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As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B 6, folic acid (vitamin B 9), and vitamin B 12 can lead to high homocysteine levels. [2] Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases. [3]
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.
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]
Blood tests may show low levels of vitamin B 12, elevated levels of methylmalonic acid or homocysteine, and a routine complete blood counts may shows anemia with an elevated mean cell volume. [141] The presence of antibodies to gastric parietal cells and intrinsic factor may indicate pernicious anemia. [2]
Otherwise, causes may include increased needs as with pregnancy, and in those with shortened red blood cell lifespan. [1] Folate deficiency can be secondary to vitamin B 12 deficiency or a defect in homocysteine methyl transferase that leads to a "folate trap" in which is an inactive metabolite that cannot be recovered. [1]
Both adults and children need folate to make normal red and white blood cells and prevent anemia, which causes fatigue, weakness, and inability to concentrate. [115] [116] Increased homocysteine levels suggest tissue folate deficiency, but homocysteine is also affected by vitamin B 12 and vitamin B 6, renal function, and
A new survey found that 1 in 5 adults “who say they have no personal or family history of heart attack or stroke,” reported “routinely” taking a low-dose aspirin
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.