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The α-tocopherol form of vitamin E.

Vitamin E is a generic term for tocopherols and tocotrienols.[1] Vitamin E is a family of α-, β-, γ-, and δ-tocopherols and corresponding four tocotrienols. Vitamin E is a fat-soluble antioxidant that stops the production of reactive oxygen species formed when fat undergoes oxidation.[2][3][4] Of these, α-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability.[5]



It has been claimed that α-tocopherol is the most important lipid-soluble antioxidant, and that it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.[3][6] This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidised α-tocopheroxyl radicals produced in this process may be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol.[7] However, the importance of the antioxidant properties of this molecule at the concentrations present in the body are not clear and it is possible that the reason why vitamin E is required in the diet is unrelated to its ability to act as an antioxidant.[8]. Other forms of vitamin E have their own unique properties. For example, γ-tocopherol (also written as gamma-tocopherol) is a nucleophile that can react with electrophilic mutagens.[5]

However, the roles and importance of all of the various forms of vitamin E are presently unclear,[9][10] and it has even been suggested that the most important function of vitamin E is as a signaling molecule, and that it has no significant role in antioxidant metabolism.[11][12]

So far, most studies about vitamin E have supplemented using only the synthetic alpha-tocopherol, but doing so leads to reduced serum gamma- and delta-tocopherol concentrations. Moreover, a 2007 clinical study involving synthetic alpha-tocopherol concluded that supplementation did not reduce the risk of major cardiovascular events in middle aged and older men.[13] For more information, read article tocopherol.


Compared with tocopherols, tocotrienols are poorly studied.[14][15][16] Less than 1% of PubMed papers on vitamin E relate to tocotrienols.[17] Current research direction are starting to give more prominence to the tocotrienols, the lesser known but more potent antioxidants in the vitamin E family. Tocotrienols have specialized roles in protecting neurons from damage[17], cancer prevention[18] and cholesterol reduction[19] by inhibiting the activity of HMG-CoA reductase[16-1];δ-tocotrienol blocks processing of sterol regulatory element‐binding proteins (SREBPs)[16-1].

Oral consumption of tocotrienols is also proven to protect against stroke-associated brain damage in vivo. Disappointments with outcomes-based clinical studies testing the efficacy of α-tocopherol need to be handled with caution and prudence recognizing the untapped opportunities offered by the other forms of natural vitamin E.[20] Toxicity studies of a specific form of tocopherol in excess should not be used to conclude that high-dosage “vitamin E” supplementation may increase all-cause mortality. Such conclusion incorrectly implies that tocotrienols are toxic as well under conditions where tocotrienols were not even considered.[21] For more info, read article tocotrienol.

Food sources of Vitamin E

Particularly high levels of vitamin E can be found in the following foods:[22]

Brackets contain the amount and proportion of the daily allowance of vitamin E.

Health effects of dietary Vitamin E


Vitamin E to prevent prostate cancer study discontinued

There have been some theories that Vitamin E, especially when coupled with selenium, may reduce the risk of prostate cancer[23] by 30 percent.[24] However, the Selenium and Vitamin E Cancer Prevention Trial, ("SELECT"), run from 2004 to 2008, found that vitamin E, whether taken alone or in combination with selenium, did not prevent prostate cancer.[25] The SELECT study was discontinued after independent reviewers determined that there was no benefit to the 35,000 men who were the subject of the study.[23]

Congenital heart defects

A case control study done in the Netherlands using food frequency questionnaires found that high maternal Vitamin E by diet and supplements is associated with an increased risk of CHD (congenital heart defects) offspring, especially when the supplements are taken in the periconception period.[26] (Note: case control studies are rated as low quality, grade 3 or 4, on a standard scale of medical evidence.[27]) The National Health Service in the United Kingdom concludes that pregnant women should: "consider avoiding taking supplemental Vitamin E tablets."[28]

Vitamin E and strokes

A Finnish study found that Vitamin E supplementation increased the risk of hemorrhagic stroke (The Alpha-Tocopherol Beta-Carotene Cancer Prevention Study Group. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 1994;330:1029–35.) Vitamin E supplementation was shown to increase the risk of heart failure in a 2005 study published in the Journal of the American Medical Association by Lonn, et al., which studied 7,000 people (JAMA. 2005 Mar 16;293(11):1338-47. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial.)

