Vitamin E benefits

How is the evidence for vitamin E supplementation read?

Three distinctions are made on this page. First, the results of observational studies (those who consumed more vitamin E had less disease) and of randomized trials (supplement or placebo given at random) are not the same; the NIH reports that lower rates of heart disease were seen in observational studies but that randomized trials cast doubt on this benefit. ^[1] Second, vitamin E obtained from foods and high-amount supplementation are different questions. Third, a trial’s main result and a subgroup finding do not carry the same weight.

Does vitamin E prevent cardiovascular disease?

In the HOPE trial, about 10,000 high-risk people were followed for 4.5 years, and among those taking 400 IU of natural vitamin E per day (268 mg), cardiovascular events, or hospitalizations for heart failure and angina, were not reduced compared with placebo. ^[1] In the extension trial HOPE-TOO, participants aged 55 and over with vascular disease or diabetes were followed for a median of 7.0 years: there was no difference in major cardiovascular events (RR 1.04; 95% CI 0.96–1.14), there was an increase in heart failure (RR 1.13; 1.01–1.26), and hospitalization for heart failure was also higher (RR 1.21; 1.00–1.47). The authors concluded that vitamin E may increase the risk of heart failure. ^[3]

The result was no different in healthy people. In the Women’s Health Study as reported by the NIH, about 40,000 healthy women aged 45 and over took 600 IU of natural vitamin E (402 mg) every other day or placebo and were followed for an average of 10 years: there was no significant difference in cardiovascular events or all-cause mortality. In the same trial, a 24% reduction in cardiovascular death and some subgroup benefits at age 65 and over were reported; these are secondary and subgroup findings and do not change the main result. In the Physicians’ Health Study II, about 15,000 healthy male physicians (aged 50 and over) took 400 IU of synthetic vitamin E every other day (mean 8 years): there was no difference in cardiovascular events and the risk of hemorrhagic stroke was significantly higher. ^[1]

USPSTF 2022 decided 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 or vitamin E supplementation (D recommendation). ^[2]

Stroke: hemorrhagic versus ischemic

In the meta-analysis by Schürks and colleagues, 9 randomized, placebo-controlled trials followed for at least one year (118,765 participants) were pooled. Vitamin E had no effect on total stroke risk (RR 0.98; 0.91–1.05). In contrast, the risk of hemorrhagic stroke increased (RR 1.22; 1.00–1.48) and the risk of ischemic stroke decreased (RR 0.90; 0.82–0.99). In absolute terms, this corresponded to one additional hemorrhagic stroke per 1,250 people taking vitamin E and one ischemic stroke prevented per 476 people. The authors cautioned against widespread use of vitamin E in everyone because hemorrhagic stroke generally runs a more severe course. ^[4]

Does vitamin E prevent cancer?

According to the NIH, no benefit has been seen between vitamin E intake and cancer incidence in most human studies. In HOPE-TOO, cancer incidence and cancer deaths were similar in the vitamin E and placebo groups. In the SELECT trial, with 400 IU of synthetic vitamin E per day in 35,533 relatively healthy men, the risk of prostate cancer was found to be 17% higher than with placebo; this increase was statistically significant. The NIH also reports that in an older study of 29,133 male smokers, prostate cancer was seen 32% less in those taking 50 mg of synthetic vitamin E per day, and that SELECT was designed partly based on this result; SELECT did not confirm this finding. ^[1]

Does vitamin E help eye health?

In AREDS, 3,640 people aged 55–80 with features such as intermediate macular degeneration, large drusen, or advanced disease in one eye were followed for an average of 6.3 years. Participants were assigned to one of four groups: antioxidants (vitamin C 500 mg, vitamin E 400 IU, beta-carotene 15 mg), zinc 80 mg with copper 2 mg, antioxidants plus zinc, or placebo. A statistically significant reduction in development of advanced macular degeneration compared with placebo was seen in the antioxidants-plus-zinc group; antioxidants alone did not provide a significant reduction. ^[5]

The NIH reports that the AREDS formula (400 IU vitamin E, 15 mg beta-carotene, 500 mg vitamin C, 80 mg zinc, 2 mg copper) reduced the risk of progression to advanced macular degeneration by 25% over 5 years, and that AREDS2 subsequently confirmed the value of this and similar formulations in reducing progression. However, in two randomized trials in which vitamin E was used alone (500 IU natural, or 50 mg synthetic together with beta-carotene), no protective effect against macular degeneration could be shown; the effect of the AREDS and AREDS2 formulations on cataract was also not found to be marked. ^[1] Therefore, vitamin E’s place in this area is as part of a multi-component formula used in people with a specific eye finding; there is no evidence for prevention in healthy eyes.

