on natural healing

as much as possible.

Patty

>

> PHYSICIANS' PROTOCOL FOR USING ANTIBIOTICS IN RHEUMATIC DISEASE

Dr. Brown's Modified Protocol For Using Antibiotics In The Treatment

Of Rheumatic Diseases As presented at the 32nd International

Congress of the Great Lakes College of Clinical Medicine

> Baltimore, land, September 25, 1999 - by Dr. ph M.

Mercola Table of Contents Introduction

> My Experience with Dr. Brown's Protocol

> Nutritional Considerations

> Antibiotic Therapy With Minocin

> Clindamycin

> What To Do If Severe Patients Fail To Respond

> Anti-Inflammatories

> Prednisone

> Remission

> Preliminary Laboratory Evaluation For Non-Rheumatologists

> Fibromyalgia

> Signs And Symptoms of Fibromyalgia

> Pain Location

> Treatment Of Fibromyalgia

> Exercise For Rheumatoid Arthritis

> The Infectious Cause Of Rheumatoid Arthritis

> Culturing Mycoplasmas From Joints Animal Evidence for The Protocol

> The Science of Why Minocycline Is Used

> Clinical Studies

> Criteria For Classification Of Rheumatoid Arthritis

> Bibliography

> Introduction Rheumatoid arthritis affects about 1 percent of

our population and at least two million Americans have definite or

classical rheumatoid arthritis. It is a much more devastating illness

than previously appreciated. Most patients with rheumatoid arthritis

have a progressive disability. More than 50% of patients who were

working at the start of their disease are disabled after five years

of rheumatoid arthritis. The annual cost of this disease in the U.S.

is estimated to be over $1 billion. There is also an increased

mortality rate. The five-year survival rate of patients with more

than thirty joints involved is approximately 50%. This is similar to

severe coronary artery disease or stage IV Hodgkin's disease. Thirty

years ago, one researcher concluded that there was an average loss of

eighteen years of life in patients who developed rheumatoid arthritis

before the age of 50. Most authorities believe that remissions

rarely occur. Some experts feel that the

> term " remission-inducing " should not be used to describe ANY

current rheumatoid arthritis treatment. A review of contemporary

treatment methods shows that medical science has not been able to

significantly improve the long-term outcome of this disease. My

Experience with the Dr. Brown's Protocol I first became aware of

Doctor Brown's protocol in 1989 when I saw him on 20/20 on ABC. This

was shortly after the introduction of his first edition of The Road

Back.The newest version is The New Arthritis Breakthrough that is

written by Henry Scammel. Unfortunately, Dr. Brown died from prostate

cancer shortly after the 20/20 program so I never had a chance to

meet him. By the year 2000, I will have treated over 1,500 patients

with rheumatic illnesses, including SLE, scleroderma, polymyositis

and dermatomyositis. My application of Dr. Brown's protocol has

changed significantly since I first started implementing it.

Initially, I followed Dr. Brown's work rigidly with very

> little modification other than shifting the tetracycline choice to

Minocin. I believe I was one of the first people who recommended the

shift to Minocin, which seems to have been widely adopted at this

time. In the early 90s, I started to integrate the nutritional

model into the program and noticed a significant improvement in the

treatment response. I cannot emphasize strongly enough the importance

of this aspect of the program. It is absolutely an essential

component of the revised Dr. Brown protocol. One may achieve

remission without it, but the chances are much improved with its

implementation. The additional benefit of the dietary changes is that

they severely reduce the risk of the two to six month worsening of

symptoms that Dr. Brown described in his book. In the late 80s, the

common retort from other physicians was that there was " no scientific

proof " that this treatment works. Well, that is certainly not true

today. If one peeks ahead at the bibliography, one

> will find over 200 references in the peer-reviewed medical

literature that supports the application of Minocin in the use of

rheumatic illnesses. The definitive scientific support for

minocycline in the treatment of rheumatoid arthritis came with the

MIRA trial in the United States. This was a double blind randomized

placebo controlled trial done at six university centers involving 200

patients for nearly one year. The dosage they used (100 mg twice

daily) was much higher and likely less effective than what most

clinicians currently use. They also did not employ any additional

antibiotics or nutritional regimens, yet 55% of the patients

improved. This study finally provided the " proof " that many

traditional clinicians demanded before seriously considering this

treatment as an alternative regimen for rheumatoid arthritis. Dr.

Brown's effort to treat the chronic mycoplasma infections

believed to cause rheumatoid arthritis is the basis for this therapy.

Dr. Brown

> believed that most rheumatic illnesses respond to this treatment.

He and others used this therapy for SLE, ankylosing spondylitis,

scleroderma, dermatomyositis and polymyositis. Dr. Osler was also a

preeminent figure of his time (1849- 1919). Many regard him as the

consummate physician of modern times. An excerpt from a commentary on

Dr. Osler provides a useful perspective on application of

alternative medical paradigms: Osler would be receptive to the

cautious exploration of nontraditional methods of treatment,

particularly in situations in which our present science has little to

offer. From his reading of medical history, he would know that many

pharmacologic agents were originally derived from folk medicine. He

would also remember that in the 19th century physicians no less

intelligent than those in our own day initially ridiculed the

unconventional practices of Semmelweis and Lister. Osler would

caution us against the arrogance of believing that only our

> current medical practices can benefit the patient. He would

realize that new scientific insights might emerge from as yet

unproved beliefs. Although he would fight vigorously to protect the

public against frauds and charlatans, he would encourage critical

study of whatever therapeutic approaches were reliably reported to be

beneficial to patients. Nutritional Considerations Limiting sugar

is a critical element of the treatment program. Sugar has multiple

significant negative influences on a person's biochemistry. Its major

mode of action is through elevation of insulin levels. However, it

has a similarly severe impairment of intestinal microflora. Patients

who are unable to decrease their sugar intake are far less likely

improve. One of the major benefits of implementing the dietary

changes is that one does not seem to develop worsening of symptoms

the first three to six months that is described in Dr. Brown's book.

