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IUPAC name (2R)-2,5,7,8-Tetramethyl-2-[(4R,8R)-4,8,12
CAS number 59-02-9
EINECS number 200-412-2
InChI InChI=1/C29H50O2/c1-20(2)
Molecular formula C29H50O2
Molar mass 430.69 g/mol
Density 0.950 g/cm³
Melting point

2.5-3.5 °C

Boiling point

200-220 °C at 0.1 mmHg

Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)

Infobox disclaimer and references

Tocopherol, a class of chemical compounds of which many have vitamin E activity, describes a series of organic compounds consisting of various methylated phenols. Because the vitamin activity was first identified in 1936 from a dietary fertility factor in rats, it was given the name "tocopherol" from the Greek words “τοκος” [birth], and “φορειν”, [to bear or carry] meaning in sum "to carry a pregnancy," with the ending "-ol" signifying its status as a chemical alcohol.

Tocotrienols, which are related compounds, also may have vitamin E activity. All of these various derivatives with vitamin activity, may correctly be referred to as "vitamin E." Tocopherols and tocotrienols are fat-soluble antioxidants.

The compound α-tocopherol, a common form of tocopherol added to food products, is denoted by the vitamin E number E307.



Natural vitamin E exists in eight different forms, four tocopherols and four tocotrienols. All feature a chromanol ring, with a hydroxyl group that can donate a hydrogen atom to reduce free radicals and a hydrophobic side chain which allows for penetration into biological membranes. Both the tocopherols and tocotrienols occur in alpha, beta, gamma and delta forms, determined by the number of methyl groups on the chromanol ring. Each form has slightly different biological activity.[2]

As a food additive, tocopherol is labeled with these E numbers: E307 (α-tocopherol), E308 (γ-tocopherol), and E309 (δ-tocopherol). Vitamin E capsules are sometimes used as visible markers in magnetic resonance imaging.[citation needed]


Alpha-tocopherol is traditionally considered the most active biological antioxidant in humans. The measurement of "vitamin E" activity in international units (IU) was based on fertility enhancement by the prevention of spontaneous abortions in pregnant rats relative to alpha tocopherol. It increases naturally to about 150% of normal in the maternal circulation during human pregnancies.

1 IU of vitamin E is defined as the biological equivalent of 0.667 milligrams of RRR-alpha-tocopherol (formerly named d-alpha-tocopherol, or of 1 milligram of all-rac-alpha-tocopheryl acetate (commercially called dl-alpha-tocopheryl acetate, the original d, l- synthetic molecular mix, properly named 2-ambo-alpha-tocopherol, is no longer manufactured).

Other R, R, R tocopherol

The other R, R, R tocopherol vitamins are slowly being recognized as research begins to elucidate their additional roles in the human body. Many naturopathic and orthomolecular medicine advocates suggest that vitamin E supplements contain at least 20% by weight of the other natural vitamin E isomers.


Tocotrienols, with four d- isomers, also belong to the vitamin E family. The four tocotrienols have structures corresponding to the four tocopherols, except with an unsaturated bond in each of the three isoprene units that form the hydrocarbon tail. Tocopherols have a saturated phytyl tail.


During feeding experiments with rats Herbert McLean Evans concluded in 1922 that besides vitamins B and C, an unknown vitamin existed.[3] Although every other nutrition was present, the rats were not fertile. This condition could be changed by additional feeding with wheat germ. It took several years until 1936 when the substance was isolated from wheat germ and the formula C29H50O2 was determined. Evans also found that the compound reacted like an alcohol and concluded that one of the oxygen atoms was part of an OH (hydroxyl) group. As noted in the introduction, the vitamin was given its name by Evans from Greek words meaning "to bear young" with the addition of the -ol as an alcohol. [4] The structure was determined shortly thereafter in 1938.[5]

Recommended amounts

The U.S. Dietary Reference Intake (DRI) Recommended Daily Amount (RDA) for a 25-year old male for Vitamin E is 15 mg/day. The DRI for vitamin E is based on the alpha-tocopherol form because it is the most active form as originally tested. Results of two national surveys, the National Health and Nutrition Examination Survey (NHANES III 1988-91) and the Continuing Survey of Food Intakes of Individuals (1994 CSFII) indicated that the dietary intakes of most Americans do not provide the recommended amounts of vitamin E. However, a 2000 Institute of Medicine (IOM) report on vitamin E states that intake estimates of vitamin E may be low because energy and fat intake is often underreported in national surveys and because the kind and amount of fat added during cooking is often not known. The IOM states that most North American adults get enough vitamin E from their normal diets to meet current recommendations. However, they do caution individuals who consume low fat diets because vegetable oils are such a good dietary source of vitamin E. "Low-fat diets can substantially decrease vitamin E intakes if food choices are not carefully made to enhance alpha-tocopherol intakes". Vitamin E supplements are absorbed best when taken with meals.[6]

