The beneficial effects of Vitamin E have bounced back and forth over the years. Lately, new data is emerging suggesting that it actually can be very beneficial. The key may be in ingesting the right forms of the vitamin and inadequate amounts.

Vitamin E is present in many foods in several forms. The most common for is alpha-tocopherol, and this is the form in most supplements. The other forms, gamma-tocopherol, delta-tocopherol and tocotrienols are also in these foods, but in lesser amounts. Most supplements contain minimal amounts of these lesser vitamin E forms.

Original studies suggested beneficial effects of vitamin E to help prevent many medical conditions. A 1993 study showed there was a reduction in heart disease (1). In 1997, a study showed that Vitamin E slowed the Progression of Alzheimer’s disease (2). In 1998, research showed a reduction in the incidence of prostate cancer by 32% and a reduction of mortality from prostate cancer up to 41% by using high doses of Vitamin E at 400 u per day (3).

Both of these studies were refuted in 2004 when another combined study suggested that high doses of Vitamin E actually did more harm than good: mortality was actually worse when high doses were used vs. not used (4). Another large study, the Woman’s Healthcare Study, showed no beneficial effects from ingesting Vitamin E (5). In 2009, more evidence appeared showing no beneficial effect of Vitamin E to reduce prostate cancer (6).

Fortunately, some recent research has been able to explain the perplexing contradictory results seen. The main reason has to do with the type of Vitamin E used. When only the alpha form is taken, no help with prevention of these medical problems seem to exist. But when the other forms are primarily ingested, there seems to be a significant reduction in medical conditions, and these are the forms we should be taken to improve our health.

In 2008 and 2009, several studies showed that gamma-tocopherol decreased sinusitis, asthma and allergic inflammation (7, 8) and that it could be helpful in these diseases. They also have been shown to decrease oxidative stress and thus could be considered a type of anti-aging supplement (9).

Another form of Vitamin E, called tocotrienols, has also been shown to be very beneficial. The Gamma-tocotrienol form has been shown to be very helpful in protecting the body from radiation injury (10). This suggests a mechanism for sun damage protection and anti-aging effects on the skin (11). These confirm the anti-oxidative and anti-inflammatory effects of gamma-tocotrienols on the body (12).

Both the above beneficial forms of vitamin E (gamma-tocopherol and gamma-tocotrienol) have recently been shown to be very effective in reducing one’s risk of developing Alzheimer’s dis. (13, 14, 15). These studies confirm the role of these forms of Vitamin E in neuroprotection and related diseases including Alzheimer’s.

Trocotrienols in high amounts have also been shown to be cardioprotective. These not only reduce abnormal blood lipids, but they also serve an antioxidative role to help prevent the deposition and oxidation of these lipids within the lining of the blood vessels; events which would otherwise have lead to atherosclerosis, hardening of the arteries, and then to heart attacks.

In conclusion, recent research has clarified the confusing findings in the past regarding the use of Vitamin E and improving ones’ health. The better forms of Vitamin E, gamma tocopherol and gamma-trienols, have been shown, in major clinical studies, and at high levels, to reduce several debilitating medical conditions that have been associated with oxidative stress and inflammation.

The new recommendations for Vitamin E are to use preparations that contain high amounts of these beneficial forms. For age <40, take 200 IU per day with 100 IU of this being the gamma forms; for age>40, take 400 IU per day with 200 IU of these as the gamma forms. Taking more than 400 IU per day is not recommended.

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2. N.Eng.J.Med, 1997, 336:1216-22.
3. J.Nat. Cancer Institute, 1998.
4. Ann Intern Med, 2005, 4:14237-46.
5. JAMA, 2005, July 6, 294:56-57.
6. JAMA, 2009, 301; 39-51.
7. Toxicol Pathol 2009,37:481-91.
8. Free Radia Bio Med, 2008, 45:40-9.
9. ClinExpAll, 2008; 38:501-11.
10. Int J Radia Bio, 2009,85:598-606.
11. J Agr Food Chem,2010,58:7013-20.
12. Exp Mol Path, 2006; 81:55-61.
13. J Alzheimer’s Dis 2010;20:1029-37
14. Am J Clin Nutr 2005; 81:508-14.
15. Neuropharmacology 2004; 47:904-15.