Fibrinogen (Blood Clots) Support -- Bromelain Enzyme

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Fibrinogen (Blood Clots) Support -- Pineapple Enzyme
Reprinted by permission from Bill Faloon of The Life Extension Foundation

Blood clots that form inside arteries are the leading cause of death in the Western world.  Most heart attacks and strokes are caused by a blood clot that obstructs the flow of blood to a portion of the heart or the brain.  No blood flow, and thus no oxygen, means no life to the heart or brain cells.  Blood clots kill more than 600,000 Americans every year.

Low-dose aspirin and certain nutrients provide partial protection against abnormal blood clots, but a newly identified clotting factor, fibrinogen, mandates that additional measures be taken to prevent heart attack and stoke.  High levels of fibrinogen predispose a person to coronary and cerebral artery disease, even when other known risk factors such as cholesterol are low.

Fibrinogen elevation in cigarette smokers, for example, has been identified as a primary mechanism causing heart disease and stroke.  Cigarette smoking increases cardiovascular disease risk and it raises fibrinogen levels in the blood.  Published studies documenting the dangers of cigarette smoking show that cigarette smokers who suffer from cardiovascular disease also have high fibrinogen levels.  In fact, high fibrinogen levels may be a more powerful predictor of cardiovascular mortality than cigarette smoking itself.

The role of fibrinogen in the development of cardiovascular disease has been fully confirmed by the results of all relevant studies conducted during the past 10 years.  High fibrinogen levels have at least as great a predictive value as any other known risk factor, such as elevated LDL cholesterol, elevated triglycerides, obesity and diabetes.

In persons with a family history of heart disease, fibrinogen levels are high.  Fibrinogen levels are primarily genetically inherited, meaning that fibrinogen may be the genetic factor causing familial premature heart disease.  Also, exposure to cold increases fibrinogen levels by 23 percent, and mortality from heart attack and stroke are higher in winter than in summer.

Fibrinogen hinders blood flow and oxygen delivery by deforming red blood cells, causing red-cell aggregation and a thickening of the blood, all of which lead to diminished circulation.  Fibrinogen binds blood platelets together, thus initiating abnormal arterial blood clots.  Fibrinogen is then converted to fibrin, which is the final step in the blood-clotting cascade.

Fibrinogen contributes to the development of atherosclerosis by incorporating itself into the arterial plaque.  Further, fibrinogen and LDL cholesterol work together to generate atherosclerotic plaques.  Fibrinogen initiates the atherosclerotic plaque, then converts to fibrin and serves as a scaffold for LDL cholesterol in the atherosclerotic plaque that slowly occludes an artery.

Fibrinogen and its derivatives trigger a variety of other mechanisms thought to be involved in the atherosclerotic process.  Fibrinogen and LDL cholesterol have a synergistic effect in promoting atherosclerosis, though fibrinogen may play a more important role in the development of atherosclerotic lesions.

Most heart attacks occur because a blood clot forms inside a coronary artery and chokes off the blood supply to the heart.  Most strokes, on the other hand, occur because a blood clot forms inside a cerebral artery and blocks the blood supply to the brain.  In either case, it is crucial to take steps to reduce the risk of fibrinogen causing an abnormal arterial clot.

Platelet-aggregation inhibitors reduce the risk that fibrinogen will cause an abnormal blood clot.  Platelet-aggregation inhibitors include aspirin, green tea, ginkgo biloba and vitamin E.  For optimal protection against the formation of arterial blood clots, it makes sense to utilize therapies that support lowering elevated fibrinogen levels.

In addition, high vitamin A and beta-carotene serum (blood) levels have been associated with reduced fibrinogen levels in humans.  For example, animals fed a vitamin A deficient diet have an impaired ability to break down fibrinogen, but when they are injected with Vitamin A, they produce tissue plasminogen activator that breaks down fibrinogen.  In addition, omega 3 fatty acids have been shown to support the lowering of fibrinogen in women with elevated fibrinogen levels.  The daily amount of omega 3 fatty acids required to produce a fibrinogen-lowering effect is 6 grams.

Elevated homocysteine levels have been shown to block the natural breakdown of fibrinogen by inhibiting the production of tissue plasminogen activator.  Folic acid and vitamin-B6 (included in Life Extension Mix -- LEM) show strong implications that may help reduce elevated homocysteine levels.

One of the more interesting studies involved the use of vitamin C to break down excess fibrinogen.  In a report published in the journal Atherosclerosis, heart-disease patients were given either 1,000 or 2,000 mg a day of vitamin C to assess its effect on the breakdown of fibrinogen.  At 1,000 mg a day, there was no detectable change in fibrinolytic activity (fibrinogen breakdown) or cholesterol.  At 2,000 mg a day of vitamin C, however, there was a 27-percent decrease in the platelet-aggregation index, a 12-percent reduction in total cholesterol, and a 45-percent increase in fibrinolytic activity.

For maximum fibrinogen-lowering support, the proteolytic enzyme bromelain may be the most effective nutrient supplement.  For those seeking to lower elevated fibrinogen levels, two to six capsules a day of standardized bromelain should be considered.

Some non-pharmacologic ways of lowering fibrinogen include stopping smoking, avoiding obesity, lowering LDL cholesterol and avoiding exposure to cold.

A European drug called Bezafibrate has been shown to lower fibrinogen levels by 25 percent in patients with fibrinogen levels between 300 and 415 mg/dL.  In patients whose fibrinogen levels were over 600, Bezafibrate lowered fibrinogen levels by 45 percent.  Bezafibrate has been used extensively in Europe since 1978 to lower LDL cholesterol by 20 to 30 percent, and increase beneficial HDL cholesterol.  It has more than 9 million patient-years of safety documentation.

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Caution:  Individuals who are taking blood-thinning medications should consult with their health care provider before taking bromelain.  Bromelain may enhance the anticoagulant activity of drugs such as warfarin and the antithrombotic activity of such drugs as aspirin.

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