Overview of vitamin e

Official reprint from UpToDatewww.uptodate.com ©2015 UpToDate

AuthorsSassan Pazirandeh, MDDavid L Burns, MD

Section EditorsTimothy O Lipman, MDKathleen J Motil, MD, PhD

Deputy EditorAlison G Hoppin, MD

Overview of vitamin E

All topics are updated as new evidence becomes available and our peer review process is complete.Literature review current through: Feb 2015. | This topic last updated: Aug 20, 2014.

INTRODUCTION — Vitamins are a number of chemically unrelated families of organic substances thatcannot be synthesized by humans but need to be ingested in the diet in small quantities to prevent disordersof metabolism. They are divided into water-soluble and fat-soluble vitamins (table 1).

In 1922, Evans and Bishop discovered a substance that was deficient in rats fed a diet that contained lardand that resulted in infertility [1]. The deficiency was corrected when a lipid extract of cereals was added tothe diet; this was termed the "anti-sterility factor" [2]. In 1925, vitamin E was officially recognized as the fifthvitamin. A few years later the name tocopherol from the Greek word of "toc" (child) and "phero" (to bringforth) was coined to describe its role as an essential dietary substance in normal fetal and childhooddevelopment [3]. In 1969, the FDA formally recognized vitamin E as an essential nutrient for humans.Vitamin E is a fat-soluble compound and an antioxidant and protects cell membranes from oxidation anddestruction.

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 minerals" and "Overview of water-soluble vitamins"and "Vitamin supplementation in disease prevention".)

SOURCES — Vitamin E is found in a variety of foods including oils, meat, eggs, and leafy vegetables. Theform that is best known for its role in human health is alpha-tocopherol, which is abundant in olive andsunflower oils, and is the predominant form in the European diet. Gamma-tocopherol is another form, whichis abundant in soybean and corn oil, and is common in the American diet.

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 intakesapply [4]. Furthermore, the RRR-isomer (formerly and incorrectly called D-alpha-tocopherol) is the only formfound in foods; it is sometimes known as “natural source” vitamin E.

Many synthetic vitamin E supplements or fortified foods contain all the eight isomers of alpha-tocopherol;these are known as "all racemic" or “DL” alpha tocopherol, and have approximately half of the activity of"natural source" vitamin E. However, all of the isomers of alpha tocopherol may contribute to the potentialadverse effects of supplemental vitamin E and are included in the calculation of an upper limit forsupplementation [4].

Vitamin E dosing is quantified by the content of the active isomer:

®®

1 mg RRR-alpha tocopherol = 1.47 international units “natural source” vitamin E (D-alpha-tocopherol) =2.2 international units “all racemic” vitamin E (DL-alpha-tocopherol).

Overview of vitamin E http://www.uptodate.com/contents/overview-of-vitamin-e?topi...

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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 datasources, often report either total tocopherol concentrations, or “alpha-tocopherol equivalents,” which adjustsfor the bioavailability for the various forms [4]. However, these measures do not reflect the bioactivity ofalpha-tocopherol, which is now used as the standard for dietary sufficiency.

Gamma-tocopherol is transported less efficiently and has lower plasma levels, but similar tissue levels ascompared with alpha-tocotrienols [5]. Because gamma-tocopherol has unique associations withinflammation and airway hyperresponsiveness (see 'Actions' below), this compound may have importantadverse or beneficial effects, although it is not currently included in the recommended daily allowance(RDA). Pharmacological 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 polyunsaturatedfatty acids (PUFA), a major structural component of the cell membranes, from peroxidation [7]. In the pastfew decades, there has been increasing interest in the role of free radicals and anti-oxidants inatherosclerosis and carcinogenesis (see "Vitamin supplementation in disease prevention"). Deficiency ofvitamin E has been connected to cardiovascular events. Low-density lipoprotein (LDL) plays a central role inthese hypotheses. When LDL is exposed to oxidative stress, it undergoes a cascade of changes affectingthe vascular endothelium, thereby facilitating atherogenesis [8-10]. This theory is referred to as the oxidativemodification hypothesis, and has fueled epidemiologic studies and clinical trials in cardiology to determinethe role of antioxidants, such as vitamin E, in prevention and treatment of atherosclerotic cardiovasculardisease [11]. However, trials of vitamin E supplementation (which typically use “all-racemic” vitamin E) havegenerally shown no effect in prevention of heart disease. (See "Nutritional antioxidants in coronary heartdisease" and "Vitamin supplementation in 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 inprostaglandin E2 [14,15]. The overall health effects of gamma-tocopherol have not been established. Highdoses of vitamin E (as alpha-tocopherol) reduce levels of gamma-tocopherol, perhaps explaining theadverse effects of pharmacological doses of the vitamin [5,6].