Most of my patients tend to not worsen once they

> start the antibiotics. I believe this is due to the beneficial

effects that the diet has on the immune response. I ask all new

patients to read my 6-page handout on the dietary changes. Rather

than repeat it here, one could obtain the current version on my web

site at www.mercola.com under the tab heading on the left side of the

page entitled Read This First. Antibiotic Therapy With Minocin

There are three different tetracyclines available: simple

tetracycline, doxycycline, or Minocin (minocycline). Minocin has a

distinct and clear advantage over tetracycline and doxycycline in

three important areas. 1. Extended spectrum of activity

> 2. Greater tissue penetrability

> 3. Higher and more sustained serum levels Bacterial cell

membranes contain a lipid layer. One mechanism of building up a

resistance to an antibiotic is to produce a thicker lipid layer. This

layer makes it difficult for an antibiotic to penetrate. Minocin's

chemical structure makes it the most lipid soluble of all the

tetracyclines. This difference can clearly be demonstrated when one

compares the drugs in the treatment of two common clinical

conditions. Minocin gives consistently superior clinical results in

the treatment of chronic prostatitis. In other studies, Minocin was

used to improve between 75-85% of patients whose acne had become

resistant to tetracycline. Strep is also believed to be a

contributing cause to many patients with rheumatoid arthritis.

Minocin has shown significant activity against treatment of this

organism. There are several important factors to consider when

using Minocin. Unlike the other tetracyclines, it tends not to cause

yeast

> infections. Some infectious disease experts even believe that it

even has a mild anti-yeast activity. Women can be on this medication

for several years and not have any vaginal yeast infections.

Nevertheless, it would be prudent to have patients on prophylactic

oral Lactobacillus acidophilus and bifidus preparations. This will

help to replace the normal intestinal flora that is killed with the

Minocin. Another advantage of Minocin is that it tends not to

sensitize patients to the sun. This minimizes the risk of sunburn and

increased risk of skin cancer. However, one must incorporate several

precautions with the use of Minocin. Like other tetracyclines, food

impairs its absorption. However, the absorption is much less impaired

than with other tetracyclines. This is fortunate because some

patients cannot tolerate Minocin on an empty stomach. They must take

it with a meal to avoid GI side effects. If they need to take it with

a meal, they will still absorb 85% of the

> medication, whereas tetracycline is only 50% absorbed. In June of

1990, a pelletized version of Minocin became available. This improved

absorption when taken with meals. This form is only available in the

non-generic Lederle brand and is a more than reasonable justification

to not substitute for the generic version. Clinical experience has

shown that many patients will relapse when they switch from the brand

name to the generic. Clinically it has been documented that it is

important to take Lederle brand Minocin. Most all generic minocycline

is clearly not as effective. A large percentage of patients will not

respond at all or not do as well with generic non-Lederle

minocycline. Traditionally it was recommended to only receive the

brand name Lederle Minocin. However, there is one generic brand that

is acceptable and that is the brand made by Lederle. The only

difference between Lederle generic Minocin and brand name Minocin is

the label and the price. The problem is

> finding the Lederle brand generic. Some of my patients have been

able to find it at Wal Mart. Since Wal Mart is one of the largest

drug chains in the US, this should make the treatment more widely

available for a reduced charge. Many patients are on NSAID's which

contribute to microulcerations of the stomach which cause chronic

blood loss. It is certainly possible they can develop a peptic

ulceration contributing to their blood loss. In either event,

patients frequently receive iron supplements to correct their blood

counts. IT IS IMPERATIVE THAT MINOCIN NOT BE GIVEN WITH IRON. Over

85% of the dose will bind to the iron and pass through the colon

unabsorbed. If iron is taken, it should be at least one hour before

the minocin or two hours after. One recent uncommon complication of

Minocin is a cell-mediated hypersensitivity pneumonitis. Most

patients can start on Minocin 100 mg. every Monday, Wednesday, and

Friday evening. Doxycycline can be substituted for patients who

> cannot afford the more expensive Minocin. It is important to not

give either medication daily, as this does not seem to provide as

great a clinical benefit. Tetracycline type drugs can cause a

permanent yellow- grayish brown discoloration of the teeth. This can

occur in the last half of pregnancy and in children up to eight years

old. One should not routinely use tetracycline in children. If

patients have severe disease, one can consider increasing the dose to

as high as 200 mg three times a week. Aside from the cost of this

approach, several problems result may result from the higher doses.

