Vitamin E

What is vitamin E, and what does it do?

Vitamin E is the common name of a group of fat-soluble compounds. In nature it has eight chemical forms: alpha-, beta-, gamma-, and delta-tocopherol and alpha-, beta-, gamma-, and delta-tocotrienol. Their biological activities differ, and according to the NIH, the only form accepted as meeting human requirements is α-tocopherol. ^[1]

The liver processes the forms absorbed from the intestine. Through the hepatic α-tocopherol transfer protein, the liver re-secretes only α-tocopherol into the blood; it metabolizes and excretes the other forms. For this reason, levels of forms other than α-tocopherol are lower in blood and cells, and these forms have been less studied. ^[1]

Vitamin E is a fat-soluble antioxidant that stops the production of reactive oxygen species formed during fat oxidation. It also plays a role in immune function; its other roles, such as cell signaling and gene expression, have been shown mainly in cell (in vitro) studies. ^[1]

Knowing these roles does not mean that taking extra in the absence of deficiency will perform the same roles better. The vitamin’s role in the body and the measured results of supplementation are separate questions; the NIH cites the lack of validated biomarkers linking vitamin E intake and status with clinical outcomes as the main obstacle to defining its role in health. ^[1]

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What is the difference between natural and synthetic vitamin E?

According to the NIH, vitamin E of natural origin is RRR-α-tocopherol (often d-α-tocopherol on labels); the synthetically produced form is all-rac-α-tocopherol (dl-α-tocopherol). Natural α-tocopherol is in the form of a single stereoisomer. Synthetic α-tocopherol contains an equal mixture of the possible eight stereoisomers; serum and tissues retain only four of them. For this reason, the synthetic form at the same weight is only half as potent as the natural form. ^[1]

This difference is also reflected in units. On labels, vitamin E is written in milligrams (mg) or international units (IU); the conversion rules given by the NIH are as follows: ^[1]

That is, the mg equivalent of the IU value on a label depends on whether the product is natural or synthetic; it cannot be calculated without knowing the form. The NIH reports that in the US, listing vitamin E in mg on food and supplement labels has been mandatory since January 2020, and that firms with annual sales under 10 million dollars could use their old IU labels until January 2021. ^[1]

α-Tocopherol in supplements and fortified foods is often esterified to extend shelf life (α-tocopheryl acetate or succinate); according to the NIH, the body hydrolyzes these esters and absorbs them as effectively as α-tocopherol. ^[1]

How much vitamin E is needed per day?

Reference values differ by organization. The US Food and Nutrition Board values reported by the NIH are RDAs set at a level to meet the needs of 97–98% of healthy people and are for α-tocopherol only. The FNB based these values on serum levels providing adequate protection in a test measuring survival of red blood cells exposed to hydrogen peroxide, and, acknowledging major uncertainties in the data, asked for other biomarkers to be investigated. ^[1]

EFSA, in its 2015 opinion, decided that an average requirement (AR) or population reference intake (PRI) could not be derived for adults, infants, and children; instead, it set adequate intake (AI) values based on observed intakes in healthy populations in the EU with no apparent α-tocopherol deficiency. ^[2]

The NIH’s RDA is 7 mg for ages 4–8 and 11 mg for ages 9–13; EFSA sets an AI of 9 mg for children from age 3 to 10, and for ages 10–18, 13 mg in males and 11 mg in females. ^{[1] [2]} Because EFSA found no evidence that α-tocopherol requirements increase in pregnancy and breastfeeding, it applies the same AI to these groups as to non-pregnant women; the NIH, however, gives an RDA of 15 mg for pregnancy and 19 mg for breastfeeding. ^[2]

The NIH states that three national surveys in the US (NHANES III, NHANES 2001–2002, and CSFII 1994–1996) show that most Americans’ diets fall below the vitamin E RDA; however, because the amount and type of fats added in cooking are not known, these estimates may have been low. No overt signs of deficiency have been detected in healthy people despite low intake from food. ^[1]

Which foods provide how much is covered on a separate page.

Detailed guideWhich foods contain vitamin E? Serving table, hazelnuts, and oils→

When does vitamin E deficiency occur?

