Michael P Lebowitz D.C.

Noah D Lebowitz

Michael Lebowitz

2550 I Road

Grand Junction, CO   81505




Hypercoagulation Disorders, a PAK Approach


Hypercoagulation is a condition that in extreme cases can lead to a deep vein thrombus, pulmonary emboli, and stroke. In less severe cases it has shown to be associated with chronic fatigue, fibromyalgia, nutrient deficiency, etc. Using Professional Applied Kinesiology the authors have developed a technique to possibly check for a patient being in a hypercoagulation state. This allows us to help the patient decrease their chance of a serious circulatory incident, or resolve chronic health issues that haven’t yet been resolved.


Hypercoagulation, deep vein thrombosis, thrombus, stroke, pulmonary embolism, chronic fatigue


Hypercoagulation is a condition manifesting in increased fibrin in ones blood and as a result the individual is at an increased risk of developing a thrombus (blood clot). If a person goes too far into a hypercoagulative state they develop deep vein thrombosis (DVT) which can be broken up and lead to pulmonary embolisms (PE), a myocardial infarction (MI), or stroke.

According to research done by David Berg, in less severe cases hypercoagulation can lead to chronic fatigue, fibromyalgia, and osteonecrosis. [1]

Checking for hyper-coagulation has never been attempted before in Professional Applied Kinesiology (PAK), even though it is a leading cause of illness in the United States. It is estimated that 300,000-600,000 suffer from a DVT in the United States each year, and that 60,000-100,000 die from a DVT or (PE) each year. [2] Well known people such as Hilary Clinton, Mariano Rivera, and Serena Williams are several of many that have suffered recently from blood clots, leading to an increased public awareness.

Hypercoagulation can be caused by a myriad of issues including: infections, metal and chemical toxicity, immobility, surgery, supplemental estrogen, malignancy, genetics, or prolonged periods of time spent at very high elevation.

Research done by Dr. Pryzdial from the Centre for Blood Research shows how certain viruses, such as herpes simplex (HHV6, EBV) or cytomegalovirus (CMV) “express phosphatidylserine like procoagulant activity, capable of binding Xa and Va to form the prothrombinase complex.” [3] David Berg went on to note that 70% of patients studied with Chronic Fatigue Syndrome as well as Multiple Sclerosis were infected with HHV6 [4]. HHV6 is known to reside in endothelial cells, causing them to lose their ability to synthesize prostacyclin, and thus have a decreased ability to deter platelet adhesion. [5] Berg also mentions how the hypercoagulative state found in patients with chronic fatigue syndrome and fibromyalgia does not result in a thrombis, though is still problematic.  While a thrombis was not formed, fibrin deposition in blood vessels can lead to hypoxia, nutrient deficiency, and a plethora of other symptoms.

By screening ones patients for hypercoagulation and giving them supplementation and lifestyle changes, one could decrease the risk of the patient developing a DVT or PE. Also by thinning out one with “thick blood” it will allow the patient to more efficiently deliver oxygen and nutrients to all parts of the body, which may have currently obstructed pathways. By doing this one can help chronic patients with conditions such as chronic fatigue, fibromyalgia, nutrient deficiencies, etc.

While the clotting pathway is quite complicated, we chose to focus on four main pro-coagulative factors and four main anti-coagulative factors.

Pro-coagulation Factors:

S  Prothrombin/Coagulation Factor II

            An inactive protein synthesized by the liver and released into the blood, which is then converted to active thrombin in the process of blood clotting.

S  Thrombin

            The active enzyme produced from Prothrombin, which acts to covert fibrinogen to fibrin.

S  Fibrinogen

            Another inactive clotting factor in blood plasma that is converted to fibrin. Produced by liver and plasma cells, fibrinogen accounts for approximately 7% of blood plasma proteins.

S  Fibrin

            The final step in the clotting cascade. Fibrin is insoluble, essential to blood clotting, and formed from fibrinogen by the action of thrombin.

Anti-coagulation Factors:

S  Antithrombin III

            An anti-coagulant, it blocks action of pro-clotting agents (factors XII, XI, IX, X and II).

S  Plasminogen

            The inactive enzyme precursor of plasmin.

S  Plasmin

            An enzyme present in blood that degrades many blood plasma proteins, most notably, fibrin clots. It activates collagenases, some mediators of the complement system, and weakens the wall of the Graafian follicle (leading to ovulation).

S  Tissue Plasminogen Activator / tPA / PLAT

            A protein involved in the breakdown of blood clots. As an enzyme, tPA catalyzes the conversion of plasminogen to plasmin. Because it works on the clotting system, tPA is used in clinical medicine to treat only embolic or thrombotic stroke. Use is contraindicated in hemorrhagic stroke and head trauma.

A person wants to have adequate pro-coagulation factors as well as anti-coagulation factors to be in proper balance for optimum body function. Just as being in a hypercoagulative state is dangerous, being in a hypo-coagulation state can be a serious health concern. If ones blood does not clot properly, a person can experience increased bruising, and the potential for excessive internal or external bleeding, such as someone suffering from hemophilia would experience.

