Version May 2024
INTRODUCTION — Vitamins are a number of chemically unrelated families of organic substances that cannot be synthesized in the human body but need to be ingested in the diet in small quantities to prevent disorders of metabolism. They are divided into water-soluble and fat-soluble vitamins (table 1). Vitamin E is a fat-soluble compound and protects cell membranes from oxidation and destruction.
In 1922, Evans and Bishop discovered that rats fed a lard-based diet developed infertility, suggesting a dietary deficiency [1]. The fertility was corrected when a lipid extract of cereals was added to the diet; this was termed the "anti-sterility factor" [2]. In 1925, vitamin E was officially recognized as the fifth vitamin. A few years later, the name tocopherol, from the Greek word of "toc" (child) and "phero" (to bring forth), was coined to describe its role as an essential dietary substance in normal fetal and childhood development [3]. In 1969, the US Food and Drug Administration (FDA) formally recognized vitamin E as an essential nutrient for humans.
This topic review will focus on vitamin E. Overviews of the other fat-soluble vitamins, minerals, and water-soluble vitamins are available elsewhere. (See "Overview of vitamin A" and "Overview of vitamin D" and "Overview of vitamin K" and "Overview of dietary trace elements" and "Overview of water-soluble vitamins" and "Vitamin intake and disease prevention".)
SOURCES — Vitamin E is found in a variety of foods including almonds, vegetable oils, and cereals. The form that is best known for its role in human health is alpha-tocopherol, which is abundant in olive and sunflower oils and is the predominant form in the European diet. Gamma-tocopherol is another form, which is abundant in soybean and corn oil and is common in the American diet.
Vitamin E is also available in supplements, either alone or as part of a multivitamin supplement.
CHEMISTRY AND NOMENCLATURE — The primary bioactive form of vitamin E is alpha-tocopherol. Alpha-tocopherol has eight isomers, but only four of these (RRR-, RSR-, RRS-, and RSS-alpha-tocopherol) are efficiently maintained in human plasma, and these are the forms to which the dietary reference intakes apply [4]. Furthermore, the RRR-isomer (formerly and incorrectly called D-alpha-tocopherol) is the only form found in foods; it is sometimes known as "natural source" vitamin E.
Many synthetic vitamin E supplements or fortified foods contain all eight isomers of alpha-tocopherol; these are known as "all-racemic" or "DL" alpha-tocopherol and have approximately one-half of the activity of "natural source" vitamin E. However, all of the isomers of alpha-tocopherol may contribute to the potential adverse effects of supplemental vitamin E and are included in the calculation of an upper limit for supplementation [4].
Vitamin E dosing is quantified by the content of the active isomer:
1 mg RRR-alpha-tocopherol
= 1.49 international units "natural source" vitamin E (D-alpha-tocopherol)
= 2.22 international units "all-racemic" vitamin E (DL-alpha-tocopherol)
Seven other naturally occurring vitamin E compounds have been described: beta-, gamma-, and delta-tocopherol and alpha-, beta-, gamma-, and delta-tocotrienols. Nutrient databases, especially older data sources, often report either total tocopherol concentrations or "alpha-tocopherol equivalents," which adjust for the bioavailability for the various forms [4]. However, these measures do not reflect the bioactivity of alpha-tocopherol, which is now used as the standard for dietary sufficiency.
Gamma-tocopherol is transported less efficiently and has lower plasma levels than alpha-tocotrienols, but tissue levels are similar [5]. Because gamma-tocopherol is associated with alterations in levels of inflammation and airway hyperresponsiveness (see 'Actions' below), this compound may have important adverse or beneficial effects, although it is not included in the recommended daily allowance (RDA). Pharmacologic doses of alpha-tocopherol taken in supplements reduce levels of gamma-tocopherol in plasma [5,6].
In most reports and in this topic review, the term "vitamin E" refers to the biologically active isomers of alpha-tocopherol, unless otherwise specified.
