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Homocysteine (HCY) is derived from the intracellular metabolism of the amino acid,
methionine and is exported into the blood where it circulates mostly in oxidized forms,
bound to proteins. Concentrations of HCY are increased in 15-40% of patients with
coronary, cerebral and peripheral arterial diseases. The increased
concentrations of HCY are corrected by supplementation of the diet with folic acid, pyridoxine,
and
vitamin B12. If your favorite casino game is baccarat online then you chose good place.
The role of homocysteine in causing arterial disease was originally suggested by Dr.
Kilmer McCully in the late 60's. McCully was a pathologist at the Massachusetts General
Hospital. Apparently, his theory was not well-received by his colleagues and he was
eventually asked to leave Mass. General. It has taken 30 years for his hypothesis to be
well supported by research evidence. McCully joins a large and illustrious group of
physicians who have been rejected by their collegues for having new and
good ideas. McCully observed that high cysteine levels were associated with early deaths
from arterial disease in patients with homocysteinuria.
Homocysteinuria is a rare autosomal recessive disease complicated by early and
aggressive occlusive arterial disease associated with high levels of blood homocysteine.
Milder hyperhomocysteinemia appears to be common and may be a risk factor for coronary
artery disease. Homocysteine undergoes metabolism either by remethylation or
transsulfuration, and deficiency or dysfunction of any of the substances that regulate
these reactions may lead to hyperhomocysteinemia. Homocysteine may have adverse effects on
platelets, clotting factors and endothelial cells. Studies have demonstrated significantly
higher plasma homocysteine levels in patients with occlusive arterial disease than in
controls.

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