When checking for adequate amounts of clotting factors in the blood via muscle testing they should neither inhibit a facilitated muscle, nor facilitate an inhibited muscle, unless something is abnormal, just as would occur in food or nutrient testing. Using PAK we can not only check for if the person has a coagulation issue, but also see if it is with clot production or clot breakdown.

The question may arise of what to do once such problems have been discovered. There are many natural substances that are known and have been used for centuries to thin the blood:

1. Ginkgo Biloba is one such which has been shown to be a potent antagonist of platelet activating factor, decreasing clot formation.

2. Ginger has been shown to have blood-thinning properties.  [6] Current research out of the University of Sydney showed ginger to inhibit arachadonic acid induced platelet aggregation via inhibition of the COX-1 gene. [7] New studies claim ginger to be a more potent anti-coagulative than aspirin.

3. Pomegranate Juice has been shown to also inhibit platelet aggregation, thus helping to deal with hyper-coagulation. [8]

4. Green Papaya has been shown to increase fibrinolysis and the break down of already formed clots. [9]

5. Bromelain, found in fresh pineapple, has been shown to decrease blood coagulation by several pathways.  Bromelain acts by inhibiting the generation of bradykinin at the inflammatory site via depletion of the plasma kallikrein system. It also limits the formation of fibrin (clots) by reduction of clotting cascade intermediates. [10] Bromelain has also been shown in multiple studies to stimulate the conversion of plasminogen to plasmin, resulting in increased fibrinolysis (dissolution of clots/fibrin). This combination of effects can make it very useful in people with hypercoagulation tendencies. [11].

6. Nattokinase can be found in supplemental form or in natto as a food and has been shown to decrease coagulation in the blood by decreasing plasma levels of fibrinogen, as well as pro-coagulation factors VII and VIII. [12] It has also been shown to increase plasma levels of tPA, thus increasing fibrinolytic activity and lysis of thrombi. [13]

7. Shochu (Japan) / Soju (Korean) is known to increase urokinase-like plasminogen activator, leading to fibrinolysis, at the highest rate among all types of liquor; and is routinely in Japan for cardiac health. [14]

Chapman Reflexes have been used in PAK to help stimulate the function of organ systems of the body. The authors have found a Chapman-like reflex that seems to negate a positive test for hypercoagulation in a high percentage of cases. The reflex is bilaterally located on the anterolateral portion of the neck over the carotid artery where the baroreceptors are found at the carotid bifurcation (approximately C4).


All patients with any of the conditions previously mentioned (stroke, DVT, fibromyalgia, miscarriage history, etc.) or a family history of any of these, should be automatically checked for a clotting disorder. For patients without these symptoms, a quick and effective pre-screen has been developed to see if further testing is necessary. As a potential “pre-screen” to see if a patient should be checked for a coagulation issue, the authors have noticed that when testing a facilitated muscle (i.e. pec major clavicular) you can squeeze the patients distal forearm firmly, decreasing circulation for approximately 10 seconds, and then re-test the patient while still squeezing. If the previously facilitated muscle is now inhibited, the patient should be checked for having a hyper-coagulation disorder as described below. This test doesn’t correlate 100% with an abnormal test for hypercoagulation but appears to be positive in most of the cases (there can be false positives due to forearm injuries, etc.). If you suspect the disorder but the patient passes the “squeeze test”, we would still recommend testing further as described next.

1. See if any of the following pro-coagulative vials inhibits a facilitated indicator muscle: Thrombin, Prothrombin Factor II, Fibrinogen, & Fibrin. If any of them weaken, it is a positive test.

2. See if any of the following anti-coagulative vials facilitate an inhibited muscle: Antithrombin III, Plasmin, Plasminogen, & Tissue Plasminogen Activator. If it does, it is a positive test.

3. See if a mixture of anti-coagulant encouraging herbs (HemoGuard Supreme 1-800-922-1744) as previously mentioned negates the positive test.

4. If severe, also consider adding systemic enzymes like nattokinase and earthworm-derived enzymes to the products in step 3. If you do, warn the patient of potential bruising from taking too large of a dose.

5. Other helpful measures include:

                   Eating raw pineapple as a snack away from other foods

                   Drinking one ounce of Shochu or Shoju daily with or without food

6. These findings (positive tests in step 1 and/or 2) are much more common when family history includes, strokes, heart attacks, clots, embolisms, or miscarriages. They are also aggravated by taking estrogen, having an infection (chronic or acute), lack of exercise, dehydration, surgery etc.

7. After identifying supplementation to negate the positive hypercoagulation reflex, see if light pressure on the carotid baroreceptors negates the positive test. If so apply light pressure rubbing over the spot for 10-20 seconds while the patient is exposed to the factors that showed positive. Re-test the vials, and they should show up negative.

8. Recheck the patient in a month. If the tests are now negative see if the supplements still strengthen a weak indicator muscle. If they do, continue with supplementation. If not just advise the patient to continue pineapple, shochu etc.

