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In the body, homocysteine can be recycled into methionine or converted into cysteine with the aid of vitamin B 6, B 9, and B 12. [3] High levels of homocysteine in the blood (hyperhomocysteinemia) is regarded as a marker of cardiovascular disease, likely working through atherogenesis, which can result in ischemic injury.
Elevated homocysteine is a known risk factor for cardiovascular disease as well as thrombosis. [7] It has also been shown to be associated with microalbuminuria which is a strong indicator of the risk of future cardiovascular disease and renal dysfunction. [8]
Homocystinuria (HCU) [2] is an inherited disorder of the metabolism of the amino acid methionine due to a deficiency of cystathionine beta synthase or methionine synthase. [3] It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene from both parents to be affected.
Methylenetetrahydrofolate reductase deficiency is the most common genetic cause of elevated serum levels of homocysteine (hyperhomocysteinemia). It is caused by genetic defects in MTHFR, which is an important enzyme in the methyl cycle. [1] Common variants of MTHFR deficiency are asymptomatic and have only minor effects on disease risk. [2]
Deficiency of vitamin B 12 can impair the remethylation of homocysteine in the methionine cycle, and result in raised homocysteine levels. [65] There is much evidence linking elevated homocysteine concentrations with an increased risk of cardiovascular disease, [ 66 ] and homocysteine lowering treatments have led to improvements in ...
This enzyme converts the S-adenosyl homocysteine into the compound homocysteine. Homocysteine may be converted back to methionine or into another amino acid, cysteine. A deficiency of any of these enzymes results in a buildup of methionine in the body, and may cause signs and symptoms related to hypermethioninemia. [citation needed]
McCully K.S., “Homocysteine, folate, vitamin B6 and cardiovascular disease”, Journal of the American Medical Association (1998), 279: pp. 392–393. McCully K.S., “Atherosclerosis, serum cholesterol and the homocysteine theory: a study of 194 consecutive autopsies”, The American Journal of the Medical Sciences.
Elevated homocysteine is an independent risk factor for cardiovascular disease and inversely correlated to consumed vitamin B12/B6 and folate levels. [37] Homocysteine methylation to methionine is catalyzed by MTR, resulting in appropriate intracellular levels of methionine and tetrahydrofolate, alongside non-toxic homocysteine levels.
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