Because vitamin E can act as an anticoagulant and may increase the risk of bleeding problems, many agencies have set an upper tolerable intake level (UL) for vitamin E at 1,000 mg (1,500 IU) per day.[7]


In foods, the most abundant sources of vitamin E are vegetable oils such as palm oil, sunflower, corn, soybean, and olive oil. Nuts, sunflower seeds, seabuckthorn berries, kiwi fruit, and wheat germ are also good sources. Other sources of vitamin E are whole grains, fish, peanut butter, and green leafy vegetables. Fortified breakfast cereals are also an important source of vitamin E in the United States. Although originally extracted from wheat germ oil, most natural vitamin E supplements are now derived from vegetable oils, usually soybean oil.

The content of Vitamin E for rich sources follows:[8]

  • Wheat germ oil (215.4 mg/100 g)
  • Sunflower oil (55.8 mg/100 g)
  • Hazelnut (26.0 mg/100 g)
  • Walnut oil (20.0 mg/100 g)
  • Peanut oil (17.2 mg/100 g)
  • Olive oil (12.0 mg/100 g)
  • Peanut (9.0 mg/100 g)
  • Pollard (2.4 mg/100 g)
  • Corn (2.0 mg/100 g)
  • Asparagus (1.5 mg/100 g)
  • Oats (1.5 mg/100 g)
  • Chestnut (1.2 mg/100 g)
  • Coconut (1.0 mg/100 g)
  • Tomatoes (0.9 mg/100 g)
  • Carrots (0.6 mg/100 g)


There are three specific situations when a vitamin E deficiency is likely to occur. It is seen in persons who cannot absorb dietary fat, has been found in premature, very low birth weight infants (birth weights less than 1500 grams, or 3.5 pounds), and is seen in individuals with rare disorders of fat metabolism. A vitamin E deficiency is usually characterized by neurological problems due to poor nerve conduction.

Individuals who cannot absorb fat may require a vitamin E supplement because some dietary fat is needed for the absorption of vitamin E from the gastrointestinal tract. Anyone diagnosed with cystic fibrosis, individuals who have had part or all of their stomach removed, and individuals with malabsorptive problems such as Crohn's disease, liver disease or pancreatic insufficiency may not absorb fat and should discuss the need for supplemental vitamin E with their physician (3). People who cannot absorb fat often pass greasy stools or have chronic diarrhea.

Very low birth weight infants may be deficient in vitamin E. A neonatologist, a pediatrician specializing in the care of newborns, typically evaluates the nutritional needs of premature infants.

Abetalipoproteinemia is a rare inherited disorder of fat metabolism that results in poor absorption of dietary fat and vitamin E. The vitamin E deficiency associated with this disease causes problems such as poor transmission of nerve impulses, muscle weakness, and degeneration of the retina that can cause blindness. Individuals with abetalipoproteinemia may be prescribed special vitamin E supplements by a physician to treat this disorder. In addition, there is a rare genetic condition termed isolated vitamin E deficiency or ataxia with isolated with vitamin E deficiency, caused by mutations in the tocopherol transfer protein gene. These individuals have an extremely poor capacity to absorb vitamin E and develop neurological complications that are reversible by supplementation with high doses of vitamin E.

Also, in adults, erythrocyte membrane fragility resuls as the erythrocytes are oxidized.


Commercial vitamin E supplements can be classified into several distinct categories:

  • Fully synthetic vitamin E, "d, l-alpha-tocopherol", the most inexpensive, most commonly sold supplement form usually as the acetate ester;
  • Semi-synthetic "natural source" vitamin E esters, the "natural source" forms used in tablets and multiple vitamins; highly fractionated natural d-alpha tocopherol
  • Less fractionated "natural mixed tocopherols" and high gamma-tocopherol fraction supplements

"Megadoses" of Vitamin E are not recommended by many government agencies, due to a possible increased risk of bleeding. Two meta-analyses have concluded that synthetic and semisynthetic vitamin E supplements increase mortality, although these meta-analyses have been challenged by the nutrition literature.

