Vitamin E

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- (respectively: alpha, beta, gamma, and delta) 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]

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 alpha-tocopherol, but doing so leads to reduced serum gamma- and delta-tocopherol concentrations. Moreover, a 2007 clinical study involving 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.

Tocotrienols

Compared with tocopherols, tocotrienols are sparsely studied.^[14][15][16] Less than 1% of PubMed papers on vitamin E relate to tocotrienols.^[17] 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^[17] and cholesterol reduction^[18] 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 thought to protect against stroke-associated brain damage in vivo. 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.^[19]

Recommended daily intake

The Food and Nutrition Board at the Institute of Medicine report the following dietary reference intakes for vitamin E:^[20]

Infants

• 0 to 6 months: 4 mg/day
• 7 to 12 months: 5 mg/day

Children

• 1 to 3 years: 6 mg/day
• 4 to 8 years: 7 mg/day
• 9 to 13 years: 11 mg/day

Adolescents and Adults

• 14 and older: 15 mg/day

Dietary sources and supplements

The following foods are rich in vitamin E:^[21]

• fortified cereals
• seeds and seed oils, like sunflower and safflower
• nuts and nut oils, like almonds and hazelnuts
• green leafy vegetables, like spinach, turnip, beet, collard, and dandelion greens
• tomato products
• pumpkin
• sweet potato
• blue crab
• canola oil
• rockfish
• mangoes
• asparagus
• broccoli
• papayas

Health effects

The consensus in the medical community is that there is no good evidence to support health benefits from vitamin E supplementation, yet there is strong evidence that taking more than 400 IU of vitamin E per day for extended periods increases the risk of death.^{[22][23][24][25]}

Deficiency

Vitamin E deficiency can cause:

• spinocerebellar ataxia^[6]
• myopathies^[26]
• peripheral neuropathy ^[27][28][23]
• ataxia^[27][28][23]
• skeletal myopathy^[27][28][23]
• retinopathy^[27][28][23]
• impairment of the immune response^[27][28][23]

References

Further reading

• Brigelius-Flohe, Regina; Kelly, F; Salonen, J; Neuzil, J; Zingg, J; Azzi, A (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. 

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