Vitamin E

Fact Sheet for Health Professionals

This is a fact sheet intended for health professionals. For a general overview, see our consumer fact sheet.

Introduction

Vitamin E is found naturally in some foods, added to others, and available as a dietary supplement. Vitamin E is the collective name for a group of fat-soluble compounds with distinctive antioxidant activities [1].

Naturally occurring vitamin E exists in eight chemical forms (alpha-, beta-, gamma-, and delta-tocopherol and alpha-, beta-, gamma-, and delta-tocotrienol) that have varying levels of biological activity [1]. Alpha- (or α-) tocopherol is the only form that is recognized to meet human requirements for vitamin E.

Serum concentrations of vitamin E (alpha-tocopherol) depend on the liver, which takes up the nutrient after the various forms are absorbed from the small intestine. The liver preferentially resecretes alpha-tocopherol via the hepatic alpha-tocopherol transfer protein [1]; the liver metabolizes and excretes the other vitamin E forms [2]. As a result, blood and cellular concentrations of other forms of vitamin E are lower than those of alpha-tocopherol and have been the subjects of less research [3,4].

Antioxidants protect cells from the damaging effects of free radicals, which are molecules that contain an unshared electron. Free radicals damage cells and might contribute to the development of cardiovascular disease (CVD) and cancer [5]. Unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species (ROS). The body forms ROS endogenously when it converts food to energy, and antioxidants might protect cells from the damaging effects of ROS. The body is also exposed to free radicals from environmental exposures, such as cigarette smoke, air pollution, and ultraviolet radiation from the sun. ROS are part of signaling mechanisms among cells.

Vitamin E is a fat-soluble antioxidant that stops the production of ROS formed when fat undergoes oxidation. Scientists are investigating whether, by limiting free-radical production and possibly through other mechanisms, vitamin E might help prevent or delay the chronic diseases associated with free radicals.

In addition to its activities as an antioxidant, vitamin E is involved in immune function and, as shown primarily by in vitro studies of cells, cell signaling, regulation of gene expression, and other metabolic processes [1]. Alpha-tocopherol inhibits the activity of protein kinase C, an enzyme involved in cell proliferation and differentiation in smooth muscle cells, platelets, and monocytes [6]. Vitamin-E-replete endothelial cells lining the interior surface of blood vessels are better able to resist blood cell components adhering to this surface. Vitamin E also increases the expression of two enzymes that suppress arachidonic acid metabolism, thereby increasing the release of prostacyclin from the endothelium, which, in turn, dilates blood vessels and inhibits platelet aggregation [6].

Assessing vitamin E status

Vitamin E status is not routinely assessed. Circulating alpha-tocopherol concentrations can be measured, but these concentrations are difficult to interpret and do not correlate well with dietary alpha-tocopherol intake. A plasma alpha-tocopherol concentration of 12 micromol/L is typically used as a cut-off for vitamin E deficiency.

Although it is not routinely measured in clinical practice, vitamin E status can be assessed by measuring plasma or serum alpha-tocopherol concentrations [7]. However, several factors make these concentrations difficult to interpret. Plasma lipid concentrations increase as a person ages, leading to higher circulating concentrations of alpha-tocopherol [8]. In addition, circulating alpha-tocopherol concentrations do not correlate well with dietary intake, suggesting that circulating alpha-tocopherol concentrations are not useful for assessing adequate vitamin E status, although they can be used to identify inadequate vitamin E status [7,8]. The mean serum alpha-tocopherol concentration in the U.S. population is about 30 micromoles/liter (micromol/L), and deficiency is typically defined as a plasma alpha-tocopherol concentration of less than 12 micromol/L [6-8].

Currently, there is a lack of research on other potential biomarkers of vitamin E status, such as adipose tissue alpha-tocopherol concentration or urinary excretion of the vitamin E metabolite alpha-carboxy-ethyl-hydroxychromanol [8].

Recommended Intakes

The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for vitamin E. These values range from 15 to 19 mg for adults and from 4 mg to 19 mg for infants, children, and adolescents, depending on age and life stage.