A 2005 meta-analysis by Miller found that high-dosage vitamin E supplements may increase all-cause mortality.[9] "High dose" vitamin E esters (>400 units/day) were also associated with an increased risk in all-cause mortality of 39 per 10,000 persons, and a statistically significant relation existed between dose and mortality, with increased risk at doses exceeding 150 units per day. These trials included synthetic beta-carotene and other cofounders.

The Miller study was rebutted by Houston in the Journal of the American Nutraceutical Association[10]. Furthermore, Rosenberg concluded that "toxicity symptoms have not been reported even at intakes of 800 IU per kilogram of body weight daily for 5 months" according to the Food and Nutrition Board (Rosenberg, et al)[citation needed], an amount that corresponds to 60,000 IU per day for a 75 kg adult.

A review of all randomized controlled trials in the scientific literature by the Cochrane Collaboration published in JAMA in 2007 also found an increase in mortality, of 4% (Relative Risk 1.04, 95% confidence interval 1.01-1.07), or 400 per 10,000 persons.[11]

Allergic Reactions

Due to its wide use as a preservative and the common belief that vitamin E is good for the skin, many cosmetics (and inexpensive foods) include it as a preservative (usually labeled tocopherol acetate in cosmetics). Despite this, individuals can still experience allergic reactions to tocopherol.


Synthetic vitamin E is now manufactured as all-racemic alpha tocopheryl acetate with three chiral centers, with only one alpha tocopherol molecule (moiety) in 8 molecules as actual R, R,R-alpha tocopherol.

Synthetic all-rac vitamin E is usually marked as d, l-tocopherol or d, l-tocopheryl acetate, with 50% d-alpha tocopherol moiety and 50% l-alpha-tocopherol moiety, as synthesized by an earlier process with only one chiral center.

The synthetic form is not as active as the natural alpha tocopherol form. Information on any side effects of the synthetic vitamin E epimers is not readily available. Naturopathic and orthomolecular medicine advocates have long considered the synthetic vitamin E forms to be with little or no merit for cancer, circulatory and heart diseases.


Semisynthetic "natural source" vitamin E, manufacturers convert the common natural beta, gamma and delta tocopherol isomers into esters using acetic or succinic acid and add methyl groups to yield d-alpha tocopheryl esters such as d-alpha tocopheryl acetate or d-alpha tocopheryl succinate. These tocopheryl esters are more stable and are easy to use in tablets and multiple vitamin pills.

Because only alpha tocopherols were officially counted as "vitamin E" in supplements, refiners and manufacturers faced enormous economic pressure to esterify and methylate the other natural tocopherol isomers, d-beta-, d-gamma- and d-delta-tocopherol into d-alpha tocopheryl acetate or succinate. However these alpha tocopheryl esters have been shown to be variably and less efficiently absorbed in humans than in the original normative tests using rats.[12] In the healthy human body, the semisynthetic forms are easily de-esterified over several days, primarily in the liver, but not for common problems in premature babies, aged or ill patients.

Tocopheryl nicotinate and tocopheryl linolate esters are used in cosmetics and some pharmaceuticals.

Mixed tocopherols

"Mixed tocopherols" in the US contain at least 20% w/w other natural R, R,R- tocopherols, i.e. R, R,R-alpha-tocopherol content plus at least 25% R, R,R-beta-, R, R,R-gamma-, R, R,R-delta-tocopherols.

Some premium brands may contain 200% w/w or more of the other tocopherols and measurable tocotrienols. Some mixed tocopherols with higher gamma-tocopherol content are marketed as "High Gamma-Tocopherol". The label should report each component in milligrams, except R, R,R-alpha-tocopherol may still be reported in IU. Mixed tocopherols can also be found in various nutritional supplements manufactured by high end supplement companies.

