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Vitamin E

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Vitamin E

Vitamin E
Drug class
The α-tocopherol form of vitamin E
Use Vitamin E deficiency, antioxidant
Biological target Reactive oxygen species
ATC code A11H
External links

Vitamin E refers to a group of ten lipid-soluble compounds that include both tocopherols and tocotrienols.[1] Of the many different forms of vitamin E, γ-tocopherol is the most common in the North American diet.[2] γ-Tocopherol can be found in corn oil, soybean oil, margarine, and dressings.[3][4] α-tocopherol, the most biologically active form of vitamin E, is the second-most common form of vitamin E in the diet. This variant can be found most abundantly in wheat germ oil, sunflower, and safflower oils.[4][5] As a fat-soluble antioxidant, it stops the production of reactive oxygen species formed when fat undergoes oxidation.[6][7][8] Regular consumption of more than 1,000 mg (1,500 IU) of tocopherols per day[9] may be expected to cause Hypervitaminosis E, with an associated risk of vitamin K deficiency and consequently of bleeding problems.


The ten forms of vitamin E are divided into two groups; five are tocopherols and five are tocotrienols. They are identified by prefixes alpha- (α-), beta- (β-), gamma- (γ-), delta- (δ-), and epsilon (ε-). Natural tocopherols occur in the RRR-configuration only. The synthetic form contains eight different stereoisomers and is called 'all-rac'-α-tocopherol.[10]


Sample of α-tocopherol, one of the various forms of vitamin E

α-Tocopherol is an important lipid-soluble antioxidant. It performs its functions as antioxidant in the glutathione peroxidase pathway,[11] and it protects cell membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction.[7][12] This would remove the free radical intermediates and prevent the oxidation reaction from continuing. The oxidized 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.[13] However, the importance of the antioxidant properties of this molecule at the concentrations present in the body are not clear and the reason vitamin E is required in the diet is possibly unrelated to its ability to act as an antioxidant.[14] Other forms of vitamin E have their own unique properties; for example, γ-tocopherol is a nucleophile that can react with electrophilic mutagens.[15]


Compared with tocopherols, tocotrienols are sparsely studied.[16][17][18] Less than 1% of PubMed papers on vitamin E relate to tocotrienols.[19] The current research direction is starting to give more prominence to the tocotrienols, the lesser known but more potent antioxidants in the vitamin E family. Some studies have suggested that tocotrienols have specialized roles in protecting neurons from damage[19] and cholesterol reduction[20] 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 thought to protect against stroke-associated brain damage in vivo.[21] Until further research has been carried out on the other forms of vitamin E, conclusions relating to the other forms of vitamin E, based on trials studying only the efficacy of α-tocopherol, may be premature.[22]


Vitamin E has many biological functions, the antioxidant function being the most important and best known.[23] Other functions include enzymatic activities, gene expression, and neurological function(s). The most important function of vitamin E has been suggested to be in cell signaling (and it may not have a significant role in antioxidant metabolism).[24][25]

  • As an antioxidant, vitamin E acts as a peroxyl radical scavenger, preventing the propagation of free radicals in tissues, by reacting with them to form a tocopheryl radical, which will then be reduced by a hydrogen donor (such as vitamin C) and thus return to its reduced state.[26] As it is fat-soluble, it is incorporated into cell membranes, which protects them from oxidative damage. Vitamin E has also found use as a commercial antioxidant in ultra high molecular weight polyethylene (UHMWPE) used in hip and knee replacements, to help resist oxidation.[27]
  • As an enzymatic activity regulator, for instance, protein kinase C (PKC), which plays a role in smooth muscle growth, can be inhibited by α-tocopherol. α-Tocopherol has a stimulatory effect on the dephosphorylation enzyme, protein phosphatase 2A, which in turn, cleaves phosphate groups from PKC, leading to its deactivation, bringing the smooth muscle growth to a halt.[28]
  • Vitamin E also has an effect on gene expression. Macrophages rich in cholesterol are found in the atherogenetic tissue. Scavenger receptor CD36 is a class B scavenger receptor found to be up-regulated by oxidized low density lipoprotein (LDL) and binds it.[29] Treatment with α-tocopherol was found to downregulate the expression of the CD36 scavenger receptor gene and the scavenger receptor class A (SR-A)[29] and modulates expression of the connective tissue growth factor (CTGF).[30][31] The CTGF gene, when expressed, is responsible for the repair of wounds and regeneration of the extracellular tissue lost or damaged during atherosclerosis.[31]
  • Vitamin E also plays a role in neurological functions,[32] and inhibition of platelet aggregation.[33][34][35]
  • Vitamin E also protects lipids and prevents the oxidation of polyunsaturated fatty acids.[36]

