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Vitamin E

Vitamin E is a fat-soluble antioxidant that stops the production of free radicals formed when fat undergoes oxidation. Researchers are still trying to determine if reducing free radical production can prevent or delay chronic diseases associated with free radical production. Many claims have been made about vitamin E’s ability to promote health and prevent and treat disease. The following discussion reviews the role of vitamin E as it pertains to heart disease and cognitive decline.

Vitamin E and Cardiovascular Diseases

Initially, it appeared that vitamin E could prevent or delay coronary heart disease (CHD). In vitro studies demonstrated Vitamin E inhibits oxidation of low-density lipoprotein (LDL) cholesterol [1]. LDL is the “bad” form of cholesterol and its oxidation is considered a crucial initiating step for atherosclerosis. Vitamin E may also have the ability to prevent the formation of blood clots which could lead to a heart attack or venous occlusion [2].

Epidemiologic studies have attributed lower rates of heart disease with higher vitamin E intakes. One study consisting of about 90,000 nurses discovered the incidence of heart disease was 30% to 40% lower in those with the highest intakes of vitamin E supplements [3]. Another study involved 5,133 Finnish people who were followed for an average of 14 years. It found higher vitamin E intakes from food was associated with decreased mortality from CHD [4].

Randomized clinical trials, however, do not demonstrate the ability of vitamin E supplements to prevent CHD [5]. For example, the Heart Outcomes Prevention Evaluation (HOPE) study, examined approximately 10,000 patients at high risk of heart attack or stroke for 4.5 years [6]. Subjects taking 400 IU/day of natural vitamin E experienced no fewer cardiovascular events than subjects taking a placebo. In the HOPE-TOO follow up study, about 4,000 of the original subjects remained on vitamin E or placebo for 2.5 more years [7]. This study determined that vitamin E provided no significant protection against heart attacks, strokes, unstable angina, or deaths from cardiovascular disease or other causes after a total of seven years of treatment.

Both of these trials (HOPE and HOPE-TOO) found that even moderately high doses of vitamin E supplements did not reduce the risk of serious cardiovascular events among men and women older than 50 with established heart disease or diabetes [8]. These studies are reinforced by findings from the Women’s Angiographic Vitamin and Estrogen study, in which 400 IU vitamin E and 500 mg vitamin C twice a day or placebo was given for more than four years to 423 postmenopausal women with some degree of coronary stenosis [9]. This study again demonstrated no cardiovascular benefits from vitamin E supplementation. Another clinical trial included almost 40,000 healthy women 45 years or older who were randomly assigned to receive either 600 IU of natural vitamin E on alternate days or placebo, and were followed for an average of 10 years [10]. No significant differences in rates of overall cardiovascular events were found.

A recent published clinical trial of vitamin E and men’s cardiovascular health involved almost 15,000 healthy physicians 50 years of age who were randomly assigned to receive 400 IU synthetic alpha-tocopherol every other day, 500 mg vitamin C daily, both vitamins, or placebo [11]. This study demonstrated neither vitamin E nor vitamin C reduced the incidence of major cardiovascular events, myocardial infarction, stroke, or cardiovascular morality.

Based on this data, one could surmise that clinical trials generally have not provided evidence that routine use of vitamin E supplements can prevent cardiovascular disease or reduce morbidity and mortality. Yet the subjects in these studies have been largely middle-aged or elderly individuals who had heart disease or risk factors for heart disease. Scientists have suggested that longer studies in younger, disease-free participants is required to fully understand the potential utility of vitamin E in preventing CHD [12]. It may be that vitamin E is beneficial in preventing cardiovascular disease and reduces its morbidity and mortality. However, to be beneficial, in may have to be given early in the disease process.

Vitamin E and Neurodegenerative Diseases

Although the brain represents only 2% of the body weight, it actually accounts for 20% of total body oxygen consumption and 25% of total body glucose utilization. Due to its high rate of oxygen consumption and abundant polyunsaturated fatty acids in the neuronal cell membranes, it is highly vulnerable to free radical damage. Researchers have postulated that this cumulative free-radical damage to neurons can contribute to cognitive decline and neurodegenerative diseases, such as Alzheimer’s disease. They also hypothesized that ingestion of supplemental antioxidants such as vitamin E might provide some protection [13].

Vitamin E from foods or supplements was associated with less cognitive decline over three years in a prospective cohort study [14]. An interesting animal study recently demonstrated the effect of vitamin on lipid peroxidation, beta-amyloid levels, and amyloid plaque deposition [15]. Animals that received vitamin E at a younger age showed a reduction in beta-amyloid levels and amyloid plaque deposition. Yet animals receiving vitamin E after amyloid plaque deposition did not demonstrate a significant difference in beta-amyloid levels or amyloid plaque deposition compared to placebo. These findings support the hypothesis that oxidative stress is an early event in the pathogenesis of Alzheimer’s disease and antioxidant therapy. To be beneficial, vitamin E must be given early in the course of the disease process.

 

    1. Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000.
    2. Glynn RJ, Ridker PM, Goldhaber SZ, Zee RY, Buring JE. Effects of random allocation to vitamin E supplementation on the occurrence of venous thromboembolism: report from the Women’s Health Study. Circulation 2007;116:1497-1503.
    3. Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary disease in women. N Engl J Med 1993;328:1444-9.
    4. Knekt P, Reunanen A, Jarvinen R, Seppanen R, Heliovaara M, Aromaa A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study. Am J Epidemiol 1994;139:1180-9.
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  1. Traber MG. Heart disease and single-vitamin supplementation. Am J Clin Nutr 2007;85:293S-9S.
  2. Jialal I, Devaraj S. Vitamin E supplementation and cardiovascular events in high-risk patients. N Engl J Med 2000;342:154-60.
  3. Lonn E, Bosch J, Yusuf S, Sheridan P, Pogue J, Arnold JM, 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;293:1338-47.
  4. Brown BG, Crowley J. Is there any hope for vitamin E? JAMA 2005;293:1387-90.
  5. Waters DD, Alderman EL, Hsia J, Howard BV, Cobb FR, Rogers WJ, et al. Effects of hormone replacement therapy and antioxidant vitamin supplements on coronary atherosclerosis in postmenopausal women: a randomized controlled trial. J Am Med Assoc 2002;288:2432-40.
  6. Lee I-M, Cook NR, Gaziano JM, Gordon D, Ridker PM, Manson JE, et al. Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women’s Health Study: a randomized controlled trial. JAMA 2005;294:56-65.
  7. Sesso HD, Buring JE, Christen WG, Kurth T, Belanger C, MacFadyen J, et al. Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians’ Health Study II randomized controlled trial. JAMA 2008;300:2123-33.
  8. Blumberg JB, Frei B. Why clinical trials of vitamin E and cardiovascular diseases may be fatally flawed. Commentary on “The relationship between dose of vitamin E and suppression of oxidative stress in humans.” Free Radic Biol Med 2007;43:1374-6.
  9. Sano M, Ernesto C, Thomas RG, Klauber MR, Schafer K, Grundman M, et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzehimer’s disease. N Engl J Med 1997;336:1216-22.
  10. Morris MC, Evand DA, Bienias JL, Tangney CC, Wilson RS. Vitamin E and cognitive decline in older persons. Arch Neurol 2002;59:1125-32.
  11. Sung S, Yao Y, Uryr K, Yang H, Lee VM, Trojanowski JQ, Pratico D: Early vitamin E supplementation in young but not aged mice reduces Abeta levels and amlyoid depostition in a transgenic model of AD. FASEB J 2004; 18:323-325