Vitamin E (Alpha-Tocopherol)

The term vitamin E describes a family of eight antioxidants, four tocopherols, alpha-, beta-, gamma- and delta-, and four tocotrienols (also alpha-, beta-, gamma- and delta-). Alpha-tocopherol is the only form of vitamin E that is actively maintained in the human body and is therefore, the form of vitamin E found in the largest quantities in the blood and tissue (1). Because alpha-tocopherol is the form of vitamin E that appears to have the greatest nutritional significance, it will be the primary topic of the following discussion. It is also the only form that meets the latest Recommended Dietary Allowance (RDA) for vitamin E.

Function

Alpha-tocopherol

The main function of alpha-tocopherol in humans appears to be that of an antioxidant. Free radicals are formed primarily in the body during normal metabolism and also upon exposure to environmental factors such as cigarette smoke or pollutants. Fats, which are an integral part of all cell membranes, are vulnerable to destruction through oxidation by free radicals. The fat-soluble vitamin, alpha-tocopherol, is uniquely suited to intercepting free radicals and preventing a chain reaction of lipid destruction. Aside from maintaining the integrity of cell membranes throughout the body, alpha-tocopherol also protects the fats in low density lipoproteins (LDLs) from oxidation. Lipoproteins are particles composed of lipids and proteins, which are able to transport fats through the blood stream. LDLs transport cholesterol from the liver to the tissues of the body. Oxidized LDLs have been implicated in the development of cardiovascular diseases (See Disease Prevention). When a molecule of alpha-tocopherol neutralizes a free radical, it is altered in such a way that its antioxidant capacity is lost. However, other antioxidants, such as vitamin C, are capable of regenerating the antioxidant capacity of alpha-tocopherol (2).

Several other functions of alpha-tocopherol have been identified, which likely are not related to its antioxidant capacity. Alpha-tocopherol is known to inhibit the actvity of protein kinase C, an important cell signaling molecule, as well as to affect the expression and activity of immune and inflammatory cells. Additionally, alpha-tocopherol has been shown to inhibit platelet aggregation and to enhance vasodilation (3, 4).

Gamma-tocopherol

The function of gamma-tocopherol in humans is presently unclear. Although the most common form of vitamin E in the American diet is gamma-tocopherol (see Food Sources), blood levels of gamma-tocopherol are generally ten times lower than those of alpha-tocopherol. This phenomenon appears due to the action of the alpha-tocopherol transfer protein (a-TTP) in the liver, which preferentially incorporates alpha-tocopherol into lipoproteins that are circulated in the blood (1) and ultimately deliver alpha-tocopherol to different tissues in the body. See the Linus Pauling Institute Newsletter for more information about a-TTP and vitamin E adequacy. Because gamma-tocopherol is initially absorbed in the same manner as alpha-tocopherol, small amounts are detectable in blood and tissue. Products of the metabolism of tocopherols, known as metabolites, can be detected in the urine. More gamma-tocopherol metabolites are excreted in the urine than alpha-tocopherol metabolites, suggesting less gamma-tocopherol is needed for use by the body (5). Limited research in the test tube and in animals indicates that gamma-tocopherol or its metabolites may play a role in the protection of the body from damage by free radicals (6, 7), but these effects have not been convincingly demonstrated in humans. Recently, concern has been raised regarding the fact that taking alpha-tocopherol supplements lowers gamma-tocopherol levels in the blood. However, no adverse effects of moderate alpha-tocopherol supplementation have been demonstrated, while many benefits have been documented (see Disease Prevention and Disease Treatment). In one recent prospective study, increased plasma gamma-tocopherol levels were associated with a significantly reduced risk of developing prostate cancer, while significant protective associations for increased levels of plasma alpha-tocopherol and toenail selenium were found only when gamma-tocopherol levels were also high (8). These limited findings, in addition to the fact that taking alpha-tocopherol supplements lower gamma-tocopherol levels in the blood, have led some scientists to call for additional research on the effects of dietary and supplemental gamma-tocopherol on health (9). For more information see the article, Which Form of Vitamin E, Alpha- or Gamma-Tocopherol, is Better? in the Linus Pauling Institute Research Report.

