The clinical and nutritional strategy aimed at lowering elevated plasma levels of the non-protein amino acid homocysteine, which is a metabolic byproduct of the methionine cycle. High homocysteine levels are considered a risk factor for cardiovascular disease, neurodegenerative conditions, and poor pregnancy outcomes due to its potential to damage the endothelial lining of blood vessels. Reduction is typically achieved through targeted supplementation with B vitamins, specifically folate (B9), B12, and B6, which are essential cofactors in its metabolic breakdown. This intervention is a focus of preventative medicine.
Origin
The concept gained prominence following the discovery of homocystinuria, a genetic disorder causing extreme elevation of homocysteine, and subsequent epidemiological studies linking moderate elevation to vascular risk. ‘Homocysteine’ is the name of the metabolite, and ‘reduction’ refers to the therapeutic goal of decreasing its concentration. This area of study bridges nutritional biochemistry and cardiovascular endocrinology.
Mechanism
Homocysteine is metabolized primarily through two pathways: remethylation to methionine or transsulfuration to cysteine. The remethylation pathway is catalyzed by methionine synthase, which requires vitamin B12 and methyl-tetrahydrofolate (the active form of folate). The transsulfuration pathway requires vitamin B6. Therefore, supplementation with these B vitamins provides the necessary cofactors to accelerate the conversion of toxic homocysteine into benign products, effectively lowering its plasma concentration and mitigating its pathological effects on vascular health.
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