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