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by Author: Jeremy Lucius Evarts
February 1, 1999
According to research performed at HEMEX Laboratories in Phoenix, Arizona, by David E. Berg, M.S., CLS (NCA), Lois Hill Berg, M.A., CLS (NCA), and John Couvaras, M.D., chronic fatigue and immune dysfunction syndrome (CFIDS) and fibromyalgia (FM) may be due to a hypercoagulable state induced by immune activation of the coagulation system. Their research is so significant it was selected for presentation at the American Association for Chronic Fatigue Syndrome (AACFS) Conference in Cambridge, Massachusetts in October 1998.
The premise of the research is that a hypercoagulable state, caused by immune activation, can be responsible for the fatigue and pain involved in CFIDS and FM. An individual's immune system can be activated by numerous events, including a virus, bacteria, or chemical exposure. According to David Berg, "Almost every CFIDS or FM patient I have ever worked with can trace their disease back to a specific event or illness."
This immune system activation causes your body to produce more immunoglobulins. These immunoglobulins punch holes in the protective proteins that cover the inside of blood vessels, ultimately resulting in excess thrombin generation which converts major blood protein (fibrinogen) into soluble fibrin monomers and/or fibrin. When fibrin coats the inside of the blood vessels, it blocks the flow of nutrients and oxygen going through the blood vessels to the tissues below, thereby starving areas of the body.
According to the Arizona Science Museum, all of the blood vessels in the human body, when stretched out, would extend over 60,000 miles. Cut open and spread out, these vessels would cover half of the surface of an entire football field. A partial clot in any area of the blood vessel system could radically affect the transport of nutrients and oxygen in that area of the body.
HEMEX Laboratories discovered the connection between hypercoagulation and CFIDS & FM while doing research on miscarriages and unwanted pregnancy terminations. Increased thrombin generation in the area of the woman's placenta caused nutrients and oxygen to be withheld from the fetus leading to its death and spontaneous abortion.
In the same way, increased thrombin levels in other parts of the body can lead to the muscle pain involved with CFIDS and FM. If immune activation causes a thrombin increase in the vicinity of a muscle, the sheath surrounding the muscle might be blocked from receiving the necessary nourishment. According to the researchers, this causes stiffness and pain in the joint that then becomes a trigger point, one of the diagnosing symptoms of the two diseases.
High thrombin levels can also have a direct impact on energy and fatigue. Elevated thrombin levels increase the viscosity, or thickness, of the blood. The thicker the blood, the harder the heart has to pump to maintain the blood's flow throughout the body. This overworking of the heart might be responsible for part of the fatigue suffered by so many patients with CFIDS and FM.
Research shows there might be a genetic disposition to hypercoagulation as well. Each human, when born, has approximately 40 genetic mutations. David Berg states that, "Out of the CFIDS and FM communities nearly two out of three patients have a specific mutation that allows the coagulation system to run easier than normal, causing hypercoaguability which makes them more susceptible to immune activation later on."
In the study at HEMEX Laboratories in Arizona, 20 patients diagnosed with CFIDS or FM were placed on an anticoagulant regimen therapy. The procedure included two main anticoagulants; heparin and coumadin. Heparin's effect as an anticoagulant is more immediate, often administered by hospitals in blood clot cases through an IV or subcutaneous injection with noticeable results within 48 hours. Coumadin is taken orally with results usually visible within one to two weeks.
The administration of heparin and coumadin was different for each patient. Initially, heparin therapy was given to all 20 patients for one month. After the first month some of the patients were then transferred to a 2 mg daily dose of coumadin. A few of the patients were maintained on low dose coumadin for up to a year.
The results of the retrospective study were staggering. Of the 20 initial test subjects, 16 of them showed improvement in the areas of fatigue, muscle pain, and headache. The research indicated that the patients' improvement might be due to simply decreasing thrombin generation through anticoagulant therapy, resulting in a decrease of blood viscosity as the soluble fibrin monomers are removed from circulation and the fibrinogen levels return to normal. This suggests that heparin and coumadin offer relief by acting on the hypercoagulable state manifested in the patients suffering from CFIDS or FM.
According to Berg, "This whole concept is just now being studied throughout the world. For now, we know that there is a large subset within the CFIDS and FM communities who suffer from this hypercoagulable state. Our next step is to find out just how large this subset actually is and how anticoagulant therapy might help them."
In January and February of 1999, HEMEX Laboratories has a randomized, controlled, double-blind study planned to determine wether soluble fibrin monomers are an indicator of excess thrombin generation, which might be responsible for the debilitating symptoms of CFIDS and FM. This further research into immune activation and hypercoagulable states might deliver a viable treatment option, or even a cure, to the patients suffering from CFIDS and FM.
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