Intake recommendations for vitamin E and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine [6]. DRI is the general term for a set of reference values used to plan and assess nutrient intakes of healthy people. These values include the following:

  • Recommended Dietary Allowance (RDA): Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals
  • Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA
  • Estimated Average Requirement (EAR): Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals
  • Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse health effects

The FNB's vitamin E recommendations are for alpha-tocopherol alone, as this is the only form that is maintained in plasma. The FNB based these recommendations primarily on the serum levels of the nutrient that provide adequate protection in a test that measures the survival of erythrocytes when exposed to hydrogen peroxide, a free radical [6]. Acknowledging great uncertainties in these data, the FNB has called for research to identify other biomarkers for assessing vitamin E requirements.

Naturally sourced vitamin E is called RRR-alpha-tocopherol (commonly labeled as d-alpha-tocopherol); the synthetically produced form is all rac-alpha-tocopherol (commonly labeled as dl-alpha-tocopherol).

RDAs for vitamin E are provided in milligrams (mg) and are listed in Table 1. One mg vitamin E (alpha-tocopherol) is equivalent to 1 mg RRR-alpha-tocopherol or 2 mg all rac-alpha-tocopherol. Because insufficient data are available to develop RDAs for infants, AIs were developed based on the amount of vitamin E consumed by healthy breastfed babies.

Table 1: Recommended Dietary Allowances (RDAs) for Vitamin E (Alpha-Tocopherol) in Milligrams (mg)[6]
Age Males Females Pregnancy Lactation
0–6 months 4 mg* 4 mg*
7–12 months 5 mg* 5 mg*
1–3 years 6 mg 6 mg
4–8 years 7 mg 7 mg
9–13 years 11 mg 11 mg
14–18 years 15 mg 15 mg 15 mg 19mg
19+ years 15 mg 15 mg 15 mg 19 mg

* Adequate Intake (AI)

Conversion between International Units and Milligrams

Vitamin E is listed on the new Nutrition Facts and Supplement Facts labels in mg [9]. The U.S. Food and Drug Administration (FDA) required manufacturers to use these new labels starting in January 2020, but companies with annual sales of less than $10 million were allowed to use the old labels that list vitamin E in International Units (IUs) until January 2021 [10]. Conversion rules are as follows:

  • To convert from mg to IU:
    • 1 mg of alpha-tocopherol is equivalent to 1.49 IU of the natural form or 2.22 IU of the synthetic form.
  • To convert from IU to mg:
    • 1 IU of the natural form is equivalent to 0.67 mg of alpha-tocopherol.
    • 1 IU of the synthetic form is equivalent to 0.45 mg of alpha-tocopherol.

For example, 15 mg of natural alpha-tocopherol would equal 22.4 IU (15 mg x 1.49 IU/mg = 22.4 IU). The corresponding value for synthetic alpha-tocopherol would be 33.3 IU (15 mg x 2.22 IU/mg).

Sources of Vitamin E

Food

Good food sources of vitamin E include nuts, seeds, and vegetable oils. Green leafy vegetables and fortified cereals also contain vitamin E.

Numerous foods provide vitamin E. Nuts, seeds, and vegetable oils are among the best sources of alpha-tocopherol, and significant amounts are available in green leafy vegetables and fortified cereals (see Table 2 for a more detailed list) [11]. Most vitamin E in American diets is in the form of gamma-tocopherol from soybean, canola, corn, and other vegetable oils and food products [4].

Table 2: Vitamin E (Alpha-Tocopherol) Content of Selected Foods [11]
Food Milligrams (mg)
per serving		 Percent DV*
Wheat germ oil, 1 tablespoon 20.3 135
Sunflower seeds, dry roasted, 1 ounce 7.4 49
Almonds, dry roasted, 1 ounce 6.8 45
Sunflower oil, 1 tablespoon 5.6 37
Safflower oil, 1 tablespoon 4.6 31
Hazelnuts, dry roasted, 1 ounce 4.3 29
Peanut butter, 2 tablespoons 2.9 19
Peanuts, dry roasted, 1 ounce 2.2 15
Corn oil, 1 tablespoon 1.9 13
Spinach, boiled, ½ cup 1.9 13
Broccoli, chopped, boiled, ½ cup 1.2 8
Soybean oil, 1 tablespoon 1.1 7
Kiwifruit, 1 medium 1.1 7
Mango, sliced, ½ cup 0.7 5
Tomato, raw, 1 medium 0.7 5
Spinach, raw, 1 cup 0.6 4

*DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for vitamin E is 15 mg for adults and children age 4 years and older [9]. One mg vitamin E = 1 mg RRR-alpha-tocopherol = 2 mg all rac-alpha-tocopherol. FDA does not require food labels to list vitamin E content unless vitamin E has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

The U.S. Department of Agriculture's (USDA's) FoodData Centralexternal link disclaimer lists the nutrient content of many foods, including, in some cases, the amounts of alpha-, beta-, gamma-, and delta-tocopherol. USDA also provides a comprehensive list of foods that contain vitamin E arranged by nutrient content and by food name.