Peyronie's Disease

Urologists commonly recommend Vitamin E supplementation as a treatment for Peyronie's disease. Some success has been reported in older trials, but those successes have not been reliably repeated in larger, newer studies.[29]


Vitamin E deficiency causes neurological problems due to poor nerve conduction. These include neuromuscular problems such as spinocerebellar ataxia and myopathies.[30] Deficiency can also cause anemia, due to oxidative damage to red blood cells.


  1. ^ Brigelius-Flohe, Regina; Traber, M (1999). "Vitamin E: function and metabolism". <I>The FASEB Journal</I> 13 (10): 1145. PMID 10385606. 
  2. ^ National Institute of Health (5/4/2009). "Vitamin E Fact Sheet". 
  3. ^ a b Herrera; Barbas, C (2001). "Vitamin E: action, metabolism and perspectives". Journal of physiology and biochemistry 57 (2): 43–56. doi:10.1007/BF03179812. PMID 11579997. 
  4. ^ Packer, Lester; Weber, S; Rimbach, G (2001). "Molecular Aspects of α-Tocotrienol Antioxidant Action and Cell Signalling". Journal of Nutrition 131 (2): 369S. PMID 11160563. 
  5. ^ a b Brigelius-Flohé; Traber, MG (1999). "Vitamin E: function and metabolism". The FASEB journal : official publication of the Federation of American Societies for Experimental Biology 13 (10): 1145–55. PMID 10385606. 
  6. ^ Traber; Atkinson, J (2007). "Vitamin E, antioxidant and nothing more". Free radical biology & medicine 43 (1): 4–15. doi:10.1016/j.freeradbiomed.2007.03.024. PMID 17561088. 
  7. ^ Wang; Quinn, PJ (1999). "Vitamin E and its function in membranes". Progress in lipid research 38 (4): 309–36. doi:10.1016/S0163-7827(99)00008-9. PMID 10793887. 
  8. ^ Brigelius-Flohé (2009). "Vitamin E: the shrew waiting to be tamed". Free radical biology & medicine 46 (5): 543–54. doi:10.1016/j.freeradbiomed.2008.12.007. PMID 19133328. 
  9. ^ Brigelius-Flohé; Davies, KJ (2007). "Is vitamin E an antioxidant, a regulator of signal transduction and gene expression, or a 'junk' food? Comments on the two accompanying papers: "Molecular mechanism of alpha-tocopherol action" by A. Azzi and "Vitamin E, antioxidant and nothing more" by M. Traber and J. Atkinson". Free radical biology & medicine 43 (1): 2–3. doi:10.1016/j.freeradbiomed.2007.05.016. PMID 17561087. 
  10. ^ Atkinson; Epand, RF; Epand, RM (2008). "Tocopherols and tocotrienols in membranes: a critical review". Free radical biology & medicine 44 (5): 739–64. doi:10.1016/j.freeradbiomed.2007.11.010. PMID 18160049. 
  11. ^ Azzi (2007). "Molecular mechanism of alpha-tocopherol action". Free radical biology & medicine 43 (1): 16–21. doi:10.1016/j.freeradbiomed.2007.03.013. PMID 17561089. 
  12. ^ Zingg; Azzi, A (2004). "Non-antioxidant activities of vitamin E". Current medicinal chemistry 11 (9): 1113–33. PMID 15134510. 
  13. ^ Sesso, H. D.; Buring, J. E.; Christen, W. G.; Kurth, T.; Belanger, C.; MacFadyen, J.; Bubes, V.; Manson, J. E. et al. (2008). "Vitamins E and C in the Prevention of Cardiovascular Disease in Men: the Physicians' Health Study II Randomized Controlled Trial". JAMA: the Journal of the American Medical Association 300: 2123. doi:10.1001/jama.2008.600. 