ACTIONS — Vitamin E (as alpha-tocopherol) works as a free radical scavenger, protecting polyunsaturated fatty acids, a major structural component of the cell membranes, from peroxidation [7]. In the past few decades, there has been increasing interest in the role of free radicals and antioxidants in atherosclerosis and carcinogenesis. Deficiency of vitamin E has been connected to cardiovascular events. Low-density lipoprotein (LDL) plays a central role in these hypotheses. When LDL is exposed to oxidative stress, it undergoes a cascade of changes affecting the vascular endothelium, thereby facilitating atherogenesis [8-10]. This theory is referred to as the oxidative modification hypothesis and has fueled epidemiologic studies and clinical trials in cardiology to determine the role of antioxidants, such as vitamin E, in prevention and treatment of atherosclerotic cardiovascular disease [11]. However, trials of vitamin E supplementation (which typically use "all-racemic" vitamin E) have generally shown no effect in prevention of heart disease. (See 'Potential benefits' below and "Vitamin intake and disease prevention".)
Gamma-tocopherol appears to promote eosinophilic lung inflammation and airway hyperresponsiveness [12,13], although it also may oppose neutrophil-mediated inflammation, mediated by reductions in prostaglandin E2 [14,15]. The overall health effects of gamma-tocopherol have not been established. High doses of vitamin E (as alpha-tocopherol) reduce levels of gamma-tocopherol, perhaps explaining the adverse effects of pharmacologic doses of the vitamin [5,6].
Some functions of vitamin E are independent of the antioxidant/radical scavenging activity, including inhibition of cell proliferation, platelet aggregation, and monocyte adhesion [16]. Several other effects at the molecular level have been identified, but the clinical implications of these actions have not been established.
METABOLISM — Like other fat-soluble vitamins, bioavailability of alpha-tocopherol depends upon physiologic mechanisms of fat digestion and absorption. This process requires lingual and gastric lipases; bile salts for solubilization and production of mixed micelles; pancreatic function; and intestinal and ileal mucosal and absorptive mechanisms. Bile salts and pancreatic enzymes are particularly important for intraluminal digestion of fat [17]. Pancreatic esterases are the enzymes responsible for breaking down the tocopheryl-ester bonds between alpha-tocopherol and fatty acids [18]. Within the intestinal mucosal cells, chylomicrons are produced from phospholipids, triglycerides, apolipoproteins, and fat-soluble vitamins. The synthesis of chylomicrons is required for transport of alpha-tocopherol via the lymphatic system to the liver [19]. Within hepatocytes, chylomicron remnants are broken down by lysosomes, and RRR-alpha-tocopherol is preferentially secreted into the bloodstream, packaged within very low-density lipoprotein molecules [20]. The transport protein for alpha-tocopherol is named alpha-tocopherol transfer protein [21].
REQUIREMENTS — Dietary vitamin E content is variable and proportional to vegetable oil intake. American diets of 2000 to 3000 kcal/day contain 7 to 10 mg of alpha-tocopherol equivalents. However, this is likely an underestimate because dietary fat intake is commonly underreported.
Healthy population — The recommended daily allowance (RDA) for vitamin E is 15 mg of dietary alpha-tocopherol for adolescents and adult males and females, as defined by the United States National Academy of Sciences Food and Nutrition Board [4]. This is the equivalent of 22 international units of RRR-alpha-tocopherol (the form that is supplied by some supplements and is marketed as "natural source" vitamin E) or 33 international units of "all-racemic" alpha-tocopherol (the synthetic form used for the majority of supplements) [4]. In children, the RDA rises from 6 mg at 1 to 3 years of age to 15 mg by 14 to 18 years (table 2). Note that although the requirements are stated in terms of alpha-tocopherol equivalents, a substantial portion of this will be provided as gamma-tocopherol if dietary sources are used. For this reason, dietary vitamin E may have advantages over vitamin E taken as a supplement. (See 'Chemistry and nomenclature' above and 'Actions' above.)