Dietary supplements

Vitamin E can be found in multivitamin/mineral supplements and in dietary supplements that contain vitamin E alone. Most vitamin E supplements provide alpha-tocopherol, although some products provide other tocopherols and tocotrienols. Both natural and synthetic forms of alpha-tocopherol are available in supplements; the synthetic form, designated as all-rac, dl, or DL, is about half as active as the natural form, designated as RRR, d, or D.

Vitamin E is available in multivitamin/mineral supplements and in dietary supplements that contain vitamin E alone. Supplements that contain vitamin E typically provide only alpha-tocopherol, although mixed products that contain other tocopherols and even tocotrienols are available. Naturally occurring alpha-tocopherol exists in one stereoisomeric form. In contrast, synthetically produced alpha-tocopherol contains equal amounts of its eight possible stereoisomers; serum and tissues maintain only four of these stereoisomers [6]. A given amount of synthetic alpha-tocopherol (all rac-alpha-tocopherol; commonly labeled as DL or dl) is therefore only half as active as the same amount (by weight in mg) of the natural form (RRR-alpha-tocopherol; commonly labeled as D or d).

Most vitamin-E-only supplements provide ≥67 mg of the nutrient (100 IU of natural vitamin E). These amounts are substantially higher than the RDAs.

Alpha-tocopherol in dietary supplements and fortified foods is often esterified to prolong its shelf life while protecting its antioxidant properties. The body hydrolyzes and absorbs these esters (alpha-tocopheryl acetate and succinate) as efficiently as alpha-tocopherol [6].

Vitamin E Intakes and Status

According to data from National Health and Nutrition Examination Survey, most people in the United States consume less than the recommended amounts of vitamin E.

Most people in the United States consume less than the recommended amounts of vitamin E. According to an analysis of data from the August 2021–August 2023 National Health and Nutrition Examination Survey (NHANES), the average daily vitamin E intake from food and beverages among people age 2 years and older is 9.8 mg for males and 8.5 mg for females [12]. These intake estimates might be low, however, because the amounts and types of fat that are added during cooking are often unknown and not accounted for [6].

The FNB suggests that mean intakes of vitamin E among healthy adults are probably higher than the RDA. However, they caution that low-fat diets might provide insufficient amounts of vitamin E unless people consciously consume good sources of vitamin E, such as nuts, seeds, fruits, and vegetables [6,13]. The 1999–2000 NHANES found that 11.3% of adults took vitamin E supplements that contained at least 400 IU [14].

Vitamin E Deficiency

The signs and symptoms of vitamin E deficiency include anemia, peripheral neuropathy, ataxia, skeletal myopathy, retinopathy, and immune system impairment. However, frank vitamin E deficiency is rare.

Frank vitamin E deficiency is rare and overt deficiency symptoms have not been found in healthy people who obtain little vitamin E from their diets [6]. However, vitamin E deficiency can occur under certain circumstances (see the next section). Deficiency symptoms include anemia, peripheral neuropathy, ataxia, skeletal myopathy, retinopathy, and impairment of the immune response [6,7,15].

Groups at Risk of Vitamin E Inadequacy

Certain groups of people are more likely than others to have inadequate vitamin E status. These include preterm infants with very low birthweight, people with fat-malabsorption disorders, people with abetalipoproteinemia, and those who have ataxia with vitamin E deficiency.

The following groups are among those most likely to have inadequate vitamin E status.

Preterm infants with very low birthweight

Preterm infants with very low birth weight (<1,500 grams) might be deficient in vitamin E. Vitamin E supplementation in these infants might reduce the risk of some complications, such as hemolytic anemia and retinopathy of prematurity, but it can also increase the risk of infections [7,16].

People with fat-malabsorption disorders

Because the digestive tract requires fat to absorb vitamin E, people with fat-malabsorption disorders are more likely to become deficient than people without such disorders. People with Crohn's disease, cystic fibrosis, or an inability to secrete bile from the liver into the digestive tract, for example, often pass greasy stools or have chronic diarrhea; as a result, they sometimes require water-soluble forms of vitamin E, such as tocopheryl polyethylene glycol-1000 succinate [1].

