Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn’s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
- Viruses, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits.
- Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it.
- Chemical exposure can result in changes that trigger the coagulation process.
The results of this thickened blood are:
- When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised.
- The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment.
- Thicker blood is harder to pump.
- By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly.
- The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin.
Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS
and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria
(for example mycoplasma or chlamydia
pneumonia) and/or transfer factor
(such as HHV6, CMV
). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus
more vulnerable, thus improving the treatment's effectiveness.
patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor
, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.