Deficiency

Vitamin E deficiency has been observed in individuals with severe malnutrition, genetic defects affecting the alpha-tocopherol transfer protein, and fat malabsorption syndromes. For example, children with cystic fibrosis or cholestatic liver disease, who have an impaired capacity to absorb dietary fat and therefore fat-soluble vitamins, may develop symptomatic vitamin E deficiency. Severe vitamin E deficiency results mainly in neurological symptoms, including impaired balance and coordination (ataxia), injury to the sensory nerves (peripheral neuropathy), muscle weakness (myopathy), and damage to the retina of the eye (pigmented retinopathy). For this reason, people who develop peripheral neuropathy, ataxia or retinitis pigmentosa should be screened for vitamin E deficiency (2). The developing nervous system appears to be especially vulnerable to vitamin E deficiency because children with severe vitamin E deficiency from birth, who are not treated with vitamin E, develop neurological symptoms rapidly. In contrast, individuals who develop malabsorption of vitamin E in adulthood may not develop neurological symptoms for 10-20 years. It should be noted that symptomatic vitamin E deficiency in healthy individuals who consume diets low in vitamin E has never been reported (10).

Although true vitamin E deficiency is rare, suboptimal intake of vitamin E is relatively common in the U.S. The National Health and Nutrition Examination Survey III (NHANES III) examined the dietary intake and blood levels of alpha-tocopherol in 16,295 multi-ethnic adults over the age of 18. Twenty seven % of white participants, 41% of African Americans, 28% of Mexican Americans and 32% of the other participants were found to have blood levels of alpha-tocopherol less than 20 micromoles/liter, a value chosen because the literature suggests an increased risk for cardiovascular disease below this level (11).

The Recommended Dietary Allowance (RDA)

The RDA for vitamin E was previously 8 mg/day for women and 10 mg/day for men. The RDA was revised by the Food and Nutrition Board of the Institute of Medicine in 2000 (3). This new recommendation was based largely on the results of studies done in the 1950s in men fed vitamin E deficient diets. In a test tube analysis, hydrogen peroxide was added to blood samples and the breakdown of red blood cells, known as hemolysis, was used to indicate vitamin E deficiency. Because hemolysis has also been reported in children with severe vitamin E deficiency, this analysis was considered to be a clinically relevant test of vitamin E status. Importantly, this means that the latest RDA for vitamin E continues to be based on the prevention of deficiency symptoms rather than on health promotion and the prevention of chronic disease.

Disease Prevention

Cardiovascular disease

The results of at least five large observational studies suggest that increased vitamin E consumption is associated with decreased risk of myocardial infarction (heart attack) or death from heart disease in both men and women. Each study was a prospective study which measured vitamin E consumption in presumably healthy people and followed them for a number of years to determine how many of them were diagnosed with, or died as a result of heart disease. In two of the studies, those individuals who consumed more than 7 mg of alpha-tocopherol in food were only approximately 35% as likely to die from heart disease as those who consumed less than 3-5 mg of alpha-tocopherol (12, 13). Two other large studies found a significant reduction in the risk of heart disease only in those women and men who consumed alpha-tocopherol supplements of at least 100 IU (67 mg of RRR-alpha-tocopherol) daily (14, 15). More recently, several studies have observed plasma or red blood cell levels of alpha-tocopherol to be inversely associated with the presence or severity of carotid atherosclerosis detected using ultrasonography (16-19). In contrast, intervention studies with vitamin E supplements in patients with heart disease have not shown vitamin E to be effective in preventing heart attacks or death (see Disease Treatment).