People with abetalipoproteinemia

Some people with abetalipoproteinemia, a rare inherited disorder resulting in poor absorption of dietary fat, require enormous doses of supplemental vitamin E (approximately 100 mg/kilogram or 5–10 g/day) [1]. Vitamin E deficiency secondary to abetalipoproteinemia causes such problems as poor transmission of nerve impulses, muscle weakness, and retinal degeneration that leads to blindness [17].

People who have ataxia with vitamin E deficiency

Ataxia with vitamin E deficiency (AVED) is another rare, inherited disorder in which the liver's alpha-tocopherol transfer protein is defective or absent. People with AVED have such severe vitamin E deficiency that they develop nerve damage and lose the ability to walk unless they take large doses of supplemental vitamin E [18].

Vitamin E and Health

Many claims have been made about vitamin E's potential to promote health and prevent and treat disease. The mechanisms by which vitamin E might provide this protection include its function as an antioxidant and its roles in anti-inflammatory processes, inhibition of platelet aggregation, and immune enhancement.

A primary barrier to characterizing the roles of vitamin E in health is the lack of validated biomarkers for vitamin E intake and status to help relate intakes to valid predictors of clinical outcomes [6]. This section focuses on four diseases and disorders in which vitamin E might be involved: CVD, cancer, eye disorders, and cognitive decline.

Cardiovascular disease

Vitamin E can inhibit the oxidation of low-density lipoprotein cholesterol and may prevent the formation of blood clots; these findings suggest that it could play a role in reducing the risk of cardiovascular disease. In addition, some observational studies have reported that higher vitamin E intakes reduce both the incidence of heart disease and the risk of death from heart disease. However, the use of vitamin E supplements has not been shown to prevent cardiovascular disease or reduce its morbidity or mortality in clinical trials.

Evidence that vitamin E could help prevent or delay CVD comes from several sources. In vitro studies have found that vitamin E inhibits oxidation of low-density lipoprotein (LDL) cholesterol, thought to be a crucial initiating step for atherosclerosis [6]. Vitamin E might also help prevent the formation of blood clots that could lead to a heart attack or venous thromboembolism [19].

Several observational studies have associated lower rates of heart disease with higher vitamin E intakes. One study of approximately 90,000 nurses found that the incidence of heart disease was 30% to 40% lower in those with the highest intakes of vitamin E, primarily from supplements [20]. Among a group of 5,133 Finnish men and women who were followed for a mean of 14 years, higher vitamin E intakes from food were associated with decreased mortality from coronary heart disease [21].

However, randomized clinical trials cast doubt on the efficacy of vitamin E supplements to prevent CVD [22]. For example, the Heart Outcomes Prevention Evaluation (HOPE) study, which followed almost 10,000 patients at high risk of heart attack or stroke for 4.5 years [23], found that participants taking 400 IU/day of natural vitamin E (268 mg) experienced no fewer cardiovascular events or hospitalizations for heart failure or chest pain than participants taking a placebo. In the HOPE-TOO follow-up study, almost 4,000 of the original participants continued to take vitamin E or placebo for an additional 2.5 years [24]. HOPE-TOO found that vitamin E provided no significant protection against heart attacks, strokes, unstable angina, or deaths from CVD or other causes after 7 years of treatment. Participants taking vitamin E, however, were 13% more likely to experience, and 21% more likely to be hospitalized for, heart failure, a statistically significant but unexpected finding not reported in other large studies.

The HOPE and HOPE-TOO trials provide compelling evidence that moderately high doses of vitamin E supplements do not reduce the risk of serious cardiovascular events among men and women older than 50 years of age with established heart disease or diabetes [25]. These findings are supported by evidence from the Women's Angiographic Vitamin and Estrogen study, in which 423 postmenopausal women with some degree of coronary stenosis took supplements with 400 IU vitamin E (form not specified) and 500 mg vitamin C twice a day or placebo for more than 4 years [26]. Not only did the supplements provide no cardiovascular benefits, but all-cause mortality was significantly higher in the women taking the supplements.