Minocin can cause quite severe nausea and vertigo. Taking the dose at

night does tend to decrease this problem considerably. However, if

one takes the dose at bedtime, one must tell the patient to swallow

the medication with TWO glasses of water. This is to insure that the

capsule doesn't get stuck in the throat. If that occurs, a severe

chemical esophagitis can result which can

> send the patient to the emergency room. For those physicians who

elect to use tetracycline or doxycycline for cost or sensitivity

reasons, several methods may help lessen the inevitable secondary

yeast overgrowth. Lactobacillus acidophilus will help maintain normal

bowel flora and decrease the risk of fungal overgrowth. Aggressive

avoidance of all sugars, especially those found in non-diet sodas

will also decrease the substrate for the yeast's growth. Macrolide

antibiotics like Biaxin or Zithromax may be used if tetracyclines are

contraindicated. They would also be used in the three pills a week

regimen. Clindamycin The other drug used to treat rheumatoid

arthritis is clindamycin. Dr. Brown's book discusses the uses of

intravenous clindamycin. It is important to use the IV form of

treatment if the disease is severe. Nearly all scleroderma patients

should take an aggressive stance and use IV treatment. Scleroderma is

a particularly dangerous form of rheumatic illness

> that should receive aggressive intervention. A major problem

with the IV form is the cost. The price ranges from $100 to $300 per

dose if administered by a home health care agency. However, if

purchased directly from Upjohn, significant savings will be

appreciated. A case of two-dozen 900 mg prefilled IV bags can be

purchased directly from Upjohn for about $200. For patients with

milder illness, the oral form is preferable. If the patient has a

mild rheumatic illness (the minority of cases), it is even possible

to exclude this from their regimen. Initial starting doses for an

adult would be a 1200 mg dose once a week. Patients do not seem to

tolerate this medication as well as Minocin. The major complaint

seems to be a bitter metallic type taste, which lasts about 24 hours

after the dose. Taking the dose after dinner does seem to help modify

this complaint somewhat. If this is a problem, one can lower the dose

and gradually increase the dose over a few weeks. Concern

> about the development of C. difficile pseudomembranous

enterocolitis as a result of the clindamycin is appropriate. This

complication is quite rare at this dosage regimen, but it certainly

can occur. It is important to warn all patients about the possibility

of developing a severe uncontrollable diarrhea. Administration of the

acidophilus seems to limit this complication by promoting the growth

of the healthy gut flora. If one encounters a resistant form of

rheumatic illness, intravenous administration should be considered.

Generally, weekly doses of 900 mg are administered until clinical

improvement is observed. This generally occurs within the first ten

doses. At that time, the regimen can be decreased to every two weeks

with the oral form substituted on the weeks where the IV is not

taken. What To Do If Severe Patients Fail To Respond The most

frequent reason for failure to respond to the protocol is lack of

adherence to the dietary guidelines. Most patients will

> be eating too many grains and sugars, which disturb insulin

physiology.It is important that patients adhere as strictly as

possible to the guidelines.A small minority, generally under 15%, of

patients will fail to respond to the protocol described above despite

rigid adherence to the diet.These individuals should already be on

the IV Clindamycin. It appears that the hyaluronic acid, which is a

potentiating agent commonly used in the treatment of cancer may be

quite useful. It seems that hyaluronic acid has very little to no

direct toxicity but works in a highly synergistic fashion when

administered directly in the IV bag with the Clindamycin. Hyaluronic

acid is also used in orthopedic procedures. The dose is generally

from 2 to 10 cc into the IV bag. Hyaluronic acid is not inexpensive

as the cost may range up to $10 per cc.One does need to exert some

caution with its use as it may precipitate a significant Herxheimer

flare reaction. Patients will frequently have

> emotional traumas that worsen their illness. Severe emotional

traumas can seriously impair the immune response to this treatment. A

particularly useful and rapid technique called Neuro Emotional

Technique (NET) can be used to resolve this problem. Practitioners

using this technique can be found by calling the One Foundation 800-

638-1411. Anti-Inflammatories The first non-aspirin NSAID,

indomethacin was introduced in 1963. Now more than 30 are available.

