TREATMENT OF RHEUMATOID ARTHRITIS: FIRST- AND SECOND-LINE DRUGS AND CORTICOSTEROIDSThe three major groups of medications prescribed for the treatment of RA are:1.  First-line drugs, which are used to reduce inflammation quickly. Aspirin and other NSAIDs are the first-line drugs.2.  Second-line drugs, which are used in an attempt to induce a remission. These are the DMARDs and the immunosuppressants.3.  Corticosteroids.We believe strongly that being aware of potential side effects from medications will help you recognize the symptoms early and will help ensure that you obtain prompt treatment if a side effect occurs. We would like to add a cautionary note about focusing too intently on the potential side effects of medications, however. Such a focus can cause unnecessary worry and stress. A proper balance is to be found somewhere between being aware of the symptoms of side effects and watching vigilantly for the possible occurrence of every one of them. Keep in mind that severe and irreversible side effects rarely happen.As stated above, new medications become available continually. In any case, please consult your doctor for more information about medications.A final note: We recommend that you use only one pharmacy to fill all of your prescriptions if possible. This allows the pharmacist to review all of the medications you are taking (possibly prescribed by more than one physician) and caution you and your physicians about potentially harmful drug interactions.*87/209/5*

TESTS USED TO SCREEN FOR COMPLICATIONS OF RA (RHEUMATOID ARTHRITIS): COMPLEMENT STUDIES AND OTHER TESTSComplement studies These blood studies, which include tests called C3, C4, and CH50, are used to determine whether a particular part of the immune system is activated. They are rarely performed for people who have an uncomplicated case of RA, but they can be helpful when a person has an unusual complication of RA called vasculitis.
Liver function tests Liver function tests are blood tests that may reflect changes in the liver, such as inflammation and organ damage. Findings of minor abnormalities in these tests are common in RA. Interestingly, though, a change in liver function tests does not necessarily mean that the liver’s functioning capacity has been altered. Elevated levels generally suggest mild liver irritation or past damage. These tests are often used to search for evidence of pre-existing liver problems or to monitor the side effects of medications. Commonly ordered liver function tests include the SGOT (or AST), SGPT (or ALT), LDH, and alkaline phosphatase.
Urinalysis and Kidney Function Tests Examination of a urine specimen is an extremely useful test that most often is requested to screen for medication-induced complications affecting the kidneys. Rarely, patients with RA have minor abnormalities in the urine unrelated to medications.The evaluation of kidney (renal) function also requires blood tests called creatinine and blood urea nitrogen (BUN). The levels of these substances present in the blood indicate how efficiently the kidney is filtering the body’s toxins. Sometimes the physician will request a twenty-four-hour urine collection and a blood test to obtain an extremely accurate assessment of kidney function. Again, these tests are undertaken to monitor for medication side effects or to look for underlying kidney problems.24/209/5*

However, when the researcher reported his remarkable findings to his superiors in an attempt to secure funding for additional research, his request was mysteriously denied. Nevertheless, struggling along without authorization, he continued his studies and reported further successes. Strangely, not only were his requests for funding continuously denied, all of his accomplishments went completely unrecognized. Though they never said so directly, it was as though the NIH wanted him to abandon the project completely. Discouraged though he was, he still continued his research as best he could with absolutely no funding at all. When he retired about a decade later, since even the mere existence of his work went completely unacknowledged by the NIH, he took his discovery with him and continued the research on his own. And well he deserved to do so. Had he not, his discovery may never have come to light.

It has been reported that some time later, one by one he went to three different major pharmaceutical companies offering to share his discovery. One by one, his offers were

rejected – not for lack of effectiveness, but because the product was derived from natural sources it could not be patented in a way to hog all the profits. The companies couldn’t care less about the fact that it worked, only that they couldn’t protect it from being manufactured by some competing company. Nor did they express any interest in funding further research on the project.