The latest published clinical trial of vitamin E's effects on the heart and blood vessels of women included almost 40,000 healthy women 45 years of age and older who were randomly assigned to receive either 600 IU of natural vitamin E (402 mg) on alternate days or placebo and who were followed for an average of 10 years [27]. The investigators found no significant differences in the rates of a composite endpoint of first major cardiovascular event (nonfatal heart attack, nonfatal stroke, or cardiovascular death) or all-cause mortality between the groups. However, the study did find two positive and significant results for women who were taking vitamin E: they had a 24% reduction in cardiovascular death rates, and those 65 years of age and older had a 26% decrease in nonfatal heart attack and a 49% decrease in cardiovascular death rates.

The most recently published clinical trial of vitamin E and men's cardiovascular health included almost 15,000 healthy physicians 50 years of age and older who were randomly assigned to receive 400 IU synthetic alpha-tocopherol (180 mg) every other day, 500 mg vitamin C daily, both vitamins, or placebo [28]. During a mean follow-up period of 8 years, intake of vitamin E (and/or vitamin C) had no effect on the incidence of major cardiovascular events, myocardial infarction, stroke, or cardiovascular morality. Furthermore, the use of vitamin E was associated with a significantly increased risk of hemorrhagic stroke.

In general, clinical trials have not provided evidence that routine use of vitamin E supplements prevents CVD or reduces its morbidity and mortality. However, participants in these studies have been largely middle-aged and older individuals with preexisting heart disease or risk factors for heart disease. Some researchers have suggested that understanding the potential utility of vitamin E in reducing the risk of CVD might require longer studies in younger participants who are taking higher doses of the supplement [29]. Further research is needed to determine whether supplemental vitamin E has any protective value for younger, healthier people with no obvious risk factors for CVD.

Cancer

Although vitamin E has some antioxidant and immune-enhancing effects that could theoretically provide some protection against cancer, the available evidence does not support the use of vitamin E supplements to prevent cancer. The findings from one large clinical trial suggest that regularly taking large doses of vitamin E supplements may even increase the risk of prostate cancer.

Antioxidant nutrients like vitamin E help protect cell constituents from the damaging effects of free radicals that might contribute to cancer development [11]. In the stomach, vitamin E might block the formation of carcinogenic nitrosamines from nitrites in foods, and it might also protect against cancer by enhancing immune function [30]. Unfortunately, the human clinical trials and surveys that have attempted to clarify the effects of vitamin E on cancer incidence have found that higher intakes of vitamin E are not beneficial in most cases.

Both the HOPE-TOO Trial and Women's Health Study evaluated whether vitamin E supplements might protect people from cancer. HOPE-TOO, which enrolled men and women 55 years of age and older with heart disease or diabetes, found no significant differences in the number of new cancers or cancer deaths after 7 years of follow up between individuals randomly assigned to take 400 IU/day of natural vitamin E (268 mg) or a placebo [24]. In the Women's Health Study, in which healthy women age 45 years and older received either 600 IU of natural vitamin E (402 mg) every other day or a placebo for 10 years, the supplement did not reduce the risk of developing any form of cancer [27].

Several studies have examined whether vitamin E intake and/or supplemental vitamin E affects the risk of developing prostate cancer. A prospective cohort study of more than 29,000 men found no association between dietary or supplemental vitamin E intake and prostate cancer risk [31]. However, among men who smoked and those who had quit, vitamin E intakes of more than 400 IU/day (form not specified) were associated with a statistically significant 71% reduction in the risk of advanced prostate cancer.

In a clinical trial that involved 29,133 men who smoked, the incidence of prostate cancer was 32% lower among men who took a daily supplement of 111 IU of synthetic vitamin E (50 mg, as dl-alpha-tocopheryl acetate) for 5 to 8 years than among those who did not take the vitamin E supplement [32]. Partially on the basis of the promising results of this study, a large randomized clinical trial, called the SELECT trial, began in 2001 to determine whether 7 to 12 years of daily supplementation with 400 IU of synthetic vitamin E (180 mg, as dl-alpha-tocopheryl acetate), with or without selenium (200 mcg, as L-selenomethionine), reduced the number of new prostate cancer cases in 35,533 healthy men age 50 and older. The trial was discontinued in October 2008, when an analysis found that vitamin E, taken alone or with selenium for about 5.5 years, did not prevent prostate cancer [33]. Results from an additional 1.5 years of follow-up from this trial (during which the subjects no longer received vitamin E or selenium) showed that the men who had taken the vitamin E had a 17% increase in the risk of prostate cancer compared to the men who had taken placebos, a statistically significant difference [34]. The risk of developing prostate cancer was also slightly increased in subjects who took vitamin E plus selenium or selenium alone, but the differences were not statistically significant. No differences were found among the groups in the incidence of lung or colorectal cancers or all cancers combined. The National Cancer Institute website provides additional information on the SELECT trialexternal link disclaimer.