Cataracts

Cataracts appear to be formed by the oxidation of proteins in the lens of the eye, which may be prevented by antioxidants such as alpha-tocopherol. To date, ten observational studies have examined the association between vitamin E consumption and the incidence and severity of cataracts. Of these studies, five found increased vitamin E intake to be associated with protection from cataracts, while five reported no association (20, 21). A recent intervention trial of a daily antioxidant supplement containing 500 mg of vitamin C, 400 IU of vitamin E, and 15 mg of beta-carotene in 4,629 men and women found that the antioxidant supplement was no different than a placebo in its effects on the development and progression of age-related cataracts over a 7-year period (22). Another intervention trial found that a daily supplement of 50 mg of synthetic alpha-tocopherol daily (equivalent to 25 mg of RRR- alpha-tocopherol) did not alter the incidence of cataract surgery in male smokers (23). Presently, the relationship between vitamin E intake and the development of cataracts requires further clarification before specific recommendations can be made.

Immune Function

Alpha-tocopherol has been shown to enhance specific aspects of the immune response that appear to decline as people age. For example, 200 mg of synthetic alpha-tocopherol (equivalent to 100 mg of RRR-alpha-tocopherol) daily for several months increased the formation of antibodies in response to hepatitis B vaccine and tetanus vaccine in elderly adults (24). Whether alpha-tocopherol associated enhancements in the immune response actually translate to increased resistance to infections such as the flu (influenza virus) in older adults remains to be determined (25).

Cancer

Many types of cancer are thought to result from oxidative damage to DNA caused by free radicals. The ability of alpha-tocopherol to neutralize free radicals has made it the subject of a number of cancer prevention studies. However, several large prospective studies have failed to find significant associations between alpha-tocopherol intake and the incidence of lung cancer or breast cancer (3). A placebo-controlled intervention study designed to look at the effect of alpha-tocopherol supplementation on lung cancer in smokers found a 34% reduction in the incidence of prostate cancer in smokers given supplements of 50 mg of synthetic alpha-tocopherol (equivalent to 25 mg of RRR-alpha-tocopherol) daily (26). Because of these findings a large randomized, placebo-controlled intervention study is currently being conducted to examine the effect of alpha-tocopherol supplementation on prostate cancer risk (27).

Disease Treatment

Cardiovascular disease

Observational studies have suggested that supplemental alpha-tocopherol might have value in the treatment of cardiovascular disease. For example, a small observational study of men who had previously undergone a coronary artery bypass surgery found a reduction in the progression of coronary artery atherosclerosis by angiography in those men who took at least 100 IU of alpha-tocopherol (67 mg of RRR-alpha-tocopherol) daily (28). A randomized, placebo-controlled intervention trial in Great Britain (the CHAOS study) found that supplementing heart diseasepatients with either 400 or 800 IU of synthetic alpha-tocopherol (equivalent to 268 or 536 mg of RRR-alpha-tocopherol) for an average of 18 months resulted in a dramatic 77% reduction in nonfatal heart attacks. However, total deaths from heart disease were not significantly reduced (29). Chronic renal dialysis patients are at much greater risk of dying from cardiovascular disease than the general population, and there is evidence that they are also under increased oxidative stress. Supplementation of renal dialysis patients with 800 IU of natural alpha-tocopherol (536 mg of RRR-alpha-tocopherol) for an average of 1.4 years resulted in a significantly reduced risk of heart attack compared to placebo (30). In contrast, three other intervention trials failed to find significant risk reductions with alpha-tocopherol supplementation. One study, which was designed mainly to examine cancer prevention, found that 50 mg of synthetic alpha-tocopherol daily (equivalent to 25 mg of RRR-alpha-tocopherol) resulted in a non-significant decrease in nonfatal heart attacks in those participants who had had previous heart attacks (31) . However, two other large trials found that daily supplements of 400 IU of natural alpha-tocopherol (equivalent to 268 mg RRR-alpha-tocopherol) and 300 mg of synthetic alpha-tocopherol (equivalent to 150 mg of RRR-alpha-tocopherol) in individuals with evidence of cardiovascular disease (previous heart attack, stroke, or evidence of vascular disease) did not significantly change the risk of a subsequent heart attack or stroke (32, 33). The results of several other large intervention trials, which are presently in progress may clarify the role of alpha-tocopherol supplementation in the treatment of cardiovascular disease.