According to the NIH, overt vitamin E deficiency is rare, and no obvious signs of deficiency have been found in healthy people who consume little from food. Because the digestive tract needs fat to absorb vitamin E, deficiency is more likely in people with fat malabsorption. Symptoms listed include peripheral neuropathy, ataxia, skeletal muscle disease (myopathy), retinopathy, and impaired immune response. Very-low-birth-weight (under 1,500 g) premature infants may also be deficient. Ataxia with vitamin E deficiency (AVED), a rare inherited disease, results from the α-tocopherol transfer protein in the liver being defective or missing; in these people, nerve damage develops and the ability to walk is lost unless high-amount supplements are taken. ^[1]

Who is affected, the symptoms, and laboratory assessment are covered on a separate page.

Detailed guideVitamin E deficiency symptoms: who gets it, how diagnosed?→

Does vitamin E supplementation work? What does the evidence say?

The summary below shows, for each claim, the group studied and the limit of the result together. Detailed results are on the benefits page.

Cardiovascular disease

Observational studies have associated higher vitamin E intake with lower heart disease; the NIH reports that randomized trials did not confirm this association. ^[1] In the HOPE trial and its extension HOPE-TOO, people aged 55 and over with vascular disease or diabetes were given 400 IU of natural vitamin E per day or placebo; median follow-up was 7.0 years. There was no difference in major cardiovascular events (RR 1.04; 95% CI 0.96–1.14). Heart failure (RR 1.13; 1.01–1.26) and hospitalization for heart failure (RR 1.21; 1.00–1.47) were higher in the vitamin E group. ^[6] The NIH describes this finding as a significant but unexpected result not reported in other large trials. ^[1]

The US Preventive Services Task Force (USPSTF) concluded with moderate certainty that vitamin E supplementation has no net benefit in preventing cardiovascular disease or cancer in community-dwelling, nonpregnant adults and issued a recommendation against beta-carotene and vitamin E supplementation for this purpose (D recommendation). ^[3]

Cancer

In the SELECT trial, 35,533 men were randomly divided into four groups (Black men aged 50 and over, other men aged 55 and over; PSA 4.0 ng/mL or below). 34,887 men were included in the analysis. The vitamin E group was given 400 IU of all-rac-α-tocopheryl acetate per day. Prostate cancer developed in 529 men in the placebo group and in 620 men in the vitamin E group (HR 1.17; 99% CI 1.004–1.36). The absolute increase was 1.6 cases per 1,000 person-years. The increases in the selenium-alone group (HR 1.09) and in the selenium-plus-vitamin E group (HR 1.05) were not statistically significant. ^[7]

In HOPE-TOO, no significant difference was found in cancer incidence (RR 0.94; 0.84–1.06) and cancer deaths (RR 0.88; 0.71–1.09). ^[6] The NIH reports that a reduction in prostate cancer was seen in an early trial (50 mg in male smokers), that SELECT was begun partly based on this result, and that the evidence ultimately changed to indicate that vitamin E does not prevent prostate cancer. ^[1]

Mortality risk

The 2005 meta-analysis by Miller and colleagues examined 19 randomized trials involving vitamin E (135,967 participants; nine tested vitamin E alone and the rest tested vitamin E together with other vitamins or minerals). In high-dose trials (400 IU per day and above; 11 trials), the difference in total mortality risk was 39 per 10,000 people (95% CI 3–74); in low-dose trials the difference was not significant (−16 per 10,000 people; CI −41 to 10). The authors note that the high-dose trials were mostly small and conducted in people with chronic disease, and that the generalizability of the results to healthy adults is uncertain. ^[4]

Cochrane’s 2012 update examined together 78 randomized trials (296,707 participants) covering vitamins A, C, and E, beta-carotene, and selenium. For antioxidant supplements, there was no difference in death in the random-effects model (RR 1.02; 0.98–1.05); in the fixed-effect model, the risk was significantly higher (RR 1.03). In 56 trials at low risk of bias, antioxidants overall increased death (RR 1.04; 1.01–1.07). For vitamin E in these trials (46 trials), RR is 1.03 (1.00–1.05); the lower bound of the confidence interval is 1.00. ^[5] The NIH also reports that the results of analyses examining the same question remain uncertain: participants were mostly middle-aged or older, had chronic disease, and most also took other supplements. ^[1]

