Physicians' Protocol For Using Antibiotics in Rheumatic Disease + My Rheumatoid

[Guest guest]

For me, I have greatly reduced arthris pain an gained a lot of joint

modility by going on a low oxalate diet, and using Magnesioum Chloride

solution topically, several times a week. I tried various

supplements for years with some success, but greatly reducing dietary

oxalates, taking Calcium Citrate with NO Magnesium or vitamin D prior

to each oxalate meal, and using transdermal Magnesium has made an

incredible difference. A decade ago I could not put on an oven mitt

or button my shirt without exteme pain. Now I can put on snug winter

gloves with minimal discomfort. I never use aspirin or other NSAIDs.

 

Alobar

 

On 11/24/08, bestsurprise2002 <bestsurprise2002 wrote:

>

> My Rheumatoid Arthritis Protocol

>

_http://articles.mercola.com/sites/articles/archive/2000/08/27/rheumatoid-arthri\'>http://articles.mercola.com/sites/articles/archive/2000/08/27/rheumatoid-arthri\

tis-part-one.aspx_

>

(http://articles.mercola.com/sites/articles/archive/2000/08/27/rheumatoid-arthri\

tis-part-one.aspx)

>

> By Dr. Mercola

> The following is a modified version of Dr. Brown's protocol.

> 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_

> (http://www.mercola.com/nutritionplan/) 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. Thomas 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. William 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.

> Revised Antibiotic-Free Approach

> Although the antibiotics frequently worked and the six-month period of

> worsening that was part of Dr. Brown's protocol was virtually eliminated, I

always

> felt like I had failed because I had to resort to the use of antibiotics.

> This has now changed, as I have been able to implement a major change in my

> revision of the protocol that allows for a completely drug-free treatment of

> RA. The major change seems to be the use of nutritional typing, along with

> energy techniques. Since we have integrated nutritional typing with full use

of

> EFT to address the stressors that seem to be universally present in RA, we

> have been able to cause RA to routinely go into remission without the use of

> antibiotics.

> To say I am excited is a serious understatement.

> nutritional typing allows each patient to get a unique diet that is right

> for their body. It is very easy to understand how a physician who successfully

> treats one patient with a particular diet would come to the conclusion that

> the diet that person was on was the " cure " for RA, when in fact nothing could

> be further from the truth. Another person with the same disease could quite

> possibly need an entirely different diet to receive any benefits, that is how

> powerful nutritional typing can be.

> If you haven't yet read the book _The nutritional typing Diet_

> (http://www.amazon.com/exec/obidos/ASIN/0767905644/optimalwellnessc) , , I

would strongly

> encourage you to do so as it reviews these topics extensively (it is

> definitely a book that belongs on the shelf of anyone with any interest in

> nutrition).

> There are some general principles that seem to hold true for all nutritional

> types and these include:

> · Eliminating sugar and grains (you can read more about this below)

> · Having unprocessed, high-quality foods, organic if possible

> · Eating your food as close to raw as possible

> · Having omega-3 fish oil

> I am overjoyed beyond belief that after 14 years of treating RA I can

> finally offer a drug-free, effective and rapid solution for most of those

with RA

> with the aid of nutritional typing. However, it is clear that a perfect diet

> alone will rarely cause the RA to go into remission.

> This is because RA is an autoimmune illness. It does indeed appear to be

> caused by an infection, as Dr. Brown speculated. But the central issue is why

> did the person acquire the infection in the first place? It is my experience

> that this infection is usually acquired when a person has a stressful event

> that causes a disruption in their bioelectrical circuits, which causes an

> impairment in their immune system. This impairment predisposes them to

developing

> the initial infection and also contributes to their relative inability to

> effectively defeat the infection.

> The antibiotics clearly seem to help most people fight the infection, but,

> as I mention above, there are better ways that address the underlying

> foundational cause of the illness.

> I am quite convinced that energy techniques are required to resolve this

> energetic disruption. Prayer can certainly be one of them. However, in my

> experience, most have not utilized prayer in a way that rallies their body's

> resources to resolve the problem.

> In my experience, energy psychology techniques are very helpful in this area

> and can be easily integrated with prayer. I happen to use EFT in my practice

> and you can download my free 25-page report

> _http://www.mercola.com/forms/eftcourse.htm_

(http://www.mercola.com/forms/eftcourse.htm) to find out more

> about this technique

> However, the emotional trauma that causes RA is nearly universally quite

> severe and is best treated by a professional. Trying to treat this trauma by

> yourself is somewhat similar to a general surgeon trying to perform an

> appendectomy on him or herself. Although it is possible, it is not generally

> recommended (Interesting aside: I read an article in JAMA about 10 years ago

in which

> a surgeon in the late 1800s actually did this. Unfortunately, he died from

> complications.).

> Dr. Partirica Carrington has actually compiled _some guidelines_

> (http://www.emofree.com/Practitioners/referralMain.aspx) on how you can

find an EFT

> practitioner.

> In the following sections I have included information about the antibiotic

> therapy for RA for anyone who is interested. However, I now recommend my

> drug-free approach for anyone fighting this illness.

> 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.

> 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.

> · Extended spectrum of activity

> · Greater tissue penetrability

> · 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. In February 2006 Wyeth sold manufacturing rights of Minocin to Triax

> Pharmaceuticals (866-488-7429).

> 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 WalMart 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.

> 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.

> Physicians' Protocol For Using Antibiotics in Rheumatic Disease

>

> _http://articles.mercola.com/sites/articles/archive/2000/08/27/rheumatoid-arth

> ritis2.aspx_

>

(http://articles.mercola.com/sites/articles/archive/2000/08/27/rheumatoid-arthri\

tis2.aspx)

>

> 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.

> 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:

> · Old age

> · Peptic ulcer history

> · Alcohol dependency

> · Cigarette smoking

> · Concurrent prednisone or corticosteroid use

> · Disability

> · High dose of the NSAID

> · 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.

> My favorite, and most profoundly beneficial treatment for fibromyalgia is

> NST.

> 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.

> 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. Thomas Brown was a rheumatologist

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

> John Hopkins Hospital and then served as chief of medicine at George

> 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.

> Presented at the 32nd International Congress of the Great Lakes College of

> Clinical Medicine. Baltimore, Maryland, September 25, 1999

> Dr. Joseph M. Mercola

>

> Using Antibiotics in Rheumatic Diseases - Bibliography

>

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> bib.aspx)

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> Presented at the 32nd International Congress of the Great Lakes College of

> Clinical Medicine. Baltimore, Maryland, September 25, 1999

> Dr. Joseph M. Mercola

>

>