For Patients & Caregivers
How It Works
A diet containing adequate amounts of vitamin E is important in maintaining general health, and may prevent against some forms of cancer. The ability of vitamin E to prevent or treat Alzheimer’s disease, rheumatoid arthritis, or heart disease requires further study.
Vitamin E, also known as alpha-tocopherol, is a natural antioxidant that is found in foods such as plant oils, eggs, nuts, green leafy vegetables, and whole grains. The major function of vitamin E is to act as a free-radical scavenger, meaning that it neutralizes free radicals and protects cells from their damaging effects. Therefore, vitamin E is being investigated in conditions such as Alzheimer’s disease and cancer, in which free radical damage is known to play a part. (See the Research Evidence section for more information about this.)
Vitamin E also lessens the blood’s ability to clot by suppressing the number of adhesion molecules on the lining of the blood vessel walls. With fewer adhesion molecules, cells in the blood are less likely to “dock” on the blood vessel wall and start forming a clot. In addition, vitamin E causes the release of prostacyclin, which itself dilates the blood vessels and inhibits blood clotting. This may be helpful in patients with coronary artery disease, in which blood clots can form around atherosclerotic plaques in coronary arteries.
Scientists think that vitamin E also inhibits a molecule called protein kinase C, which is involved in cell proliferation and differentiation in smooth muscle, platelets, and monocytes (a type of immune cell). Although in theory this would be helpful against cancer cells, this effect has not been strongly shown in humans. An animal study shows NAC can speed up the growth of lung cancer cells due to its antioxidant activity.
To prevent the progression of Alzheimer’s disease
One clinical trial showed that vitamin E helped prevent progression of Alzheimer’s disease. A few population-based studies have suggested that high intake of vitamin E in the diet is associated with a lower risk of developing Alzheimer’s disease.
To treat arthritis
One clinical trial suggested that vitamin E can relieve pain in patients with rheumatoid arthritis, but has no anti-inflammatory effect. No other clinical trials have tested this use.
To prevent cancer
Large population-based studies in Finland found that taking vitamin E supplements reduced the risk of prostate and colorectal cancers in male smokers. However, initial data from the large-scale SELECT (Selenium and Vitamin E Cancer Prevention) Trial shows vitamin E taken alone or with selenium for five years, did not reduce the risk of prostate cancer. Vitamin E supplementation had no effect on lung, urinary tract, pancreas, mouth or stomach cancer risks. Another trial in patients with head and neck cancers found that patients who received vitamin E had a higher rate of second primary cancers compared with those on placebo, and that vitamin E may interfere with radiation therapy.
To manage heart disease
Data from clinical trials show that vitamin E does not help prevent heart disease.
To prevent cataracts
Two clinical trials do not support this use
To prevent the cardiovascular complications of diabetes
Several clinical trials have shown that vitamin E supplements may be helpful in preventing LDL oxidation in patients with diabetes, which may help prevent progression to atherosclerosis.
- To treat liver diseases
- Vitamin E can be used to treat fatty liver disease not caused by alcohol in adults
To stimulate the immune system
No scientific evidence supports this use.
To prevent the progression of Parkinson’s disease
Clinical trials do not support this use.
To improve wound healing
No scientific evidence supports this use.
To reduce hot flashes
A clinical trial showed that vitamin E reduces hot flashes in breast cancer survivors somewhat, but most patients did not prefer vitamin E over placebo at the end of the study and.
- A recent analysis of seven brands of commercially available vitamin E found their actual content to vary considerably from the labeled dosage, from 41% less than the labeled amount, to 57% more.
- This product is regulated by the FDA as a dietary supplement. Unlike approved drugs, supplements are not required to be manufactured under specific standardized conditions. This product may not contain the labeled amount or may be contaminated. In addition, it may not have been tested for safety or effectiveness.
Do Not Take If
- Natural vitamin E supplements that are derived from plant oils contain d-alpha-tocopherol, which is believed to be the active form, while synthetic vitamin E supplements are a mixture of d-alpha-tocopherol and l-alpha-tocopherol (inactive forms).
- It is controversial whether antioxidants like vitamin E can lessen or negate the effects of chemotherapy and radiation therapy. Because these therapies work by creating free radicals that kill cancer cells, some physicians have suggested that high levels of antioxidants can neutralize these free radicals and thereby protect cancer cells from these therapies. So what protects healthy cells may protect cancer cells as well. This question is still not fully understood and patients who are interested in taking more than the RDA of any antioxidant should consult with their doctor.
For Healthcare Professionals
Vitamin E is a fat-soluble vitamin derived from plant. Natural food sources include plant oils, wheat germ, eggs, green leafy vegetables, and whole grains (3). Vitamin E acts as an antioxidant and is thought to help prevent and treat many diseases. Although available in a variety of formulations, only the d-isomer is considered active (1).
