Hypercoagulability: ‘Sticky’ Blood Is Present in Nearly all Chronically Ill Patients, This Is Why

Acute or chronic innate immune system activation, heavy metal toxins, and inflammation may result in the generation of excess soluble fibrin. The presence of this excess causes hypercoagulability

The treatment of hypercoagulability involves helping the body degrade the excessive soluble fibrin it has produced, heal blood vessel damage, and stopping the eitiology of hypercoagulability. Tatiana Belova

Hypercoagulability is present to some degree at one time or another in almost every chronically ill patient. Everyone has experienced a flu-like illness with fever, headache, body aches and pains, fatigue, nausea and insomnia in their lives. When we acquire an acute infection, our bodies respond with a brisk innate immune system response. Part of the body’s inflammatory response includes activation of the coagulation cascade, a domino of protein production, whereby the body creates more soluble fibrin. Flu-like headaches, aches and pains, fatigue, nausea, and insomnia can be partially attributed to this excess soluble fibrin. Acute or chronic innate immune system activation, heavy metal toxins, mold toxins, Herxheimer reactions (symptom flare after killing off certain infections), and inflammation of any cause may result in the generation of excess soluble fibrin. The presence of excess soluble fibrin causes hypercoagulability.

What Is Hypercoagulability?

Through a very complex and redundant system, the body maintains a very delicate balance in the production of molecules that either encourage or discourage blood clotting. After injury, we must be immediately able to stop bleeding by plugging holes in our blood vessel walls, and we must also be ready to thin the blood and contain blood clot formation to avoid blocking life-giving blood flow to organs and tissues. When this delicate seesaw system is tilted towards being on the “sticky” side, with an abundance of molecules encouraging blood clotting over blood thinning, we are in a hypercoagulable state.

The body’s coagulation system depends on both platelet activation and fibrin production. When small blood cells called platelets get activated, they clump or aggregate and stick or adhere together, releasing chemical messengers that encourage blood clot formation. Fibrin is produced or formed when the coagulation cascade is activated. The breakdown or degradation of fibrin can be slowed and weakened by different hereditary or genetic weaknesses.

What Is Soluble Fibrin?

The coagulation cascade is a series of molecular reactions that result in the production of a protein called fibrin. Fibrin molecules can be either soluble and free floating in the blood, or insoluble, becoming linked together by bonds—analogous to interlocking Lego™ toy pieces—to form a blood clot.

Generally, in the absence of a tear in a blood vessel wall, only soluble fibrin is produced. In the majority of patients who are hypercoagulable as a result of chronic illness, soluble fibrin is produced. This soluble fibrin accumulates in the blood, overwhelms the body’s ability to break it down, and ends up creating a sludge-like layer along the inner surface of blood vessel walls, especially smaller blood vessels or capillaries. Just one micron (one millionth of a meter) thick layer of soluble fibrin along the inner lining of a capillary wall reduces the diffusion of oxygen molecules out of the blood into tissues by 500% with the resulting tissue hypoxia (lack of oxygen) creating clinical symptoms.

Fibrin Deposition Model.

Additionally, the delivery of nutrients, growth factors, hormones, and minerals to tissues, and the removal of wastes from tissues, can be significantly affected by excess soluble fibrin. This can result in tissue congestion and overwhelm the lymphatic system’s ability to drain toxins and waste from the periphery of the body back into the blood stream. Once in the blood stream, toxins and waste undergo detoxification in the liver with fat soluble debris being dumped into the bile for excretion and water-soluble debris returned to the blood for the kidneys to filter out.

Once a pro-coagulant environment with excess soluble fibrin is set up, it creates a self-perpetuating positive feedback cycle. The layer of fibrin sludge on the inner lining of blood vessel walls makes the small vessels called arterioles stiff and less able to constrict or dilate in response to neuroendocrine control of blood pressure. Therefore, hypercoagulable people can be prone to high blood pressure.

To make matters worse, about 20% of the general population have an inherited genetic variation in different parts of the genes coding for the coagulation system that makes them more prone to developing hypercoagulability.

Interestingly, a 2003 study of over a thousand chronic Lyme patients found nearly 90% were hypercoagulable and also had one or more hereditary defects in the coagulation system.

A study of over a thousand chronic Lyme patients found 9 in 10 were hypercoagulable.

