Are B-complex vitamins (i.e., vitamins B12, B9, and B6) effective in primary or secondary prevention of myocardial infarction (MI) or stroke?
Eight randomized clinical trials that included 24,210 patients did not show a reduction in MI, stroke, or all-cause mortality with B-complex vitamin therapy. (Strength of Recommendation = A, based on consistent and good quality patient-oriented evidence)
A high level of circulating total homocysteine is associated with an increased risk of cardiovascular disease. Levels of homocysteine in the blood are influenced by serum levels of vitamins B12, B9, and B6. For example, folic acid (B9) supplementation reduces circulating total homocysteine levels. Therefore, supplementation with B-complex vitamins is plausible as a primary or secondary prevention measure. However, this Cochrane review confirms that supplementation with B-complex vitamins is not an effective strategy for reducing cardiovascular events.
Patients were followed for one to 7.3 years. Results of eight randomized controlled trials were consistent despite different risk factors for cardiovascular disease, baseline total homocysteine levels, access to foods fortified with folic acid, dose of vitamin, and duration of treatment.
Although they acknowledge the lack of evidence, the American Heart Association and American Stroke Association recommend that all persons meet current dietary guidelines for foods rich in folate and vitamins B6 and B12.1,2 They recommend that, given their safety and low cost, supplementation with folic acid and B vitamins may be useful in patients with elevated homocysteine levels.1 For patients who have had an ischemic stroke or transient ischemic attack with hyper-homocysteinemia (i.e., homocysteine levels greater than 1.35 mg per L [10 μmol per L]), they recommend standard vitamin preparations, yet acknowledge that there is no evidence that the vitamins will reduce the occurrence of stroke.2
The authors of this review point out that the United States is the only country with mandatory fortification of foods with folic acid. The justification for this was to modify risk of neural tube defects. Fortification reduced the prevalence of low folic acid levels and either did not change or reduced homocysteine levels. However, it did not influence death from cardiovascular causes, MI, or stroke. On the other hand, high folic acid levels can mask vitamin B12 deficiency. Therefore, the effects of mandatory folic acid fortification deserve further evaluation.