Some functions of vitamin E are independent of the antioxidant/radical scavenging activity, includinginhibition of cell proliferation, platelet aggregation, and monocyte adhesion [16]. Several other effects at themolecular 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 uponphysiologic mechanisms for fat digestion and absorption. This process requires lipolytic function ofpancreatic enzymes [17]. Pancreatic esterases are the enzymes responsible for breaking down thetocopheryl-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. Thesynthesis 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-tocopherolis preferentially secreted into the bloodstream, packaged within very-low-density lipoprotein (VLDL)molecules [20]. The transport protein for alpha-tocopherol is named alpha-tocopherol transfer protein(A-TTP) [21].


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REQUIREMENTS — Dietary vitamin E content is variable and proportional to vegetable oil intake. Americandiets of 2000 to 3000 kcal/day contain 7 to 10 mg of alpha-tocopherol equivalents. However, this is likely anunderestimate because dietary fat intake is commonly under-reported.

Healthy population — The recommended daily allowance (RDA) for vitamin E is 15 mg of dietary alpha-tocopherol per day for adolescents and adult men and women, as defined by the United States NationalAcademy of Sciences Food and Nutrition Board [4]. This is the equivalent of 22 international units ofRRR-alpha-tocopherol (the form that is supplied by some supplements and is marketed as "natural-source"vitamin E), or 33 international units of all-rac-alpha-tocopherol (the synthetic form used for the majority ofsupplements) [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, asubstantial 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 andnomenclature' above and 'Actions' above.)

Cholestatic disease — Patients with cholestasis or pancreatic exocrine insufficiency are at risk for vitaminE deficiency because of malabsorption of fat and fat-soluble vitamins. Patients with cholestasis also tend tohave hyperlipidemia, which strongly influences vitamin E levels, so assessment of their vitamin E statusrequires simultaneous measurement of alpha-tocopherol and serum lipids (see 'Measurement' below).

If vitamin E deficiency is diagnosed, these patients are treated with large oral doses of vitamin E. Water-miscible vitamin E (d-alpha-tocopherol glycol 1000 succinate, TPGS) is most effective in these patients [22].However, water-miscible preparations have not been shown to be superior for patients with cystic fibrosiswho are taking concurrent pancreatic enzyme supplements [23,24].

Typical supplementation regimens for infants and children with cholestasis are 25 to 50 int. units/kg/day ofvitamin E (alpha tocopherol), or 15 to 25 international units/kg/day of water-miscible vitamin E [25,26].

The prevalence of vitamin E deficiency in adults with cholestatic liver diseases has not been well defined. Itis probably most common in patients with severe and prolonged primary biliary cirrhosis, in whom estimatesof vitamin E deficiency range from 10 to 50 percent [27-29]. For patients with significant cholestasis (eg,bilirubin >2.0 mg/dL), routine monitoring of vitamin E levels is recommended, with vitamin E replacement asneeded [30].

