Scientific Name(s): Alpha-tocopherol Common Name(s): Vitamin E
Routine use of high-dose vitamin E for cancer, cardiovascular disease, diabetes, and epilepsy is not recommended. Vitamin E supplementation may have a role in treating age-related macular degeneration, dysmenorrhea, preeclampsia, rheumatoid arthritis, and tardive dyskinesia. Topical use of vitamin E has been investigated for the reduction of scarring.
Doses in clinical trials range from 400 to 1,600 units/day. The established safe upper limit is 1,000 mg/day (1,500 units/day), but consequent to the findings from meta-analyses, a lower safe dosage of 150 to 200 units/day has been suggested.
Contraindications have not been identified.
Trials have been conducted in pregnant women (see Uses and Pharmacology). The majority of trials report no increase in negative fetal outcome, but results regarding birth-weight are conflicting. Considering the evidence of harm (all-cause mortality), high-dose vitamin E supplementation, should be used with caution. Natural food sources are preferred.
Orlistat may reduce vitamin E absorption. Vitamin E may increase the anticoagulant effect of warfarin and may decrease the benefits of atorvastatin therapy.
Meta-analyses of trials investigating high-dose vitamin E supplementation have found evidence of harm. Low-dose vitamin E supplementation (150 mg/day) does not appear to have any serious adverse reactions. High doses of vitamin E may prolong bleeding time.
Vitamin E is a known antioxidant. However, it may be a pro-oxidant, causing oxidation and consequent damage to cells. The use of high-dose vitamin E supplementation may increase the risk of cancer in certain populations and also increase mortality.
Vitamin E was discovered in 1922 when reproductive abnormalities in rats reared on a basic diet were cured by a substance isolated from vegetable oils. A pure fraction was chemically identified in 1938 and named tocopherol after the Greek words tokos and phero meaning "child birth" and "to bring forth."1
Vitamin E is a generic term for a group of tocol and tocotrienol derivatives. It is a fat-soluble vitamin that exists in a variety of forms in many foods (eg, asparagus, mangoes, nuts, olives, spinach, sunflower seeds, vegetable oils, wheat germ, whole-wheat breads). Its most common form in a Western diet is alpha-tocopherol.2 The most important chemical characteristic is its antioxidant property.
Vitamin E is fairly stable to heat and acids, but unstable to alkalis, ultraviolet light, and oxygen. It is destroyed when in contact with rancid fats, lead, and iron. Esters of tocopherol are more stable, with tocopherol acetate accounting for the most common, naturally occurring form.1
Uses and Pharmacology
Vitamin E has been extensively studied for several decades, with the large number of clinical trials making animal experiments largely redundant.
A number of meta-analyses and systematic reviews have found no positive effect of vitamin E on mortality in cardiovascular disease or cancer.3, 4, 5, 6 Furthermore, high-dose vitamin E supplementation has been associated with increased risk of morbidity and mortality.3, 4, 6, 7 A Cochrane meta-analysis of all randomized clinical trials evaluating the effect of antioxidant supplements on primary and secondary disease prevention found that antioxidants had no significant effect on all-cause mortality (relative risk [RR] 1.02; 95% confidence interval [CI] = 0.99 to 1.06). Supplementation with vitamin E alone in trials with a low risk of bias showed significantly increased mortality (RR 1.04; 95% CI = 1.01 to 1.07).6
Conflicting evidence exists. Epidemiological data suggest vitamin E supplementation taken for longer than 10 years is associated with a 50% decreased risk of death from amyotrophic lateral sclerosis than in those individuals not taking supplementation.55 However, a review of available data found poor methodology and insufficient evidence for antioxidants in general for motor neuron disease.61
Despite epidemiological studies suggesting favorable outcomes with vitamin E supplementation in reducing the risks and mortality of cancer, meta-analyses of clinical trials12, 13, 14, 15, 16, 17, 18 found no beneficial effect and suggest evidence for harm.3, 4, 5, 6, 7, 19, 20, 112
A role in reducing the risk of prostate cancer is possible, with limited smaller trials showing a protective, but not statistically significant, effect.21, 22 The SELECT (Selenium and Vitamin E Cancer Prevention Trial) study was halted earlier than planned because of a lack of positive effect, and in the vitamin E monotherapy group, there was a small increase (17%) in prostate cancer incidence.22, 112 Among Finnish smokers, a high baseline alpha-tocopherol level was associated with a lower total mortality risk23 despite negative findings for pancreatic cancer from the same trial.15 In the Women's Health Study, vitamin E 600 units on alternate days did not increase the risk of cancer or death from cancer, nor did it increase total mortality.24
