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Multivitamins and Cardiovascular Disease (CVD)

Introduction

Evidence from large-scale observational studies suggests that multivitamin use may have a positive effect on the development of cardiovascular disease, but no impact on mortality. No intervention studies directly examining the effect of multivitamins on CVD risk have been published, although a limited number of clinical trials have shown an improved risk factor profile.

Epidemiological Studies

Rimm et al. [1] first reported a significant reduction in coronary events with multivitamin use in their 14 y follow up study of 80,082 females from the Nurses’ Health Study who had no history of cancer, angina, MI, stroke, CVD, hypercholesterolemia or diabetes at baseline. More recently, Osganian et al. [2] reported a significantly lower risk of CHD with the use of multivitamins and other dietary supplements containing vitamin C in women from the same cohort.

Large-scale observational studies by Muntwyler et al. [3] and Watkins et al. [4], reported no effect on CVD or CHD mortality with multivitamin use. However, the multivariate adjusted risk for multivitamin users who reported a history of ischemic heart disease in the Watkins et al. study was significantly lower than in non-users. In addition, multivitamin use combined with antioxidant supplements (carotenoids and/or vitamins C or E) reduced ischemic heart disease and stroke mortality by 15%. In their review of the available evidence regarding the effectiveness of vitamin supplementation in preventing CVD, Morris and Carson [5] attributed the discrepancies in these results to unreported differences in the multivitamin combinations used.

Results from the Stockholm Heart Epidemiology Program (SHEEP) study [6]indicate that the use of dietary supplements may aid in the primary prevention of myocardial infarction (MI). The most commonly reported dietary supplement among users in this study (80%) was a multivitamin preparation formulated at ~ 100% DV.

In a prospective cohort study of 51,529 male health professionals enrolled in the Physicians’ Health study, Merchant et al. [7] observed an inverse association between folate intake from supplements and peripheral artery disease (PAD) risk. The primary source of supplemental folate in this study was a multivitamin supplement.

Multivitamin use has also been associated with low homocysteine concentrations in several observational studies [8-10], and lower levels of interleukin (IL) -6, a marker of the inflammatory process associated with atherosclerotic cardiovascular disease (ACVD) and its clinical sequelae [11].

Clinical Trials

In a randomized, placebo controlled clinical trial of a 100% DV multivitamin/mineral preparation, McKay et al.[12] demonstrated the effectiveness of this formulation in reducing total plasma homocysteine levels among healthy older adults who were already consuming a folate fortified diet. There is, however, no conclusive evidence that lowering homocysteine levels reduces CVD risk.

In this same study, multivitamin supplementation also elevated the mean serum vitamin E concentration of subjects to a level (> 30 μmol/L) often associated with CVD prevention [13-14] and improved folate and vitamin B6 status to levels associated with reduced risk for vascular disease [15].

Critical Thinking Questions

Can the observed effects of supplementation on CVD risk in epidemiological studies be attributed to multivitamins?

Would a long term clinical trial examining the effects of multivitamins on CVD be practical or feasible?

Would the presence of vitamin K in multivitamin supplements interact with oral anticoagulant therapy?

Which micronutrients might be present in multivitamin preparations marketed to “help support a healthy heart?”

Professional Societies, Agencies, and Government Organizations:

American Heart Association
http://www.americanheart.org/presenter.jhtml?identifier=4788
U.S. Preventive Services Task Force http://www.aafp.org/afp/20031215/usx.html