DEFICIENCY — Vitamin E deficiency is uncommon in humans except in unusual circumstances. This is dueto the abundance of tocopherols in the diet. Individuals eating a vegetarian or vegan diet typically are not atincreased risk for vitamin E deficiency. Individuals with fat malabsorption and steatorrhea are at risk fordeficiency of all lipid-soluble vitamins [31]. These disorders include cirrhosis, cholestatic liver disease, cysticfibrosis, small bowel bacterial overgrowth, pancreatic insufficiency, celiac disease, and Crohn disease. Thedegree of deficiency is generally proportional to the magnitude and the duration of steatorrhea [32]. (See'Cholestatic disease' above.)

There are also several genetic disorders that lead to vitamin E deficiency. As an example, a mutation in thegene encoding hepatic alpha-tocopherol transfer protein (TTPA) is associated with neurologic deficits and isknown as ataxia with vitamin E deficiency (AVED). Affected patients have symptoms similar to Friedreich'sataxia [33]. These patients sometimes respond to oral supplementation of vitamin E in doses of 800 to 1500mg per day (or 40 mg/kg/day in children) of alpha-tocopherol [34-36]. More often, supplementation serves toprevent progression of the disease [37]. (See "Overview of the hereditary ataxias", section on 'Treatablediseases'.)


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In adults and children, vitamin E deficiency can cause neuromuscular disorders and hemolysis. Low serumlevels of vitamin E (defined as below 0.5 mg/dL) may cause no appreciable symptoms, or may manifest assubtle neurologic abnormalities. Neuromuscular disorders associated with vitamin E deficiency are mostly ofthe neuropathic and myopathic type [37]. The neuropathy generally consists of a spinocerebellar syndrome,with variable involvement of the peripheral nerves. Clinical manifestations include ataxia, hyporeflexia, andloss of proprioceptive and vibratory sensation [38]. A skeletal myopathy and pigmented retinopathy also maybe present [37,38].

Vitamin E deficiency can shorten the lifespan of red blood cells. In premature infants, vitamin E deficiencymay cause a hemolytic anemia [39]. Congenital hemolytic disorders such as thalassemia, sickle cell anemia,glucose-6-phosphate dehydrogenase deficiency (G6PD), and spherocytosis may be associated with lowvitamin E plasma levels, likely because of increased oxidant stress and antioxidant consumption [40-42].Oral therapy with vitamin E supplementation may be of benefit, but efficacy has not been proven [43,44].

EXCESS AND TOXICITY — The long-term effects and the safety of vitamin E supplementation are unclear[45]. The Tolerable Upper Intake Level (UL) for vitamin E consumption from supplements is based primarilyon concerns for hemorrhagic effects [4]. The recommended UL is 1000 mg of alpha-tocopherol daily(approximately 1,500 international units of natural source or 2,200 international units of synthetic vitamin E)for adults without fat malabsorption or other cause of vitamin E malabsorption. The UL in children rises from200 mg daily at 1 to 3 years to 600 mg daily at 9 to 13 years (table 2). Because of increasing evidenceshowing adverse effects of pharmacologic doses of vitamin E, it is possible that this UL is too high [46,47].We do not recommend supplementation near this level except when necessary to correct a deficiency state.

Most studies suggest that pharmacological doses of vitamin E supplementation in doses of 100 to 400international units (67 to 272 mg RRR-alpha tocopherol) per day are safe for most patients [11]. However,other reports caution against the use of higher doses. One study, for example, found a higher evidence ofmortality due to hemorrhagic strokes in vitamin E supplementation [8]. Other studies caution against the useof vitamin E in patients with an increased propensity to bleeding or those taking vitamin K antagonistanticoagulants such as warfarin. Animal models have demonstrated impaired absorption of fat-solublevitamins A and K with large vitamin E supplements. Large oral supplements of vitamin E have beenassociated with necrotizing enterocolitis in infants [48]. Vitamin E may impair the hematologic response toiron in children with iron-deficiency anemia.

