Main articles: tocopherol and tocotrienol
Vitamin E is a generic term for tocopherols and tocotrienols. 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. Of these, α-tocopherol (also written as alpha-tocopherol) has been most studied as it has the highest bioavailability.
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. 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. 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.. 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.
However, the roles and importance of all of the various forms of vitamin E are presently unclear, 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.
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. For more info, read article tocopherol.
Compared with tocopherols, tocotrienols are poorly studied. Less than 1% of PubMed papers on vitamin E relate to tocotrienols. 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, cancer prevention and cholesterol reduction by inhibiting the activity of HMG-CoA reductase;δ-tocotrienol blocks processing of sterol regulatory element‐binding proteins (SREBPs).
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. 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. For more info, read article tocotrienol.
Food sources of Vitamin E
Particularly high levels of vitamin E can be found in the following foods:
- Asparagus
- Avocado
- Egg
- Milk
- Nuts, such as almonds or hazelnuts
- Seeds
- Spinach and other green leafy vegetables
- Unheated vegetable oils
- Wheat germ
- Wholegrain foods
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 by 30 percent. However, the Sel enium and Vitamin E C ancer Prevention T rial, ("SELECT"), run from 2004 to 2008, found that vitamin E, whether taken alone or in combination with selenium, did not prevent prostate cancer. 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.
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. (Note: case control studies are rated as low quality, grade 3 or 4, on a standard scale of medical evidence.) The National Health Service in the United Kingdom concludes that pregnant women should: "consider avoiding taking supplemental Vitamin E tablets."
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: 10.1016/j.freeradbiomed.2007.03.024 . PMID 17561088.
- ^ Wang (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.
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