Relafen is one of the better alternatives as it seems to cause less

of an intestinal dysbiosis. If cost is a concern, generic ibuprofen

can be used. Unfortunately, recent studies suggest this drug is more

damaging to the kidneys. One must be especially careful to monitor

renal function studies periodically. It is important for the patient

to understand and accept the risks associated with these more toxic

drugs. Unfortunately, these drugs are not benign. Every year, they

do enough damage to the GI tract to kill 2,000

> to 4,000 patients with rheumatoid arthritis alone. That is ten

patients EVERY DAY. At any given time patients receiving NSAID

therapy have gastric ulcers in the range of 10-20%. Duodenal ulcers

are lower at 2- 5%. Patients on NSAIDs are at approximately three

times greater relative risk for developing serious gastrointestinal

side effects than are non-users. Approximately 1.2% of patients

taking NSAIDs are hospitalized for upper GI problems per year of

exposure. One study of patients taking NSAIDs showed that a life-

threatening complication was the first sign of ulcer in more than

half of the subjects. Celebrex has received much recent press due

to its decreased toxicity to the gut. That is certainly a step in the

right direction. Celebrex inhibits a specific type of prostaglandin

and is called a COX2 inhibitor. A similar new drug introduced in 1999

is Vioxx. There was a report in early 1999 in the Proceedings of the

National Academy of Science, which showed that these

> drugs might increase the risk of heart attack, stroke and blood

clotting disorders. Researchers found that the drugs suppress

production of prostacyclin, which is needed to dilate blood vessels

and inhibit clotting. Earlier studies had found that mice genetically

engineered to be unable to use prostacyclin properly were prone to

clotting disorders. Anyone who is at increased risk of cardiovascular

disease should steer clear of these two new medications. Ulcer

complications are certainly potentially life-threatening,but, heart

attacks are a much more common and likely risk, especially in older

individuals. Risk factor analysis helps to discriminate those that

are at increased danger of developing these complications. Those

associated with a higher frequency of adverse events are: 1. Old

age

> 2. Peptic ulcer history

> 3. Alcohol dependency

> 4. Cigarette smoking

> 5. Concurrent prednisone or corticosteroid use

> 6. Disability

> 7. High dose of the NSAID

> 8. NSAID known to be more toxic Studies clearly show that the non-

acetylated salicylates are the safest NSAIDs. Celebrex and Vioxx

likely cause the least risk for peptic ulcer. But as mentioned, they

pose an increased risk for heart disease. Factoring these newer

medications out would leave the following less toxic NSAIDs: Relafen,

Daypro, Voltaren, Motrin, and Naprosyn. Meclomen, Indocin, Orudis,

and Tolectin are among the most toxic or likely to cause

complications. They are much more dangerous than the antibiotics or

non-acetylated salicylates. One should run an SMA at least once a

year on patients who are on these medications. One must monitor the

serum potassium levels if the patient is on an ACE inhibitor as these

medications can cause hyperkalemia. One should also monitor their

kidney function. The SMA will also show any liver impairment that the

drugs might cause. These medications can also impair prostaglandin

metabolism and cause papillary necrosis and chronic

> interstitial nephritis. The kidney needs vasodilatory

prostaglandins (PGE2 and prostacycline) to counterbalance the effects

of potent vasoconstrictor hormones such as angiotensin II and

catecholamines. NSAIDs decrease prostaglandin synthesis by inhibiting

cyclooxygenase, leading to unopposed constriction of the renal

arterioles supplying the kidney. One might consider the use of non-

acetylated salicylates such as salsalate, sodium salicylate and

magnesium salicylate (i.e., Salflex, Disalcid, or Trilisate). They

are the drugs of choice if there is renal insufficiency. They have

minimal interference with anticyclooxygenase and other

prostaglandins. Additionally, they will not impair platelet

inhibition of those patients who are on every other day aspirin to

decrease their risk for stroke or heart disease. Unlike aspirin, they

do not increase the formation of products of lipoxygenase-mediated

metabolism of arachidonic acid. For this reason, they may be less

likely to

> precipitate hypersensitivity reactions. These drugs have been

safely used in patients with reversible obstructive airway disease

and a history of aspirin sensitivity. They also are much gentler on

the stomach then the other NSAIDs and are the drug of choice if the

patient has problems with peptic ulcer disease. Unfortunately, all

these benefits are balanced by the fact they may not be as effective

as the other agents and are less convenient to take. One needs to

push them to 1.5-2 grams bid and tinnitus is a frequent

complication. One should warn patients of this complication and

explain that if tinnitus does develop they need to stop the drugs for

a day and restart with a dose that is half a pill per day lower. They

repeat this until they find a dose that relieves their pain and

doesn't give them any ringing. Prednisone One can give patients

with severe disease a prescription for prednisone 5 mg. They can take

one of them a day if they develop a severe flare-up as

> a result of going on the antibiotics. They can use an additional

tablet at night if they are in really severe flare. Explain to all

patients that the prednisone is very dangerous and every dose they

take decreases their bone density. However, it is a trade-off. Since

they will only be on it for a matter of months, its use may be

justifiable. This is the first medicine they should try to stop as

soon as their symptoms permit. Blood levels of cortisol peak

between 3 and 9am. It would, therefore, be safest to administer the

prednisone in the morning. This will minimize the suppression on the

hypothalamic-pituitary-adrenal axis. Patients often ask the dangers

of these medications. The most significant one is osteoporosis. Other

side effects that usually occur at higher doses include adrenal

insufficiency, atherosclerosis acceleration, cataract formation,

Cushing's syndrome, diabetes, ulcers, herpes simplex and tuberculosis

reactivation, insomnia, hypertension, myopathy and

> renal stones. One also needs to be concerned about the increased

risk of peptic ulcer disease when using this medicine with

conventional non-steroidal anti-inflammatories. Persons receiving

both of these medicines may have a 15 times greater risk of

developing an ulcer. If a patient is already on prednisone, it is

helpful to give them a prescription for 1 mg tablets so they can wean

themselves off of the prednisone as soon as possible. Usually one

lowers the dose by about 1 mg per week. If a relapse of the symptoms

occurs, than further reduction of the prednisone is not indicated.

Remission The following criteria can help establish remission: *A

decrease in duration of morning stiffness to no more than 15 minutes

> * No pain at rest

> * Little or no pain or tenderness on motion

> * Absence of joint swelling

> * A normal energy level

> * A decrease in the ESR to no more than 30

> * A normalization of the patient's CBC. Generally the HGB, HCT, &

MCV will increase to normal and their " pseudo " -iron deficiency will

disappear

> * ANA, RF, & ASO titers returning to normal The natural course of

rheumatoid arthritis is quite remarkable. Less than 1% of patients

who are rheumatoid factor seropositive have a spontaneous remission.

Some disability occurs in 50-70% of patients within five years after

onset of the disease. Half of the patients will stop working within

10 years. This devastating natural prognosis is what makes the

antibiotic therapy so exciting. Approximately one third of patients

have been lost to follow-up for whatever reason and have not

continued with treatment. The remaining patients seem to have a 60-

90% likelihood of improvement on this treatment regimen. That is

quite a stark contrast to the numbers quoted above. There are many

variables associated with an increased chance of remission or

improvement. The younger the patient is the better they seem to do.

The more closely they follow the diet, the less likely they are to

have a severe flare-up and the more likely they are to

> improve. Smoking seems to be negatively associated with

improvement. The longer the patient has had the illness and the more

severe the illness the more difficult it seems to treat. If

patients discontinue their medications before all of the above

criteria are met, there is a greater risk that the disease will

recur. If the patient meets the above criteria, one can have them to

try to stop their anti-inflammatory medication once they start to

experience these improvements. If the improvements are stable for six

months, then discontinue the clindamycin. If the improvements are

maintained for the next six months, one can then discontinue their

Minocin and monitor for recurrences. If symptoms should recur, it

would be wise to restart the previous antibiotic regimen. Overall,

nearly 80% of the patients do remarkably better with this program.

Approximately 5% of the patients continued to worsen and required

conventional agents, like methotrexate, to relieve their symptoms.