A meta-analysis examined the dose-response relationship between vitamin E and overall mortality in a totalof 19 randomized clinical trials which included a total of 135,967 participants [46]. Doses of vitamin E rangedfrom 16.5 to 2000 IU/day (median, 400 IU). Vitamin E supplementation with a dose ≥400 IU/day wasassociated with a significantly increased risk of all-cause mortality (95% CI 3-74 per 10,000 persons). Thus,patients without special indications should not take vitamin E supplements for disease prevention. (See"Vitamin supplementation in disease prevention", section on 'Vitamin E'.)

Although significant, these findings should be interpreted with some caution since trials of high dose vitaminE were small, and most of these included patients with chronic diseases. Furthermore, there washeterogeneity among the studies that showed an increase in all-cause mortality.

THERAPEUTIC ROLES — The benefit of vitamin E supplementation in pharmacologic doses on cancer,cardiovascular disease, stroke, dementia, and liver disease (such as nonalcoholic fatty liver disease)continue to be evaluated. A benefit of supplementation in cardiovascular disease appears to be unlikely.(See "Vitamin supplementation in disease prevention" and "Nutritional antioxidants in coronary heartdisease" and "Chemoprevention strategies in prostate cancer" and "Natural history and management of


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nonalcoholic fatty liver disease in adults".)

In premature infants, hemolytic anemia is a common abnormality encountered in the presence of vitamin Edeficiency. Vitamin E therapy slightly increases hemoglobin concentrations and reduces the incidence ofperiventricular hemorrhage [49]. However, the risk of sepsis also was increased with high-dosesupplementation, regardless of whether administered by intravenous or oral routes. A few studies suggestsome benefit in preventing retinopathy of prematurity, but overall the evidence is inconclusive [49-52].

Some studies suggest some association between development of Alzheimer disease and vitamin Edeficiency [53]. However, randomized trials suggest that vitamin E supplementation does not affect the riskof cognitive impairment or dementia [54], but a possible role for slowing progression of Alzheimer disease.(See "Vitamin supplementation in disease prevention" and "Treatment of dementia", section on 'Antioxidanttherapy'.)

Although controversial, a few studies support potential benefits of vitamin E supplementation in treatingcataracts or age-related macular degeneration [51,55,56]. (See "Age-related macular degeneration: Clinicalpresentation, etiology, and diagnosis", section on 'Risk factors'.)

Some studies suggest benefit in preventing or treating tardive dyskinesia [57]. A meta-analysis concludedthat it may protect against deterioration of tardive dyskinesia, but probably does not improve symptoms [58].(See "Pharmacotherapy for schizophrenia: Side effect management", section on 'Tardive dyskinesia'.)

MEASUREMENT — Serum vitamin E levels are strongly influenced by concentration of serum lipids, and donot accurately reflect tissue vitamin levels. Therefore, effective vitamin E levels are calculated as thefollowing ratio:

Effective serum vitamin E level = Alpha-tocopherol / (cholesterol + triglycerides)

A normal ratio is >0.8 mg alpha-tocopherol/gram total lipids.

For patients with normal levels of serum lipids, serum alpha-tocopherol levels provide an adequate estimateof vitamin E sufficiency. Alpha-tocopherol levels of less than 0.5 mg/dL (5 µg/mL, or 11.5 µmol/L) areconsidered deficient. In a United States national survey, the 5th percentile for serum levels of vitamin E was0.62 mg/dL (14.3 µmol/L), and the 25th percentile was 0.79 mg/dL (18.5 µmol/L) [4].

SUMMARY AND RECOMMENDATIONS

Vitamin E (tocopherol) is a fat-soluble vitamin with antioxidant properties; it protects cell membranesfrom oxidation and destruction. Vitamin E is found in a variety of foods including oils, meat, eggs, andleafy vegetables. (See 'Requirements' above and 'Actions' above.)

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There are multiple forms and isomers of tocopherol and the related compounds, tocotrienols. The bestcurrent evidence suggests that the primary bioactive form of Vitamin E is alpha-tocopherol. This isquantified according to the presence of the RRR-isomer, which is the only form found in nature, and isalso called “natural source vitamin E”, or D-alpha-tocopherol. Synthetic vitamin E contains seven otherisomers (termed “all-racemic vitamin E” or DL-alpha-tocopherol), and has lower activity and possiblymore toxic potential than the RRR-isomer. (See 'Chemistry and nomenclature' above and 'Actions'above.)