Patients with fat malabsorption — Patients with fat malabsorption are at risk for vitamin E deficiency because of malabsorption of fat and fat-soluble vitamins; in most cases, this is caused by a pancreatic, hepatic, or intestinal disorder. Rarely, vitamin E deficiency is caused by a genetic disorder that affects vitamin E transport. (See 'Causes' below.)
For patients with pancreatic insufficiency due to cystic fibrosis, guidelines recommend routine supplements with vitamin E and other fat-soluble vitamins. Dosing and monitoring are discussed separately. Similar strategies are likely to be appropriate for patients with other causes of severe pancreatic exocrine insufficiency. (See "Cystic fibrosis: Nutritional issues", section on 'Fat-soluble vitamins'.)
Prevention and management of vitamin E deficiency depends upon the severity of the fat malabsorption, as discussed below. (See 'Treatment' below.)
DEFICIENCY — Vitamin E deficiency is uncommon in humans except in unusual circumstances. This is due to the abundance of tocopherols in a wide variety of diets, including vegetarian and vegan diets. It occasionally occurs in individuals with severe protein-energy malnutrition [22].
Causes — Vitamin E deficiency is most commonly seen in patients with medical conditions that cause fat malabsorption. The degree of deficiency is generally proportional to the magnitude and duration of steatorrhea. Important causes of fat malabsorption are:
●Pancreatic exocrine insufficiency – In which there is insufficient lipase to enable optimal fat absorption. Important causes are cystic fibrosis, pancreatectomy, and chronic pancreatitis.
●Cholestatic liver disease – In which there is insufficient bile in the intestinal lumen to permit fat solubilization and absorption. Important causes include biliary atresia, primary sclerosing cholangitis, primary biliary cholangitis, and familial intrahepatic cholestasis. Fat malabsorption may also occur in other types of cirrhosis, although typically late in the course of the liver disease (decompensated cirrhosis). Patients with cholestasis also tend to have hyperlipidemia, which influences vitamin E levels, so assessment of their vitamin E status requires simultaneous measurement of alpha-tocopherol and serum lipids. (See 'Measurement' below.)
Although cholestasis is a risk factor for fat-soluble vitamin deficiencies, vitamin E deficiency is uncommon except in patients with severe and prolonged cholestasis. Most cases arise in patients with severe and prolonged primary biliary cholangitis, typically in those with cirrhosis and hyperbilirubinemia [23-26]. However, it is considerably less common than other fat-soluble vitamin deficiencies [26]. For patients with significant cholestasis (eg, bilirubin >2 mg/dL), routine monitoring of fat-soluble vitamin levels is recommended, although deficiencies of vitamin E are uncommon [27].
●Extensive resection or disease affecting small intestine – In which there is insufficient intestinal absorptive area to permit fat absorption. If there is loss or disease of the terminal ileum, this may also cause malabsorption of bile acids and a diminished bile acid pool, which further contributes to fat malabsorption. Important causes include short bowel syndrome, congenital intestinal lymphangiectasia, infiltrative diseases such as amyloid or lymphoma, and Crohn disease.
Patients with these conditions typically require high maintenance doses of vitamin E. (See 'Patients with fat malabsorption' above.)
There are also several genetic disorders that lead to vitamin E deficiency, including:
●Ataxia with vitamin E deficiency, due to a mutation in the gene encoding hepatic alpha-tocopherol transfer protein (TTPA). Affected patients have neurologic deficits including symptoms similar to Friedreich ataxia [28]. These patients sometimes respond to oral supplementation of vitamin E in doses of 800 to 1500 mg/day (1200 to 2200 international units/day) of alpha-tocopherol for adults or 40 mg/kg/day (60 international units/kg/day) for children [29-32]. More often, supplementation serves to prevent progression of the disease [33]. (See "Overview of the hereditary ataxias", section on 'Treatable diseases'.)