  14. ^ Traber, MG; Packer, L (1995). "Vitamin E: beyond antioxidant function". American Journal of Clinical Nutrition 62 (6): 1501S. PMID 7495251. 
  15. ^ Traber; Sies, H (1996). "Vitamin E in humans: demand and delivery". Annual review of nutrition 16: 321–47. doi:10.1146/ PMID 8839930. 
  16. ^ Sen; Khanna, S; Roy, S (2004). "Tocotrienol: the natural vitamin E to defend the nervous system?". Annals of the New York Academy of Sciences 1031: 127–42. doi:10.1196/annals.1331.013. PMID 15753140. 
  17. ^ a b Sen; Khanna, S; Roy, S (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life sciences 78 (18): 2088–98. doi:10.1016/j.lfs.2005.12.001. PMID 16458936. 
  18. ^ Malafa (2008). "New insights and gains in pancreatic cancer". Cancer control : journal of the Moffitt Cancer Center 15 (4): 276–7. PMID 18813194. 
  19. ^ Das; Lekli, I; Das, M; Szabo, G; Varadi, J; Juhasz, B; Bak, I; Nesaretam, K et al. (2008). "Cardioprotection with palm oil tocotrienols: comparision of different isomers". American journal of physiology. Heart and circulatory physiology 294 (2): H970–8. doi:10.1152/ajpheart.01200.2007. PMID 18083895. 
  20. ^ Sen, C; Khanna, S; Roy, S (2007). "Tocotrienols in health and disease: the other half of the natural vitamin E family". Molecular Aspects of Medicine 28 (5-6): 692. doi:10.1016/j.mam.2007.03.001. PMID 17507086. 
  21. ^ Sen; Khanna, S; Rink, C; Roy, S (2007). "Tocotrienols: the emerging face of natural vitamin E". Vitamins and hormones 76: 203–61. doi:10.1016/S0083-6729(07)76008-9. PMID 17628176. 
  22. ^ USDA National Nutrient Database
  23. ^ a b American Cancer Society, Vitamin E, updated Oct. 27, 2008
  24. ^ National Cancer Institute, The SELECT Prostate Cancer Prevention Trial, Oct. 27, 2008
  25. ^ National Cancer Institute, Selenium and Vitamin E Cancer Prevention Trial (SELECT), Oct. 31, 2008
  26. ^ Smedts; De Vries, JH; Rakhshandehroo, M; Wildhagen, MF; Verkleij-Hagoort, AC; Steegers, EA; Steegers-Theunissen, RP (2009). "High maternal vitamin E intake by diet or supplements is associated with congenital heart defects in the offspring". BJOG : an international journal of obstetrics and gynaecology 116 (3): 416–23. doi:10.1111/j.1471-0528.2008.01957.x. PMID 19187374. 
  27. ^ Bob Phillips; Chris Ball, Dave Sackett, Doug Badenoch, Sharon Straus, Brian Haynes, Martin Dawes (May 2001). "Levels of Evidence". Oxford Centre for Evidence-based Medicine.
  28. ^
  29. ^ L A Mynderse and M Monga. "Oral therapy for Peyronie's disease".
  30. ^ Brigelius-Flohé R, Traber MG (1 July 1999). "Vitamin E: function and metabolism". FASEB J. 13 (10): 1145–55. PMID 10385606. 

Further reading

External links

Simple English

Vitamin E (which is also called Tocopherol or Tocotrienol, E307, E308,E309) is a vitamin. There are eight forms of it, E1 to E8. It can be found in vegetable oils. Very often it is also added to lotions and creams for the skin. It is supposed to help the healing of the skin, after burns and injuries, and lower the risk of heart disease and cancer.[1]

Vitamin E is claimed to help Anti-Aging.[needs proof]


  1. Anderson J, Young L. "Fat-Soluble Vitamins". Colorado State University, Cooperative Extension. Retrieved 2007-5-30. 


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