One of the most fascinating aspects of pharmaceutical drugs is that the “method” or “mode of action” of most drugs is unknown. Reading the “Physicians’ Desk Reference” (PDR), which every doctor has in their office, you find “Mode of Action” to which is listed “Unknown”. Instead, one reads phrases like “is believed to cause” or “is thought to act” to describe what is believed, not proven, to be the action of a drug. In other words, no one fully understands or knows how a drug works. And so it is with coumadin. Coumadin “is thought to interfere with clotting factor synthesis by inhibition of the regeneration of vitamin K1 epoxide.”
Coumadin appears to inhibit the effects of Vitamin K. Vitamin K is a group name for protein-related compounds with similar molecular structures. It is necessary for blood clotting as in the healing of a wound or cut. Vitamin K1 is found in dark green, leafy vegetables while K2 is found in animals and bacteria. K2 is manufactured by the beneficial bacteria that inhabit our digestive tract. It has been recently discovered K2 directs calcium into the bones to build proper bone matrix.
This is very important because coumadin causes arterial calcification. An over accumulation of calcium in the arteries leads to plaque, then athersclerosis and can trigger a heart attack or stroke. Everyone on coumadin is expected to be diligent in their vitamin K intake and may even for periods at a time stop foods rich in vitamin K. This can be very stressful on a patient.
More so, here is the irony. Vitamin K prevents calcification in the arteries by moving calcium into the bones. Coumadin can cause arterial calcification. Those on coumadin most often are deficient in the very nutrient (vitamin K) that prevents arterial calcification. In elderly patients on coumadin there is an increased risk of hip fractures and cardiovascular disease because of vitamin K deficiency.
“The effects of coumadin may become more pronounced as effects of daily maintenance doses overlap. Anticoagulants have no direct effect on an established thrombus (blood clot already formed), nor do they reverse ischemic (deficiency of blood and oxygen deprived) tissue damage.”
There is an accumulative affect taking coumadin which poses an additional problem in itself. An accumulation of a blood thinner will lead to a greater chance for bleeding, especially when it interferes with vitamin K dependent clotting factors.
There are a few inherited genetic traits that prevent adequate clotting and need to be tested and considered before deciding to use either anticoagulant drugs or other natural methods for treating potential life-threatening conditions. These include:
|Methylene tetrahydrofolate Reductase (MTHFR) C677T mutation|
|Elevated levels of homocysteine|
|Factor V Leiden R506Q mutation|
|Prothrombin gene mutation|
|“Sticky” platelet syndrome|
|Elevated levels of fibrinogen or dysfunctional fibrinogen (dysfibrinogenemia)|
|Abnormal fibrinolytic system, including hypoplasminogenemia, dysplasmino-genemia and elevation in levels of plasminogen activator inhibitor (PAI-1 )|
|Deficiencies of natural proteins that prevent clotting (such as antithrombin, protein C and protein S)|
|Elevated levels of factor VIII (still being investigated as an inherited condition) and other factors including factor XI|
MTHFR is an inherited failure of utilizing folate (folic acid) from supplementation or food. It represents an inability to methylate. Methylation is a process by which specific chemicals called ‘methyl groups’ are added to DNA, proteins and other molecules. Methyl groups are necessary for a variety of metabolic functions to take place.
One of the more commonly known folic acid deficiency conditions is spina bifida, a type of neural tube disease in fetuses. Folic acid deficiency is known to cause this and supplementation has only recently been recommended for pregnant women. However, if the mother has the MTHFR mutation the fetus may present with this congenital disease because the mother cannot process folic acid properly.
Testing blood homocysteine levels is now used to screen patients for cardiovascular disease. Folate is required for the metabolism of several important amino acids. The synthesis of methionine from homocysteine requires folate coenzyme and a vitamin B12-dependent enzyme. Folate deficiency can result in decreased synthesis of methionine and a buildup of homocysteine. Elevated levels of homocysteine are known to create blood clots and are associated with other chronic diseases.
Healthy individuals use two different pathways to metabolize homocysteine. One pathway synthesizes methionine (a sulfur amino acid) from homocysteine. The other converts homocysteine to another amino acid, cysteine, (sulfur) and requires two other vitamin B6-dependent enzymes. Thus, the amount of homocysteine in the blood is regulated by three vitamins: folate (folic acid), vitamin B12 and vitamin B6.
Those tested with the genetic trait MTHFR, cannot process folate (folic acid) and must use methylated forms of folate (L-5-MTHF) and vitamin B12 (methylcobalamin). These methylated forms assure processing the two B-vitamins and prevent elevated homocysteine levels and may prevent clotting problems.
The Factor V Leiden R506Q mutation and prothrombin gene mutation present a bigger challenge. One might not be able to get off coumadin in these cases, however, finding a hematologist or cardiologist well versed in alternative medicine could help one to minimize the use of coumadin or find a different anti-coagulant drug instead.
Elevated levels of fibrinogen, dysfunctional fibrinogen, abnormal fibrinolytic system, or elevation in levels of plasminogen activator inhibitor, may respond well with use of highly concentrated proteolytic (protein-digesting) enzymes. Fibrinogen is a normal part of human plasma. Fibrin is a protein formed from fibrinogen and is the primary portion of a blood clot. It is like a web “cementing” red blood cells together creating a matrix that seals off damaged tissue. It is essential in the healing process.