●Abetalipoproteinemia, due to mutations in the microsomal triglyceride transfer protein. This disorder is characterized by very low or absent levels of low-density lipoprotein (LDL) and fat-soluble vitamin deficiencies. Symptoms may include progressive ataxia, sensory-motor neuropathy, and vision impairment with retinitis pigmentosa. Less severe deficits of LDL and fat-soluble vitamins are seen in hypobetalipoproteinemia. (See "Neuroacanthocytosis", section on 'Abetalipoproteinemia' and "Low LDL-cholesterol: Etiologies and approach to evaluation", section on 'Homozygous familial hypobetalipoproteinemia' and "Low LDL-cholesterol: Etiologies and approach to evaluation", section on 'Abetalipoproteinemia'.)
Clinical manifestations — In adults and children, vitamin E deficiency can cause neuromuscular disorders and hemolysis. Low serum levels of vitamin E (defined as below 0.5 mg/dL) may cause no appreciable symptoms or may manifest as subtle neurologic abnormalities. Neuromuscular disorders associated with vitamin E deficiency are mostly of the neuropathic and myopathic type [33]. The neuropathy generally consists of a spinocerebellar syndrome, with variable involvement of the peripheral nerves. Clinical manifestations include ataxia, hyporeflexia, and loss of proprioceptive and vibratory sensation [34]. A skeletal myopathy and pigmented retinopathy may also be present [34]. Brown bowel syndrome (intestinal lipofuscinosis) is a brown pigmentation of the bowel that occasionally presents with bowel dilatation and pseudo-obstruction [35,36]. It is a rare complication of chronic vitamin E deficiency and is thought to be caused by lipofuscin accumulation within the smooth muscle mitochondria.
Vitamin E deficiency can shorten the lifespan of red blood cells. In premature infants, vitamin E deficiency may cause a hemolytic anemia [37]. Congenital hemolytic disorders such as thalassemia, sickle cell anemia, glucose-6-phosphate dehydrogenase (G6PD) deficiency, and spherocytosis may be associated with low vitamin E plasma levels, likely because of increased oxidant stress and antioxidant consumption [38-40]. Oral therapy with vitamin E supplementation may be of benefit, but efficacy has not been proven [41,42].
Treatment — Patients with documented vitamin E deficiency should be treated with large oral doses of vitamin E.
For infants and children with cholestasis, typical supplementation regimens are 17 to 35 mg/kg/day of RRR-alpha-tocopherol (25 to 50 international units/kg/day of RRR-alpha-tocopherol, or "natural source" vitamin E) [43,44]. If this form is used, some patients may require incremental increases up to 70 to 130 mg/kg/day (100 to 200 international units/kg/day) to achieve normal serum measurements of alpha-tocopherol (or ratio of alpha-tocopherol/total lipids).
Water-miscible vitamin E (RRR-alpha-tocopherol polyethylene glycol 1000 succinate [TPGS]) also may be used; typical doses for cholestatic conditions are 10 to 17 mg/kg/day (15 to 25 international units/kg/day) [45]. TPGS is available as an over-the-counter nutritional supplement in the United States (brand names: DEKAs [provides multiple fat-soluble vitamins], Aqua-E), but no pharmaceutical-grade preparation is approved by the US Food and Drug Administration (FDA). A pharmaceutical-grade form of TPGS (Vedrop) is available in Europe. TPGS may be more effective than other types of vitamin E supplements for treatment of some of the most severe chronic cholestatic conditions, such as Alagille syndrome, biliary atresia, and progressive familial intrahepatic cholestasis [45].
For adults with fat malabsorption due to cholestasis, pancreatic insufficiency, or intestinal disease or resection, vitamin E requirements are variable. If vitamin E replacement is needed, doses are typically started at 50 to 500 mg/day (75 to 800 international units/day), then adjusted as needed to achieve normal serum measurements of alpha-tocopherol (or ratio of alpha-tocopherol/total lipids), assuming that albumin levels are normal. (See 'Measurement' below.)
