Also indexed as: Alpha Tocopherol, Tocopherol, Tocopheryl
(Acetate, Succinate)
What does it do?
Vitamin E is an antioxidant that protects cell
membranes and other fat-soluble parts of the body, such as low-density lipoprotein (LDL;
“bad” cholesterol) cholesterol, from
damage.
Only when LDL is damaged does cholesterol appear to lead to heart disease, and vitamin E is an important
antioxidant protector of LDL.1 Several studies,2 3 including
two double-blind trials,4 5 have reported that 400 to 800 IU of natural
vitamin E per day reduces the risk of heart attacks. Other recent double-blind trials have
found either limited benefit6 or no benefit at all from supplementation with
synthetic vitamin E.7 One of the negative trials used 400 IU of natural vitamin
E8 —a similar amount and form to previous successful trials. In attempting to
make sense of these apparently inconsistent findings, the following is clear: less than 400 IU
of synthetic vitamin E, even when taken for years, does not protect against heart disease.
Whether 400 to 800 IU of natural vitamin E is, or is not, protective remains unclear.
Vitamin E also plays some role in the body’s ability to process glucose. Some, but
not all, trials suggest that vitamin E supplementation may eventually prove to be helpful in
the prevention and treatment of diabetes.
In the last ten years, the functions of vitamin E in the cell have been further clarified.
In addition to its antioxidant functions, vitamin E is now known to act through other
mechanisms, including direct effects on inflammation, blood cell regulation, connective tissue
growth, and genetic control of cell division.9
Where is it found?
Wheat germ oil, nuts and seeds, whole grains, egg yolks,
and leafy green vegetables all contain vitamin E.
Certain vegetable oils should contain
significant amounts of vitamin E. However, many of the vegetable oils sold in supermarkets
have had the vitamin E removed in processing. The high amounts found in supplements, often 100
to 800 IU per day, are not obtainable from eating food.
Vitamin E has been used in
connection with the following conditions (refer to the individual
health concern for complete information):
Who is likely to be deficient?
Severe vitamin E deficiencies are rare. People with a genetic defect in a vitamin E
transfer protein called thrombotic thrombocytopenic purpura (TTP) have severe vitamin E
deficiency, characterized by low blood and tissue levels of vitamin E and progressive nerve
abnormalities.10 11
Low vitamin E status has been associated with an increased risk of rheumatoid arthritis12 and major depression.13 Women with preeclampsia have been found to have lower blood levels of
vitamin E than women without the condition.14
Very old people with type 2 diabetes have shown a
significant age-related decline in blood levels of vitamin E, irrespective of their dietary
intake.15
How much is usually taken?
The recommended dietary allowance for vitamin E is low, just 15 mg or approximately 22
International Units (IU) per day. The most commonly recommended amount of supplemental vitamin
E for adults is 400 to 800 IU per day. However, some leading researchers suggest taking only
100 to 200 IU per day, since trials that have explored the long-term effects of different
supplemental levels suggest no further benefit beyond that amount. In addition, research
reporting positive effects with 400 to 800 IU per day has not investigated the effects of
lower intakes.22 For tardive
dyskinesia, the best results have been achieved from 1,600 IU per day,23 a
large amount that should be supervised by a healthcare practitioner.
Are there any side effects or interactions?
Vitamin E toxicity is very rare and supplements are widely considered to be safe. The
National Academy of Sciences has established the daily tolerable upper intake level for adults
to be 1,000 mg of vitamin E, which is equivalent to 1,500 IU of natural vitamin E or 1,100 IU
of synthetic vitamin E.24
In a double-blind study of healthy elderly people, supplementation with 200 IU of vitamin E
per day for 15 months had no effect in the incidence of respiratory infections, but increased
the severity of those infections that did occur.25 For elderly individuals, the
risks and benefits of taking this vitamin should be assessed with the help of a doctor or
nutritionist.
In contrast to trials suggesting vitamin E improves glucose tolerance in people with diabetes, one trial reported that 600 IU per day of vitamin
E led to impairment in glucose tolerance in obese people with diabetes.26 The
reason for the discrepancy between reports is not known.
In a double-blind study of people with established heart disease or diabetes, participants who took 400 IU of vitamin E per day for
an average of 4.5 years developed heart failure
significantly more often than did those taking a placebo.27 Hospitalizations for
heart failure occurred in 5.8% of those in the vitamin E group, compared with 4.2% of those in
the placebo group, a 38.1% increase. Considering that some other studies have shown a
beneficial effect of vitamin E against heart disease, the results of this study are difficult
to interpret. Nevertheless, individuals with heart disease or diabetes should consult their
doctor before taking vitamin E.
Patients on kidney dialysis who are given injections of iron
frequently experience “oxidative stress.” This is because iron is a pro-oxidant,
meaning that it interacts with oxygen molecules in ways that may damage tissues. These adverse
effects of iron therapy may be counteracted by supplementation with vitamin
E.28
A diet high in unsaturated fat increases vitamin E requirements. Vitamin E and selenium work together to protect fat-soluble parts of the
body.
Are there any drug
interactions?
Certain medicines may interact with vitamin E. Refer to drug interactions for a list of those medicines.
References
1. Balz F. Antioxidant vitamins and heart disease. Presented at the 60th
Annual Biology Colloquium, Oregon State University, Corvallis, Oregon, February 25, 1999.
2. Rimm EB, Stampfer MJ, Ascherio A, et al. Vitamin E consumption and the
risk of coronary heart disease in men. N Engl J Med 1993;328:1450–6.