So far, most human supplementation studies about vitamin E have used only α-tocopherol. This can affect levels of other forms of vitamin E, e.g. reducing serum γ- and δ-tocopherol concentrations. Moreover, a 2007 clinical study involving α-tocopherol concluded supplementation did not reduce the risk of major cardiovascular events in middle-aged and older men.[37]


Vitamin E deficiency can cause:


While vitamin E supplementation was initially hoped to have a positive effect on health, research has not supported this hope.[40] Vitamin E does not decrease mortality in adults, even at large doses,[41] and high-dosage supplementation may slightly increase it.[42][43] It does not improve blood sugar control in an unselected group of people with diabetes mellitus[41] or decrease the risk of stroke.[44] Daily supplementation of vitamin E does not decrease the risk of prostate cancer and may increase it.[45] Studies on its role in age-related macular degeneration are ongoing as, though it is of a combination of dietary antioxidants used to treat the condition, it may increase the risk.[46] A Japanese study in 2012 found vitamin E may contribute to osteoporosis.[47]

In a 2013 study, 613 people with "mild to moderate Alzheimer's disease" were given either a daily dose of vitamin E, memantine, both vitamin E and memantine, or a placebo. Those given vitamin E had slower cognitive decline than those given the placebo. Although the study suggests that vitamin E supplementation may slow the progression of dementia, the dosage was very high and may be unsafe in the long term. Furthermore, Dr. Eric Karran, director of research at Alzheimer's Research UK, stated that "until the findings from this trial have been replicated, we would not encourage people to take high doses of vitamin E supplements to try to prevent or treat Alzheimer's."[48]

A 2012 Cochrane Review examined the potential effectiveness of antioxidant vitamin supplementation in preventing and slowing the progression of age-related cataract. The included studies involved supplementation of vitamin E, along with β-carotene and vitamin C, either dosed independently or in combination, and compared to the placebo. The systematic review showed that vitamin E supplementation had no protective effect on reducing the risk of cataract, cataract extraction, progression of cataract, and slowing the loss of visual acuity.[49]


Vitamin E can act as an anticoagulant, increasing the risk of bleeding problems. As a result, many agencies have set a tolerable upper intake levels (UL) at 1,000 mg (1,500 IU) per day.[9] In combination with certain other drugs such as aspirin, hypervitaminosis E can be life-threatening. Hypervitaminosis E may also counteract vitamin K, leading to a vitamin K deficiency.

Dietary sources

mg/(100 g)
[note 1]
Some foods with vitamin E content[6]
low high
150 Wheat germ oil
41 Sunflower oil
95 Almond oil
34 Safflower oil
15 26 Nuts and nut oils, such as almonds and hazelnuts[note 2]
15 Palm oil[50]
14 Olive oil
12.2 Common purslane[51]
1.5 3.4 High-value green, leafy vegetables: spinach, turnip, beet greens, collard greens, and dandelion greens[note 3]
2 Avocados[52]
1.4 Sesame oil[53]
1.1 1.5 Asparagus[note 4]
1.5 Kiwifruit (green)
0.78 1.5 Broccoli[note 5]
0.8 1 Pumpkin[note 6]
0.26 0.94 Sweet potato[note 7]
0.9 Mangoes
0.54 0.56 Tomatoes[note 8]
0.36 0.44 Rockfish[note 9]
0.3 Papayas
0.13 0.22 Low-value green, leafy vegetables: lettuce[note 10]

Butter and egg yolk are the only food containing vitamin E and free from phytate

Recommended daily intake

The Food and Nutrition Board at the Institute of Medicine (IOM) of the US National Academy of Sciences reported the following dietary reference intakes for vitamin E:[6][54]

mg/day Age
4 0 to 6 months
5 7 to 12 months
6 1 to 3 years
7 4 to 8 years
11 9 to 13 years
Adolescents and adults
15 14 and older

One IU of vitamin E is defined as equivalent to either: 0.67 mg of the natural form, RRR-α-tocopherol, also known as d-α-tocopherol; or 0.45 mg of the synthetic form, all-rac-α-tocopherol, also known as dl-α-tocopherol.[6]


Vitamin E was discovered in 1922 by Herbert McLean Evans and Katharine Scott Bishop[55] and first isolated in a pure form by Gladys Anderson Emerson in 1935 at the University of California, Berkeley.[56] Erhard Fernholz elucidated its structure in 1938 and shortly afterwards the same year, Paul Karrer and his team first synthesized it.[57]

