16 Facts About Vitamin E

Vitamin E is a group of eight fat soluble compounds that include four tocopherols and four tocotrienols.

Vitamin E was discovered in 1922, isolated in 1935 and first synthesized in 1938.

The thus-generated tocopheryl radical is recycled to tocopherol by a redox reaction with a hydrogen donor, such as vitamin C As it is fat-soluble, vitamin E is incorporated into cell membranes, which are therefore protected from oxidative damage.

Vitamin E affects gene expression and is an enzyme activity regulator, such as for protein kinase C – which plays a role in smooth muscle growth – with vitamin E participating in deactivation of PKC to inhibit smooth muscle growth.

Vitamin E biosynthesis occurs in the plastid and goes through two different pathways: the Shikimate pathway and the Methylerythritol Phosphate pathway.

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Vitamin E deficiency is rare in humans, occurring as a consequence of abnormalities in dietary fat absorption or metabolism rather than from a diet low in vitamin E One example of a genetic abnormality in metabolism is mutations of genes coding for alpha-tocopherol transfer protein.

In multiple clinical trials, vitamin E lowered blood concentration of the immunosuppressant medication, cyclosporine A The US National Institutes of Health, Office of Dietary Supplements, raises a concern that co-administration of vitamin E could counter the mechanisms of anti-cancer radiation therapy and some types of chemotherapy, and so advises against its use in these patient populations.

Vitamin E is fat soluble, so dietary supplement products are usually in the form of the vitamin, esterified with acetic acid to generate tocopheryl acetate, and dissolved in vegetable oil in a softgel capsule.

Various forms of vitamin E are common food additive in oily food, used to deter rancidity caused by peroxidation.

Additionally, vitamin E is excreted by the liver via bile into the intestinal lumen, where it will either be reabsorbed or excreted via feces, and all of the vitamin E vitamers are metabolized and then excreted via urine.

An older meta-analysis had concluded high-dosage vitamin E was associated with an increase in all-cause mortality.

In 2017, a consensus statement from the British Association for Psychopharmacology concluded that, until further information is available, vitamin E cannot be recommended for treatment or prevention of Alzheimer's disease.

Synthetic, racemic mixtures of vitamin E isomers are not bioequivalent to natural, non-racemic mixtures, yet are widely used in clinical trials and as dietary supplement ingredients.

Vitamin E status has been implicated in the maintenance of normal endothelial cell function of cells lining the inner surface of arteries, anti-inflammatory activity and inhibition of platelet adhesion and aggregation.

The review identified only three small trials in which vitamin E was supplemented without co-supplementation with vitamin C None of these trials reported any clinically meaningful information.

Vitamin E was discovered in 1922 by Herbert McLean Evans and Katharine Scott Bishop and first isolated in a pure form by Evans and Gladys Anderson Emerson in 1935 at the University of California, Berkeley.