Symptoms of hypercoagulability

The symptoms of hypercoagulability or the presence of excessive soluble fibrin that the body cannot break down itself may include: insomnia; restless legs; stiffness upon awakening or after being sedentary; morning nausea with poor breakfast appetite; nausea after eating; brain fog; irritability; anxiety and/or panic; depression; mood swings; fatigue; generalized pain that can be debilitating; painful numbness or “pins and needles”; sharp stabbing shooting pains; deep aching pains, particularly of the arms and legs; limbs that “fall asleep” easily; and the inability to tolerate aerobic exercise with worsening of fatigue and pain after exercise.

• Physical signs of hypercoagulability

Physical signs of hypercoagulability may include: mottled skin; cold, sometimes clammy hands and feet; prolonged capillary refill in fingers and toes; pale, swollen tongue with scalloped edges; full sublingual veins; doughy abdomen with peri-umbilical (belly button) tenderness, and generalized soft tissue congestion. The head and neck may become red or ruddy in color upon laying down, the feet may get deep purple or red with dependency, and there is often compromise of cognitive function or brain fog with irritability and emotional lability.

• Laboratory work-up

The laboratory work-up to determine if a patient is hypercoagulable and may have a genetic predisposition to become hypercoagulable includes: fibrinogen, antithrombin activity III; D-dimer; protein C activity; protein S activity; activated protein C resistance; factor II activity; alpha-2 antiplasmin; plasminogen activase inhibitor–1 (PAI-1); lipoprotein-a; homocysteine; lipid panel; prothrombin fragments 1&2; and thrombin-antithrombin complexes (TATs).

Causes of hypercoagulability

Naturally, blood gets stickier as part of the aging process. Normal pregnancy is a hypercoagulable state. About 20% of the population have a genetic fault that predisposes them to hypercoagulability, especially when they are under any kind of significant stress.

Just about anything that causes inflammation can lead to hypercoagulability: both acute and chronic infections, cancer, exogenous toxins (mold toxins, heavy metals, chemicals), allergens, physical trauma, vaccinations, biologically imcompatible frequencies from wireless radiation (wifi, 5G), and biowarfare agents such as trichothecenes.

Hypercoagulability is made worse by: acute and chronic inflammation; infections, especially those with fever; severe physical trauma from accidents; heart disease; diabetes; cancer; vasculitis; and even gut dysbiosis, dental cavitations, and toxic loads. When inflammatory cytokines are released due to Herxheimer reactions, exposure to indoor toxic mold in susceptible individuals, detoxificiation protocols that move toxins too fast, and even glyphosate-induced sulfate deficiency (see “Toxic Legacy” by Dr. Stephanie Seneff), that damages the endothelial membrane of inner lining of all blood vessel walls.

Several scientific papers have substantiated that hypercoagulation has been a significant contributor to the demise of many COVID-19 patients as well as those injured or killed by the COVID-19 injections. These include the following:

Scientific papers have substantiated that hypercoagulation has been a contributor to the demise of many COVID-19 patients.

“Our data suggest that microvascular thrombosis should be entertained as a likely cause of cardiac injury in hospitalized patients with COVID-19.”

The first study to show that the spike protein damages the endothelial lining of blood vessel walls.

This was the first study to show that the spike protein damages the endothelial lining of blood vessel walls.

A study found that SARS-CoV-2 infection is associated with an increased risk of arterial and venous thrombotic events.

This study found that “SARS-CoV-2 infection is associated with an increased risk of arterial and venous thrombotic events.The pathophysiological mechanisms underlying thrombotic events in SARS-CoV-2 infection include platelet activation, triggering of the coagulation cascade, the formation of neutrophil extracellular traps and ‘cytokine storm’ syndromes. Anti-thrombotics, such as low-molecular-weight heparin or unfractionated heparin, are used for thromboprophylaxis or for the treatment of thrombotic events related to SARS-CoV-2 infection.”

German pathologist Prof. Dr. A. Burkhardt, in his Notes and recommendations for conducting post-mortem examination (autopsy) of persons deceased in connection with COVID vaccination – Updated. Doctors for Covid Ethics. March 2022, stated that he and his colleagues performed 17 autopsies on persons deceased within days to months of vaccination. They found widespread vasculitis with microthrombi as well as intense lymphocytic infiltration of multiple, which led them to conclude that, in most patients, the vaccines were likely the cause of death.

