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One of the most frequently studied natural compounds is vitamin E. It is a family of molecules that have a potent antioxidant effect in fat rich tissues such as skin, nerves and vital organs. A number of studies have found that vitamin E supplementation reduces lipid peroxidation, improves cognitive performance after brain injury, improves hot flashes in menopause, and lowers cholesterol.1 Vitamin E deficiency has been linked to Alzheimer’s disease; however, supplementation has not shown clear and consistent benefit.2 Population studies suggest that vitamin E may have a preventative role in cancer. However, several recent large-scale human trials with ?-tocopherol, the most commonly used form of vitamin E, failed to show a cancer preventive effect.1 The recently published Selenium and Vitamin E Cancer Prevention Trial (SELECT) even showed higher prostate cancer incidence in subjects who supplemented with ?-tocopherol.3 Vitamin E possesses therapeutic potential based on its proposed action in the body, but there is growing negative and conflicting evidence. What can be concluded about its health benefits? Is it safe to be used as supplement?

Some of the conflicting results may be due to a number of flaws that exist in the use of vitamin E as an intervention in research trials. Vitamin E is a family of 8 molecules (four tocopherols and four tocotrienols) that function synergistically in human physiology.1 Most studies have only used low doses of ?-tocopherol, which has been thought to be the active form in human physiology, since it’s the most common form found in tissues. Many studies state they use vitamin E, but in reality they are only supplementing with one form and not the full group of molecules that makes up vitamin E. While tocotrienols represent 50% of the vitamin E molecules, over 95% of all studies to date have only used ?-tocopherol.4 There also is evidence that the natural form has a more detrimental effect than synthetic ?-tocopherol.1 While this flies in the face of the notion that natural forms are usually more bioavailable, the evidence suggests that both forms of ?-tocopherol have a negative effect on mortality. The reason that ?-tocopherol may have a detrimental effect on mortality is that it strongly binds to a vitamin E transfer protein in the liver which prevents the absorption and distribution of other forms of tocopherols and tocotrienols.1,5

The other forms of tocopherols and tocotrienols have been shown to have a better chemo-protective and anti-inflammatory effect than ?-tocopherol. While ?-tocopherol does have an anti-thrombotic effect, ?-tocopherol is the main anti-inflammatory component of the vitamin E family and has been found to be more effective than the alpha form in scavenging free radicals that cause inflammation. ?-tocopherol is more protective against certain types of cancer and myocardial infarction than ?-tocopherol.6

Emerging evidence suggests that the tocotrienol family has even more benefits than the tocopherols in stroke recovery, cancer prevention and vascular health.4 Preclinical and animal studies have shown tocotrienols are able to lower cholesterol and protect cellular membranes through a powerful antioxidant effect. Like ?-tocopherol, tocotrienols possess powerful anti-inflammatory effects, which represent promising application in brain injury and cancer prevention.4 The question arises, why are tocotrienols superior to ?-tocopherol? The answer is not completely clear but it appears they are better distributed throughout fatty tissue, and unlike ?-tocopherol they do not inhibit the transport and bioavailability of other forms.

In addition, vitamin E works with other antioxidants such as vitamin C and Coenzyme Q10 as part of an antioxidant network. Supplementation with a single antioxidant can lead to itself becoming oxidized if adequate levels of supporting antioxidants are not present.7 The fact that studies have only used ?-tocopherol and not the full spectrum of vitamin E molecules and supportive antioxidants, may be the reason that have led to poor outcomes in research trials. A number of negative studies have put the whole vitamin E family in a negative light while the true culprit is only ?-tocopherol. The synergistic nature of the vitamin E family highlights the need to supplement antioxidants together in order to support their proper biological function in the body. Recent evidence is starting to support the benefit of all the forms of vitamin E in cognitive decline and obesity related diseases, although more is needed to vindicate this misunderstood vitamin.8,9

The full spectrum of tocopherols and tocotrienols offer unique and pronounced health benefits if we can adopt the reality that they must be supplemented together. Whenever looking for a vitamin E supplement, make sure that it contains all 8 forms for vitamin E, with high amounts of tocopherol and tocotrienols, to harness all the beneficial effects.


1. Gee PT . Unleashing the untold and misunderstood observations on vitamin E. Genes Nutr. 2011 Feb;6(1):5-16.
2. Joshi YB, Praticò D. Vitamin E in aging, dementia, and Alzheimer’s disease. Biofactors. 2012 Mar-Apr;38(2):90-7.
3. Yang CS, Suh N, Kong AN. Does vitamin E prevent or promote cancer? Cancer Prev Res (Phila). 2012 May;5(5):701-5.
4. Sen CK, Khanna S, Roy S (2007) Tocotrienols in health and disease: the other half of the natural vitamin E family. Mol Aspects of Med 28:693–728.
5. Huang H-Y, Appel LJ (2003) Supplementation of diets with a-tocopherol reduces serum concentrations of c- and d-tocopherol in humans. J Nutr 133:3137–3140
6. Wagner KH, Kamal-Eldin A, Elmadfa I. Gamma-tocopherol–an underestimated vitamin? Ann Nutr Metab. 2004; 48(3):169-88.
7. Usoro OB, Mousa SA. Vitamin E forms in Alzheimer’s disease: A review of controversial and clinical experiences. Crit Rev Food Sci Nutr. 2010;50:414–9
8. Mangialasche et al. Tocopherols and tocotrienols plasma levels are associated with cognitive impairment. Neurobiol Aging. 2012 Oct;33(10):2282-90
9. Yachi R, Muto C, Ohtaka N, Aoki Y, Koike T, Igarashi O, Kiyose C. Effects of tocotrienol on tumor necrosis factor-?/d-galactosamine-induced steatohepatitis in rats. J Clin Biochem Nutr. 2013 Mar;52(2):146-53.

Dr. Paul Hrkal

About The Author

Dr. Paul Hrkal is a board-certified Naturopathic doctor with a passion to apply innovative and evidence-based nutritional, biological, and supplemental interventions to address underlying metabolic, endocrine and immunological dysfunctions. He is strong advocate of integrative medical education frequently writing and lecturing to both healthcare practitioners and public audiences. He also is the medical director for Advanced Orthomolecular Research, a leading Canadian natural health product company, and maintains a clinical practice in the Toronto area.

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