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impossible
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Ive been doing some reading the last few days and wanted to throw another angle your way. MTHFR is known as a risk factor for thrombosis. You also have another homozygous mutation (dont remember which off the top of my head, computer wants me to download your results again to view them) that is a considerable risk factor as well. This page sums up the pieces I was trying to put together perfectly, and then some. Im so glad I found it.

http://www.anapsid.org/cnd/diffdx/hypercoagulation.html

The first excerpt:

A simplified introduction into hypercoagulable state…

Research conducted by Dr. David Berg and others at Hemex Laboratories1 has found hypercoagulation to be a factor in many patients with chronic fatigue syndrome (CFS), fibromyalgia (FM), myofascial pain syndrome (MPS), and other disorders such as osteonecrosis (bone loss due to inadequate blood supply), and fetal loss.

Hypercoagulation (thickened blood) results from fibrin being deposited in small blood vessels. Fibrin is the body’s natural bandaid: strands of fibrin form across a defect (wound, tear) in the walls of blood vessels, forming a mesh that holds platelets and blood cells. This beneficial clotting of cellular matter and fibrin strands plugs the leak, so to speak, holding things together until the body starts to repair itself.

Fibrin production is the last stage in a complex clotting process. The process itself starts off with the release of thrombin which in turn results in the production of soluble fibrin monomer (SFM), a sticky protein that increases blood viscosity. This leads to the deposit of fibrin on the endothelial cells that line the wall of the blood vessels. Under the normal conditions, it takes only a single burst of thrombin to generate a large amount of SFM which in turns produces sufficient amounts of fibrin to clot the defect. Testing of many patients diagnosed with CFS, FM, MPS shows that the thrombin-SFM-fibrin process is not working properly. Instead of a single burst of thrombin producing the amount of SFM needed, the thrombin keeps being produced at low levels. Instead of clots being formed, however, the result is that blood becomes increasingly thickened. The body’s own ability to thin blood and break up clots is impaired because the fibrin smothering the endothelial cells prevents those cells from releasing heparans.

There are two different ways this scenario can be played out. The first is thrombinphilia, “thrombin loving”, where the body keeps producing thrombin because the normal control that would prevent excessive or inappropriate thrombin generation fail, do not exist, or have somehow been overridden so the body keeps producing thrombin at low levels. The controller is anti-thrombin (AT). AT combines with thrombin to form thrombin/anti-thrombin (T/AT). Normally, when the endothelial cells release heparans, the release activates the AT, which acts slowly to reduce the thrombin. Not enough AT may be produced, or the amount may not be enough to keep up with the continuous thrombin production. Another possible cause is hypofibrinolysis, where too little heparans, the body’s natural clot busters, is produced or circulated. So, in the (simplified) three part process (thrombin, antithrombin, heparans), one or more parts is dysregulated or rendered insufficient, leading to hypercoagulation.

Berg states that there are at least three possible causes for this thrombin malfunction:

Viruses, bacteria and/or parasites can activate certain antibodies in the immune system, which in this case trigger the continual production of thrombin, generating excessive SFM and fibrin.
Predispositional genetic defect in coagulation regulatory proteins (protein C, protein S, Factor VL, prothrombin gene mutation, PAI-1, Lp(a), or elevated homocysteine.
Chemical exposure can result in changes that trigger the coagulation process.

The results of this thickened blood are widespread, due to the role blood plays as the major transport of nutrients and oxygen throughout the body:

Thicker blood is harder to pump.
Muscle, nerve, bone and organs function is impaired because of the inability of sufficient nutrients and oxygen to pass through the capillaries.
The fibrin coating the vessel walls, the endothelial cells are no longer able to release heparans, the body’s natural blood thinner.
Hypercoagulation, by depriving the bowel of blood, may be a major factor in Irritable Bowel Disease.
Viruses and bacteria may be hidden under the fibrin layer coating the vessel walls, essentially hiding them from antibiotic and antiviral treatments.

Some of the symptoms associated with hypercoagulation will surprise few with CFS and/or FM: brainfog, cognitive dysfunction, digestion problems, fatigue, and generalize malaise.

Because this hypercoagulability does not result in an immediate thrombosis (100% occlusion), but rather in fibrin deposition (50-95%), Berg, et al.2 suggest that an appropriate name for this antiphospholipid antibody process would be Immune System Activation of Coagulation (ISAC) syndrome.

Hyperoagulation Testing
As a part of Hemex’s research, they have developed a test to determine if a patient has this hypercoagulation disorder. The Immune System Activation of Coagulation (ISAC) tests five substances; abnormal results on any two of the five is considered to be a positive indicator of hypercoagulation. Their results thus far have found 79-92 percent of the CFS and/or FM patients they tested have hypercoagulation. As with many of the more detailed blood tests developed in the past decade, the defects causing hypercoagulation are rarely or not at all detectable by the standard laboratory tests performed at general labs, such as Unilab, Quest Diagnostics, etc. The standard coagulation workup done by these labs assess only the risk of actual clotting, whereas the ISAC panel is 10-20 times more sensitive.