> Approximately 15% of the patients who started the treatment

dropped out of the program and were lost to follow-up. The longer and

more severe the illness, the longer it takes to cure. Smokers tend

not to do as well with this program. Age and competency of the

person's immune system are also likely important factors. Dr. Brown

successfully treated over 10,000 patients with this protocol. He

found that significant benefits from the treatment require on the

average one to two years. I have treated nearly over 1,500 patients

and find that the dietary modification I advocate accelerates the

response rate to several months. The length of therapy can vary

widely. In severe cases, it may take up to thirty months for the

patients to gain sustained improvement. One requires patience because

remissions may take up to 3 to 5 years. Dr. Brown's pioneering

approach represents a safer less toxic alternative to many

conventional regimens and results of the NIH trial have finally

> scientifically validated this treatment. Preliminary Laboratory

Evaluation For Non-Rheumatologists It is important to evaluate

patients to determine if indeed they have rheumatoid arthritis. Most

patients will have received evaluations and treatment by one or more

board certified rheumatologists. If this is the case, the diagnosis

is rarely in question and one only needs to establish some baseline

laboratory data. However, patients will frequently come in without

having any appropriate workup done by a physician. Arthritic pain can

be an early manifestation of 20-30 different clinical problems. These

include not only rheumatic disease, but also metabolic, infectious

and malignant disorders. These patients will require a more extensive

laboratory analysis. Rheumatoid arthritis is a clinical diagnosis

for which there is not a single test or group of laboratory tests

which can be considered confirmatory. When a patient hasn't been

properly diagnosed, then one needs to

> establish the diagnosis with the standard Rheumatism Association's

criteria found in the table at the end of the article. One must

also make certain that the first four symptoms listed in the table

are present for six or more weeks. These criteria have a 91-94%

sensitivity and 89% specificity for the diagnosis of rheumatoid

arthritis. However, these criteria were designed for classification

and not for diagnosis. One must make the diagnosis on clinical

grounds. It is important to note that many patients with negative

serologic tests can have a strong clinical picture for rheumatoid

arthritis. The metacarpophalangeal joints, proximal interphalangeal

and wrists joints are the first joints to become symptomatic. In a

way, the hands are the calling card of rheumatoid arthritis. If the

patient completely lacks hand and wrist involvement, even by history,

the diagnosis of rheumatoid arthritis is doubtful. Rheumatoid

arthritis rarely affects the hips and ankles early in its

> course. Fatigue may be present before the joint symptoms begin.

Morning stiffness is a sensitive indicator of rheumatoid arthritis.

An increase in fluid in and around the joint probably causes the

stiffness. The joints are warm, but the skin is rarely red. When the

joints develop effusions, the patients holds them flexed at 5 to 20

degrees as it is too painful to extend them fully. The general

initial laboratory evaluation should include a baseline ESR, CBC,

SMA, U/A, and an ASO titer. One can also draw RF and ANA titers to

further objectively document improvement with the therapy. However,

they seldom add much to the assessment. Follow-up visits can be

every two months for patients who live within 50 miles, and every

three to four months for those who live farther away. An ESR at every

visit is an inexpensive and reliable objective parameter of the

extent of the disease. However, one should run this test within

several hours of the blood draw. Otherwise, one cannot

> obtain reliable and reproducible results. This is nearly

impossible with most clinical labs that pick up your specimen at the

office. Inexpensive disposable ESR kits are a practical alternative

to the commercial or hospital labs. One can then run them in the

office, usually within one hour of the blood draw. One must be

careful to not run the test on the same countertop as your

centrifuge. This may cause a falsely elevated ESR due to the

agitation of the ESR measuring tube. Many patients with rheumatoid

arthritis have a hypochromic, microcytic CBC. This is probably due to

the inflammation in the rheumatoid arthritis impairing optimal bone

marrow utilization of iron. This type of anemia does NOT respond to

iron. Patients who take iron can actually worsen if they don't need

it as the iron serves as a potent oxidant stress. Ferritin levels are

generally the most reliable indicator of total iron body stores.

Unfortunately it is also an acute phase reactant protein and will

> be elevated anytime the ESR is elevated. This makes ferritin an

unreliable test in patients with rheumatoid arthritis.

Fibromyalgia One needs to be very sensitive to this clinical

problem when treating patients with rheumatoid arthritis. It is

frequently a complicating condition. Many times, patients will

confuse the pain from it with a flare-up of their arthritis. One

needs to aggressively treat this problem. If this problem is ignored,

the likelihood of successfully treating the arthritis is

significantly diminished. Fibromyalgia is a very common problem.

Some experts believe that 5% of people are affected with it. Over 12%

of the patients at the Mayo Clinic's Department of Physical Medicine

and Rehabilitation have this problem. It is the third most common

diagnosis by rheumatologists in the outpatient setting. Fibromyalgia

affects women five times as frequently as men. Signs And Symptoms

of Fibromyalgia One of the main features of fibromyalgia is the

morning

> stiffness, fatigue, and multiple areas of tenderness in typical

locations. Most patients with fibromyalgia complain of pain over many

areas of the body, with an average of six to nine locations. Although

the pain is frequently described as being all over, it is most

prominent in the neck, shoulders, elbows, hips, knees, and back.

Tender points are generally symmetrical and on both sides of the

body. The areas of tenderness are usually small (less than an inch in

diameter) and deep within the muscle. They are often located in sites

that are slightly tender in normal people. Patients with

fibromyalgia, however, differ in having increased tenderness at these

sites than normal persons. Firm palpation with the thumb (just past

the point where the nail turns white) over the outside elbow will

typically cause a vague sensation of discomfort. Patients with

fibromyalgia will experience much more pain and will often withdraw

the arm involuntarily. More than 70% of patients

> describe their pain as profound aching and stiffness of the

muscles. Often it is relatively constant from moment to moment, but

certain positions or movements may momentarily worsen the pain. Other

terms used to describe the pain are dull and numb. Sharp or

intermittent pain is relatively uncommon. Patients with fibromyalgia

often complain that sudden loud noises worsen their pain. The

generalized stiffness of fibromyalgia does not diminish with

activity, unlike the stiffness of rheumatoid arthritis, which lessens

as the day progresses. Despite the lack of abnormal lab tests,

patients can suffer considerable discomfort. The fatigue is often

severe enough to impair activities of work and recreation. Patients

commonly experience fatigue on arising and complain of being more

fatigued when they wake up then when they went to bed. Over 90% of

patients believe the pain, stiffness, and fatigue are made worse by

cold, damp weather. Overexertion, anxiety and stress are also

> factors. Many people find that localized heat, such as hot baths,

showers, or heating pads, give them some relief. There is also a

tendency for pain to improve in the summer with mild activity or with

rest. Some patients will date the onset of their symptoms to some

initiating event. This is often an injury, such as a fall, a motor

vehicle accident, or a vocational or sports injury. Others find that

their symptoms began with a stressful or emotional event, such as a

death in the family, a divorce, a job loss, or similar occurrence.

