The antioxidant that protects the fats in your cell membranes.
Mechanisms, studies and evidence grades for each claim above.
Cell membranes are made of fats, and the polyunsaturated ones (PUFAs, mainly linoleic acid and the omega-3s) have weak spots. A carbon sitting between two double bonds gives up a hydrogen atom easily. Once a free radical takes it, the fatty acid becomes a radical itself, reacts with oxygen to form a lipid peroxyl radical, and takes a hydrogen from the next PUFA. This lipid peroxidation chain reaction can run through hundreds of fatty acids from a single starting event, damaging membranes and producing toxic aldehydes such as 4-HNE and malondialdehyde.1
Alpha-tocopherol stops the chain. It sits inside the membrane with its reactive ring near the surface, where peroxyl radicals form. It gives them a hydrogen atom about 1,000 times faster than a PUFA would, which ends the chain. The tocopheryl radical left behind is stable and doesn't continue the reaction. Vitamin C then restores it at the membrane surface, and glutathione and NADPH in turn restore vitamin C (see Vitamin C). Traber's review puts it plainly: vitamin E's essential job is to be a fat-soluble chain-breaking antioxidant, and nothing more.1
That makes the requirement depend on PUFA intake. The more PUFA in your membranes, the more targets for peroxidation, and the more vitamin E you need. The usual estimate is about 0.6 mg of vitamin E per gram of linoleic acid, more for fats with three or more double bonds.2 A diet high in seed oils raises vitamin E needs even as the oils supply it. A diet low in linoleic acid needs less. That's the link to this site's Linoleic Acid paper.
The clearest human evidence is from genetic disease. People with defects in the liver's vitamin E transfer protein (α-TTP), or who can't absorb fat, develop a progressive ataxia (loss of coordination) and peripheral neuropathy as the long, PUFA-rich nerve fibres slowly oxidise. Vitamin E supplements stop it.1
↑ back to summaryImmune cells have more vitamin E than almost any other cells in the body, and they need it. T cell membranes are rich in PUFA and exposed to the oxidative bursts that immune cells use to kill germs. As we age, T cells respond less well, partly because of more oxidative stress and more prostaglandin E2 (which suppresses T cells) from macrophages. Vitamin E lowers PGE2 production and helps T cells form the contact points (immune synapses) they need to activate.
Human trials in older adults. In a randomised trial in healthy people over 65, 200 mg/day of vitamin E for 4 months raised skin-test immune responses by 65% and antibody response to hepatitis B vaccine six-fold. Oddly, 800 mg/day worked less well than 200.3 In nursing-home residents, a year of 200 IU/day didn't reduce lower respiratory infections. It did slightly reduce the share of people who caught at least one infection (60% vs 68%), mostly colds.4 So the benefit is real but modest and seen in older people, whose immune systems are under the most oxidative strain.
↑ back to summaryThe RDA is 15 mg/day of alpha-tocopherol. Other forms of vitamin E in food (gamma-tocopherol and tocotrienols) are poorly kept by the body, because the liver's transfer protein strongly prefers the natural RRR-alpha form. Synthetic "dl-alpha" is about half as active.
Seed oils and nuts, which top most vitamin E lists, are left off on purpose. They are also the richest sources of linoleic acid, and the extra PUFA they bring raises the demand for the vitamin E they supply (see above and Linoleic Acid).
↑ back to summaryDeficiency from diet alone is rare. It happens with fat malabsorption (cystic fibrosis, cholestatic liver disease, pancreatic insufficiency, bariatric surgery), genetic α-TTP deficiency, and in premature infants. Signs develop slowly: loss of reflexes and position sense, unsteady gait, peripheral neuropathy, muscle weakness, retinal damage, red cells that break apart under oxidative stress, and weaker immunity.1
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