One could also speculate on the likelihood that by making available a product that potentially reverses the arthritic process permanently, it would kill their annual multi-billion dollar sales of existing arthritis products – all of which must be taken repeatedly for the rest of the arthritis victims’ lives. Quite understandably, of course, the pharmaceutical companies love products that lead to a lifetime of repeat sales.

After its rejection by the pharmaceutical companies the project lay fallow for several years. No further attempts were made to explore its potential.

The chain of events that followed have never been made crystal clear. It has been reported that as some years passed, the researcher himself began to suffer terribly from arthritis and was receiving conventional medical therapy to treat it. It is important to note that despite the fact that he had explored the safety and effectiveness of his discovery on lower animals at the NIH, research had never reached the level of testing on higher animals. But once his arthritis reached excruciating extremes and his physician told him that he was beyond any effective help, the researcher decided to take a risk. He brewed up a batch of cetylmyristoleate at home and injected himself. Thus, he became the first person ever to receive the substance as a test of the discovery on human beings. We honour his courage.

It was a historic moment. He began to feel symptomatic relief the very next day, and soon he reached a point where he experienced total reversal of his arthritis. His doctor was astonished when he subsequently examined his patient and heard the whole story of the discovery.

The doctor was so impressed that he persuaded him to write an account of his research project. The doctor promised to help him get it published in the Journal of Pharmaceutical Sciences, hoping that the article might stimulate someone into continuing the exploration of the project. Then, early in 1995, a few months after the article appeared, that’s exactly what happened. The San Diego Clinic International Immunological Centre (SDC) embarked on a project to develop the discovery into a usable product.

But long before that, it seems that several years had intervened between the self-injection and the actual publication of the article. Meanwhile, it has been reported, even though the substance was provided quite informally to a couple hundred more arthritis victims with astounding success, there was no formal progress in research or development.

The journal article itself didn’t seem to stimulate much interest either. Perhaps that’s because it was only three pages long and dealt solely with mouse model studies. Besides, it was reporting on research that took place over twenty years before. Perhaps the readers thought there couldn’t be much value to something that had lain dormant so very long. Or maybe they thought there must have been more recent research that refuted the early findings. Nor did the article provoke questions about why it had been ignored by the NIH and how it came to buried for so

long – except in one instance.

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CMO, on the other hand, corrects autoimmune programs within the memory T-cells themselves rather than just temporarily suppressing or stimulating immune system activities. That is why a single CMO therapy program can correct memory T-cell faults without any need to continually apply the therapy or use any additional medication of any kind.

CMO is not an immunosuppressant, nor an immunostimulant. Nor is it a pharmaceutical. It is a naturally derived substance. Some practitioners have speculated that, in the case of arthritis for example, CMO merely acts upon pain receptors at the arthritic site. If that were so, CMO’s effects would not be so permanent. Furthermore, that theory cannot explain:

• how CMO lowers blood sedimentation rates in lupus patients,

• or how it reverses lung inflammation in emphysema,

• or how it lowers the need for insulin in diabetics,

• or how it reverses prostate inflammation,

• or how it relieves certain symptoms of multiple sclerosis,

• or how it corrects Crohn’s disease,

• or how it reverses fibromyalgia

• or how it lowers high blood pressure yet elevates low blood pressure,

• or how it benefits virtually any ailment with autoimmune components.

Obviously, CMO is a general remedial immunomodulator that acts upon the memory T-cells which control the autoimmune processes within our bodies. Those who speculate otherwise have misunderstood the physiological actions of CMO within the body.

It is also important to understand that CMO acts only upon memory T-cells and does not inhibit the activities of any of the several other types of T-cells or protective immune system agents that are responsible for combating invading microorganisms or intrusive substances.

Unlike the immunosuppressants commonly used to try to temporarily control the symptoms of autoimmune diseases, CMO does not leave the body vulnerable to attack by disease-causing agents. Nor does it inhibit the body’s resistance to tumor formation, as do the dangerous tumor necrosis factor (TNF) suppressants of some new arthritis drugs

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The Autoimmune-Arthritic Process – Step-By-Step

The following is an overview of the autoimmune-arthritic process. The process is explained in eleven steps. It all starts with initiation of altered autoimmune system function.

