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[1] By normalising homocysteine levels, B12 supplementation may reduce this toxic burden and support nerve recovery
This page is for general educational purposes only and is not medical advice
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Reference: Nicotinamide N-Methyltransferase in Cardiovascular Diseases: Metabolic Regulator and Emerging Therapeutic Target (2025)
One possible explanation is that low serum vitamin B12 levels would trap folate as 5-methyltetrahydrofolate, prevent the generation of methionine from homocysteine, and therefore reduce protein synthesis and lean tissue deposition
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