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The proposed mechanism for hyperhomocysteinaemia on inducing endothelial dysfunction and thus atherosclerosis includes homocysteine-induced endoplasmic reticulum stress, oxidative stress, and proinflammatory response.48 Animal models of hyperhomocysteinaemia have confirmed the causal relationship between hyperhomocysteinaemia and the development of endothelial dysfunction and accelerated atherosclerosis.48 Although meta-analyses have shown reduction of cardiovascular risk with reduction of homocysteine levels,46 47 vitamin supplementation (with vitamin B 6 , vitamin B 12 , and folic acid) to lower homocysteine in the body may not be transformed into clinically beneficial vascular outcomes

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As a result, it can take more than 48 hours for cyanocobalamin to eventually convert to usable B12, and even then only a small amount of converted and absorbed