A more thorough discussion of the complex issues involved in analyzing the results of recent trials of vitamin E in heart disease can be found in the Fall/Winter 1999 issue of the Linus Pauling Institute Newsletter: Fish Oil, Vitamin E, Genes, Diet, and CHAOS. For a discussion of some of the limitations of the HOPE study see the article, Vitamin E: Hope or Hopeless, in the Spring/Summer 2000 issue of the Linus Pauling Institute Newsletter.

Diabetes mellitus

Alpha-tocopherol supplementation of individuals with diabetes has been proposed because diabetes appears to increase oxidative stress and because cardiovascular complications (heart attack and stroke) are among the leading causes of death in diabetics. A recent study found a biochemical marker of oxidative stress to be elevated in diabetic individuals (34). Supplementation with 600 mg of synthetic alpha-tocopherol daily (equivalent to 300 mg of RRR-alpha-tocopherol) for 14 days resulted in a reduction in the oxidative stress marker. Studies of the effect of alpha-tocopherol supplementation on blood glucose control have been contradictory. One study reported improved control of blood glucose levels with supplementation of only 100 IU of synthetic alpha-tocopherol daily (equivalent to 45 mg RRR-alpha-tocopherol) (35), while studies using 900 to 1,600 IU of synthetic alpha-tocopherol daily (equivalent to 405 to 720 mg RRR-alpha-tocopherol) found either minimal or no improvement, respectively (36, 37). Although there is reason to suspect that alpha-tocopherol supplementation may be beneficial for individuals with diabetes, evidence from well-controlled clinical trials is lacking.

Dementia (impaired cognitive function)

The brain is particularly vulnerable to oxidative stress, which is thought to play a role in the pathology of neurodegenerative diseases, such as Alzheimer's disease (38). In a large placebo-controlled intervention trial, supplementation of individuals who had moderate neurological impairment with 2,000 IU of synthetic alpha-tocopherol daily for two years (equivalent to 900 mg/day of RRR-alpha-tocopherol) resulted in a significant slowing of the progression of Alzheimer's dementia (39). After Alzheimer's disease, vascular dementia (dementia resulting from strokes) is the most common cause of dementia in the U.S. A case-control study examining risk factors for vascular dementia in elderly Japanese-American men found that supplemental vitamin E and vitamin C intake was associated with a significantly decreased risk of vascular and other types of dementia, but not Alzheimer's dementia (40). Among those without dementia, vitamin E supplement use was associated with better scores on cognitive tests. Although these findings are promising, further studies are required to determine the role of alpha-tocopherol supplementation in the treatment of Alzheimer's disease and other types of dementia.

Cancer

Cancer cells proliferate rapidly and are resistant to death by apoptosis (programmed cell death). Cell culture studies indicate that the vitamin E ester, alpha-tocopheryl succinate, can inhibit proliferation and induce apoptosis in a number of cancer cell lines (41, 42). The ester form, alpha-tocopheryl succinate, not alpha-tocopherol, is required to effectively inhibit proliferation or induce cancer cell death (43). Although the mechanisms for the effects of alpha-tocohpheryl succinate on cancer cells are not yet clear, the fact that the ester form has no antioxidant activity argues against an antioxidant mechanism (44). Limited data from animal models of cancer indicate that alpha-tocopheryl succinate administered by injection may inhibit tumor growth (45-47), but much more research is required to determine whether alpha-tocopheryl succinate will be a useful adjunct to cancer therapy in humans. Certainly, administration by injection will be necessary for any benefit, because alpha-tocopheryl succinate is cleaved to form alpha-tocopherol in the intestine when taken orally (48). There is currently no evidence in humans that taking oral alpha-tocopheryl succinate supplements delivers alpha-tocopheryl succinate to tissues.

Sources

Food sources

Major sources of alpha-tocopherol in the American diet include vegetable oils (olive, sunflower, safflower oils), nuts, whole grains, and green leafy vegetables. All eight forms of vitamin E (alpha-, beta, gamma-, and delta-tocopherols and tocotrienols) occur naturally in foods, but in varying amounts.