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Gamma-tocopherol is also present in foods. It is transported less efficiently and has lower plasmalevels than alpha-tocopherol, but similar tissue levels are achieved. The overall health effects ofgamma-tocopherol have not been established. (See 'Chemistry and nomenclature' above and 'Actions'

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REFERENCES

Traber MG. Vitamin E. In: Modern Nutrition in Health and Disease, Shils M, Olson J, Shike M, et al(Eds), Lippincott, Philadelphia 2000.

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Evans HM. The pioneer history of vitamin E. Vitam Horm 1963; 20:379.2.

Mason, KE. The first two decades of vitamin E history. In: Vitamin E: A Comprehensive Treatise,Machlin, LJ (Eds), Marcel Dekker, New York 1980. p.1.

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above.)

Serum vitamin E levels are strongly influenced by concentration of serum lipids, and do not accuratelyreflect tissue vitamin levels. Effective vitamin E levels are calculated as the ratio of serum alpha-tocopherol per gram total lipids. (See 'Measurement' above.)

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Absorption of dietary vitamin E requires effective pancreatic exocrine function and fat absorption,unless provided in a synthetic water-soluble form. In addition, a specific protein (alpha-tocopheroltransfer protein) is required for effective transport and use. (See 'Metabolism' above.)

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Signs and symptoms of vitamin E deficiency include hemolysis, neuromuscular disorders, ataxia, andperipheral neuropathy. Because of an abundance of tocopherols in the human diet, vitamin Edeficiency is rare except in individuals with pancreatic insufficiency or other conditions causingsubstantial fat malabsorption, or protein-energy malnutrition. Vitamin E deficiency also may be causedby rare genetic defects affecting vitamin E metabolism or transport. (See 'Deficiency' above.)

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No syndrome of acute vitamin E toxicity has been described. In premature infants, high-dose vitamin Etreatment was associated with increased risk for sepsis (see 'Therapeutic roles' above). Chronic intakeof supplements of pharmacologic doses in excess of 400 international units (272 mg RRR-alpha-tocopherol) daily has been associated with increased risk of hemorrhage and all-cause mortality. (See'Excess and toxicity' above.)

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There is no evidence that supplementation of vitamin E improves health outcomes in healthy childrenor adults. We suggest that patients without special indications avoid taking daily supplementscontaining high doses (>400 IU) of vitamin E (Grade 2B). (See 'Excess and toxicity' above.)

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Individuals with severe pancreatic insufficiency or cholestatic liver disease may have vitamin Edeficiency due to fat malabsorption. For these individuals, we recommend vitamin E supplementation(Grade 1A). Doses of about 25 to 50 international units/kg/day (17 to 34 mg RRR-alpha-tocopherol)are generally effective in children. Alternatively, water miscible vitamin E can be used to maximizeabsorption, at a dose of 15 to 25 international units/kg/day. (See 'Requirements' above.)

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Current evidence does not support a role for vitamin E supplementation in the prevention or treatmentof cancers, cardiovascular and cerebrovascular disease, dementia, and retinopathy of prematurity.Weak evidence suggests a possible role in slowing the progression of Alzheimer disease, tardivedyskinesia, and macular degeneration. In premature infants, vitamin E supplementation may reducethe risk of periventricular hemorrhage, but also increases the risk of sepsis. (See 'Therapeutic roles'above.) See associated topic reviews.

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Jiang Q, Elson-Schwab I, Courtemanche C, Ames BN. gamma-tocopherol and its major metabolite, incontrast to alpha-tocopherol, inhibit cyclooxygenase activity in macrophages and epithelial cells. ProcNatl Acad Sci U S A 2000; 97:11494.

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Zingg JM, Azzi A. Non-antioxidant activities of vitamin E. Curr Med Chem 2004; 11:1113.16.