One study of women in Iowa provides evidence that higher intakes of vitamin E from foods and supplements could decrease the risk of colon cancer, especially in women less than 65 years of age [35]. The overall relative risk for the highest quintile of intake (>35.7 IU/day, form not specified) compared to the lowest quintile (<5.7 IU/day, form not specified) was 0.32. However, prospective cohort studies of 87,998 women in the Nurses' Health Study and 47,344 men in the Health Professionals Follow-up Study failed to replicate these results [36]. Although some research links higher intakes of vitamin E with decreased incidence of breast cancer, an examination of the impact of dietary factors, including vitamin E, on the incidence of postmenopausal breast cancer in more than 18,000 women found no benefit from the vitamin [37].

The American Cancer Society conducted an epidemiologic study that examined the association between use of vitamin C and vitamin E supplements and bladder cancer mortality. Of the almost one million adults who were followed between 1982 and 1998, adults who took supplemental vitamin E for 10 years or longer had a reduced risk of death from bladder cancer [38]; vitamin C supplementation provided no protection.

The evidence to date is insufficient to support taking vitamin E to prevent cancer. In fact, daily use of large-dose vitamin E supplements (400 IU of synthetic vitamin E [180 mg]) may increase the risk of prostate cancer.

Eye disorders

Because the cumulative effects of oxidative stress are thought to play a role in the development of age-related macular degeneration and cataracts, nutrients with antioxidant functions, such as vitamin E, have been evaluated as potential treatments for these conditions. The AREDS and AREDS2 clinical trials found that taking a daily supplement that contained vitamin E and other nutrients slowed the progression of age-related macular degeneration in people who had a high risk of developing the advanced form of this condition. However, it is unclear whether vitamin E supplements can reduce the risk of developing age-related macular degeneration or cataracts.

Age-related macular degeneration (AMD) and cataracts are among the most common causes of significant vision loss in older people. Their etiologies are usually unknown, but the cumulative effects of oxidative stress have been postulated to play a role. If so, nutrients with antioxidant functions, such as vitamin E, could be used to prevent or treat these conditions.

Prospective cohort studies have found that people with relatively high dietary intakes of vitamin E (e.g., 20 mg/day [30 IU]) have an approximately 20% lower risk of developing AMD than people with low intakes (e.g., <10 mg/day [<15 IU]) [39,40]. However, two randomized, placebo-controlled trials failed to show a protective effect for vitamin E on AMD. In one of these trials, participants received 500 IU/day (335 mg) d-alpha-tocopherol [41]: in the other, they received 111 IU/day (50 mg) dl-alpha-tocopheryl acetate combined with 20 mg/day beta-carotene [42]. The Age-Related Eye Disease Study (AREDS), a large randomized clinical trial, found that participants who were at high risk of developing advanced AMD (i.e., those with intermediate AMD or those with advanced AMD in one eye) reduced their risk of developing advanced AMD by 25% at 5 years by taking a daily supplement that contained vitamin E (400 IU [180 mg] dl-alpha-tocopheryl acetate), beta-carotene (15 mg), vitamin C (500 mg), zinc (80 mg), and copper (2 mg) compared to participants who took a placebo [43]. A follow-up AREDS2 study confirmed the value of this and similar supplement formulations in reducing the progression of AMD over a median follow-up period of 5 years [44].

Several observational studies have revealed a potential relationship between vitamin E supplements and the risk of cataract formation. One prospective cohort study found that lens clarity was superior in participants who took vitamin E supplements and those with higher blood levels of the vitamin [45]. In another study, long-term use of vitamin E supplements was associated with slower progression of age-related lens opacification [46]. However, in the AREDS trial, the use of a supplement that contained vitamin E (in the form of dl-alpha-tocopheryl acetate) had no apparent effect on the development or progression of cataracts over an average of 6.3 years [47]. The AREDS2 study, which also tested formulations that contained 400 IU (180 mg) vitamin E, confirmed these findings [48].