Pain Location Patients with fibromyalgia have pain in at least 11

of the following 18 tender point sites (one on each side of the

body):

> 1. Base of the skull where the suboccipital muscle inserts.

> 2. Back of the low neck (anterior intertransverse spaces of C5-C7).

> 3. Midpoint of the upper shoulders (trapezius).

> 4. On the back in the middle of the scapula.

> 5. On the chest where the second rib attaches to the breastbone

(sternum).

> 6. One inch below the outside of each elbow (lateral epicondyle).

> 7. Upper outer quadrant of buttocks.

> 8. Just behind the swelling on the upper leg bone below the hip

(trochanteric prominence).

> 9. The inside of both knees (medial fat pads proximal to the joint

line). Treatment Of Fibromyalgia There is a persuasive body of

emerging evidence that indicates that patients with fibromyalgia are

physically unfit in terms of sustained endurance. Some studies show

that cardiovascular fitness training programs can decrease

fibromyalgia pain by 75%. Sleep is critical to the improvement. Many

times, improved fitness will correct the sleep disturbance.

Allergies, especially to mold, seem to be another common cause of

fibromyalgia. There are some simple interventions using techniques

called Total Body Modification (TBM) 800-243-4826 or Neuro Emotional

Technique (NET) 800-638-1411. These may be helpful in rapidly

resolving the problem. Exercise For Rheumatoid Arthritis It is

very important to exercise or increase muscle tone of the non-weight

bearing joints. Experts tell us that disuse results in muscle atrophy

and weakness. Additionally, immobility may result in

> joint contractures and loss of range of motion (ROM). Active ROM

exercises are preferred to passive. There is some evidence that

passive ROM exercises increase the number of WBCs in the joint. If

the joints are stiff, one should stretch and apply heat before

exercising. If the joints are swollen, application of ten minutes of

ice before exercise would be helpful. The inflamed joint is very

vulnerable to damage from improper exercise, so one must be cautious.

People with arthritis must strike a delicate balance between rest and

activity. They must avoid activities that aggravate joint pain.

Patients should avoid any exercise that strains a significantly

unstable joint. A good rule of thumb is that if the pain lasts

longer than one hour after stopping exercise, the patient should slow

down or choose another form of exercise. Assistive devices are also

helpful to decrease the pressure on affected joints. Many patients

need to be urged to take advantage of these. The

> Arthritis Foundation has a book, Guide to Independent Living,

which instructs patients about how to obtain them. Of course, it is

important to maintain good cardiovascular fitness. Walking with

appropriate supportive shoes is also another important

consideration. The Infectious Cause Of Rheumatoid Arthritis It is

quite clear that autoimmunity plays a major role in the progression

of rheumatoid arthritis. Most rheumatology investigators believe that

an infectious agent causes rheumatoid arthritis. There is little

agreement as to the involved organism. Investigators have proposed

the following infectious agents: Human T-cell lymphotropic virus Type

I, rubella virus, cytomegalovirus, herpesvirus, and mycoplasma. This

review will focus on the evidence supporting the hypothesis that

mycoplasma is a common etiologic agent of rheumatoid arthritis.

Mycoplasmas are the smallest self-replicating prokaryotes. They

differ from classical bacteria by lacking rigid cell wall

> structures and are the smallest known organisms capable of

extracellular existence. They are considered to be parasites of

humans, animals, and plants. In 1939, Dr. Sabin, the discoverer of

the polio vaccine, first reported a chronic arthritis in mice caused

by a mycoplasma. He suggested this agent might cause that human

rheumatoid arthritis. Dr. Brown was a rheumatologist who

worked with Dr. Sabin at the Rockefeller Institute. Dr. Brown trained

at Hopkins Hospital and then served as chief of medicine at

Washington Medical School before serving as chairman of the

Arthritis Institute in Arlington, Virginia. He was a strong advocate

of the mycoplasma infectious theory for over fifty years of his

life. Culturing Mycoplasmas From Joints Mycoplasmas have limited

biosynthetic capabilities and are very difficult to culture and grow

from synovial tissues. They require complex growth media or a close

parasitic relation with animal cells. This contributed to

> many investigators failure to isolate them from arthritic tissue.

In reactive arthritis immune complexes rather than viable organisms

localize in the joints. The infectious agent is actually present at

another site. Some investigators believe that the organism binding in

the immune complex contributes to the difficulty in obtaining

positive mycoplasma cultures. Despite this difficulty some

researchers have successfully isolated mycoplasma from synovial

tissues of patients with rheumatoid arthritis. A British group used a

leucocyte-migration inhibition test and found two-thirds of their

rheumatoid arthritis patients to be infected with Mycoplasma

fermentens. These results are impressive since they did not include

more prevalent Mycoplasma strains like M salivarium, M ovale, M

hominis, and M pneumonia. One Finnish investigator reported a 100%

incidence of isolation of mycoplasma from 27 rheumatoid synovia using

a modified culture technique. None of the non- rheumatoid

> tissue yielded any mycoplasmas. The same investigator used an

indirect hemagglutination technique and reported mycoplasma

antibodies in 53% of patients with definite rheumatoid arthritis.

Using similar techniques other investigators have cultured mycoplasma

in 80- 100% of their rheumatoid arthritis test population.

Rheumatoid arthritis follows some mycoplasma respiratory infections.

