Healthy Decisions for the Love of Health

Fibrinogen Levels More Important than Cholesterol in Heart Attack and Stroke Risk

 The blood clotting process: Blood has a natural tendency to clot and does so rapidly if removed from the body. This is normally prevented by natural anti-coagulants, the most powerful of which is heparin, stored mostly in the liver and lungs. However, there are times when clotting is essential, for example to stem the loss of blood in cases of tissue injury. There are three phases of clotting following injury:

  • the vasoconstriction phase
  • the platelet phase (divided into adhesion, activation and aggregation stages)
  • the coagulation phase

The vasoconstriction phase refers to blood vessels clamping shut following damage by contraction of their muscle walls. It is brought about by chemicals released at the site of injury and by nerve impulses arising from the pain response. This is followed by the platelet phase in which platelets clump together and form a platelet plug. If this fails to control blood loss, then the coagulation phase is triggered in which a complex cascade of reactions leads to the formation of an insoluble blood clot. If clotting happens abnormally inside a blood vessel, then the resulting thrombus can restrict or block blood flow, resulting in a heart attack, a stroke or another problem.

The platelet phase is central to thrombus formation inside blood vessels. Important triggers of platelet aggregation are found in the wall of blood vessels, especially a substance called collagen, a main constituent of many body tissues. Normally, collagen is separated from the platelets by the inner lining of cells, rather like the teflon coating in a frying pan, which prevents platelet triggering.

Damage to the cell lining by plaque often exposes collagen, to which platelets stick, using specialised receptors (the adhesion stage). This activates the platelets and they change shape, putting out extensions which cover the exposed or damaged collagen areas. In the process, they come into close contact with each other and chemicals called adenosine diphosphate (ADP) and thromboxane A2 (TXA2) are released (the activation stage). These substances attract other platelets and cause them to bind fibrin from the blood to their so-called GPIIb/IIIa receptors, to stick together and add to the growing blood clot (the aggregation stage).

The coagulation phase is very complex, but ends with the conversion of a protein dissolved in the blood called fibrinogen into insoluble hair-like strands of fibrin. This is brought about by the enzyme thrombin. The fibrin entangles platelets and red blood cells into a solid mass.

Plasmin, a thrombolytic (clot-dissolving) enzyme, is made from plasminogen through the action of an enzyme, tissue plasminogen activator (TPA). Thromobolytic enzymes are produced in blood vessel linings, and their production drops with age. To make matters worse, even in healthy people fibrinogen levels rise by 25 mg/dl per decade.2 “There are several pathways by which acute or chronic increase in fibrinogen levels can lead to a cardiovascular [or cerebrovascular] event…, including…increased platelet aggregation and thrombus formation, and increased fibrin formation.”

In other words, high fibrinogen levels tend to promote the spontaneous formation of unnecessary fibrin-clots. High fibrinogen (and thus implicitly, high fibrin) levels are such a serious risk factor for heart attacks and strokes that one major study of 2,116 men found that those who had high LDL (“bad”) cholesterol—but low fibrinogen levels—had only one-sixth the heart attack risk of men with high LDL and high fibrinogen levels.

Checking your fibrinogen level during your regular blood test is essential, according to many experts. Fibrinogen is a protein produced by the liver and it plays a role in development of atherosclerotic plaque and can contribute to acute blood clot formation, which can cause a heart attack or ischemic stroke. Reports link elevated fibrinogen levels to increased heart attack risk and stroke risk.

The standard reference range for fibrinogen is 193-423 mg/dL. But studies have shown that those with fibrinogen levels of 300 or more are at greatly increased risk for heart attack, stroke and cardiovascular disease. The ideal range for health is a fibrinogen level of 200-300 mg/dL.

Increased rates of cancer incidence are also found in those with high fibrinogen levels. Fibrinogen is the precurser to fibrin, which cancer cells use to coat themselves in order to hide from the immune system. Fibrin also is part of a signaling system to cancer cells to begin antiogenesis, the growth of new blood vessels into the tumor, which contributes to the growth and spread of the tumor.

Compounds that can help lower fibrinogen levels include: fish oil, olive oil, carotenoid complex, folic acid, B12, B6, green tea, ginkgo. There are other helpful compounds and specific herbal medicines.

Serrapeptase, is one of the many potent proteolytic enzymes available today that exhibits an unusually high fibrinolytic activity and is generally well-tolerated.* This enzyme breaks down "non living" matter in the human body. This action may promote a reduction in levels of dead tissue, and may also promote normal mucous levels both in the sinus and lung.* Serrapeptase is a super protein digesting enzyme which has many implications as to its high level of performance.* 

Copyright © 2005 HealthSmart Nutrition. All rights reserved.
Revised: June 24, 2006

Target Stroke - Stroke and the pharmaceutical industry
placeholder image
placeholder image