Patients with severe cholestasis or genetic disorders that interfere with vitamin E transport might not respond to even high doses of oral alpha-tocopherol. Intramuscular vitamin E is effective, but it is not widely available and is somewhat impractical as it requires frequent (weekly) dosing [46]. (See 'Causes' above.)
MEASUREMENT
Indications — Monitoring of vitamin E status is not necessary in healthy patients but is appropriate for patients with risk factors for vitamin E deficiency, which include (see 'Causes' above):
●Chronic cholestatic liver disease such as primary biliary cholangitis or primary sclerosing cholangitis when disease is in its advanced stage (eg, bilirubin >2 mg/dL).
●Severe cholestatic diseases (mostly in pediatrics) such as Alagille syndrome and biliary atresia.
●Pancreatic exocrine insufficiency (patients with steatorrhea due to chronic pancreatitis or cystic fibrosis).
●Extensive disease or resection of the small intestine (eg, patients with short bowel syndrome, those who have had gastric bypass surgery, and selected patients with Crohn disease).
●Patients with unexplained spinocerebellar neuropathy or ataxia. These symptoms may be caused by severe nutritional deficiency or acquired or hereditary malabsorption of vitamin E. (See "Overview of the hereditary ataxias", section on 'Treatable diseases'.)
If vitamin E deficiency is identified, the patient should be treated with high-dose supplements. (See 'Treatment' above.)
Method — For patients with normal levels of serum lipids and carrier proteins, serum alpha-tocopherol levels provide an adequate estimate of vitamin E sufficiency. Alpha-tocopherol levels of less than 0.5 mg/dL (5 mcg/mL or 11.5 micromol/L) are considered deficient. In a United States national survey, the 5th percentile for serum levels of vitamin E was 0.62 mg/dL (14.3 micromol/L) and the 25th percentile was 0.79 mg/dL (18.5 micromol/L) [4].
For patients with marked hyperlipidemia, the serum vitamin E level does not accurately reflect tissue vitamin levels. In these patients, the patient's vitamin E status can be estimated using the following ratio [47]:
●Effective serum vitamin E level = alpha-tocopherol (mg) / total lipids (g)
Where total lipids = cholesterol + triglycerides.
A normal result is >0.8 mg.
Low levels of vitamin E should be interpreted with caution in hypoproteinemic states because fat-soluble vitamins are transported bound to carrier proteins. We are not aware of data that define target levels from which to determine sufficiency in the hypoproteinemic state. Further, estimates of adequacy based on blood levels do not account for populations with low carrier protein levels.
RISKS AND BENEFITS OF SUPPLEMENTATION
Potential risks — For adults without fat malabsorption, the tolerable upper intake level (UL) is 1000 mg/day for any form of alpha-tocopherol (approximately 1500 international units of "natural source" or 2200 international units of synthetic vitamin E). The UL in children rises from 200 mg/day at 1 to 3 years to 600 mg/day at 9 to 13 years (table 2). These ULs are based primarily on concerns for hemorrhagic effects [4]. We do not recommend supplementation near this level except when necessary to correct a deficiency state.
While pharmacologic doses of up to 270 mg/day RRR-alpha-tocopherol (400 international units/day of "natural source" vitamin E) are probably safe for most patients, we recommend supplementation doses remain below this level. Some meta-analyses suggest that doses above this range may increase all-cause mortality, although these analyses are limited because the trials of high-dose vitamin E were small and most included patients with chronic diseases [48,49]. Other studies suggested doses at or above this range significantly increase the risk for prostate cancer [50]. Therefore, we suggest that doses in this range be used only for patients with specific indications, such as selected patients with nonalcoholic fatty liver disease or age-related macular degeneration, as outlined below. Patients without special indications should not take vitamin E supplements for disease prevention. (See 'Potential benefits' below and "Vitamin intake and disease prevention", section on 'Vitamin E'.)
