Can vitamin E affect the overall risk of heart failure?

March 28, 2012

According to new US research, long-term increased vitamin E intake may not be associated with a reduced risk of developing systolic heart failure but may help against diastolic heart failure by 40% in healthy women.

To examine the potential effect of vitamin E on heart failure risk, vitamin intakes and cases of heart failure were examined in a randomized controlled trial including 39,815 initially healthy women (mean age 54.6 years) who received 600 IU vitamin E every other day or placebo over a median of 10.2 years (1). The study results showed that there was no significant difference in the incidence of heart failure (HF) between the vitamin E and placebo groups. However, although vitamin E did not influence the risk of developing systolic HF, it was associated with a significant 40% reduction in the risk of developing diastolic HF.

The researchers commented that this is the only data available regarding the influence of vitamin E on HF risk in apparently healthy people ( primary prevention). The findings differed from prior data from a clinical trial with patients (comparatively small population of women) with preexisting vascular disease or diabetes ( secondary prevention) speculating that vitamin E supplementation has no effect or even may increase HF risk (2). Potential protective effects of vitamin E on diastolic HF needed to be confirmed in additional clinical trials, according to the researchers.

Experts commented that several factors may explain the inconclusive outcomes of vitamin E supplementation in human studies, in particular, the relatively short duration of supplementation (3). Furthermore, it would be a miscalculation to expect additional preventive effects from supplementation in cases where high baseline levels of vitamin E in the normal diet are sufficient to prevent disease (4). The dosage of antioxidant vitamin E supplementation moreover may have been too low, since a detectable reduction in the biomarkers of oxidative damage has only been achieved with much higher doses of vitamin E (>1600 IU) than those used in most primary and secondary prevention studies (5,6). The potential health effects of vitamin E supplemen-tation may become evident only under specific environmental and patho-physiological circumstances, such as local depletion of vitamin E by free radicals associated with inflammation, infection, smoking or UV irradiation.

Heart failure (HF)with normal ejection fraction, where the primary abnormality is related to diastolic dysfunc-tion or impaired relaxation, represents approximately half of all cases of the disease. Diastolic HF is increasing in prevalence and is more common in women than in men. Although associated with similar biological disorders and adverse prognosis to those of systolic HF, fewer effective therapies exist. Recent animal studies have demonstrated that oxidative stress may play an important role in diastolic dysfunction and that therapies with antioxidants such as vitamin E may improve diastolic performance in conditions including hypertension, insulin resistance and diabetes, and hypercholesterolemia (7,8).


  1. Chae C. U. et al. Vitamin E Supplementation and the Risk of Heart Failure in Women. Circ Heart Fail. 2012; 5:176–182.
  2. Lonn E. et al. HOPE and HOPE-TOO Trial Investigators. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. JAMA. 2005; 293:1338–1347.
  3. Hayden K. M. et al. Risk of mortality with vitamin E supplements: the Cache County study. Am J Med. 2007; 120:180–184.
  4. Robinson I. et al. Vitamin E in humans: an explanation of clinical trial failure. Endocr Pract. 2006; 12:576–582.
  5. Roberts 2nd L. J. et al. The relationship between dose of vitamin E and suppression of oxidative stress in humans. Free Radic Biol Med. 2007; 43:1388–1393.
  6. Devaraj S. et al. Effect of high-dose alpha-tocopherol supplementation on biomarkers of oxidative stress and inflammation and carotid atherosclerosis in patients with coronary artery disease. Am J Clin Nutr. 2007; 86:1392–1398.
  7. Silberman G. A. et al. Uncoupled cardiac nitric oxide synthase mediates diastolic dysfunction. Circulation. 2010; 121:519–528.
  8. Zhou Z. et al. Nebivolol improves diastolic dysfunction and myocardial remodeling through reductions in oxidative stress in the Zucker obese rat. Hypertension. 2010; 55:880–888.