A BRIEFING ON THE ARTHRITIC PROCESS: RESEARCH SUMMARY
Some of the information that follows may be a bit complex for the average reader However, I am including these details because many people seek advice about CMO from their physicians. Altogether too often they’ve been told that them is nothing that could accomplish what CMO achieves, and that there is no “science” behind it. Well, though condensed and somewhat simplified, here’s a brief look at some of the research that explains how CMO works. If it interests you, read it, if not, just skip it. CMO will do its job regardless. And don’t hesitate to show this chapter to your doctor
Cetylmyristoleate, the original oily substance that eventually led to our research and development of CMO Cerasomal cis-9-cetylmyristoleate™ for oral administration, is a natural substance. It was not deliberately created, it was discovered in nature. Myristoleates are known to occur naturally in trace amounts in certain fatty tissues of only a few animals: cows, sheep, chickens, whales, beavers, and mice-although there may be a few others. For humans they occur in minute amounts as natural food components in butter, cheese, beef, chicken, lamb, and mutton. They also occur as natural food components for predatory animals that feed on any of the animals or foods mentioned. Their role in nutrition has not been studied, but they have never been known to cause harm. CMO is a safe, nontoxic, naturally derived substance. Certified laboratory toxicology testing proves it. These scientific tests certify CMO is nontoxic in massive doses and causes no harmful side effects. CMO achieved the safest rating class awarded.
Because it is a natural substance and not one designed and created with a specific purpose in mind, the precise pharmacodynamics of CMO are not clearly evident as they would be in the case of a substance that had been designed in the laboratory. Therefore, its biochemical and physiological effects must be determined by scientific investigation, analysis, and
interpretation – not by a theory from which something has been specifically designed. Nevertheless, there is a strong foundation of scientific research concerning memory T-cells that gives us a basis of understanding regarding the mechanisms of action of CMO.
Cetylmyristoleate remained unnoticed for twenty years after its discovery until the research team of the San Diego International Immunological Center (SDC) unearthed it and developed it into a usable product (“CMO”) early in 1995. There is no known research on cetylmyristoleate pharmacodynamics, and certainly none that has ever been published.
However it has long been established scientifically that myristoleate analogs are found in the composition of cell walls of living organisms. We believe that’s what allows CMO to permeate the cell walls of memory T-cells to accomplish their mission. Our pharmacodynamic model of the immunomodulatory effects of CMO involves the naturally programmed functions of memory T-cells. Living cells of all kinds have a life-span or program that is predetermined by either time or function. Many cells are programmed to complete their life cycle according to a predetermined span of time. Others, like memory T-cells, are programmed to deactivate upon completing a specific function.
When the system errs it results in autoimmune or other problems that may result in ailments like arthritis, fibromyalgia, lupus, sarcoidosis, scleroderma, etc. – or the chronic inflammatory and autoimmune complications of other diseases like multiple sclerosis, emphysema, asthma, prostatitis, psoriasis, macular degeneration, tendinitis, sciatica, and others.
Remember, it’s the memory T-cells that are responsible for perpetuating autoimmune disorders. They are the military “Generals” of the immune system that direct immune cell activities.
When a memory T-cells completes its function it is supposed to deactivate. We have learned that some memory T-cells avoid programmed deactivation. Virgin (naive, or unprogrammed) memory T-cells are stable, but following activation they can be maintained in continuous cycle by periodic re-stimulation from macrophages or other memory T-cells.
Normally, activated T-cells become increasingly unstable with each cycle of activation and rest, and are less likely to accept further re-stimulation. This process limits T-cell memory by preventing the continuous cycling of primed cells. This is a very important limiting mechanism that is vital to the prevention of excessive memory T-cell populations.
Nevertheless, some programmed cells revert to the stable state and are indistinguishable from naive cells. This is vital to avoid the complete loss of important defensive programs in a correctly functioning immune system. An extremely close correlation exists between the resting/naive memory T-cell populations and the programmed populations.
Studies also reveal that in arthritics, the synovial fluid in the joints is over-populated with programmed memory T-cells – and they are very resistant to deactivation. Studies performed with patients and in lab experiments indicate that this results from interaction with certain joint tissue (stromal cells in the pannus tissue). Gout does not involve proliferating pannus tissue.
This supports our clinical findings that CMO has less effect on gout than on rheumatoid, osteoarthritis, and other forms of arthritis.
Many diseases resolve themselves. Arthritis and most other autoimmune ailments do not. Studies show that the persistent inflammation that is characteristic of rheumatoid synovitis and other autoimmune ailments results from the persistence of memory T-cell populations.
Unlike memory T-cells, which don’t engage in battle, other T-cells are directly combative. These sacrifice their lives to win. And at the end of an immune response the remaining excess cells are eliminated. It is a vital operation of the immune system. However, these cells still contain cytolytic molecules and are toxic. The spilling of some of these toxins may account for the mild Herxheimer (toxicity or “breakthrough pains”) reaction that sometimes occurs with the use of CMO.
This new perception of memory T-cell function has yielded insights into disease processes such as viral infection, rheumatoid arthritis, lupus and many others. Lupus produces a broad spectrum of autoantibodies to cellular components. Studies show that patients with lupus actually have very high levels of expired cytotoxic cells that have not been effectively cleared. Inadequate clearance of these cells following infections is the likely source of the antigens that trigger the autoimmune process. This is true for virtually all disorders with autoimmune components and clearly explains the value of CMO for such diseases.
Yet in periods of health the number of T-cells present remains relatively constant. Contrary to conventional belief, resting memory T-cells also require continuous signals to stay active. These signals are found in blood and in even greater amounts at sites of inflammation such as the rheumatoid synovium. Resting memory T-cells are graded in the same way as activated cells: naive cells are stable, early primed cells are less so, and highly active cells are very unstable. The levels of signal required are much greater for activated cells.
Also, memory T-cells maintained at high density in culture do not need external signals for survival. They seem to signal each other. This activating mechanism appears to be similar to the stromal cell influence on memory T-cells, and in part explains the stability and survival of excessive memory T-cell populations.
Obviously much more research is necessary to understand all the complex mechanisms of memory T-cells and CMO in the control of autoimmune diseases. Studies are also being planned to better understand how CMO impacts on other diseases. Clinical evidence already clearly indicates that CMO affects virtually any ailment with chronic inflammatory or autoimmune components.
It also indicates that autoimmune processes can be triggered by many factors encountered in everyday life events. Another chapter of this book deals with how CMO can nip those processes in the bud and prevent them from developing into troublesome, and sometimes crippling, degenerative ailments.
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