Studies evaluating vitamin E supplementation suggest that it may improve immune response in the elderly. Vitamin E may slow the progression of Alzheimer’s disease (9) (15) (16) (18); however, conflicting data from another study do not support the utility of antioxidants (vitamin E, vitamin C, lipoid acid, and Coenzyme Q) (43). It was also ineffective in arresting the development or progression of macular degeneration (14) and Early Parkinson’s Disease (21).
Vitamin E did not decrease the incidence of acute respiratory tract infections (12), reduce mortality, or reduce the risk of cardiovascular death or cerebrovascular accident (26). When taken along with vitamin C, vitamin E may increase mortality and nonfatal myocardial infarction in patients with coronary artery disease (13). Further, findings from the recent Physicians’ Health Study II show that neither vitamin E nor C is beneficial in preventing cardiovascular events; vitamin E may actually increase the risk of stroke (36). The Women’s Health Study also failed to find any benefit of vitamin E supplementation in lowering the risk of heart failure in healthy women (42). A meta-analysis showed that vitamin E increases the risk for hemorrhagic stroke but reduces the risk of ischemic stroke (38). Vitamin E can reduce signs and symptoms of nonalcoholic steatohepatitis in adults (45), but not in children and adolescents (46) .
Vitamin E was shown to reduce the risk of some cancers (19) (20). It may help to relieve hot flashes in breast cancer survivors (27), and to reduce the incidence of cisplatin-induced neurotoxicity (22). However, data suggest that supplementation with vitamins C, E, and beta carotene is not beneficial in preventing cancer incidence or affecting cancer mortality (37). Furthermore, vitamin E when used alone or with other supplements did not prevent gastrointestinal cancer (28). A large scale clinical Selenium and Vitamin E Cancer Prevention Trial (SELECT) evaluated the role of vitamin E in prostate cancer prevention. Initial review shows that vitamin E taken alone or with selenium for 5 years did not reduce the risk of prostate cancer (35); observational data from 7 years of participant follow-up indicate a significant increase in the risk of prostate cancer with vitamin E supplementation (41). Vitamin E, when used together with soy and selenium, did not prevent prostate cancer progression (40). Further, findings from other studies indicate vitamin E may actually increase risk of lung cancer (33) and overall mortality (28). At the same time, conflicting data suggest an association between dietary tocopherol and a reduction in risk of lung cancer (38) (48). Also, both dietary and supplemental form of vitamin E may reduce the risk of liver cancer (44).
Toxicity may occur with chronic supplementation of vitamin E with doses greater than 800 IU. Daily supplementation over 400 IU may increase all-cause mortality (29). Vitamin E may also enhance the activity of warfarin, but data are inconsistent (7) (8).
Mechanism of Action
Vitamin E is a fat soluble vitamin that acts as an antioxidant. The natural form of vitamin E is composed of 4 different tocopherols and 4 different tocotrienol homologues (alpha, beta, delta and gamma). All 8 forms have antioxidant activity but recent data indicate that the different homologues have different activities unrelated to antioxidant effects (34).
Gamma-tocopherol is a stronger inhibitor of cyclooxygenase and traps reactive oxygen species more effectively than alpha-tocopherol. In vitro and in vivo, gamma-tocopherol exhibits anti-proliferative and pro-apoptotic effects where alpha-tocopherol does not (34) . While both alpha- and gamma-tocopherols exhibit anti-inflammatory effects in vitro and in vivo, gamma-enriched mixed tocopherols may be more potent compared to alpha-tocopherols. This may help explain the negative outcomes of recent large-scale intervention studies that used only the alpha homologue (34).
The d-alpha-tocopherol isomer is believed to be the active principle. Natural vitamin E supplements contain d-alpha-tocopherol derived from plant oil sources, whereas synthetic supplements are composed of a racemic mixture of d- and l-alpha-tocopherols. The major function of d-alpha-tocopherol is to prevent the propagation of free radical reactions by acting as a peroxyl radical scavenger and protecting polyunsaturated fatty acids (PUFAs) within membrane phospholipids and in plasma lipoproteins. Alpha-tocopherol reportedly causes inhibition of protein kinase C activity, which is involved in cell proliferation and differentiation in smooth muscle cells, human platelets, and monocytes. Vitamin E enrichment of endothelial cells, down regulates the expression of intercellular adhesion molecule (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby decreasing the adhesion of blood cell components to the endothelium. Vitamin E also upregulates the expression of cytosolic phospholipase A2 and cyclooxegenase-1, which leads to the release of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation in humans (3).
In an animal study, vitamin E increased lung cancer cell proliferation due to its antioxidant activity by reducing reactive oxygen species (ROS), DNA damage and p53 expression (47).
Although many research protocols use milligrams of vitamin E, most commercial products are sold in international units (IU). One IU natural vitamin E equals 0.67 mg d-alpha-tocopherol and one IU of synthetic vitamin E equals 0.45 mg d-alpha-tocopherol.