The first use for vitamin E as a therapeutic agent was conducted in 1938 by Widenbauer, who used wheat germ oil supplement on 17 premature newborn infants suffering from growth failure. Eleven of the original 17 patients recovered and were able to resume normal growth rates.[23]

In 1945, Drs. Evan V. Shute and Wilfred E. Shute, siblings from Ontario, Canada, published the first monograph arguing that megadoses of vitamin E can slow down and even reverse the development of atherosclerosis.[58] Peer-reviewed publications soon followed.[59][60] The same research team also demonstrated, in 1946, that α-tocopherol improved impaired capillary permeability and low platelet counts in experimental and clinical thrombocytopenic purpura.[61]

Later, in 1948, while conducting experiments on hemolysis than those that did not receive tocopherol.[62] In 1949, Gerloczy administered all-rac-α-tocopheryl acetate to prevent and cure edema.[63][64] Methods of administration used were both oral, that showed positive response, and intramuscular, which did not show a response.[23] This early investigative work on the benefits of vitamin E supplementation was the gateway to curing the vitamin E deficiency-caused hemolytic anemia described during the 1960s. Since then, supplementation of infant formulas with vitamin E has eradicated this vitamin’s deficiency as a cause for hemolytic anemia.[23]


  1. ^ "USDA Nutrient Data Laboratory".  In notes 2–11, USDA NDL Release 24 numbers are given as mg/(100 g). Low and high values vary some by raw versus cooked and by variety.
  2. ^ 26 almonds, 15 hazelnuts
  3. ^ Spinach (2.0 raw, 2.1 cooked), turnip (2.9 raw, 1.9 cooked), beet (1.5 raw, 1.8 cooked), collard (2.3 raw, 0.88 cooked), and dandelion greens (3.4 raw, 2.4 cooked)
  4. ^ 1.1 raw, 1.5 cooked
  5. ^ 0.78 raw, 1.5 cooked
  6. ^ 1. raw, 0.8 cooked
  7. ^ 0.26 raw, 0.94 boiled
  8. ^ 0.54 raw, 0.56 cooked
  9. ^ 0.36 raw, 0.44 cooked
  10. ^ Lettuce (0.18 iceberg, 0.22 green leaf, 0.13 romaine, 0.15 red leaf, 0.18 butterhead)