Eye diseases

In the Age-Related Eye Disease Study AREDS, 3,640 participants (ages 55–80) were followed for an average of 6.3 years. In high-risk people with intermediate macular degeneration or advanced disease in one eye, a formula containing antioxidants (vitamin C, vitamin E 400 IU, beta-carotene) plus zinc and copper significantly reduced progression to advanced macular degeneration compared with placebo; antioxidants alone did not provide a statistically significant reduction in progression. ^[8] The NIH reports that in AREDS this formula reduced the risk by 25% and that AREDS2 confirmed the value of similar formulations in reducing progression; the same source adds that the formula containing vitamin E had no marked effect on the development or progression of cataract and that there are two randomized trials in which vitamin E supplementation (alone in one, together with beta-carotene in the other) showed no protective effect against macular degeneration. ^[1]

The evidence on cognitive function, fatty liver, and skin is covered on the benefits page.

Detailed guideVitamin E benefits: evidence, harm signals, and limits→

Is too much vitamin E harmful?

The NIH reports that no adverse effects of vitamin E obtained from food have been detected. For supplements, it is stated that high-amount α-tocopherol has caused bleeding and impaired clotting in animals and that in vitro data show reduced platelet aggregation. In two clinical trials, the risk of hemorrhagic stroke increased: with 50 mg per day in Finnish male smokers (mean 6 years) and with 400 IU of synthetic vitamin E every other day in US male physicians (8 years); in the second trial, most participants were also using aspirin. ^[1]

This signal is also supported by a 2010 meta-analysis; its details are given on the benefits page. The upper limits (UL) reported by the NIH are based on bleeding effects and apply to all supplemental α-tocopherol forms:

For adults, 1,000 mg corresponds to 1,500 IU in the natural form and 1,100 IU in the synthetic form. The NIH states that amounts up to 1,000 mg per day appear safe but that the data are limited and based on small groups taking up to 3,200 mg per day for only a few weeks or months, and that long-term intakes above the upper limit increase the risk of adverse effects. An upper limit has not been set for infants. ^[1] The NIH also reports that most supplements containing only vitamin E contain 67 mg (100 IU natural vitamin E) and above, which is far above the RDA. ^[1]

Risk questions are also being debated at amounts below the upper limit: in HOPE-TOO described above, 400 IU of natural vitamin E per day was used, and in SELECT 400 IU of synthetic. These trials were conducted in people with chronic disease (HOPE-TOO) and in relatively healthy men (SELECT), and the generalization of the findings is limited.

With which medications does vitamin E interact?

The NIH’s interactions section gives three examples: ^[1]

• Anticoagulant and antiplatelet drugs: Vitamin E can inhibit platelet aggregation and can antagonize vitamin K–dependent clotting factors. Taking large amounts together with drugs such as warfarin, especially when vitamin K intake is low, can increase bleeding risk. The amount needed for a clinically significant effect is not known but is probably above 400 IU per day.
• Simvastatin and niacin: Combined use of antioxidants such as vitamin E, vitamin C, selenium, and beta-carotene blunted the rise in HDL cholesterol (especially HDL2) in people receiving simvastatin-niacin therapy.
• Chemotherapy and radiotherapy: Oncologists generally advise against the use of antioxidant supplements during chemotherapy and radiotherapy on the grounds that they may also block oxidative damage in cancer cells and reduce treatment efficacy. A systematic review of randomized trials has questioned this concern; the NIH states that more research is needed.

In people who regularly use medications, every product containing vitamin E is evaluated together with prescription drugs by a physician or pharmacist.

What is looked at on a supplement label?

The label answers at three points: the unit of the amount (mg or IU), the form (natural d- or synthetic dl-), and whether the product contains only α-tocopherol or mixed tocopherols and tocotrienols. Writing the amount in mg makes comparison easier; when IU is written, the conversion table above cannot be used without knowing the form. In mixed products, forms other than α-tocopherol are not included in the RDA and UL calculation; these values are set only for α-tocopherol. ^[1]

As reported by the NIH, the US federal Dietary Guidelines (2020–2025) state that nutrient requirements should primarily be met with foods, and that fortified foods and supplements may be helpful when needs cannot be met in another way. ^[1] This guide does not recommend a personal dose; the decision on a supplement is made with a physician, taking into account test results, medications used, and accompanying diseases.