Therapeutic Uses of Vitamin E
in Prevention of Atherosclerosis

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:    Frankp@chiro.org

FROM:   Alternative Medicine Review 1999 (Dec); 4 (6): 414–423 ~ FULL TEXT

Randall A. Swain, MD, and Barbara Kaplan-Machlis, PharmD

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Introduction

Coronary artery disease is the number one cause of death in the United States and other industrialized countries. Hence, correspondingly greater attention is being focused on prevention of this chronic degenerative disease. In this arena, antioxidants such as vitamin E may serve an important role. Vitamin E acts as an antioxidant by donating an electron to neutralize reactive oxygen species and prevent oxidative damage thought to be responsible for atherosclerosis, oncogenesis, various neurologic problems and ophthalmic disorders. As a result, vitamin E is being investigated as a potential preventive nutrient for these common clinical disorders. Vitamin E has a favorable side effect profile and relatively low cost, making it an ideal part of a disease prevention program, provided it is indeed efficacious. This review examines the available scientific evidence for vitamin E administration in the prevention of coronary artery, and cerebro- and peripheral vascular disease.

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Vitamin E Metabolism and Deficiency States

Vitamin E is a lipid soluble micronutrient containing eight active, naturally occurring plant constituents - tocopherols and tocotrienols. Vitamin E is an essential element of human nutrition and exerts its effects in the body via a number of different mechanisms. The most abundant and active isomer is d-alpha-tocopherol, which is used to calculate the vitamin E content of food; other tocopherols include the beta, gamma, and delta isomers. Vitamin E functions primarily as an antioxidant, protecting cellular membranes from oxidative damage or destruction, and red blood cells from hemolysis. Vitamin E is also thought to enhance vitamin A utilization and, at high doses, may be involved in the inhibition of platelet aggregation. Foods rich in vitamin E include vegetable oils, green vegetables, nuts, wheat germ, and whole grains. Vitamin E distributes to all body tissues, especially adipose tissue where it is stored. Tocopherols are metabolized by the liver to glucuronides and eliminated in feces and bile.

Vitamin E deficiency in the United States is rare. Murphy et al reported that 96 percent of men and 88 percent of women achieved the RDA through diet alone in their population-based report. [1] Dietary manipulations are largely unsuccessful in increasing serum vitamin E levels significantly. [2] However, absorption may be as low as 10 percent, even when doses of 200 mg are administered (1 mg=1.5 IU). [3] In general, vitamin E absorption (unless taken as a water-miscible supplement) is dependent on pancreatic enzymes and bile salts which enhance absorption of fats in the small intestine. Two general patient populations are at risk for vitamin E deficiency: premature, very low birth-weight infants, and patients with fat malabsorption syndromes (e.g., pancreatic insufficiency, cystic fibrosis, betalipoproteinemia, or small intestinal resection). Premature neonates are at risk due to low fat stores, low transmission of fat across the placenta, and initial problems with intestinal absorption. Infants may develop hemolytic anemia or retrolental fibroplasia, a severe retinal disease thought to originate from oxygen therapy, in the absence of sufficient internal antioxidants.

Characteristics of vitamin E deficiency include a variety of symptoms such as areflexia, psychological syndromes, cognitive dysfunction, nystagmus, ataxia, muscle weakness, and sensory loss in the arms or legs. [4] Manifestations of vitamin E deficiency may not be completely reversible. Diagnosis is often made using serum vitamin E levels obtained as a result of clinical suspicion in high-risk individuals.

Vitamin E is well tolerated in large oral doses; up to 3200 IU per day have been administered to humans without adverse effects. [5] Historically, experts thought vitamin E would increase the effects of warfarin by causing vitamin K deficiency. In a recent study of patients on chronic warfarin treatment, no significant effect on prothrombin times was observed when 800-1200 mg of vitamin E per day was administered. [6] Conversely, if tissues are already vitamin K deficient, some experts suggest alpha-tocopherol may increase bleeding tendency through its mild effect on platelet aggregation at larger dosages (> 800 IU/day). [7] Even though vitamin E is relatively nontoxic, the potential risks of long-term, mega-dose therapy (> 1000 IU/day) are unknown.

Natural source vitamin E (d-alpha-tocopherol) differs from synthetic vitamin E (dl-alpha-tocopherol) in its stereoisomer formation. Synthetic vitamin E is a mixture of isomers. It is thought that the bioavailability of synthetic vitamin E is essentially one-half that of natural vitamin E.

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Since 12-07-2001