Other uses

Conventional medical studies on vitamin E, as of 2006 and as below, use either a synthetic all-racemic ("d, l-") alpha tocopheryl ester (acetate or succinate) or a semi-synthetic d-alpha tocopheryl ester (acetate or succinate). Proponents of megavitamin, orthomolecular and naturally based therapies have advocated, for the last two thirds of a century, and have used the natural tocopherols, often mixed tocopherols with an additional 25% - 200% w/w d-beta-, d-gamma-,[13][14] and d-delta-tocopherol. Based on various clinical, experimental, patent, and individual data, natural health proponents have long held[15][16] that the other poorly studied tocopherols, especially the abundant d-gamma-tocopherol,[17] in combination with other antioxidants such as selenium, coQ10, vitamin C, vitamin K2, mixed carotenoids, and lipoic acid, provide unique biochemical benefits.[10] The methodology, interpretation and reporting of conventional vitamin E studies have even become contentious within conventional medicine circles.[18]

As a Preservative

Vitamin E is widely used in industry as an inexpensive preservative (namely for cosmetics and foods).

Reduce scarring

Topical use of Vitamin E is often claimed by manufacturers of skin creams and lotions to play a role in encouraging skin healing and reducing scarring after injuries such as burns on the basis of limited research,[19] but the weak evidence of a benefit of silicon gel sheeting with or without added Vitamin E is limited by the poor quality of the research.[20] Indeed one study found that it did not improve or worsened the cosmetic appearance in 90% of patients, with a third developing contact dermatitis.[21]

During pregnancy

Recent studies into the use of both vitamin C and the single isomer vitamin E esters as possible help in preventing oxidative stress leading to pre-eclampsia has failed to show significant benefits,[22]but did increase the rate of babies born with a low birthweight in one study.[23] However, earlier work that suggested vitamin K (similar structures to natural E isomers) and C together have 91% benefit in nausea and vomiting remains unaddressed.[24]

Heart disease

Preliminary research has led to a widely held belief that vitamin E may help prevent or delay coronary heart disease, but larger controlled studies have not shown any benefit. Many researchers advance the belief that oxidative modification of LDL-cholesterol (sometimes called "bad" cholesterol) promotes blockages in coronary arteries that may lead to atherosclerosis and heart attacks[citation needed]. Vitamin E may help prevent or delay coronary heart disease by limiting the oxidation of LDL-cholesterol. Vitamin E also may help prevent the formation of blood clots, which could lead to a heart attack. Observational studies have associated lower rates of heart disease with higher vitamin E intake. A study of approximately 90,000 nurses suggested that the incidence of heart disease was 30% to 40% lower among nurses with the highest intake of vitamin E from diet and supplements. The range of intakes from both diet and supplements in this group was 21.6 to 1,000 IU (32 to 1,500 mg), with the median intake being 208 IU (139 mg). A 1994 review of 5,133 Finnish men and women aged 30 - 69 years suggested that increased dietary intake of vitamin E was associated with decreased mortality (death) from heart disease.

But even though these observations are promising, randomized clinical trials have consistently shown lack of benefit to the role of vitamin E supplements in heart disease. The Heart Outcomes Prevention Evaluation (HOPE) Study followed almost 10,000 patients for 4.5 years who were at high risk for heart attack or stroke. In this intervention study the subjects who received 265 mg (400) IU of vitamin E daily did not experience significantly fewer cardiovascular events or hospitalizations for heart failure or chest pain when compared to those who received a sugar pill. The researchers suggested that it is unlikely that the vitamin E supplement provided any protection against cardiovascular disease in the HOPE study. This study is continuing, to determine whether a longer duration of intervention with vitamin E supplements will provide any protection against cardiovascular disease.

Furthermore, meta analysis of several trials of antioxidants, including vitamin E, have not shown any benefit to vitamin E supplementation for preventing coronary heart disease.[25] Indeed, one study suggested that vitamin E supplementation may increase the risk for heart failure.[26]

Orthomolecular and naturopathic medicine use much different types of vitamin E, the natural mixed tocopherols, and other supportive cofactors such as, selenium, vitamin C, carnitine, lysine, and co-Q10 for various cardiovascular diseases.[27][28] See also Orthomolecular medicine:Vitamin E controversy.

On September 10, 2007, the American Heart Association (in its journal Circulation) stated that women taking regular doses of vitamin E or Tocopherol were 21% less likely to suffer a blood clot. Dr. Robert Glynn of Harvard Medical School said (it was an interesting finding but not yet proven and) further research must confirm the link in the prevention of venous thromboembolism, and patients must not stop taking prescribed blood thinners.[29]


Antioxidants such as vitamin E help protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. Vitamin E also may block the formation of nitrosamines, which are carcinogens formed in the stomach from nitrites consumed in the diet. It also may protect against the development of cancers by enhancing immune function. To date, human trials and surveys that have tried to associate vitamin E with incidence of cancer remain generally inconclusive.