Overall, the available evidence is inconsistent with respect to whether vitamin E supplements, taken alone or in combination with other antioxidants, can reduce the risk of developing AMD or cataracts. However, the formulations of vitamin E, other antioxidants, zinc, and copper that were used in AREDS can slow the progression of AMD in people who are at high risk of developing advanced AMD.

Cognitive decline

Because antioxidants, such as vitamin E, might help prevent free-radical damage to neurons, researchers have examined whether they might protect the brain against cognitive decline and certain neurodegenerative diseases. While some evidence supports this idea, most studies have found that the use of vitamin E supplements does not help maintain cognitive function or slow its decline in healthy or mildly impaired individuals.

The brain has a high oxygen consumption rate and abundant polyunsaturated fatty acids in the neuronal cell membranes. Researchers hypothesize that if cumulative free-radical damage to neurons over time contributes to cognitive decline and neurodegenerative diseases, such as Alzheimer's disease, then ingesting sufficient or supplemental antioxidants (such as vitamin E) might provide some protection [49]. This hypothesis was supported by the results of a clinical trial in 341 patients with Alzheimer's disease of moderate severity who were randomly assigned to receive a placebo, vitamin E (2,000 IU/day dl-alpha-tocopherol), a monoamine oxidase inhibitor (selegiline), or vitamin E and selegiline [49]. Over 2 years, treatment with vitamin E and selegiline, separately or together, significantly delayed functional deterioration and the need for institutionalization compared to placebo. However, participants who were taking vitamin E experienced significantly more falls.

Vitamin E consumption from foods or supplements was associated with less cognitive decline over 3 years in a prospective cohort study of free-living individuals age 65 to 102 years [50]. However, a clinical trial in primarily healthy older women who were randomly assigned to receive 600 IU (402 mg) d-alpha-tocopherol every other day or a placebo for 4 years or less found that the supplements provided no apparent cognitive benefits [51]. In another trial, 769 men and women with mild cognitive impairment were randomly assigned to receive 2,000 IU/day vitamin E (form not specified), a cholinesterase inhibitor (donepezil), or placebo [52]. This trial found no significant differences in the progression rate of Alzheimer’s disease between the vitamin E and placebo groups.

In summary, most research results do not support the use of vitamin E supplements by healthy or mildly impaired individuals to maintain cognitive function or slow its decline with normal aging [53]. More research is needed to identify the role of vitamin E, if any, in the management of cognitive impairment [54].

Health Risks from Excessive Vitamin E

No adverse effects have been reported from consuming large amounts of vitamin E from food. However, clinical trials have reported an increased risk of hemorrhagic stroke from high doses of vitamin E from supplements. The Tolerable Upper Intake Level for supplemental vitamin E is 1,000 mg for adults, and it ranges from 200 to 800 mg for children and adolescents, depending on age.

Research has not found any adverse effects from consuming large amounts of vitamin E from food [6]. However, high doses of alpha-tocopherol supplements can cause hemorrhage and interrupt blood coagulation in animals, and in vitro data suggest that high doses inhibit platelet aggregation. Two clinical trials found an increased risk of hemorrhagic stroke in participants who took alpha-tocopherol; one trial included Finnish men who smoked and who consumed 50 mg/day for an average of 6 years [55] and the other trial involved a large group of male physicians in the United States who consumed 400 IU (180 mg) of synthetic vitamin E every other day for 8 years [28]. Because the majority of physicians in the latter study were also taking aspirin, this finding could indicate that vitamin E has a tendency to cause bleeding.

The FNB has established ULs for vitamin E based on the potential for hemorrhagic effects (see Table 3). The ULs apply to all forms of supplemental alpha-tocopherol, including the eight stereoisomers present in synthetic vitamin E. Doses of up to 1,000 mg/day (1,500 IU/day of the natural form or 1,100 IU/day of the synthetic form) appear to be safe for adults, although the data are limited and based on small groups of people who took up to 3,200 mg/day of alpha-tocopherol for only a few weeks or months. Long-term intakes above the UL increase the risk of adverse health effects [6]. Vitamin E ULs for infants have not been established.

Table 3: Tolerable Upper Intake Levels (ULs) for Vitamin E in Milligrams (mg) [6]
Age Male Female Pregnancy Lactation
0–6 months Not possible to establish* Not possible to establish*
7–12 months Not possible to establish* Not possible to establish*
1–3 years 200 mg 200 mg
4–8 years 300 mg 300 mg
9–13 years 600 mg 600 mg
14–18 years 800 mg 800 mg 800 mg 800 mg
19+ years 1,000 mg 1,000 mg 1,000 mg 1,000 mg

* Breast milk, formula, and food should be the only sources of vitamin E for infants.

