Homocysteine is a naturally occurring, sulfur containing amino acid, formed from methionine, an essential amino acid, via transmethylation. Homocysteine may be irreversibly metabolized to cysteine or can be converted back to methionine by transfer a methyl group from a derivative of the vitamin, folic acid) in a reaction that involves Vitamin B12.
Experiments on arteries of both animals and humans with an elevated level of homocysteine showed that homocysteine level in blood is an independent risk factor for atherosclerotic vascular disease affecting the coronary (arteries supplying the heart), cerebral (arteries supplying the brain) and peripheral arteries (supplying the rest of the body). Homocysteine contributes to in many ways that lead to this disease.
Homocysteine prevents small arteries from dilating, thereby making them more vulnerable to obstruction by clot or plaque
Homocysteine changes coagulation factor levels, which encourages blood clot formation
Homocysteine generates superoxide and hydrogen peroxide, both of which have been linked to damage the endothelial lining of arterial vessels.
Homocysteine causes the smooth muscle cells that support the arterial wall to multiply, which is part of the narrowing process.
In its reactive form, homocysteine thiolactone, causes platelets to aggregate, which is part of the clotting process.
The active form of excess homocysteine reacts with Low Density Lipoprotein (LDL, which is sometimes referred to as the ‘bad’ cholesterol) to form LDL-homocysteine thiolactone aggregates. These are taken up by macrophages, which in turn promotes atherothrombosis.
Elevated homocysteine levels also may be associated with spina bifida. rheumatoid arthritis and some cancers. Elevated homocysteine levels, has inverse relationship to the plasma levels of both folate and vitamin B12. Dietary supplementation with foIic acid B 12 and B6 reduces the plasma homocysteine levels by about 30% in almost all subjects.
Who should have their Homocysteine level tested?
“Anyone who has early symptoms or strong family history of atherosclerosis should be screened for elevated homocysteine”
“In populations with low plasma levels of vitamin B6, vitamin B12 and folic acid, homocysteine levels and incidence of atherosclerosis are high”
Homocysteine occurs in plasma as the free thiol (free homocysteine about 1%), its symmetrical disulfide (homocysteine) asymmetrical disulfide and conjugated with protein through disulfide link-age. The bulk of plasma homocysteine thus occurs in conjugated form, making it inaccessible to common analytical techniques. Sample must therefore be treated with reacting agent before analysis to liberate homocysteine as the free thiol.
A study on about 600 Norwegian patients with coronary heart disease, heart attacks and deaths rose in straight line relation to plasma homocysteine level. In other words, the higher the homocysteine the higher the risk for death from heart disease. (Stampfer MJ. Malinow MR- Willett WC, et al. A prospective study of plasma homocysteine and risk of myocardial infarction in US physicians. JAMA. 1992:268-877-881.)
An international study of healthy middle aged men from 11 countries convincingly shows that the risk of dying from arteriosclerotic cardiovascular disease (ACVD) increased with average homocysteine level in a given nation. (Alfthan G. Aro A. Gey KF. Plasma Homocysteine and cardiovascular disease mortality. Lancet 1997:349:397.)
For each 5-umolA increase in blood homocysteine content, the risk of middle-aged men dying of ischemic heart diseases by one third. (Wald NJ, Watt HC. Law MR- et al. homocysteine and ischemic heart disease: results of prospective study with implications regarding prevention. Arch lnternal Med. 1998:158:862-867.)
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