In vitro studies are directing attention to the role of vitamin E analogs, especially alpha-tocopheryl succinate, on inducing apoptosis of malignant cells, but clinical trials are lacking.25, 26, 27, 28, 29, 30 Complications from chemotherapy, such as mucositis31, 32 and paclitaxel-induced peripheral neuropathy33 may benefit from vitamin E supplementation, but data from quality trials are limited. The American Society of Clinical Oncology clinical practice guidelines for prevention and management of chemotherapy-induced peripheral neuropathy (CIPN) in survivors of adult cancers (2014) advise against the use of vitamin E for the prevention of CIPN in patients undergoing treatment with neurotoxic agents (low-quality evidence, inconclusive).113
Despite epidemiological studies in favor of vitamin E supplementation in reducing the risks of cardiovascular disease4, 34, 35, 36 and as a plausible mechanism for antioxidant action37, 38, 39, 40 meta-analyses of landmark trials41, 42, 43, 44, 45, 46, 47, 48, 49 found no evidence for effect and suggested evidence for harm.3, 4, 5, 6, 34, 35, 50 The American Heart Association does not support the routine use of antioxidants in people with cardiovascular disease.51
Trials evaluating subgroup populations subsequent to the Cochrane meta-analysis6 have found varying effects. In men and women with hypercholesterolemia, no effect documented cardiovascular risk despite a variety of tocotrienol isomers tested.52 In smokers 50 years of age or older, ultrasound showed no effect on atherosclerosis after 5 years of vitamin E supplementation.35 In the Women's Antioxidant and Cardiovascular Study, no impact from supplementation on total mortality was observed in women at high risk for cardiovascular events, but a marginal effect was reported in women with a previous cardiovascular event.53 A null effect was documented in another study for vitamin E supplementation, with increased mortality in certain disease groups and a reduced risk in others.54
A 2013 randomized controlled trial in Iranian patients on maintenance hemodialysis found that 2 months of supplementation with 400 units of vitamin E alone and combined with 600 mg of alpha-lipoic acid significantly decreased one inflammation biomarker, interleukin-6. Biomarkers for lipid peroxidation, malnutrition, and another inflammation biomarker (C-reactive protein) were not significantly affected. Although, subjective nutritional scores increased significantly with supplement monotherapy or combination therapy.111
The American College of Cardiology Foundation/American Heart Association Guideline for the management of peripheral artery disease (2005/2011) stated that vitamin E is not recommended as a treatment for patients with intermittent claudication (level of evidence: C).104
Animal experiments and epidemiological studies suggest a correlation between low-serum vitamin E levels and memory performance in elderly patients.55 However, clinical trials demonstrate equivocal results. A trial evaluating vitamin E supplementation (2,000 units/day) showed no difference in conversion from mild cognitive impairment to Alzheimer disease over 2 years compared with donepezil or placebo56, 57; other trials found a prolonged time to end point for vitamin E but no improvement in cognitive tests.55, 58 A Cochrane review reported few trials meeting the inclusion criteria. In 1 trial, fewer patients on vitamin E supplementation reached end point (death, institutionalization, or loss of 2 out of 3 basic activities) within 2 years but experienced more falls. Overall, the review revealed no statistically significant difference compared with placebo, in the probability of progression from mild impairment to Alzheimer disease.59 If vitamin E supplementation is considered beneficial (versus the potential for harm), then low-dose supplementation is recommended.60 Similar results were found from the Prevention of Alzheimer’s Disease by Vitamin E and Selenium (PREADViSE) primary prevention trial, which enrolled 3,786 of the 7,450 men from the parent prostate cancer prevention study (Selenium and Vitamin E Cancer Prevention Trial). Depending on the particular analysis, hazard ratios for dementia incidence over a 7-year period ranged from 0.8 to 0.97 for vitamin E alone and 0.97 to 1.18 for the combination of selenium plus vitamin E.121
