Vitamin E

Vitamin E refers to a group of eight fat-soluble compounds that include four tocopherols and four tocotrienols (alpha, beta, gamma, and delta forms). Alpha-tocopherol is the most biologically active form in humans and the form preferentially absorbed and maintained in the body.

The primary function of vitamin E is as a lipid-soluble antioxidant. It protects cell membranes from oxidative damage by neutralizing free radicals, particularly reactive oxygen species (ROS) that can damage polyunsaturated fatty acids in cell membranes. This protective role extends to all cells but is especially important for cells with high metabolic activity and abundant membranes, such as nerve cells, red blood cells, and immune cells.

Beyond its antioxidant function, vitamin E plays important roles in immune function, cellular signaling, gene expression, and metabolic processes. It enhances immune responses, particularly in older adults, and helps maintain healthy skin by protecting against UV damage and supporting wound healing. Vitamin E also influences the expression of genes involved in inflammation, cell cycle regulation, and cell adhesion.

The body stores vitamin E primarily in adipose tissue, with smaller amounts in the liver, muscle, and other tissues. Unlike water-soluble vitamins, vitamin E can be stored for extended periods, and deficiency typically takes months to develop when intake is inadequate.

While vitamin E deficiency is rare in healthy individuals with adequate fat absorption, certain conditions increase risk, including fat malabsorption disorders, genetic defects in vitamin E transport proteins, and very low-fat diets. Deficiency primarily affects the nervous system and can cause serious neurological symptoms.

Vitamin E functions primarily as a lipid-soluble antioxidant. Alpha-tocopherol, the most active form, incorporates into cell membranes where it donates hydrogen atoms to neutralize lipid peroxyl radicals, preventing the chain reaction of lipid peroxidation that damages cell membranes. After donating an electron, vitamin E is regenerated by other antioxidants, particularly vitamin C, allowing it to be reused.

In immune function, vitamin E modulates T-cell function and enhances the proliferative response of lymphocytes. It reduces production of prostaglandin E2, an immunosuppressive compound, and enhances interleukin-2 production, which promotes T-cell growth and differentiation. These effects are particularly important in older adults, where immune function naturally declines.

Vitamin E influences gene expression through several mechanisms. It can activate protein kinase C, a signaling enzyme involved in cell proliferation and differentiation. It also affects the activity of transcription factors including NF-kappaB and AP-1, which regulate genes involved in inflammation and cell growth. Through these pathways, vitamin E can modulate expression of genes involved in immune response, cell adhesion, and inflammatory processes.

In the skin, vitamin E absorbs UVB radiation and acts as a photoprotectant. It reduces UV-induced free radical damage to skin cells and helps maintain the skin's barrier function by protecting lipids in cell membranes. When applied topically or consumed orally, vitamin E supports wound healing by reducing oxidative stress and promoting tissue repair.

Absorption of vitamin E requires dietary fat and intact pancreatic function and bile secretion. Alpha-tocopherol is absorbed in the small intestine, incorporated into chylomicrons, and transported to the liver. The liver selectively retains alpha-tocopherol (via alpha-tocopherol transfer protein, alpha-TTP) for distribution in lipoproteins, while other tocopherols and tocotrienols are preferentially metabolized and excreted.

Vitamin E is found in a variety of foods, with the highest concentrations in plant oils, nuts, seeds, and green leafy vegetables. Wheat germ oil is particularly rich in vitamin E. Animal products generally contain lower amounts, primarily in the fatty portions.

Vitamin E deficiency is rare but can cause serious neurological problems when it occurs. Primary deficiency results from fat malabsorption disorders, genetic defects affecting vitamin E transport, or very low-fat diets. The nervous system is most affected due to high lipid content of neuronal membranes.

Vitamin E requirements are based on the amount needed to prevent deficiency symptoms in healthy individuals. Requirements increase with higher polyunsaturated fat intake because vitamin E protects these fats from oxidation. The RDA is expressed as milligrams of alpha-tocopherol.

Vitamin E supplements contain either natural (d-alpha-tocopherol) or synthetic (dl-alpha-tocopherol) forms. Natural vitamin E has approximately twice the bioactivity of synthetic forms. Mixed tocopherol supplements provide gamma, delta, and beta tocopherols in addition to alpha-tocopherol.