Traber MG, Goldberg I, Davidson E, et al. Vitamin E uptake by human intestinal cells during lipolysis invitro. Gastroenterology 1990; 98:96.

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GRAPHICS

Clinical symptoms of selected vitamin deficiencies

Function Deficiency syndrome

Water-soluble vitamins

Vitamin B1(thiamine)

Thiaminepyrophosphate

Beriberi - congestive heart failure (wet beriberi),aphonia, peripheral neuropathy, Wernickeencephalopathy (nystagmus, opthalmoplegia,ataxia), confusion, or coma

Vitamin B2(riboflavin)

Flavine adeninedinucleotide

Nonspecific symptoms including edema of mucusmembranes, angular stomatitis, glossitis, andseborrheic dermatitis (eg, nose, scrotum)

Niacin(nicotinic acid)

Nicotinamideadeninedinucleotide

Pellagra - dermatitis on areas exposed to sunlight;diarrhea with vomiting, dysphagia, mouthinflammation (glossitis, angular stomatitis, cheilitis);headache, dementia, peripheral neuropathy, loss ofmemory, psychosis, delirium, catatonia

Vitamin B6(pyroxidine,pyridoxal)

Transaminasecofactor

Anemia, weakness, insomnia, difficulty walking,nasolabial seborrheic dermatitis, cheilosis, stomatitis

Vitamin B12(cobalamin)

One carbontransfer

Megaloblastic anemia (pernicious anemia). Peripheralneuropathy, with impaired proprioception, andslowed mentation.

Folate One carbontransfer

Megaloblastic anemia

Biotin Pyruvatecarboxylasecofactor

Nonspecific symptoms including altered mentalstatus, myalgia, dysesthesias, anorexia,maculosquamous dermatitis

Pantothenate Coenzyme A Nonspecific symptoms including paresthesias,dysesthesias ("burning feet"), anemia,gastrointestinal symptoms

Vitamin C(ascorbate)

Antioxidant,collagensynthesis

Scurvy - fatigue, petechiae, ecchymoses, bleedinggums, depression, dry skin, impaired wound healing

Fat-soluble vitamins

Vitamin A(retinol,retinal, retinoicacid)

Vision, epithelialdifferentiation

Night blindness, xerophthalmia, keratomalacia,Bitot's spot, follicular hyperkeratosis


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Vitamin D(cholecalciferol,ergocalciferol)

Prohormone forcalciumregulation

Rickets, osteomalacia, craniotabes, rachitic rosary

Vitamin E(tocopherols)

Antioxidant Sensory and motor neuropathy, ataxia, retinaldegeneration, hemolytic anemia

Vitamin K(phylloquinone,menaquinone,menadione)

Clotting factors,bone proteins

Hemorrhagic disease

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Dietary reference intakes for fat-soluble vitamins

Nutrient Age group RDA*/AI ULAdverse

effects ofexcess

Vitamin A

1 mcg retinolactivityeqivalent =3.3 unitvitamin A

Micrograms

dailyMicrograms

dailyAtaxia, alopecia,hyperlipidemia,hepatotoxicity,bone andmuscle pain;teratogenic

Infants

0 to 6 months 400 600

7 to 12 months 500 600

Children

1 to 3 years 300 600

4 to 8 years 400 900

Males

9 to 13 years 600 1700

14 to 18 years 900 2800

≥19 years 900 3000

Females

9 to 13 years 600 1700

14 to 18 years 700 2800

≥19 years 700 3000

Pregnancy

<18 years 750 2800

≥19 years 770 3000

Lactation

<18 years 1200 2800

≥19 years 1300 3000

Vitamin D

(calciferol)

1 mcgcalciferol =40 int. unit

Micrograms

dailyMicrograms

dailyHypercalcemia,hypercalciuria,polydipsia,polyuria,confusion,anorexia,vomiting, bonedemineralization

Infants

0 to 12 months 10 (400 int. unit) 0 to 6 months: 25(1000 int. unit)