Several guidelines have been published discussing vitamin E use in Alzheimer disease and dementia. The European Federation of Neurological Sciences guidelines on the management of Alzheimer disease (2010) offers a strong recommendation that there is insufficient evidence to support the use of Vitamin E for primary prevention of dementia and it should not be used in treatment of patients with mild cognitive impairment. An additional recommendation states that Vitamin E should not be used in the treatment of Alzheimer disease.105 The British Association for Psychopharmacology (BAP) consensus statement on the clinical practice with anti-dementia drugs (2006) states that there is type 1b evidence (well-designed quasi-experimental study) of a delay in the progression of Alzheimer B disease with high dose vitamin E alone, but not when combined with selegiline. In addition, this statement also notes that in type 1b evidence that vitamin E is not effective in reducing the risk of developing Alzheimer disease.106 The American Academy of Neurology (AAN) practice parameter for the management of dementia (2001) states that some patients with Alzheimer disease may benefit from vitamin E and it should be considered as an option to slow progression of the disease (Guideline level; Class II or III).126 However, the American Academy of Neurology (AAN) updated practice guideline for mild cognitive impairment (2018) notes that vitamin E 2,000 units/day in patients with mild cognitive impairment is possibly ineffective for reducing progression to Alzheimer disease (Low Level, Class II). Similarly, the combination of vitamin E 300 mg plus vitamin C 400 mg daily over 12 months is of uncertain efficacy (Very Low Level, Class III).122 The American Association for Geriatric Psychiatry (AAGP) position statement for patients with dementia resulting from Alzheimer disease (2006) states that vitamin E may be considered for prevention of functional decline; doses should not to exceed 400 units/day based on data of possible increased mortality in the elderly.123 The American Psychiatric Association (APA) practice guideline for the treatment of patients with Alzheimer disease and other dementias (2007) no longer recommends vitamin E for treatment of cognitive symptoms of dementia due to limited evidence for efficacy plus safety concerns, including dose-dependent mortality (Class II; Level A x 2, Level E x 1, Level G x 2).124 The American Psychiatric Association (APA) guideline watch for the treatment of patients with Alzheimer disease and other dementias (2014) did not find enough definitive new evidence to change the 2007 guideline recommendations for alternative agents, including vitamin E.125
Compared with placebo and alpha-lipoic acid (ALA), supplementation with alpha-tocopherol (400 Units/day) × 4 months significantly decreased urinary concentrations of the oxidative stress biomarker 8=hydroxyl-2'-deoxyguanosine (8OHdG) in children with Down syndrome (P < 0.01) in a randomized controlled trial (n = 93). Because Down syndrome children have higher baseline levels of oxidative stress than their siblings, the authors suggested that alpha-tocopherol supplementation may reduce oxidative stress at the DNA level.116
A Cochrane review of trials from 1966 through 2006 discusses poor trial methodology and did not find sufficient evidence to support routine use of vitamin E in the management of epilepsy.62
Animal studies have produced conflicting results. In humans receiving alpha-tocopherol 2,000 units/day, no benefit was demonstrated in 1 trial, whereas high-dose vitamin E (3,200 units/day) with vitamin C (3 g/day) delayed the progression of Parkinson disease by 2.5 years.55
A meta-analysis of neuroleptic-induced tardive dyskinesia, including 10 studies from 1966 through 2001, showed that vitamin E protected against deterioration but did not improve the symptoms of tardive dyskinesia.63 A trial evaluating vitamin E 1,200 units/day versus placebo over 12 weeks reported a mean improvement in Abnormal Involuntary Movements Scale (AIMS) scores.64 In combination with vitamin C 200 mg/day, vitamin E 1,800 mg/day reduced tardive symptoms in a small trial (N = 8). Theoretically, the combination reduces vitamin E radicals formed when vitamin E scavenges oxygen radicals.65
The American Academy of Neurology guidelines for the treatment of tardive syndromes (2013), including tardive dyskinesia, concludes that data are conflicting and insufficient to determine the efficacy of vitamin E in the management of tardive dyskinesia syndrome.107
The role of vitamin E in diabetes was not determined in any of the major meta-analyses3, 5, 6; however, the risk of harm raised in these analyses should not be overlooked. A number of clinical trials found no effect of vitamin E on outcomes66, 67, 68, 69, 70 while others showed unexpected increases in blood pressure.71, 72 Some small trials have reported improvements in surrogate outcomes.47, 48, 70 The American Diabetes Association does not consider the evidence to be sufficient to support routine use of antioxidants in people with diabetes.73 As a component of medical nutrition therapy for patients with type 1 or type 2 diabetes, the American Diabetes Association Standards of Care (2014 and 2015) does not recommend routine supplementation with vitamin E due to a lack of efficacy and uncertainty regarding long-term safety (high- and low-quality evidence).112, 115
