Synopsis

Source of validity: Scientific
Rating (out of 5): 2

Vitamin B12 (hydroxycobalamin) has been investigated for its role in cardiovascular disease (CVD) primarily due to its involvement in homocysteine metabolism. Elevated homocysteine levels are an independent risk factor for CVD, as they are associated with endothelial dysfunction and atherosclerosis. Vitamin B12, along with folate and vitamin B6, is required for the conversion of homocysteine to methionine, thereby lowering plasma homocysteine levels.

Several randomized controlled trials and meta-analyses have demonstrated that supplementation with vitamin B12 (often in combination with folic acid and B6) can lower homocysteine concentrations. However, despite this biochemical effect, large-scale clinical trials—including the HOPE-2 and NORVIT studies—have not shown that reducing homocysteine with B vitamin supplementation translates to a significant reduction in major cardiovascular events such as myocardial infarction, stroke, or cardiovascular mortality in the general population.

Therefore, while there is scientific evidence supporting vitamin B12’s effect on homocysteine metabolism (a CVD risk marker), there is only weak evidence that this translates into meaningful clinical benefits for cardiovascular outcomes. Supplementation may be justified in individuals with documented B12 deficiency, which itself can be associated with increased homocysteine and other health issues, but routine use in CVD prevention or treatment in the absence of deficiency is not strongly supported by current evidence.

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