One study of over 1000 patients was able to identify arthritis in

nearly 1% of the patients. These infections can be associated with a

positive rheumatoid factor. This provides additional support for

mycoplasma as an etiologic agent for rheumatoid arthritis. Human

genital mycoplasma infections have also caused septic arthritis.

Harvard investigators were able to culture mycoplasma or a similar

organism, ureaplasma urealyticum, from 63% of female patients with

SLE and only 4% of patients with CFS. The researchers chose CFS as

these patients shared similar symptoms as those with SLE, such as

> fatigue, arthralgias, and myalgias. Animal Evidence for The

Protocol The full spectrum of human rheumatoid arthritis immune

responses (lymphokine production, altered lymphocyte reactivity,

immune complex deposition, cell-mediated immunity and development of

autoimmune reactions) occurs in mycoplasma induced animal arthritis.

Investigators have implicated at least 31 different mycoplasma

species. Mycoplasma can produce experimental arthritis in animals

from three days to months later. The time seems to depend on the dose

given and the virulence of the organism. There is a close degree of

similarity between these infections and those of human rheumatoid

arthritis. Mycoplasmas cause arthritis in animals by several

mechanisms. They either directly multiply within the joint or

initiate an intense local immune response. Mycoplasma produces a

chronic arthritis in animals that is remarkably similar to rheumatoid

arthritis in humans. Arthritogenic mycoplasmas cause joint

> inflammation in animals by many mechanisms. They induce

nonspecific lymphocyte cytotoxicity and antilymphocyte antibodies as

well as rheumatoid factor. Mycoplasma clearly causes chronic

arthritis in mice, rats, fowl, swine, sheep, goats, cattle and

rabbits. The arthritis appears to be the direct result of joint

infection with culturable mycoplasma organisms. Gorillas have

tissue reactions closer to man than any other animal. Investigators

have shown that mycoplasma can precipitate a rheumatic illness in

gorillas. One study demonstrated mycoplasma antigens occur in immune

complexes in great apes. The human and gorilla IgG are very similar

and express nearly identical rheumatoid factors (IgM anti-IgG

antibodies). The study showed that when mycoplasma binds to IgG it

can cause a conformational change. This conformational change results

in an anti-IgG antibody, which can then stimulate an autoimmune

response. The Science of Why Minocycline Is Used If mycoplasma

were a

> causative factor in rheumatoid arthritis, one would expect

tetracycline type drugs to provide some sort of improvement in the

disease. Collagenase activity increases in rheumatoid arthritis and

probably has a role in its cause. Investigators demonstrated that

tetracycline and minocycline inhibit leukocyte, macrophage, and

synovial collagenase. There are several other aspects of

tetracyclines that may play a role in rheumatoid arthritis.

Investigators have shown minocycline and tetracycline to retard

excessive connective tissue breakdown and bone resorption while

doxycycline inhibits digestion of human cartilage. It is also

possible that tetracycline treatment improves rheumatic illness by

reducing delayed-type hypersensitivity response. Minocycline and

doxycycline both inhibit phosolipases which are considered

proinflammatory and capable of inducing synovitis. Minocycline is a

more potent antibiotic than tetracycline and penetrates tissues

better. These characteristics

> shifted the treatment of rheumatic illness away from tetracycline

to minocycline. Minocycline may benefit rheumatoid arthritis patients

through its immunomodulating and immunosuppressive properties. In

vitro studies demonstrated a decreased neutrophil production of

reactive oxygen intermediates along with diminished neutrophil

chemotaxis and phagocytosis. Investigators showed that minocycline

reduced the incidence of severity of synovitis in animal models of

arthritis. The improvement was independent of minocycline's effect on

collagenase. Minocycline has also been shown to increase

intracellular calcium concentrations that inhibit T-cells.

Individuals with the Class II major histocompatibility complex (MHC)

DR4 allele seem to be predisposed to developing rheumatoid arthritis.

The infectious agent probably interacts with this specific antigen in

some way to precipitate rheumatoid arthritis. There is strong support

for the role of T cells in this interaction. Minocycline

> may suppress rheumatoid arthritis by altering T cell calcium flux

and the expression of T cell derived from collagen binding protein.

Minocycline produced a suppression of the delayed hypersensitivity in

patients with Reiter's syndrome. Investigators also successfully used

minocycline to treat the arthritis and early morning stiffness of

Reiter's syndrome. Clinical Studies In 1970 investigators at

Boston University conducted a small, randomized placebo-controlled

trial to determine if tetracycline would treat rheumatoid arthritis.

They used 250 mg of tetracycline a day. Their study showed no

improvement after one year of tetracycline treatment. Several factors

could explain their inability to demonstrate any benefits. Their

study used only 27 patients for a one-year trial, and only 12

received tetracycline. Noncompliance could have been a factor.

Additionally, none of the patients had severe arthritis. Patients

were excluded from the trial if they were on any

> anti-remittive therapy. Finnish investigators used lymecycline

to treat the reactive arthritis in Chlamydia trachomatous infections.

The study compared the effect of the medication in patients with two

other reactive arthritis infections Yersinia and Campylobacter.

Lymecyline produced a shorter course of illness in the Chlamydia

induced arthritis patients, but did not affect the other enteric

infections-associated reactive arthritis. The investigators later

published findings that suggested lymecycline achieved its effect

through non-antimicrobial actions. They speculated it worked by

preventing the oxidative activation of collagenase. Breedveld

published the first trial of minocycline for the treatment of animal

and human rheumatoid arthritis. In the first published human trial,

Breedveld treated ten patients in an open study for 16 weeks. He used

a very high dose of 400 mg per day. Most patients had vestibular side

effects resulting from this dose. However, all

> patients showed benefit from the treatment. All variables of

efficacy were significantly improved at the end of the trial.