3. Stampfer MJ, Hennekens CH, Manson JE, et al. Vitamin E consumption and
the risk of coronary heart disease in women. N Engl J Med 1993;328:1444–9.
4. Stephens NG, Parsons A, Schofield PM, et al. Randomised controlled
trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study
(CHAOS). Lancet 1996;347:781–6.
5. Boaz M, Smetana S, Weinstein T, et al. Secondary prevention with
antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised
placebo-controlled trial. Lancet 2000;356:1213–8.
6. GISSI-Prevenzione Investigators. Dietary supplementation with n-3
polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the
GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto
miocardico. Lancet 1999; 354:447–55.
7. Collaborative Group of the Primary Prevention Project (PPP). Low-dose
aspirin and vitamin E in people at cardiovascular risk: a randomized trial in general
practice. Lancet 2001;357:89–95.
8. Yusuf S, Dagenais G, Pogue J, et al. Vitamin E supplementation and
cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study
Investigators. N Engl J Med 2000;342:154–60.
9. Azzi A, Breyer I, Feher M, et al. Specific cellular responses to
a-tocopherol. J Nutr 2000;130:1649–52.
10. Traber MG. Vitamin E. In: Shils ME, Olsen JA, Shike M, Ross AC (eds).
Modern Nutrition in Health and Disease. Baltimore: Williams & Wilkins, 1999,
347–62.
11. Cavalier L, Ouahchi K, Kayden HJ, et al. Ataxia with isolated vitamin
E deficiency: heterogeneity of mutations and phenotypic variability in a large number of
families. Am J Hum Genet 1998;62:301–10.
12. Knekt P, Heliovaara M, Aho K, et al. Serum selenium, serum
alpha-tocopherol, and the risk of rheumatoid arthritis. Epidemiology
2000;11:402–5.
13. Maes M, De Vos N, Pioli R, et al. Lower serum vitamin E
concentrations in major depression. Another marker of lowered antioxidant defenses in that
illness. J Affect Disord 2000;58:241–6.
14. Kharb S. Total free radical trapping antioxidant potential in
pre-eclampsia. Int J Gynaecol Obstet 2000;69:23–6.
15. Polidori MC, Mecocci P, Stahl W, et al. Plasma levels of lipophilic
antioxidants in very old patients with type 2 diabetes. Diabetes Metab Res Rev
2000;16:15–9.
16. VERIS Research Information Service. Summary finds superiority of
natural vitamin E supplements over synthetic forms. Townsend Letter for Doctors &
Patients 1999;July:100–5 [review].
17. Acuff RV, Thedford SS, Hidiroglou NN, et al. Relative bioavailability
of RRR- and all-rac-alpha-tocopheryl acetate in humans: studies using deuterated compounds.
Am J Clin Nutr 1994;60:397–402.
18. Christen S, Woodall AA, Shigenaga MK, et al. Gamma-tocopherol traps
mutagenic electrophiles such as NO+ and complements alpha-tocopherol: physiological
implications. Proc Natl Acad Sci 1997;94:3217–22.
19. Morinobu T, Yoshikawa S, Hamamura K, Tamai H. Measurement of vitamin
E metabolites by high-performance liquid chromatography during high-dose administration of
alpha-tocopherol. Eur J Clin Nutr 2003;57:410–4.
20. Beijersbergen van Henegouwen GM, Junginger HE, de Vries H. Hydrolysis
of RRR-alpha-tocopheryl acetate (vitamin E acetate) in the skin and its UV protecting activity
(an in vivo study with the rat). J Photochem Photobiol B 1995;29:45–51.
21. Norkus EP, Bryce GF, Bhagavan HN. Uptake and bioconversion of
alpha-tocopheryl acetate to alpha-tocopherol in skin of hairless mice. Photochem
Photobiol 1993;57:613–5.
22. Rimm E. Micronutrients, coronary heart disease and cancer: should we
all be on supplements? Presented at the 60th Annual Biology Colloquium, Oregon State
University, February 25, 1999.
23. Hashim S, Sajjad A. Vitamin E in the treatment of tardive dyskinesia:
a preliminary study over 7 months at different doses. Int Clin Psychopharmacol
1988;13:147–55.
24. Panel on Dietary Antioxidants and Related Compounds, Food and
Nutrition Board, Institute of Medicine, National Academy of Sciences. Dietary Reference
Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, D.C.: National
Academy Press, 2000, 249–59.
25. Graat JM, Schouten EG, Kok FJ. Effect of daily vitamin E and
multivitamin-mineral supplementation on acute respiratory tract infections in elderly persons:
a randomized controlled trial. JAMA 2002;288:715–21.
26. Skrha J, Sindelka G, Kvasnicka J, Hilgertova J. Insulin action and
fibrinolysis influenced by vitamin E in obese type 2 diabetes mellitus. Diabetes Res Clin
Pract 1999;44:27–33.
27. Zoler ML. Supplemental vitamin E linked to heart failure. Fam
Pract News 2003 (October 1):28 [News report].
28. Roob JM, Khoschsorur G, Tiran A, et al. Vitamin E attenuates
oxidative stress induced by intravenous iron in patients on hemodialysis. J Am Soc
Nephrol 2000;11:539–49.
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The information presented in Healthnotes is for informational
purposes only. It is based on scientific studies (human, animal, or in vitro),
clinical experience, or traditional usage as cited in each article. The results reported may
not necessarily occur in all individuals. For many of the conditions discussed, treatment with
prescription or over-the-counter medication is also available. Consult your doctor,
practitioner, and/or pharmacist for any health problem and before using any supplements or
before making any changes in prescribed medications. Information expires March 2005.
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