Treatment

The treatment of hypercoagulability involves not only helping the body degrade the excessive soluble fibrin it has produced and heal blood vessel damage, but also to stop the eitiology of hypercoagulability.

Excess soluble fibrin is best dissolved with fibrinolytic enzymes. Those readily available for oral administration include nattokinase and lumbrokinase. The enzymes, urokinase or streptokinase, are fibrinolytic enzymes that have been used in hospitals to treat strokes and heart attacks caused by blood clots.

Nattokinase works primarily inside blood vessels while lumbrokinase, nearly 30 times more powerful, works both inside and outside blood vessels. Dosages must start low and gradually increase as the debris, toxins, and infective agents, released as soluble fibrin is dissovled, can easily overwhelm the body’s ablities to detoxify. Other proteolytic enzymes, such as serrapeptidases, may be helpful adjuncts. Sometimes, subcutaneous or intravenous heparin is required.

Other homeopathic immune modulators, herbs, and nutriceuticals, such as omega-3 fats and vitamin E, can help to control both the coagulation cascade and platelet activation, as well as contribute to healing of blood vessel walls.

It must be remembered that, in addition to chronic inflammation from infections, the movement of heavy metals during chelation and the exposure to mold toxins in susceptible individuals can seriously exacerbate hypercoagulablity. Additionally, many of the symptoms of Herxheimer reactions result not only from inflammatory cytokine release, but also from hypercoagulability. Symptoms can often be significantly reduced with the addition of sufficient doses of fibrinolytic enzymes and appropriate detoxification.

Luckily, treatment of hypercoagulability, the breakdown of blood clots and rebalancing the coagulation system, is being included by some doctors besides myself in the treatment of those injured by COVID-19 jabs. The FLCCC’s recently released guidelines include the use of lumbrokinase. In an interview with Dr. Mercola, pediatrician Dr. Michelle Perro mentions fibrinolytic enzymes as well.

References:

Researched Nutritionals’ Conferences:

• Role of Hypercoagulation & Biofilms in Chronic Illness
• Decoding the Mystery of Chronic Illness

Allergy Research Group’s Focus Newsletter:

• January 2003: Hypercoagulation Linked to Chronic Fatigue, Fibromyalgia, MS, Infertility, Chronic Illness
• November 2008: Nattokinase: Clinical Updates from Doctors Support its Safety and Efficacy
• March 2009: New Enzyme Complex Isolated from Earthworms is Potent Fibrinolytic Lumbrokinase has Anti-Platelet, Anti-Thrombotic Activity
• 40th Anniversary Edition 2019: Potent, Natural Fibrinolytic Enzymes Safely Reduce Clotting Risk

Hsia CH, et al. Nattokinase decreases plasma levels of fibrinogen, factor VII, and factor VIII in human subjects. Nutr Res. 2009 Mar 1;29(3):190-6.

Milner M, Makise K. Natto and its active ingredient nattokinase: A potent and safe thrombolytic agent. Alt Comp Ther. 2002 Jun 1;8(3):157-64.

Cooper EL. Leukocyte activity during earthworm inflammatory reactions. Int J Tis React. 1986;8(3):175-84.

Dong Q, et al. The efficacy and safety of lumbrokinase capsule in treatment of cerebral infarction. Chinese New Drug J. 2004; 13:257-9.

Verma MK, Pulicherla KK. Lumbrokinase-a potent and stable fibrin-specific plasminogen activator. Int J Bio-Sci Bio-Tech. 2011 Jun; 3(2):57-69.

Ding SQ, et al. A Clinical Study of Therapeutic Effectiveness in Treating Ischemic Cerebrovascular Disease with Lumbrokinase. Chinese J Neurol Psych. 1993;26(4).

Mihara H, et al. Novel thrombolytic therapy discovered from traditional oriental medicine using the earthworm. Southeast Asian J Trop Med Public Health. 1992;23 Suppl 2:131-40.

Jin L, et al. Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase. Clin Hemorheol Microcirc. 2000; 23(2-4):213-8.

Cao YJ, et al. Oral fibrinogen-depleting agent lumbrokinase for secondary ischemic stroke prevention: results from a multicenter, randomized, parallel-group and controlled clinical trial. Chin Med J (Engl). 2013 Nov; 126(21):4060-5.