Macular degeneration, cataracts, and visual loss
Systematic reviews report the effects of vitamin E on the prevention and progression of age-related macular degeneration.8, 9 The majority of trials were conducted by the Age-Related Eye Disease Study Research Group.10 The analyses conclude that vitamin E supplementation has a modest, borderline protective effect (odds ratio [OR] 0.83; 95% CI = 0.69 to 1.01)9 and people with moderate to severe degeneration may experience a slight delay in progression of disease with antioxidant supplementation.8 Harm from long-term use should be considered.8 However, eye end point data (n = 11,267) from a large prostate cancer cohort (SELECT study) with a mean follow-up of 5.6 years indicated that vitamin E 400 units/day and/or selenium 200 mcg/day supplementation was not likely to have beneficial effects on age-related cataracts in healthy men.112
A similar, small study investigated the effect of 4 months of therapy with high-dose vitamin E (1,600 units/day) for uveitis-associated macular edema. Supplementation did not affect visual acuity or retinal thickening, and the study was terminated early.11
A meta-analysis of 13 observational studies (n = 18,999) evaluated the association between blood levels of antioxidants and vitamins to the risk of age-related cataract. Based on the results of 8 relevant studies with no substantial heterogeneity, vitamin E showed a significant inverse association with cataract risk.109
Pregnancy and preeclampsia
As a consequence of earlier trials and a meta-analysis revealing a reduction in the risk of preeclampsia78, 79, 80 several large multicenter and international trials have been or are being conducted to investigate the effect of antioxidant supplementation on the rate of preeclampsia.81, 82 Of the available data, vitamin E 400 units in combination with vitamin C 1,000 mg does not affect the risk of preeclampsia versus placebo.83, 84, 85, 86 A meta-analysis of trials from 2006 found no effect of antioxidant supplementation on the rate of preeclampsia versus placebo.87
The outcomes of ongoing preeclampsia trials, together with the findings of harm for vitamin E supplementation in large meta-analyses3, 6 will need to be considered when data are available.81
Varying results on fetal outcomes have been obtained from these trials, with most showing no effect.83, 84, 85, 86 A study investigating the effect of maternal concentrations of alpha-tocopherol on fetal growth suggested a positive relationship, with a decreased risk for small-for-gestational-age births.88 A negative association was suggested for wheeze (in the absence of a cold) in the second year of life in children of mothers who took vitamin E supplements during pregnancy.89 A follow-up at 5 years exposed an association between childhood asthma and low maternal vitamin E intake.90 Similarly, a negative association for childhood eczema and maternal vitamin E intake was found.89
The use of vitamin E for the prevention of morbidity and mortality in preterm infants has been investigated. A meta-analysis concluded that routine use of vitamin E supplementation via the intravenous route is not supported by evidence because of the increased risk for harm.2, 91 A small study evaluated the effects of vitamin E supplementation (50 units/day) on erythropoiesis in premature infants. No effect was reported at that dosage, and no increased harm was detected.92
A 2012 Cochrane review identified 2 randomized clinical trials evaluating vitamin E for atopic eczema/dermatitis that met criteria for analysis.110 A significant reduction was noted with vitamin E monotherapy (600 units alpha-tocopherol) in lichenification and dryness in 52 adults and children older than 13 years of age. Additionally, vitamin D (cholecalciferol 1,600 units) and E combination therapy resulted in a significant difference in severity scores at the end of 60-day treatment as well as improvements in pruritis and erythema compared with placebo, whereas vitamin D supplementation alone did not provide significant benefit over placebo in any of the measured outcomes. No significant differences were found in mean disease severity scores in 60 adults treated with vitamin E plus selenium.110
A few trials demonstrated a reduction in menstrual pain, with maximum effect after 3 months of vitamin E at dosages up to 200 units for 5 days, when starting 2 days prior to menses.74, 75 A meta-analysis confirms evidence for effect. Harm or adverse reactions, however, were not reported.76, 77 In contrast, a Cochrane systematic review and meta-analysis of dietary supplements for dysmenorrhea identified only low or very low quality studies with very small sample sizes. No evidence of effectiveness was found for the treatment of primary dysmenorrhea with vitamin E compared to placebo or no treatment (2 randomized clinical trials, N = 135), no difference was found when vitamin E was compared to fennel (1 randomized clinical trial, n = 42), and data were unsuitable for analysis in the studies that compared vitamin E with vitamin B1 and vitamin E plus fennel to ibuprofen.117