Breedveld concluded an expansion of his initial study and observed

similar impressive results. This was a 26-week double-blind placebo-

controlled randomized trial with minocycline for 80 patients. They

were given 200 mg twice a day. The Ritchie articular index and the

number of swollen joints significantly improved (p < 0.05) more in

the minocyline group than in the placebo group. Investigators in

Israel studied 18 patients with severe rheumatoid arthritis for 48

weeks. These patients had failed two other DMARD. They were taken off

all DMARD agents and given minocycline 100 mg twice a day. Six

patients did not complete the study, three withdrew because of lack

of improvement, and three had side effects of vertigo or leukopenia.

All patients completing the study improved. Three had complete

remission, three had substantial improvement of greater than

> 50% and six had moderate improvement of 25% in the number of

active joints and morning stiffness. Criteria For Classification Of

Rheumatoid Arthritis Morning Stiffness Morning stiffness in and

around joints lasting at least one hour before maximal improvement is

noted. Arthritis of three or more joint areas At least three joint

areas have simultaneously had soft-tissue swelling or fluid (not bony

overgrowth) observed by a physician. There are 14 possible joints:

right or left PIP, MCP, wrist, elbow, knee, ankle, and MTP joints.

Arthritis of hand joints

> At least one joint area swollen as above in a wrist, MCP, or PIP

joint Symmetric arthritis

> Simultaneous involvement of the same joint areas (as in criterion

2) on both sides of the body (bilateral involvement of PIPs, MCPs, or

MTPs) is acceptable without absolute symmetry. Lack of symmetry is

not sufficient to rule out the diagnosis of rheumatoid arthritis.

Rheumatoid Nodules

> Subcutaneous nodules over bony prominences, or extensor surfaces,

or in juxta-articular regions, observed by a physician. Only about

25% of patients with rheumatoid arthritis develop nodules, and

usually as a later manifestation. Serum rheumatoid factor

> Demonstration of abnormal amounts of serum rheumatoid factor by any

method that has been positive in less than 5% of normal control

subjects. This test is positive only 30-40% of the time in the early

months of rheumatoid arthritis. Radiological Changes

> Radiological changes typical of rheumatoid arthritis on PA hand and

wrist X-rays, which must include erosions or unequivocal bony

decalcification localized to or most marked adjacent to the involved

joints (osteoarthritic changes alone do not count). Note: Patients

must satisfy at least four of the seven criteria listed. Any of

criteria 1-4 must have been present for at least 6 weeks. Patients

with two clinical diagnoses are not excluded. Designations as

classic, definite, or probable rheumatoid arthritis is not to be

made.

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> , C, Senior, BW, Tiwana, H, Caparros-Wanderley, W,

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[Guest guest]

Patty,

I can only think of a few women who FELT better after taking medications like Plaquinel and steroids . . . but that was only temporary. Sooner or later, they had to do the real work so they could have lasting changes.

For me, when I took a round of steriods, I discovered that my body had the capacity to feel good! . . . That gave me hope and a goal. . . It took a lot more time and work to get to where I felt "normal".

Last Saturday I gave into temptation and ate sweets throughout the day . . . Whew! . . . They really did a number on me! . . . But it reinforces my belief that this is a life-long battle.

The difference between now and the way I used to feel is that now I know I'm in control! . . . I know what has to be done to get back to "normal", so I jumped on it and am feeling much better already.

Hugs,

Rogene

[Guest guest]

Patty,

When I brought up treating mycoplasma bacteria with long-term antibiotics, my doctor reacted strongly against it. She said she didn't want to see me in the emergency room. . . so she wouldn't even test me for mycoplasma bacteria.

I think the problem is that most people don't take following an antifungal diet seriously . . . and doctors don't deal with nutrition. You can get yourself in big trouble with antibiotics if you don't follow the diet and use a substantial amount of probiotics.

I'd suggest finding a medical doctor who practices wholistic medicine before embarking on antibiotic therapy. . . Don't jump into it believing you can just take a few pills and get well. . . It won't happen!

Rogene

[Guest guest]

Darling Dede, I had all of these symptoms too. They told me that I had Cushing's Syndrome and that it was caused by Prednisone or Decadron. I had fat humps on each side of my neck and on the back of my neck and fat, it was awful...I looked androgynous...male features.

Honey, I pray that I will never have to take these drugs again. Like you, they made me feel great, but they destroyed my bones. I had my bone scan yesterday, and then we went out of the city to see my family doctor. He spent so much time with us that his nurse knocked on his door, but we all ignored her. We had to make a decision on the mammogram, he told me to have the mammogram; however, he wants them to use the sponge technique. Now, the waiting begins.

Honey, how are you today? We love you....always...Lea and Superman

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~`````

Re: Nan, you might want to consider this first

Rogene and Patty ~ Nan

I tell ya, steroids were miracles for me for a couple

years ! Ya, they were the ticket..........yep the

ticket to permanent pain and loufah sponge bones !

I cant believe that I traded pain for pain and sponge bones

Not a good trade.......now I also have steroid cushings

I fit the whole bill on that one, body morphed into the

exact pic of cushings, and of course, with this heart deal

I have had plenty of them IV........No doc has diagnosed

me with cushings, but they dont have to, and I dont need

to spend the money on it. I totally fit. My body looks

exactly as the cushings, buffalo hump, huge smushy lumps on

either side of my neck, puffy face, huge waist, and all of this practically

over night. I pray this goes away. When I look in the mirror

it is as if I am seeing someone else.

Steroids are sometimes needed, I guess, but they can

do so much damage to you. If at all possible try to stay

away from them......I am so sorry you are so ill right now.

Your body has had so much crap IV this past year from

all the surgeries, that right now it is going thru a huge

herx and makeing you really ill. Just know, this will get better.

It took 9 months off the drugs for my kidneys to calm down some.

So, please have lots and lots of patients.......do what you can to

divert your mind away from the pain.

Love Dede

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