  1. ^ Brigelius-Flohé R, Traber MG (1999). "Vitamin E: function and metabolism". FASEB J. 13 (10): 1145–1155.  
  2. ^ Traber, MG (1998). "The biological activity of vitamin E". The Linus Pauling Institute. Retrieved 6 March 2011. 
  3. ^ Bieri JG, Evarts RP (1974). "γ-Tocopherol: metabolism, biological activity and significance in human vitamin E nutrition". American Journal of Clinical Nutrition 27 (9): 980–986.  
  4. ^ a b c Brigelius-Flohé R, Traber MG (1 July 1999). "Vitamin E: function and metabolism". FASEB J. 13 (10): 1145–55.  
  5. ^ Reboul E, Richelle M, Perrot E, Desmoulins-Malezet C, Pirisi V, Borel P (15 November 2006). "Bioaccessibility of carotenoids and vitamin E from their main dietary sources". Journal of Agricultural and Food Chemistry 54 (23): 8749–8755.  
  6. ^ a b c d e f g h i National Institute of Health (4 May 2009). "Vitamin E fact sheet". 
  7. ^ a b Herrera E, Barbas C (2001). "Vitamin E: action, metabolism and perspectives". Journal of Physiology and Biochemistry 57 (2): 43–56.  
  8. ^ Packer L, Weber SU, Rimbach G (2001). "Molecular aspects of α-tocotrienol antioxidant action and cell signalling". Journal of Nutrition 131 (2): 369S–73S.  
  9. ^ a b Vitamin E Fact sheet
  10. ^ Traber, MG. "Chapter 15: vitamin E". In Bowman BA and Russell RM. Current Knowledge in Nutrition I (9 ed.). Washington DC, USA: ILSI.  
  11. ^ Wefers H, Sies H (1988). "The protection of ascorbate and glutathione against microsomal lipid peroxidation is dependent on Vitamin E". European Journal of Biochemistry 174 (2): 353–357.  
  12. ^ a b Traber MG, Atkinson J (2007). "Vitamin E, Antioxidant and Nothing More". Free radical biology & medicine 43 (1): 4–15.  
  13. ^ Wang X, Quinn PJ (1999). "Vitamin E and its function in membranes". Progress in Lipid Research 38 (4): 309–36.  
  14. ^ Brigelius-Flohé R (2009). "Vitamin E: the shrew waiting to be tamed". Free radical biology & medicine 46 (5): 543–54.  
  15. ^ Brigelius-Flohé R, Traber MG (1999). "Vit amin E: function and metabolism". FASEB J. 13 (10): 1145–55.  
  16. ^ Traber MG, Packer L; Packer, L (1995). "Vitamin E: beyond antioxidant function". American Journal of Clinical Nutrition 62 (6): 1501S–1509S.  
  17. ^ Traber MG, Sies H; Sies, H (1996). "Vitamin E in humans: demand and delivery". Annual review of nutrition 16: 321–47.  
  18. ^ Sen CK, 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.  
  19. ^ a b Sen CK, Khanna S, Roy S (2006). "Tocotrienols: Vitamin E Beyond Tocopherols". Life Sciences 78 (18): 2088–98.  
  20. ^ Das S, Lekli I, Das M, Szabo G, Varadi J, Juhasz B, Bak I, Nesaretam K, Tosaki A, Powell SR, Das DK (2008). "Cardioprotection with palm oil tocotrienols: comparison of different isomers". American journal of physiology. Heart and circulatory physiology 294 (2): H970–8.  
  21. ^ Khanna S, Roy S, Slivka A, Craft TK, Chaki S, Rink C, Notestine MA, DeVries AC, Parinandi NL, Sen CK (2005). "Neuroprotective Properties of The Natural Vitamin E α-Tocotrienol". Stroke 36 (10): 2258–64.  
  22. ^ Sen CK, 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): 692–728.  
  23. ^ a b c d Bell EF (1987). "History of vitamin E in infant nutrition". American Journal of Clinical Nutrition 46 (1 Suppl): 183–186.  
  24. ^ Azzi A (2007). "Molecular mechanism of alpha-tocopherol action". Free radical biology & medicine 43 (1): 16–21.  
  25. ^ Zingg JM, Azzi A (2004). "Non-antioxidant activities of vitamin E". Current medicinal chemistry 11 (9): 1113–33.  
  26. ^ Traber MG, Stevens JF (2011). "Free Radical Biology and Medicine – Vitamins C and E: Beneficial effects from a mechanistic perspective". Free Radical Biology and Medicine 51 (5): 1000–13.  
  27. ^ UHMWPE Biomaterials Handbook, 2nd Edition, Kurtz ed. (2009)
  28. ^ Schneider C (2005). "Chemistry and biology of vitamin E". Mol Nutr Food Res 49 (1): 7–30.  
  29. ^ a b Devaraj S, Hugou I, Jialal I (2001). "-Tocopherol decreases CD36 expression in human monocyte-derived macrophages". J Lipid Res 42 (4): 521–527.  
  30. ^ Azzi A, Stocker A (2000). "Vitamin E: non-antioxidant roles". Prog Lipid Res 39 (3): 231–255.  
  31. ^ a b Villacorta L, Graça-Souza AV, Ricciarelli R, Zingg JM, Azzi A (2003). "α-Tocopherol induces expression of connective tissue growth factor and antagonizes tumor necrosis factor-α-mediated downregulation in human smooth muscle cells". Circ. Res. 92 (1): 104–110.  
  32. ^ Muller DP (2010). "Vitamin E and neurological function. Review". Mol. Nutr. Food Res 54 (5): 710–718.  
  33. ^ Dowd P, Zheng ZB (1995). "On the mechanism of the anticlotting action of vitamin E quinone". Proc Natl Acad Sci U S A. 92 (18): 8171–8175.  
  34. ^ Brigelius-Flohé R, 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.  
