Deficiencies in B6, B12 and folate are mc non genetic causes of elevated ___________

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Multiple Choice

Deficiencies in B6, B12 and folate are mc non genetic causes of elevated ___________

Explanation:
Homocysteine levels rise when the body’s ways of removing it from metabolism are slowed. Those removal pathways depend on vitamins B6, B12, and folate. For remethylation, folate (as 5-methyl-THF) and vitamin B12 are required to convert homocysteine back to methionine. For the transsulfuration route, vitamin B6 is needed to turn homocysteine into cystathionine. If any of these vitamins are deficient, the pathways don’t work efficiently, causing homocysteine to accumulate in the blood. This makes elevated homocysteine the most common non-genetic cause of hyperhomocysteinemia. Other options—bilirubin reflects liver function or hemolysis, while calcium and potassium are not directly tied to homocysteine metabolism. Clinically, high homocysteine is a marker of these vitamin deficiencies and is associated with cardiovascular risk.

Homocysteine levels rise when the body’s ways of removing it from metabolism are slowed. Those removal pathways depend on vitamins B6, B12, and folate. For remethylation, folate (as 5-methyl-THF) and vitamin B12 are required to convert homocysteine back to methionine. For the transsulfuration route, vitamin B6 is needed to turn homocysteine into cystathionine. If any of these vitamins are deficient, the pathways don’t work efficiently, causing homocysteine to accumulate in the blood. This makes elevated homocysteine the most common non-genetic cause of hyperhomocysteinemia. Other options—bilirubin reflects liver function or hemolysis, while calcium and potassium are not directly tied to homocysteine metabolism. Clinically, high homocysteine is a marker of these vitamin deficiencies and is associated with cardiovascular risk.

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