However, when there is too much fibrin produced, on-going production of fibrin or the body fails to break it down in a timely manner; clots remain, accumulate and pose life-threatening conditions. This is the danger posed by an abnormal fibrnolytic system. Being protein, however, fibrin can be broken down by the action of supplemental enzymes. Enzymes that have proven fibrinolytic activity are streptokinase, urokinase, and bromelain from pineapple. Added to that are the more powerful enzymes nattokinase from natto (a fermented soy food) and lumbrokinase from red earthworms. The latter have been tested extensively and show excellent results at dissolving blood clots in pulmonary embolisms and deep vein thrombosis.
There are other natural substances listed that affect coumadin. While a few may interfere with coumadin’s actions, others have properties of increasing the thinning action of coumadin. This makes the risk of bleeding much greater.
Omega-3 fats, as found in fish oils, have blood thinning properties as does vitamin E, evening primrose oil, garlic, ginseng and other foods and herbs. Contrary, excessive refined sugar and simple/refined carbohydrate intake, together with an inability to digest proteins and fats efficiently leads to “thick” blood. Platelets become “sticky” as a result and clots can be formed more easily. Using digestive enzymes before meals to improve digestion and reducing or eliminating refined sugar and carbohydrate intake thins the blood. It also stops platelets from sticking together and reduces the potential for clotting.
The question arises, “If food nutrients, herbs and enzymes have anticoagulant and blood thinning actions, why not use them and decrease the amount of coumadin used?” For most doctors, nutritional and other alternative therapies are outside their realm of knowledge. They are not well informed about alternative treatments.
With all the potential dangers posed by coumadin it is worth one’s while to educate yourself to what alternatives are available, especially if you do not have any of the genetic traits. Even then, there are substances, especially enzymes, with proven studies that could be incorporated into a regime with the help of an educated health care professional.
Often patients explore alternatives, especially when their physician will avoid treatments not fitting the “standard of medicine”. In the case of coumadin, patients may be fortunate to find a health care professional willing to work with them.
An excellent monograph is titled “Living with Warfarin” by Hans R. Larsen MSc Ch E. Another is “Vitamin K Functions and Functional Markers” by the company Metagenics. There are many clinical studies available on the therapeutic use of enzymes in cardiovascular disease. Many can be sent via email if you request them from me.
“Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study”; Johanna M. Geleijnse, Cees Vermeer, Diederick E. Grobbee, Leon J. Schurgers, Marjo H. J. Knapen, Irene M. van der Meer, Albert Hofman, and Jacqueline C. M. Witteman; The Journal of Nutrition; August 25, 2005, 3100-3106
“Beyond Deficiency: Potential benefits of increased intakes of vitamin K for bone and vascular health”, Cees Vermeer, Martin J. Shearer, Armin Zittermann, Caroline Bolton-Smith, Pawel Szulc,
Stephen Hodges, Paul Walter, Walter Rambeck, Elisabeth Stocklin, Peter Weber; Eur J Nutr (2004) 43: 325–33
“Vitamin K2”, Alternative Medicine Review Volume 14, Number 3 2009
“Activation of Plasminogen”, Sten Mullertz, Annals New York Academy of Sciences, pg 38-51
“Biochemical, experimental, and clinical studies of proteolytic enzymes: with particular reference to the Fibrinolytic enzyme of human plasma”, Sol Sherry and Norma Alkjaersig; Annals New York Academy of Sciences, pg 52-66
“Clinical and experimental studies on Fibrinolytic enzymes”, Julian L. Ambrus, Clara M. Ambrus, Nathan Back, Joseph E. Sokal, and George L. Collins, Annals New York Academy of Sciences, pg 97-137
“Earthworm Protease”, Rong Pan, Zi-Jian Zhang, and Rong-Qiao He, Applied and Environmental Soil Science Volume 2010, Article ID 294258, 13 pages
“Fibrinolytic activity of earthworms extract (G-90) on lysis of fibrin clots originated from the venous blood of patients with malignant tumors”, Terezija M. Hrzenjak, Maja Popovic, Ljerka Tiska-Rudman, Pathology Oncology Research Vol 4, No 3, 1998, pg 206-211
“Rapid purification and biochemical characteristics of lumbrokinase III from earthworm for use as a fibrinolytic agent”, Yong-Doo Park, Jong-Won Kim, Byong-Goo Min, Jeong-Won Seo, and Jong-Moon Jeong, Biotechnology Letters, Vol 20, NO 2, February 1998, pp. 169-172
“Studies on the Thrombolytic Activity of a Protease from Aspergillus Oryzae”, Rolf Bergkvist, and Par Olvo Svard, Acta Physiol. Scand 1964, Vol 60, pg 363-371
“Effects of Omega-3 fatty acids, especially considering their impact on blood coagulation”, Jasmin Stieger, University of Salzburg
“Variable Hypocoagulant Effect of Fish Oil Intake in Humans: Modulation of Fibrinogen Level and Thrombin Generation”, Kristof Vanschoonbeek, Marion A.H. Feijge, Martine Paquay, Jan Rosing, Wim Saris, Cornelis Kluft, Peter L.A. Giesen, Moniek P.M. de Maat and Johan W.M. Heemskerk, Arterioscler Thromb Vasc Biol 2004;24;1734-1740
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