Vitamin E
From Wikipedia, the free encyclopedia
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 info, 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[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.
Contents |
[edit] Food sources of Vitamin E
Particularly high levels of vitamin E can be found in the following foods:[23]
- Asparagus
- Avocado
- Egg
- Milk
- Nuts, such as almonds or hazelnuts
- Seeds
- Spinach and other green leafy vegetables
- Unheated vegetable oils
- Wheat germ
- Wholegrain foods
[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] References
- ^ Brigelius-Flohe, Regina (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.
- ^ National Institute of Health (5/4/2009). "Vitamin E Fact Sheet". http://ods.od.nih.gov/factsheets/VitaminE.asp.
- ^ a b Herrera (2001). "Vitamin E: action, metabolism and perspectives". Journal of physiology and biochemistry 57 (2): 43–56. PMID 11579997.
- ^ Packer, Lester (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.
- ^ a b Brigelius-Flohé (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.
- ^ Traber (2007). "Vitamin E, antioxidant and nothing more". Free radical biology & medicine 43 (1): 4–15. doi:. PMID 17561088.
- ^ Wang (1999). "Vitamin E and its function in membranes". Progress in lipid research 38 (4): 309–36. doi:. PMID 10793887.
- ^ Brigelius-Flohé (2009). "Vitamin E: the shrew waiting to be tamed". Free radical biology & medicine 46 (5): 543–54. doi:. PMID 19133328.
- ^ Brigelius-Flohé (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:. PMID 17561087.
- ^ Atkinson (2008). "Tocopherols and tocotrienols in membranes: a critical review". Free radical biology & medicine 44 (5): 739–64. doi:. PMID 18160049.
- ^ Azzi (2007). "Molecular mechanism of alpha-tocopherol action". Free radical biology & medicine 43 (1): 16–21. doi:. PMID 17561089.
- ^ Zingg (2004). "Non-antioxidant activities of vitamin E". Current medicinal chemistry 11 (9): 1113–33. PMID 15134510.
- ^ Sesso, H. D. (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:.
- ^ Traber, MG (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.
- ^ Traber (1996). "Vitamin E in humans: demand and delivery". Annual review of nutrition 16: 321–47. doi:. PMID 8839930.
- ^ Sen (2004). "Tocotrienol: the natural vitamin E to defend the nervous system?". Annals of the New York Academy of Sciences 1031: 127–42. doi:. PMID 15753140.
- ^ Sen (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life sciences 78 (18): 2088–98. doi:. PMID 16458936.
- ^ Sen (2006). "Tocotrienols: Vitamin E beyond tocopherols". Life sciences 78 (18): 2088–98. doi:. PMID 16458936.
- ^ 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.
- ^ Das (2008). "Cardioprotection with palm oil tocotrienols: comparision of different isomers". American journal of physiology. Heart and circulatory physiology 294 (2): H970–8. doi:. PMID 18083895.
- ^ Sen, C (2007). "Tocotrienols in health and disease: the other half of the natural vitamin E family". Molecular Aspects of Medicine 28 (5-6): 692. doi:. PMID 17507086.
- ^ Sen (2007). "Tocotrienols: the emerging face of natural vitamin E". Vitamins and hormones 76: 203–61. doi:. PMID 17628176.
- ^ USDA National Nutrient Database
- ^ a b American Cancer Society, Vitamin E, updated Oct. 27, 2008
- ^ National Cancer Institute, The SELECT Prostate Cancer Prevention Trial, Oct. 27, 2008
- ^ National Cancer Institute, Selenium and Vitamin E Cancer Prevention Trial (SELECT), Oct. 31, 2008
- ^ Smedts (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:. PMID 19187374.
- ^ 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.
- ^ http://www.nhs.uk/news/2009/04April/Pages/VitaminEPregnancyRisk.aspx
[edit] Further reading
- Brigelius-Flohe, Regina (2002). "The European perspective on vitamin E: current knowledge and future research". American Journal of Clinical Nutrition 76 (4): 703. PMID 12324281. http://www.ajcn.org/cgi/pmidlookup?view=long&pmid=12324281.
[edit] External links
- Vitamin E Medline Plus, Medical Encyclopedia, U.S. National Library of Medicine
- Vitamin E Office of Dietary Supplements, National Institutes of Health
- Jane Higdon, "Vitamin E", Micronutrient Information Center, Linus Pauling Institute
|
|||||||||||||||||||||||||||