Homocysteine is a sulphur-containing amino acid and is an intermediate metabolite of methionine metabolism.
Homocysteine is a well-known cardiovascular disease risk factor.
– Metabolized by two pathways; trans-methylation and trans-sulphation pathways.
– Regulation of homocysteine depends on certain key nutrients, including vitamin B12, vitamin B6 and folic acid.
– High homocysteine levels are an important biomarker in risk assessment for CVD, strokes and other inflammatory diseases.
– Functional biomarker for low B6, B9 and B12; also excess methionine.
– It may also give indications of polymorphisms affecting methylation
Age, gender, folate, serum vitamin B12, serum creatinine and multivitamin usage are determinants of plasma homocysteine concentration. In population studies, total plasma homocysteine concentrations are higher in men than in women, increase markedly with age and are inversely correlated with blood folate, serum vitamin B12 and serum creatinine. Users of multivitamins have a lower homocysteine levels than nonusers.
Although high plasma homocysteine is widely recognized as a cardiovascular disease risk factor, individuals with low homocysteine are also at risk of other conditions related to sulfur amino acid metabolism. The risk of hypohomocysteinemia derives from the fact that homocysteine is the normal precursor for formation of cysteine and thus production of glutathione, taurine and sulfate from methionine.
Individuals with low homocysteine have limited capacity for up-regulation of glutathione synthesis in response to oxidative stress and certain kinds of toxin exposure. The most common treatment for low homocysteine is administration of sulfur-containing amino acids such as N-acetylcysteine and taurine. Preformed glutathione and inorganic sulfate salts (postassium salts) may also be employed to support hepatic and renal demands for toxin removal through sulfation and mercaptan formation.
Hypohomocysteinemia causes reduced availability of cysteine. Cysteine restriction causes limitation in production of sulfate, taurine and glutathione. The limited production ability is exacerbated in conditions that cause increased demand for any of the sulfur compounds produced from homocysteine, such as alcohol intake.
The most common dietary deficiency leading to homocysteine elevation and the associated increase in heart disease risk involves vitamin B12 and folic acid. You can have normal blood levels of these vitamins but still not have enough for your body’s enzymes to function properly. Dietary deficiency of vitamin B12 and folic acid are associated with increased risk of many diseases, including anemia and the associated chronic fatigue.
Vitamin B6 deficiency may also result in elevated concentrations of homocysteine in blood, which leads to increased risk of heart disease.
A high level of homocysteine in the blood (hyperhomocysteinemia) makes a person more prone to endothelial cell injury, which leads to inflammation in the blood vessels, which in turn may lead to atherogenesis, which can result in ischemic injury. Abnormally high levels of homocysteine in the serum, above 15 µmol/L, are a medical condition called hyperhomocysteinemia.
Hyperhomocysteinemia is a possible risk factor for coronary artery disease. Coronary artery disease occurs when an atherosclerotic plaque blocks blood flow to the coronary arteries, which supply the heart with oxygenated blood.
High levels of homocysteine can also be a risk factor for the development of a wide range of diseases, including thrombosis, neuropsychiatric illness, and fractures.
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