A 2014 Cochrane systematic review and meta-analysis on antioxidants for use in male subfertility identified 2 trials (N=117) that investigated vitamin E and although an apparent association between vitamin E and an increase in live birth rates appeared to exist (P=0.006, I2=0%), risk of bias was high. One trial also reported a significantly lower sperm DNA fragmentation with administration of vitamin E plus vitamin C compared to placebo (n=64). Vitamin E was also one of 2 antioxidants associated with an increase in clinical pregnancy rate based on evidence from analyses of specific antioxidants.120
The Endocrine Society clinical practice guidelines for the treatment of symptoms of the menopause (2015) recommend counseling patients on the lack of consistent evidence for benefit of complementary medicine therapies, including vitamin E, as an alternative nonhormonal therapy for vasomotor symptoms (weak recommendation; low quality evidence).119
Restless legs syndrome
A joint European task force developed evidence-based guidelines on the management of restless legs syndrome (2012) and stated that insufficient evidence was available regarding vitamin E in the management of restless legs syndrome.108
Clinical trials present conflicting results.49, 93, 94 Overall, vitamin E supplementation exhibits a low level of evidence for effectiveness in rheumatoid arthritis. The value of vitamin E may only be evident in patients with increased oxidative stress or at dosages higher than the 400 units/day.95
Vitamin E has been evaluated for use in immunodeficient states and for topical use in reducing scarring.96
Deficiencies in vitamin E are uncommon, and dietary sources are preferred over supplementation.97
Doses in clinical trials range from 400 to 1,600 units/day. Higher doses have been used in some trials.3, 6
The established safe upper limit is 1,000 mg/day (1,500 units/day)97 but consequent to the findings from meta-analyses, a lower safe dosage of 150 to 200 units/day has been suggested.3, 6 The American Heart Association's guidelines for prevention of heart disease and stroke in women advise against antioxidant use, and the Alzheimer's Association recommends use only under the care of a health care provider.97
In the 2016 Scientific Statement by the American Heart Association regarding drugs that may cause or exacerbate heart failure, supplementation with 400 units/day or more of vitamin E was not advised in patients with established disease based on evidence indicating a possible increased risk of new-onset heart failure.118
Pregnancy / Lactation
Trials have been conducted in pregnant women (see Uses and Pharmacology). The majority of trials report no increase in negative fetal outcome, but results regarding birth-weight are conflicting.83, 84, 85, 86, 87, 88, 89, 90
Considering the evidence of harm (all-cause mortality), high-dose vitamin E supplementation, should be used with caution. Natural food sources are preferred.3, 4, 5, 6
Vitamin E at 400 units/day impaired the positive endothelial effects of low-dose atorvastatin in a trial of patients with heart failure.98
Orlistat administration may reduce the biologic and therapeutic effect of vitamin E by decreasing GI absorption of the vitamin. In 12 healthy subjects receiving Orlistat (120 mg 3 times daily for 4 days), administration of vitamin E (400 units alpha-tocopheryl acetate) on the fourth day of Orlistat treatment decreased the area under the curve and peak plasma level of vitamin E 60% and 43%, respectively, compared with placebo.99, 100
Vitamin E may interfere with vitamin K-dependent clotting factors, adding to the anticoagulant effects of warfarin. A markedly prolonged prothrombin time and bleeding occurred in a 55-year-old man stabilized on warfarin for 2 months after he started taking vitamin E supplementation (1,200 units/day or less). Taking more than vitamin E 400 units/day may cause additive hypo-prothrombinemic effects to occur.101, 102
High levels of vitamin E can adversely affect the absorption of vitamins A and K. Long-term use of high doses may cause nausea, diarrhea, blurred vision, and prolonged bleeding time.103
In the 2016 Scientific Statement by the American Heart Association regarding drugs that may cause or exacerbate heart failure, supplementation with 400 units/day or more of vitamin E was not advised in patients with established disease based on evidence indicating a possible increased risk of new-onset heart failure.118
Vitamin E is a known antioxidant. However, it may be a pro-oxidant, causing oxidation and consequent damage to cells.7 The use of high-dose vitamin E supplementation may increase the risk of cancer in certain populations7 and also increase mortality.6
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