9. CoQ10 can increase coagulation and supplementation containing it should be discouraged in these type of patients.

             10. If the patient is already on pharmaceutical anti-coagulants it is not advisable to supplement further as it can

increase the risk of bleeding disorders. The authors though have seen many people on these medications that still

fail the above PAK screening test and they fell are still at risk. If you are not licensed to prescribe it is difficult to make any recommendations in these cases.

The above procedure can be reversed checking a patient for hypo-coagulation.

            1. See if any of the following pro-coagulative vials facilitate an inhibited indicator muscle:

Thrombin, Prothrombin Factor II, Fibrinogen, & Fibrin. If any of them

strengthen, it is a positive test.

2. See if any of the following anti-coagulative vials inhibit a facilitated indicator muscle: Antithrombin III, Plasmin, Plasminogen, & Tissue Plasminogen Activator. If it does, it is a positive test.

Discussion While working with this technique for the past year we have found that most people with family histories of coagulation abnormalities, strokes, miscarriages, etc- will test positive on at least one of the above screening tests and often times many of them. Using the therapies outlined above most often lead to a return to normal testing within a month’s time. While we cannot be positive what we are accomplishing we think we are making a positive impact on returning the person to a normal state of coagulation and thus helping prevent potentially lethal events in their future health.

There are many lab tests that check for genetic tendencies to hypercoagulate and much controversy exists on interpretation, strategies etc. The recommendations above come from the personal research of one of the above authors who almost died from massive pulmonary embolisms secondary to a West Nile Virus infection in 2011.

Conclusion Screening for hypercoagulation is a quick and easy test that may potentially be life saving for your patients. It is well worth the minute or two it takes and it may help also aid in resolution of certain unresolved symptoms in the chronic patient.


1. Berg D, Berg LH, Couvaras J, Harrison H. Chronic fatigue syndrome &/or fibromyalgia as a variation of antiphospholipid antibody syndrome (APS): An explanatory model and approach to laboratory diagnosis. Blood Coagulation and Fibrinolysis 1999: 10 435-438.

2. "For Patients." Get Involved. UNC Blood Clot Research Program, n.d. Web. 07 Jan. 2013.

3. Pryzdial ELG, Wright JF. Prothrombinase assembly on an enveloped virus: evidence that the CMV surface contains procoagulant phospholipid. Blood 1994; 84 (11):3749-3757.

4. Berg, D., L. H. Berg, J. Couvaras, and H. Harrison. "Chronic Fatigue Syndrome And/or Fibromyalgia as a Variation of Antiphospholipid Antibody Syndrome." Blood Coagulation & Fibrinolysis 10.7 (1999): 435-38. Print.

5. Nicholson AC, Hajjar DP.  Herpes viruses in atherosclerosis and thrombosis: etiologic agents or ubiquitous bystanders? Arteriosclerosis Thromb Vasc Biol 1998; IS: 339-348.

6. Bordia A, Verma SK, Srivastava KC. Effect of ginger (Zingiber officinale Rosc.) and fenugreek (Trigonella foenumgraecum L.) on blood lipids, blood sugar, and platelet aggregation ion patients with coronary heart disease. Prostaglandins Leukot Essent Fatty Acids. 1997;56(5):379-384.

7. Nurtjahja-Tjendraputra, Effie, Alaina J. Ammit, Basil D. Roufogalis, Van H. Tran, and Colin C. Duke. "Effective Anti-platelet and COX-1 Enzyme Inhibitors from Pungent Constituents of Ginger." Thrombosis Research 111.4-5 (2003): 259-65. Print.

8. Teresa Mattiello, Elisabetta Trifirò, Gloria Saccani Jotti, and Fabio M. Pulcinelli. Journal of Medicinal Food. April 2009, 12(2): 334-339. doi:10.1089/jmf.2007.0640.

9. Robertson, Virginia. Studies on Papaya Leaf Tea. N.p.: n.p., n.d. Print.

10. Maurer, H.R. "Bromelain: Biochemistry, Pharmacology and Medical Use." Cellular and Molecular Life Sciences 58.9 (2001): 1234-245. Print.

11. Maurer H. R., Eckert K., Grabowska E., Eschmann K. (2000) Use of bromelain proteases for inhibiting blood coagulation. Patent WO PCT/EP 98/04406

12. Hsia, Chien-Hsun, Ming-Ching Shen, Jen-Shiou Lin, Yao-Ke Wen, Kai-Lin Hwang, Thau-Ming Cham, and Nae-Cherng Yang. "Nattokinase Decreases Plasma Levels of Fibrinogen, Factor VII, and Factor VIII in Human Subjects." Nutrition Research 29.3 (2009): 190-96. Print.

13. Sumi, Hiroyuki, Hiroki Hamada, Koichiro Nakanishi, and Hajime Hiratani. "Enhancement of the Fibrinolytic Activity in Plasma by Oral Administration of Nattokinases." Acta Haematologica 84.3 (1990): 139-43. Print.

14. Sumi H, Hamada  H, Tsushima  H, Mihara  H. Urokinase-like plasminogen  activator increased  in plasma  after  alcohol drinking.  Alcohol 1988;23:33-43.