Supplements

Alpha-tocopherol

The average intake of alpha-tocopherol from food in the U.S. is approximately 9 mg daily for men and 6 mg daily for women, well below the RDA of 15 mg/day of RRR-alpha-tocopherol (3). Many scientists believe it is difficult for an individual to consume more than 15 mg/day of alpha-tocopherol from food alone, without also increasing fat intake above recommended levels. All alpha-tocopherol in food is the form of the isomer, RRR-alpha-tocopherol. The same is not always true for supplements. Vitamin E supplements generally contain from 100 IU to 1000 IU of alpha-tocopherol. Supplements made from entirely natural sources contain only RRR-alpha-tocopherol (also labeled d-alpha-tocopherol). RRR-alpha-tocopherol is the isomer preferred for use by the body, making it the most bioavailable form of alpha-tocopherol. Synthetic alpha-tocopherol, which is often found in food additives and nutritional supplements, is usually labeled all-rac-alpha-tocopherol or dl-alpha-tocopherol, meaning that all eight isomers of alpha-tocopherol are present in the mixture. Because half of the isomers of alpha-tocopherol present in all-rac-alpha-tocopherol are not usable by the body, synthetic alpha-tocopherol is less bioavailable and only half as potent. To calculate the number of mg of bioavailable alpha-tocopherol present in a supplement, use the following formulas:

RRR-alpha-tocopherol (natural or d-alpha-tocopherol):
IU x 0.67 = mg RRR-alpha-tocopherol.
Example: 100 IU = 67 mg
all-rac-alpha-tocopherol (synthetic or dl-alpha-tocopherol):
IU x 0.45 = mg RRR-alpha-tocopherol.
Example: 100 IU = 45 mg
For more information on the Biological Activity of Vitamin E, see the article by Dr. Maret Traber in the Linus Pauling Institute Newsletter.

Alpha-tocopheryl succinate and alpha-tocopheryl acetate (alpha-tocopheryl esters)

Alpha-tocopherol supplements are available in the ester forms, alpha-tocopheryl succinate and alpha-tocopheryl acetate. Tocopherol esters are more resistant to oxidation during storage than unesterified tocopherols. When taken orally, the succinate or acetate moiety is removed from alpha-tocopherol in the intestine. The bioavailability of alpha-tocopherol from alpha-tocopheryl succinate and alpha-tocopheryl acetate is equivalent to that of free alpha-tocopherol. Because international units (IU) for alpha-tocopherol esters are adjusted for molecular weight, the conversion factors for determining the amount of bioavailable alpha-tocopherol provided by alpha-tocopheryl succinate and alpha-tocopheryl acetate are not different than those used for alpha-tocopherol (see formulas) (3). The ester, alpha-tocopheryl succinate, not alpha-tocopherol, is required to effectively inhibit growth and induce death in cancer cells grown in culture (see Disease Treatment: Cancer). However, there is currently no evidence in humans that taking oral alpha-tocopheryl succinate supplements delivers alpha-tocopheryl succinate to tissues.

Alpha-tocopheryl phosphates (Ester-E®)

Despite a six million dollar marketing campaign to launch a supplement containing alpha-tocopheryl phosphates in the U.S. (49), there is currently no evidence that supplements containing alpha-tocopheryl phosphates are more efficiently absorbed or have greater bioavailability in humans than supplements containing alpha-tocopherol.

Gamma-tocopherol

Gamma-tocopherol supplements and mixed tocopherol supplements are also commercially available (50). The amounts of alpha- and gamma-tocopherol vary in mixed tocopherol supplements, so it is important to read the label to determine the amount of each tocopherol present in the supplement.