Two meta-analyses of randomized trials have also raised questions about the safety of large doses of vitamin E, including doses lower than the UL. These meta-analyses linked supplementation to small but statistically significant increases in all-cause mortality. One analysis found an increased risk of death at doses of 400 IU/day (form not specified), although the risk began to increase at 150 IU [56]. In the other analysis, which evaluated studies that used antioxidant supplements for disease prevention, the highest quality trials revealed that administering vitamin E alone (dose range 10 IU–5,000 IU/day; mean 569 IU [form not specified]) or with up to four other antioxidants, significantly increased mortality risk [57].

The implications of these analyses for the potential adverse effects of high-dose vitamin E supplements are unclear [58-61]. The participants in the studies that were included in these analyses were typically middle-aged or older and had chronic diseases or related risk factors. These participants often consumed other supplements in addition to vitamin E. Some of the studies took place in developing countries in which nutritional deficiencies are common. A review of the subset of studies in which vitamin E supplements were given to healthy individuals for the primary prevention of chronic disease found no convincing evidence that the supplements increased mortality [62].

However, results from the SELECT trial show that vitamin E supplements (400 IU/day [180 mg] as dl-alpha-tocopheryl acetate) may harm adult men in the general population by increasing their risk of prostate cancer [34]. Follow-up studies are assessing whether the cancer risk was associated with baseline blood levels of vitamin E and selenium prior to supplementation as well as whether changes in one or more genes might increase a man's risk of developing prostate cancer while taking vitamin E.

Interactions with Medications

Vitamin E supplements can interact with certain medications, including anticoagulants, antiplatelets, simvastatin, and niacin. These supplements also have the potential to interact with the medications used for chemotherapy and radiotherapy.

Vitamin E supplements have the potential to interact with several types of medications. A few examples are provided below. People who are taking these and other medications on a regular basis should discuss their vitamin E intakes with their health care providers.

Anticoagulant and antiplatelet medications

Vitamin E can inhibit platelet aggregation and antagonize vitamin K-dependent clotting factors. As a result, taking large doses of vitamin E with anticoagulant or antiplatelet medications, such as warfarin (Coumadin), can increase the risk of bleeding, especially in conjunction with low vitamin K intake. The amounts of supplemental vitamin E needed to produce clinically significant effects are unknown but probably exceed 400 IU/day [63].

Simvastatin and niacin

Some people take vitamin E supplements with other antioxidants, such as vitamin C, selenium, and beta-carotene. This collection of antioxidant ingredients blunted the rise in high-density lipoprotein (HDL) cholesterol levels among people who were treated with a combination of simvastatin (brand name Zocor) and niacin [64,65]. This effect was especially pronounced for levels of HDL2, the most cardioprotective HDL component.

Chemotherapy and radiotherapy

Oncologists generally advise against the use of antioxidant supplements during cancer chemotherapy or radiotherapy because they might reduce the effectiveness of these therapies by inhibiting cellular oxidative damage in cancerous cells [66,67]. Although a systematic review of randomized controlled trials has called this concern into question [68], further research is needed to evaluate the potential risks and benefits of concurrent antioxidant supplementation with conventional therapies for cancer.

Vitamin E and Healthful Diets

In general, a person’s nutritional needs should be met primarily through the diet, including fortified foods. Dietary supplements may be useful in cases where it is not possible to meet the needs for specific nutrients through food alone, especially during certain life stages. The Dietary Guidelines for Americans offers a general description of healthy dietary patterns.

For more information about building a healthy dietary pattern, refer to the Dietary Guidelines for Americansexternal link disclaimer.

References

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Disclaimer

This fact sheet by the National Institutes of Health (NIH) Office of Dietary Supplements (ODS) provides information that should not take the place of medical advice. We encourage you to talk to your health care providers (doctor, registered dietitian, pharmacist, etc.) about your interest in, questions about, or use of dietary supplements and what may be best for your overall health. Any mention in this publication of a specific product or service, or recommendation from an organization or professional society, does not represent an endorsement by ODS of that product, service, or expert advice.

Updated: October 19, 2026 History of changes to this fact sheet