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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]

Contents

[edit] α-tocopherol

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 info, read article tocopherol.

[edit] Tocotrienols

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[18], cancer prevention[19] and cholesterol reduction[20] 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.[21] 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.[22] For more info, read article tocotrienol.

[edit] Food sources of Vitamin E

Particularly high levels of vitamin E can be found in the following foods:[23]

[edit] Health effects of dietary Vitamin E

[edit] 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[24] by 30 percent.[25] 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.[26] 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. [24]

[edit] 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.[27] (Note: case control studies are rated as low quality, grade 3 or 4, on a standard scale of medical evidence.[28]) The National Health Service in the United Kingdom concludes that pregnant women should: "consider avoiding taking supplemental Vitamin E tablets."[29]

[edit] 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.)

[edit] References

  1. ^ Brigelius-Flohe, Regina; Traber, M (1999). "Vitamin E: function and metabolism". <I>The FASEB Journal</I> 13 (10): 1145. PMID 10385606. http://www.fasebj.org/cgi/content/short/13/10/1145. 
  2. ^ National Institute of Health (5/4/2009). "Vitamin E Fact Sheet". http://ods.od.nih.gov/factsheets/VitaminE.asp. 
  3. ^ a b Herrera; Barbas, C (2001). "Vitamin E: action, metabolism and perspectives". Journal of physiology and biochemistry 57 (2): 43–56. 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. http://jn.nutrition.org/cgi/content/full/131/2/369S. 
  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. http://www.ajcn.org/cgi/content/abstract/62/6/1501S. 
  15. ^ Traber; Sies, H (1996). "Vitamin E in humans: demand and delivery". Annual review of nutrition 16: 321–47. doi:10.1146/annurev.nu.16.070196.001541. 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. ^ 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. ^ 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. 
  19. ^ Malafa (2008). "New insights and gains in pancreatic cancer". Cancer control : journal of the Moffitt Cancer Center 15 (4): 276–7. PMID 18813194. http://www.moffitt.org/CCJRoot/v15n4/pdf/276.pdf. 
  20. ^ 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. 
  21. ^ 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. 
  22. ^ 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. 
  23. ^ USDA National Nutrient Database
  24. ^ a b American Cancer Society, Vitamin E, updated Oct. 27, 2008
  25. ^ National Cancer Institute, The SELECT Prostate Cancer Prevention Trial, Oct. 27, 2008
  26. ^ National Cancer Institute, Selenium and Vitamin E Cancer Prevention Trial (SELECT), Oct. 31, 2008
  27. ^ 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. 
  28. ^ 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. http://www.cebm.net/index.aspx?o=1047.
  29. ^ http://www.nhs.uk/news/2009/04April/Pages/VitaminEPregnancyRisk.aspx

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