  35. ^ Atkinson J, Epand RF, Epand RM (2008). "Tocopherols and tocotrienols in membranes: a critical review". Free radical biology & medicine 44 (5): 739–64.  
  36. ^ a b Whitney, Ellie; Sharon Rady Rolfes (2011). Peggy Williams, ed. Understanding Nutrition (Twelfth ed.). California: Wadsworth,Cengage Learning.  
  37. ^ Sesso HD, Buring JE, Christen WG, Kurth T, Belanger C, MacFadyen J, Bubes V, Manson JE, Glynn RJ, Gaziano JM (2008). "Vitamins E and C in the Prevention of Cardiovascular Disease in Men: The Physicians' Health Study II Randomized Trial". JAMA: the Journal of the American Medical Association 300 (18): 2123–33.  
  38. ^ a b c d e Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press, 2000.
  39. ^ a b c d e Kowdley KV, Mason JB, Meydani SN, Cornwall S, Grand RJ (1992). "Vitamin E deficiency and impaired cellular immunity related to intestinal fat malabsorption". Gastroenterology 102 (6): 2139–42.  
  40. ^ Haber, David (2006). Health promotion and aging: practical applications for health professionals (4th ed.). New York, NY: Springer Pub. p. 280.  
  41. ^ a b Abner EL, Schmitt FA, Mendiondo MS, Marcum JL, Kryscio RJ (July 2011). "Vitamin E and all-cause mortality: a meta-analysis". Current aging science 4 (2): 158–70.  
  42. ^ Miller ER, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E (2005). "Meta-analysis: High-dosage vitamin E supplementation may increase all-cause mortality". Annals of internal medicine 142 (1): 37–46.  
  43. ^ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (16 April 2008). Bjelakovic, Goran, ed. "Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases". Cochrane database of systematic reviews (Online) (2): CD007176.  
  44. ^ Bin Q, Hu X, Cao Y, Gao F (April 2011). "The role of vitamin E (tocopherol) supplementation in the prevention of stroke. A meta-analysis of 13 randomized controlled trials". Thrombosis and haemostasis 105 (4): 579–85.  
  45. ^ Haederle, Michael. "Vitamin E Supplements Raise Risk of Prostate Cancer". Health Discovery.  
  46. ^ Olson JH, Erie JC, Bakri SJ (May 2011). "Nutritional supplementation and age-related macular degeneration". Seminars in ophthalmology 26 (3): 131–6.  
  47. ^ "Taking vitamin E linked to osteoporosis: research|". 
  48. ^ "Vitamin E 'beneficial' in dementia". BBC News. 
  49. ^ Mathew MC, Ervin AM, Tao J, Davis RM (2012). "Routine Antioxidant vitamin supplementation for preventing and slowing the progression of age-related cataract". Cochrane Database Syst Rev 6: CD004567.  
  50. ^ "Wolfram Alpha". 
  51. ^ Simopoulos AP, Norman HA, Gillaspy JE, Duke JA. Common purslane: a source of omega-3 fatty acids and antioxidants. J Am Coll Nutr. 1992;11(4):374-82.
  52. ^ "09038, Avocados, raw, California". National Nutrient Database for Standard Reference, Release 26. United States Department of Agriculture, Agricultural Research Service. Retrieved 14 August 2014. 
  53. ^ USDA List for Vitamin E in Vegetable Oils
  54. ^ Institute of Medicine. Food and Nutrition Board. (2000). Dietary Reference Intakes: Applications in Dietary Assessment. Washington, DC: National Academy Press. p. 289.  
  55. ^ Evans HM, Bishop KS (1922). "On the existence of a hitherto unrecognized dietary factor essential for reproduction".  
  56. ^ Oakes, Elizabeth H. (2007). "Emerson, Gladys Anderson". Encyclopedia of World Scientists. p. 211.  
  57. ^ Subcommittee on Vitamin Tolerance, Committee on Animal Nutrition, National Research Council (1987). "Vitamin E, in Vitamin Tolerance of Animals". National Academy of Sciences. Retrieved December 22, 2013. 
  58. ^ Shute, W. E.; Shute, E. V.; et al., Alpha Tocopherol (Vitamin E) in Cardiovascular Disease. Toronto, Ontario, Canada: Ryerson Press, 1945
  59. ^ Vogelsang A, Shute EV (June 1946). "Effect of vitamin E in coronary heart disease". Nature 157: 772.  
  60. ^ Shute EV, Vogelsang AB, Skelton FB, Shute WE (January 1948). "The influence of vitamin E on vascular disease". Surg Gynecol Obstet 86 (1): 1–8.  
  61. ^ Skelton F, Shute E, Skinner HG, Waud RA (1946). "Antipurpuric Action of A-Tocopherol (Vitamin E)". Science 103 (2687): 762.  
  62. ^ György P, Rose CS (1948). "Effect of dietary factors on early mortality and hemoglobinuria in rats following administration of alloxan". Science 108 (2817): 716–718.  
  63. ^ Gerloczy F (1949). "Clinical and pathological role of d, 1-alpha tocopherol in premature infants; studies on the treatment of scleroedema". Ann Paediatr 173 (3): 171–86.  
  64. ^ Brion LP, Bell EF, Raghuveer TS (2003). Brion, Luc P, ed. "Vitamin E supplementation for prevention of morbidity and mortality in preterm infants". Cochrane Database Syst Rev (4): CD003665.  

Further reading

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