Some evidence associates higher intake of vitamin E with a decreased incidence of prostate cancer (see ATBC study) and breast cancer. Some studies correlate additional cofactors, such as specific vitamin E isomers, e.g. gamma-tocopherol, and other nutrients, e.g. selenium, with dramatic risk reductions in prostate cancer.[30] However, an examination of the effect of dietary factors, including vitamin E, on incidence of postmenopausal breast cancer in over 18,000 women from New York State did not associate a greater vitamin E intake with a reduced risk of developing breast cancer. A study of the effect on lung cancer in smokers also showed no benefit.[31]

A study of women in Iowa provided evidence that an increased dietary intake of vitamin E may decrease the risk of colon cancer, especially in women under 65 years of age.[citation needed] On the other hand, vitamin E intake was not statistically associated with risk of colon cancer in almost 2,000 adults with cancer who were compared to controls without cancer.[clarify][citation needed] At this time there is limited evidence to recommend vitamin E supplements for the prevention of cancer.


A cataract is a condition of clouding of the tissue of the lens of the eye. They increase the risk of disability and blindness in aging adults. Antioxidants are being studied to determine whether they can help prevent or delay cataract growth. Observational studies have found that lens clarity, which is used to diagnose cataracts, was better in regular users of vitamin E supplements and in persons with higher blood levels of vitamin E. A study of middle aged male smokers, however, did not demonstrate any effect from vitamin E supplements on the incidence of cataract formation. The effects of smoking, a major risk factor for developing cataracts, may have overridden any potential benefit from the vitamin E, but the conflicting results also indicate a need for further studies before researchers can confidently recommend extra vitamin E for the prevention of cataracts.

It is important to note that the term "cataract" may be used in common parlance for an opacity involving any tissue of the eye, for example a corneal scar. Thus a character in theater or on television who is blind from cataracts might have white instead of clear corneas, covering over the iris and pupil. Since the lens is behind the pupil, real cataracts are difficult to see without special instrumentation, so people with cataracts have rather normally appearing eyes.

Age-related macular degeneration (AMD)

Age-related macular degeneration (AMD) is the leading cause of visual impairment and blindness in the United States and the developed world among people 65 years and older. It has been shown that vitamin E alone does not attenuate the development or progression of AMD.[32]

However, studies focusing on efficacy of Vitamin E combined with other antioxidants, like zinc and vitamin C, indicate a protective effect against the onset and progression of AMD[33][34][35]


A 2007 study published in the European Journal of Ophthalmology found that, along with other treatments for glaucoma, adding alpha-tocopherol appeared to help protect the retina from glaucomatous damage. Groups receiving 300 mg and 600 mg per day of alpha-tocopherol, delivered orally, showed statistically significant decreases in the resistivity index in the posterior ciliary arteries and in the pulsatility index in the ophthalmic arteries, after six and twelve months of therapy. Alpha-tocopherol-treated patients also had significantly lower differences in mean visual field deviations."[36]

Alzheimer's disease

Alzheimer's disease is a wasting disease of the brain. An observational trial conducted by The Johns Hopkins University Bloomberg School of Public Health found that when vitamin E is taken daily in large doses (400-1000IU) in combination with vitamin C (500-1000mg) the onset of Alzheimer's was reduced between 64 and 78%.[37]

Parkinson's disease

In May 2005, The Lancet Neurology published a study suggesting that vitamin E may help protect against Parkinson's disease.[38] Individuals with moderate to high intakes of dietary vitamin E were found to have a lower risk of Parkinson's. No conclusion was drawn about whether supplemental vitamin E has the same effect, however.[39]


A 1998 Journal of Neuroscience article on hippocampal neurotoxicity, it is suggested that Vitamin E, among other substances, might inhibit the neural death caused in the hippocampus by THC, which is the main psychoactive component of cannabis. "Neuron death induced by THC was inhibited by nonsteroidal anti-inflammatory drugs, including indomethacin and aspirin, as well as vitamin E and other antioxidants." [40]

See also

  • Alkylresorcinols


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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Tocopherol". A list of authors is available in Wikipedia.
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