1. First, infection, trauma, or excessive wear affects the joints. The usual infections are rheumatic fever, flu, or bacteria. Traumas include events such as, jolts or injuries from auto wrecks, falls, sports injuries, jogging, etc. Excessive joint wear comes from being overweight, or from repetitive use of keyboards, jackhammers, knitting needles, screwdrivers etc.

2. The effects of #1 cause damaged or infected cartilage particles to be dislodged from their normal site. This happens regardless of whether it’s rheumatoid, reactive, or osteoarthritis.

3. Macrophages of the immune system begin a cleanup of these dislodged cartilage particles. That’s a normal part of their job.

4. Macrophages report their activities to dormant memory T-cells, which are the commanding “generals” of the immune system that direct the activities of other immune cells.

5. The reports from the macrophages activate the dormant memory T-cells, then develop aggressive anti-cartilage cleanup programs. Unfortunately, these programs do not distinguish between healthy and damaged cartilage.

6. The memory T-cell programs stimulate more macrophage activity which, in turn, activates even more dormant memory T-cells.

7. The increased memory T-cell population continues to stimulate more macrophage activity, and the self-perpetuating cycle of cartilage destruction expands. Because the memory T-cell programs don’t limit macrophage activity to damaged cartilage only, destruction of healthy cartilage also occurs. It has now developed into a destructive autoimmune process. But, until sufficient cartilage has been destroyed, symptoms are not evident. The individual is unaware that the destructive process is occurring.

8. The initiating factor (infection, trauma, weight) taking place in # 1, may have disappeared many months or years ago, but the destructive autoimmune process remains active. It is self perpetuating and no longer dependent upon the initiating factor. When this happens it has become a pure autoimmune disease.

9. The cycle is compounded by the fact that the mechanism which should deactivate certain memory T-cells (those that have completed their mission) fails to function. The constant macrophage re-stimulation of the memory T-cells keeps them active. The memory T-cells also re-stimulate each other. So now there is an overabundance of memory T-cells propelling macrophage cartilage destruction. The immune system is now totally out of control and massive cartilage destruction often begins. Early symptoms of pain and inflammation often appear.

10. Cartilage destruction accelerates. The cycle reaches an explosive critical mass. Macrophages are now scouring the body to find and destroy any cartilage anywhere it can be found. Symptoms become more severe. Pain, inflammation, and joint deformity intensify at old sites and now appear at new sites as they suffer macrophage attacks. Any or all joints may be affected, including the spine.

11. Symptoms of pain, stiffness, swelling, nodules, and deformation often reach intolerable and crippling levels-especially as joint cartilage disappears and bone-on-bone erosion occurs. Conventional arthritis medications also take their toll on the liver, kidneys, and heart. Normal life span is often shortened by ten or twenty years not only from the ravages of arthritis, but from the side effects of both prescription and over-the-counter medications as well.

By deactivating the memory T-cells, CMO intervention (the sooner the better) can stop the autoimmune process at any point.

Current medical dogma holds that only rheumatoid arthritis is an autoimmune disease. On the contrary, the above explanation makes it evident that osteoarthritis is an autoimmune disease as well. The sooner the medical community accepts that fact, the better they may be able to treat their arthritis patients effectively.

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It seems that it is the inflammatory process itself that initiates the arthritic process, regardless of what triggers the inflammation. In other words, the arthritic process can start whether the particles of cartilage result from an attack by certain pathogenic micro-organisms (leading to rheumatoid arthritis) or by a trauma (developing into osteoarthritis)!

In either case, rheumatoid or osteoarthritis, it results in a vicious cycle. As more macrophages bring back messages to the memory T-cells, more and more T-cells develop programs that direct attacks against the cartilage and arthritis continues to get progressively worse. You almost never hear of arthritis getting better. Now you’ve learned why.

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