Theoretical concerns have been raised that vitamin E supplementation might increase the risk for operative bleeding because vitamin E is known to inhibit platelet aggregation and adhesion in vitro [51]. However, studies in humans give no evidence that supplements (eg, 500 mg [800 international units]/day) prolong bleeding propensity or alter platelet aggregation in the absence of aspirin or anticoagulant therapy [52,53]. Other studies caution against the use of vitamin E in patients with an increased propensity to bleeding or those taking aspirin or vitamin K antagonist anticoagulants such as warfarin [54,55]. In animal models, high-dose vitamin E supplements impaired absorption of fat-soluble vitamins A and K [56]. Large oral supplements of vitamin E have been associated with necrotizing enterocolitis in infants [57].
Potential benefits — Diseases for which high-dose vitamin E supplementation may be beneficial for selected patients are:
●Nonalcoholic fatty liver disease – High-dose vitamin E supplementation may be beneficial for selected patients with nonalcoholic fatty liver disease. Studies have suggested improvements in aminotransferase abnormalities and/or some histologic outcomes, although long-term benefits on disease outcomes have not been demonstrated. (See "Management of nonalcoholic fatty liver disease in adults", section on 'Potential pharmacologic therapies' and "Metabolic dysfunction-associated steatotic liver disease in children and adolescents", section on 'Pharmacotherapy'.)
●Age-related macular degeneration – For patients with established age-related macular degeneration, supplementation with antioxidant vitamins and zinc appears to delay progression of the disease [58]. Supplements for this purpose provide 400 international units of synthetic alpha-tocopherol (approximately 180 mg), which is generally considered safe, although higher doses may be associated with complications (see 'Potential risks' above). There is no evidence that supplementation with vitamin E or other antioxidant vitamins is effective for prevention of this disorder [59].
Vitamin E supplementation is probably not beneficial for the following conditions:
●Cardiovascular disease – A benefit of vitamin E supplementation in preventing cardiovascular disease appears to be unlikely. (See "Vitamin intake and disease prevention", section on 'Cardiovascular disease'.)
●Cancer – Vitamin E supplementation has been evaluated for prevention of prostate cancer and several other common neoplasms. A benefit seems unlikely, and there is some evidence that supplementation may actually increase the risk for prostate cancer. (See "Chemoprevention strategies in prostate cancer", section on 'Vitamin E' and "Vitamin intake and disease prevention", section on 'Cancer'.)
●Premature infants – In premature infants, hemolytic anemia is a common abnormality encountered in the presence of vitamin E deficiency [37]. Vitamin E therapy at standard doses slightly increases hemoglobin concentrations and reduces the incidence of periventricular hemorrhage [60]. However, the risk of sepsis also was increased with high-dose supplementation, regardless of whether administered by intravenous or oral routes. A few studies suggest some benefit in preventing retinopathy of prematurity, but overall the evidence is inconclusive [60]. (See "Retinopathy of prematurity (ROP): Treatment and prognosis", section on 'Prevention' and "Parenteral nutrition in premature infants", section on 'Vitamins'.)
●Dementia – Some studies suggest some association between development of Alzheimer disease and vitamin E deficiency [61]. Randomized trials suggest that high-dose vitamin E supplementation does not affect the risk of cognitive impairment or dementia but may slow progression of Alzheimer disease [62]. (See "Vitamin intake and disease prevention" and "Treatment of Alzheimer disease", section on 'Antioxidants'.)
●Tardive dyskinesia – Limited evidence suggests that vitamin E supplementation probably does not improve symptoms of tardive dyskinesia induced by neuroleptic medications [63]. (See "Tardive dyskinesia: Prevention, treatment, and prognosis", section on 'Initial management'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Vitamin deficiencies".)
SUMMARY AND RECOMMENDATIONS
●Vitamin E (tocopherol) is a fat-soluble vitamin with antioxidant properties; it protects cell membranes from oxidation and destruction. Vitamin E is found in a variety of foods including oils, meat, eggs, and leafy vegetables. (See 'Requirements' above and 'Actions' above.)
