Moderator: ofonorow
Fibrinogen is the main protein involved in the clotting mechanism in the blood plasma, and it also factors directly into how viscous ("thick") the blood is. Fibrinogen can also play a role in how readily the platelets in the blood will stick together and promote the initiation of blood clots. Fibrin, a very important component in the blood clot, results from the direct conversion of fibrinogen when the clotting mechanism in the blood as been initiated.
We have recently presented ascorbate deficiency as the primary cause of human CVD. We proposed that the most frequent pathomechanism leading to the development of atherosclerotic plaques is the deposition of Lp(a) and fibrinogen/fibrin in the ascorbate-deficient vascular wall (1, 2). In the course of this work we discovered that virtually every pathomechanism for human CVD known today can be induced by ascorbate deficiency. Beside the deposition of Lp(a) this includes such seemingly unrelated processes as foam cell formation and decreased reverse-cholesterol transfer, and also peripheral angiopathies in diabetic or homocystinuric patients. We did not accept this observation as a coincidence.
In ascorbate deficiency Lp(a) is selectively retained in the vascular wall. Apo(a) counteracts increased permeability by compensating for collagens, by its binding to fibrin, as a proteinthiol and antioxidant, and as an inhibitor of plasmin-induced proteolysis (1). Moreover, as an adhesive protein apo(a) is effective in tissue-repair processes (8). Chronic ascorbate deficiency leads to a sustained accumulation of Lp(a) in the vascular wall. This leads to the development of atherosclerotic plaques and premature CVD particularly in individuals with genetically determined high plasma Lp(a) levels. Because of its association with apo(a), Lp(a) is the most specific repair particle among all lipoproteins. Lp(a) is predominantly deposited at predisposition sites and it is therefore found to be significantly correlated with coronary, cervical, and cerebral atherosclerosis but not with peripheral vascular disease.
can identify the condition even before a patient experiences noticeable symptoms. This allows physicians to take steps to treat this disease in its earliest stages, before it can cause a heart attack."
Return to “Heart Disease: Linus Pauling's Vitamin C/Lysine Therapy”
Users browsing this forum: Ahrefs [Bot] and 5 guests