Written by Amy Kosowski, M.S., LDN. Vitamin E plays a role in the prevention of colon, breast, and skin cancers.   

Vitamin E refers to a group of fat-soluble compounds called tocopherols and tocotrienols. There are four major dietary tocopherols, α, β, δ, and γ, and four forms of tocotrienols, also called α, β, δ, and γ. Of these forms, α-tocopherol has historically received the most attention, however recent scientific research has revealed that the other forms of Vitamin E possess properties equally important to human health (1,2). Vitamin E is an antioxidant, which means that it protects cells from the effects of oxidation. Oxidant species attack other molecules, removing an electron, forming what are known as free radicals. Free radicals are highly destructive molecules that can cause extensive damage to the body if left unchecked.

Fatty acids are particularly vulnerable to attack by free radicals. Because lipid is the main constituent of all cell membranes, a major function of Vitamin E is to protect cell membranes from oxidative stress. Free radical injury to cell membranes has been implicated in many disease processes and a wide variety of epidemiological and prospective studies have shown health benefits associated with higher than average Vitamin E consumption.

Free radical formation and oxidation are tied to cancer development, therefore antioxidants, including Vitamin E, may help in preventing tumor growth. Some experimental evidence supports a role for Vitamin E in the prevention of colon (3), breast (4), and skin cancers (5). Vitamin E also possesses immunomodulatory effects, which may also help to protect against the development of cancer (6).

That Vitamin E protects against cardiovascular disease is well supported in the scientific literature. In simple terms, Vitamin E’s function is to modify and stabilize blood lipids, thereby protecting the blood vessels, heart and brain from free radical injury. There are at least three mechanisms by which Vitamin E protects against atherosclerosis and age-related neurological dysfunction. First, as an antioxidant, it helps limits LDL oxidation, a major risk factor in the development of cardiovascular disease and neurodegenerative disorders (7,8). Second, Vitamin E has been shown to reduce platelet aggregation and platelet adhesiveness, thereby reducing the risk of blood clot development (9). Finally, Vitamin E exhibits immunomodulatory effects that enhance its anti-atherogenic properties (10).

It is important to note that Vitamin E interacts with other antioxidant nutrients within an antioxidant network. When Vitamin E quenches a free radical, a Vitamin E radical is formed. The Vitamin E radical can then be reduced by one or more lipid or water soluble antioxidants such as Coenzyme Q10, α-Lipoic Acid, Ascorbic Acid (Vitamin C), or Vitamin A (11). It is therefore important that other antioxidants are present in the body along with Vitamin E. Furthermore, although research has been focused on α-tocopherol, recent studies have revealed that γ-tocopherol and the tocotrienols also play an important role in the prevention of cancer and cardiovascular disease (1,2). Therefore, a Vitamin E supplement containing mixed tocopherols and tocotrienols may be more beneficial than one containing only α-tocopherol.

Safety: Side effects associated with Vitamin E supplements are exceedingly rare. Unlike other fat-soluble vitamins, such as A, D, and K, Vitamin E is relatively non-toxic, even at doses of 1000 or more percent of the current DV of 30 IU (12). Caution is advised, however, in those individuals at risk for prolonged bleeding, such as those taking anticoagulant medications, because Vitamin E supplementation can decrease blood clotting ability by reducing platelet aggregation.

Posted September 19, 2008

References:

  1. Jiang Q, Christen S, Shigenaga MK, Ames BN (2001) Am J Clin Nutr 74:714-22.
  2. Theriault A, Chao J-T,Wang Q, Gapor A, Adeli K (1999) Clin Biochem 32(5):309.
  3. Bostick RM, Potter JD, McKenzie DR, Sellers TA, Kushi LH, Steinmetz KA, Folsom AR (1993) Cancer Res 53(18):4230.
  4. Schwenke DC (2001) J Nutr Biochem 13:2-20.
  5. Gensler HL, Magdaleno M (1991) Nutr Cancer 15(2):97-106.
  6. Meydani SN, et al. (1990) Am J Clin Nutr 52(3):557-63.
  7. Jialal I and Fuler CJ (1995) Can J Cardiol 11(supplG):97G-103G.
  8. Schippling S, et al. (2000) Free Radic Biol Med 28(3):351-60.
  9. Szczeklik A, Gryglewski RJ, Domagala B, Dworski R, Basista M (1985) Thromb Haemost 54:425-30.
  10. Neuzil J, Weber C, Kontush (2001) Atherolsclerosis 157:257-283.
  11. Packer L, Kraemer, K Rimbach G (2001) Nutrition 17:888-895.
  12. Kappus H, Diplock AT (1992) Free Radic Biol Med 13(1):55-74.