●There are multiple forms and isomers of tocopherol and the related compounds, tocotrienols. The best evidence suggests that the primary bioactive form of vitamin E is alpha-tocopherol. This is quantified according to the presence of the RRR-isomer, which is the only form found in nature and is also called "natural source" vitamin E or D-alpha-tocopherol. Synthetic vitamin E contains seven other isomers (termed "all-racemic" vitamin E or DL-alpha-tocopherol) and has lower activity and possibly more toxic potential than the RRR-isomer. (See 'Chemistry and nomenclature' above and 'Actions' above.)
•Measurement of serum alpha-tocopherol concentrations provides an accurate measure of vitamin E status for most patients in the absence of hyperlipidemia. For patients with hyperlipidemia, effective vitamin E levels are calculated as the ratio of serum alpha-tocopherol per gram total lipids. (See 'Measurement' above.)
•Gamma-tocopherol is also present in foods. It is transported less efficiently and has lower plasma levels than alpha-tocopherol, but similar tissue levels are achieved. The overall health effects of gamma-tocopherol have not been established.
●Absorption of dietary vitamin E requires fully functional mechanisms for fat absorption, including lingual and gastric lipases; bile salts for solubilization and production of mixed micelles; pancreatic function; and intestinal and ileal mucosal and absorptive mechanisms, unless provided in a synthetic water-soluble form. In addition, a specific protein (alpha-tocopherol transfer protein) is required for effective transport and use. (See 'Metabolism' above.)
●Signs and symptoms of vitamin E deficiency include hemolysis, neuromuscular disorders, ataxia, and peripheral neuropathy. Because of an abundance of tocopherols in the human diet, vitamin E deficiency is rare except in individuals with cholestatic liver disease, pancreatic insufficiency, or other conditions causing substantial fat malabsorption or protein-energy malnutrition. Vitamin E deficiency also may be caused by rare genetic defects affecting vitamin E metabolism or transport. (See 'Deficiency' above.)
●No syndrome of acute vitamin E toxicity has been described. In premature infants, high-dose vitamin E treatment was associated with increased risk for sepsis. Chronic intake of supplements of pharmacologic doses in excess of 270 mg/day RRR-alpha-tocopherol (400 international units/day) has been associated with increased risk of all-cause mortality and possibly prostate cancer. (See 'Potential risks' above.)
●There is no evidence that supplementation of vitamin E improves health outcomes in healthy children or adults. We suggest that patients without special indications avoid taking daily supplements containing high doses (≥400 international units) of vitamin E (Grade 2B). (See 'Potential risks' above.)
●Individuals with severe pancreatic insufficiency or cholestatic liver disease may have vitamin E deficiency due to fat malabsorption. For these individuals, we recommend vitamin E supplementation (Grade 1A).
•For children with severe cholestasis, a suggested starting dose is 17 to 35 mg/kg/day of RRR-alpha-tocopherol (25 to 50 international units/kg/day), with titration up if the ratio of alpha-tocopherol/total lipids does not normalize. Alternatively, water-miscible vitamin E can be used to maximize absorption, given at a dose of 10 to 17 mg/kg/day (15 to 25 international units/kg/day).
•For adults with pancreatic disease or cholestasis, vitamin E requirements vary and supplements should be based on serum measurements of alpha-tocopherol. (See 'Treatment' above.)
●Evidence does not support a role for vitamin E supplementation in the prevention or treatment of cancers, cardiovascular and cerebrovascular disease, dementia, and retinopathy of prematurity. Weak evidence suggests a possible role in managing nonalcoholic fatty liver disease and in slowing the progression of macular degeneration and Alzheimer disease. In premature infants, vitamin E supplementation may reduce the risk of periventricular hemorrhage but also increases the risk of sepsis. (See 'Potential benefits' above.)
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