6 to 12 months:37.5 (1500 int.unit)

• Δ


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Children and adolescents

1 to 18 years 15 (600 int. unit) 1 to 3 years: 62.5(2500 int. unit)

4 to 8 years: 75(3000 int. unit)

9 to 18 years: 100(4000 int. unit)

Males and females (including pregnancy and lactation)

19 to 50 years 15 (600 int. unit) 100 (4000 int.unit)

50 to 70 years 15 100

>70 years 20 (800 int. unit) 100

Vitamin E

(alpha-tocopherol)

1 mg = 1.47int. unit"naturalsource"vitamin E, or2.2 int. unitsyntheticvitamin E

Milligrams daily Milligrams daily Increased risk ofbleeding;possiblyincreased risk ofnecrotizingenterocolitis ininfants

Infants

0 to 6 months 4 ND

7 to 12 months 5 ND

Children

1 to 3 years 6 200

4 to 8 years 7 300

Males and females (including pregnancy)

9 to 13 years 11 600

14 to 18 years 15 800

>18 years 15 1000

Lactation

≤18 years 19 800

>19 years 19 1000

Vitamin K

Microgramsdaily

Microgramsdaily

No adverseeffectsassociated withvitamin Kconsumptionfrom food orsupplementshave beenreported,however data

Infants

0 to 6 months 2 ND

7 to 12 months 2.5 ND

Children

1 to 3 years 30 ND

4 to 8 years 55 ND


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are limitedMales

9 to 13 years 60 ND

14 to 18 years 75 ND

>19 years 120 ND

Females (including pregnancy and lactation)

9 to 13 years 60 ND

14 to 18 years 75 ND

>19 years 90 ND

Vitamin A doses given as retinol activity equivalents (RAE). 1 RAE = 1 mcg retinol, 12 mcgbeta-carotene, 14 mcg alpha-carotene, or 24 mcg beta-cryptoxanthin.

RDA: recommended dietary allowance; AI: adequate intake; UL: upper tolerable level.* The RDA is the level of dietary intake that is sufficient to meet the daily nutrient requirements of97 percent of the individuals in a specific life stage group.• The AI represents an approximation of the average nutrient intake that sustains a definednutritional state, based on observed or experimentally determined values in a defined population.Δ The UL is the maximum level of daily nutrient intake that is likely to pose no risk of adversehealth effects in almost all individuals in the specified life-stage or gender group.

Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Otten JJ, Hellwig JP,Meyers LD (Eds), The National Academies Press, Washington, DC 2006. pp.530-541. Modified withpermission from the National Academies Press, Copyright © 2006, National Academy of Sciences.Sources: Dietary reference intakes for Thiamin, Riboflavin, Niacin, Vitamin B , Folate, Vitamin B ,Panthothenic acid, Biotin, and Choline (1998); Dietary reference intakes for Vitamin C, Vitamin E,Selenium, and Carotenoids (2000); Dietary Reference Intake reports of the Food and NutritionBoard, Institute of Medicine (2010). These reports may be accessed via www.nap.edu.

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Disclosures: Sassan Pazirandeh, MD Nothing to disclose. David L Burns, MD Nothing to disclose. Timothy O Lipman, MD OtherFinancial Interest: GI Board Review Lecturer [Clinical nutrition]; Audio Journal Club Practice Reviews in Gastroenterology [Clinicalnutrition, gut microbiome, complementary and alternative medicine, critical reading skills]. Kathleen J Motil, MD, PhDConsultant/Advisory Boards: NPS Pharmaceuticals [Short gut syndrome (Teduglutide)]. Alison G Hoppin, MD Employee ofUpToDate, Inc.Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vettingthrough a multi-level review process, and through requirements for references to be provided to support the content. Appropriatelyreferenced content is required of all authors and must conform to UpToDate standards of evidence.Conflict of interest policy

Disclosures


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Overview of vitamin e

Food

Transcript of Overview of vitamin e