Does vitamin E work in dementia and cognitive decline?

The 2017 Cochrane review examined trials in Alzheimer’s disease (AD) or mild cognitive impairment (MCI) in which vitamin E was compared with placebo in double-blind randomized trials. Four trials met the criteria, but protocol-compliant data could be extracted from only two: one was an AD (304 people) trial and the other an MCI (516 people) trial. In AD, no clinically important effect was found on cognitive function (ADAS-Cog) (mean difference −1.81; 95% CI −3.75 to 0.13; single trial, 272 people; moderate-certainty evidence). In the same trial, functional decline on the activities of daily living scale was less in the vitamin E group (mean difference 3.15; CI 0.07–6.23; single trial, 280 people; moderate-certainty evidence). In MCI, the likelihood of progression to dementia at 36 months did not change (RR 1.03; 0.79–1.35). The authors found no evidence that it improves cognitive function or prevents progression from MCI to dementia. ^[6]

The NIH reports that in an earlier trial (341 patients with moderately severe Alzheimer’s disease, 2 years, 2,000 IU dl-α-tocopherol per day), a delay in functional deterioration was accompanied by significantly more falls among those taking vitamin E; and that in healthy older women, no cognitive benefit was found with 600 IU d-α-tocopherol every other day for up to 4 years. ^[1]

Does vitamin E work in fatty liver (NASH)?

In the PIVENS trial, 247 adults without diabetes who had nonalcoholic steatohepatitis (NASH) were divided into three groups: 800 IU vitamin E per day (84 people), 30 mg pioglitazone (80 people), or placebo (83 people); duration was 96 weeks. The primary outcome was improvement on a histologic measure combining steatosis, lobular inflammation, hepatocyte ballooning, and fibrosis. The improvement rate was 43% in the vitamin E group and 19% in the placebo group (P = 0.001); it was 34% versus 19% with pioglitazone (P = 0.04); because the significance threshold was set at 0.025 for the two primary comparisons, this difference was not considered significant. Transaminase levels, hepatic steatosis, and lobular inflammation decreased with vitamin E and pioglitazone compared with placebo; no significant improvement in fibrosis scores was seen with either drug. The authors reported that vitamin E was superior to placebo in the treatment of NASH in adults without diabetes. ^[7]

This finding rests on a single randomized trial; people with diabetes were not included in the trial, and the results are read together with the hemorrhagic stroke, heart failure, and prostate cancer signals described on this page. The decision to use it is made by a physician according to the diagnosis of liver disease.

Does vitamin E help the skin?

For the skin, vitamin E is one of the areas with the weakest evidence in this guide. The abstract of a review published in Clinics in Dermatology in 2026 states that vitamin E is a fat-soluble antioxidant that has been used in dermatology for more than 50 years, but that there is a lack of research and evidence for its photoprotective (sun-protective) and tumor-preventing properties. ^[8] The same abstract also states that it discusses the relationship of oral and topical vitamin E with improvement in various dermatologic conditions; however, it does not report a systematic search or a measured effect size. The benefit of vitamin E taken by mouth or applied to the skin for skin appearance, aging, or scarring has not been demonstrated as a result measured in controlled trials.

Who benefits? Diagnosed deficiency

In vitamin E deficiency (fat malabsorption, abetalipoproteinemia, AVED), replacement is needed: the NIH reports that some people with abetalipoproteinemia need very high amounts of supplements, and that people with AVED develop nerve damage and lose the ability to walk unless they take large amounts of supplements. ^[1] These situations are a separate clinical area in which dose and form choice are made by a physician; details are covered on the deficiency symptoms page.

The balance of benefit and harm and the interaction with bleeding medications are summarized in the vitamin E main guide. This page does not recommend a personal dose.