Safety

Toxicity

Few side effects have been noted in adults taking supplements of less than 2,000 mg of alpha-tocopherol daily (RRR- or all-rac-alpha-tocopherol). However, most studies of toxicity or side effects of alpha-tocopherol supplementation have lasted only a few weeks to a few months, and side effects occurring as a result of long-term alpha-tocopherol supplementation have not been adequately studied. The most worrisome possibility is that of impaired blood clotting resulting in an increased likelihood of hemorrhage in some individuals. The Food and Nutrition Board of the Institute of Medicine established a tolerable upper intake level (UL) for alpha-tocopherol supplements, based on the prevention of hemorrhage (see table below). The Board felt that 1,000 mg/day of alpha-tocopherol of any form (equivalent to 1,500 IU/day of RRR-alpha-tocopherol or 1,100 IU/day of all-rac-alpha-tocopherol) would be the highest dose unlikely to result in hemorrhage in almost all adults (3). Although only certain isomers of alpha-tocopherol are retained in the circulation, all forms are absorbed, and the liver must break them down and eliminate them. The rationale that any form of alpha-tocopherol (natural or synthetic) that can be absorbed could potentially have adverse effects is the basis for a UL that refers to all forms of alpha-tocopherol.

Some physicians recommend that high-dose vitamin E supplementation be discontinued one month before elective surgery to decrease the risk of hemorrhage. Premature infants appear to be especially vulnerable to adverse effects of alpha-tocopherol supplementation, which should be used only under controlled supervision by a pediatrician (50). Supplementation with 400 IU/day of vitamin E has been found to accelerate the progression of retinitis pigmentosa that is not associated with vitamin E deficiency (51).

Vitamin E Supplementation and All-Cause Mortality

A recent meta-analysis that combined the results of 19 clinical trials of vitamin E supplementation for various diseases, including heart disease, end-stage renal failure and Alzheimer's disease, reported that adults who took supplements of 400 IU/day or more were 6% more likely to die from any cause than those who did not take vitamin E supplements (52). However, further breakdown of the risk by vitamin E dose and adjustment for other vitamin and mineral supplements revealed that the increased risk of death was statistically significant only at a dose of 2,000 IU/day, which is higher than the UL for adults. Furthermore, three other meta-analyses that combined the results of randomized controlled trials designed to evaluate the efficacy of vitamin E supplementation for the prevention or treatment of cardiovascular disease found no evidence that vitamin E supplementation up to 800 IU/day significantly increased or decreased cardiovascular disease mortality or all-cause mortality (53-55). At present, there is no convincing evidence that vitamin E supplementation up to 800 IU/day increases the risk of death from cardiovascular disease or other causes.

Drug interactions

Individuals on anticoagulant therapy (blood thinners) or individuals who are vitamin K deficient should not take alpha-tocopherol supplements without close medical supervision because of the increased risk of hemorrhage (3). A number of medications may decrease the absorption of vitamin E, including cholestyramine, colestipol, isoniazid, mineral oil, orlistat, sucralfate, and the fat substitute, olestra. Anticonvulsant drugs such as phenobarbitol, phenytoin, or carbamazepine may decrease plasma levels of vitamin E (3, 50).

Antioxidants and HMG-CoA reductase inhibitors (statins)

A 3-year randomized controlled trial in 160 patients with documented coronary heart disease (CHD) and low HDL levels found that a combination of simvastatin (Zocor) and niacin increased HDL2 levels, inhibited the progression of coronary artery stenosis (narrowing), and decreased the frequency of cardiovascular events, such as myocardial infarction and stroke (56). Surprisingly, when an antioxidant combination (1000 mg vitamin C, 800 IU alpha-tocopherol, 100 mcg of selenium, and 25 mg beta-carotene daily) was taken with the simvastatin-niacin combination, the protective effects were diminished. However, in a much larger randomized controlled trial of simvastatin and an antioxidant combination (600 mg vitamin E, 250 mg vitamin C, and 20 mg beta-carotene daily) in more than 20,000 men and women with coronary artery disease or diabetes, the antioxidant combination did not adversely affect the cardioprotective effects of simvastatin therapy over a 5-year period (57). These contradictory findings indicate that further research is needed on potential interactions between antioxidant supplementation and cholesterol-lowering agents, such as HMG-CoA reductase inhibitors (statins).

Linus Pauling Institute Recommendation

Scientists at the Linus Pauling Institute feel there exists credible evidence that taking a supplement of 200 IU of natural source d-alpha-tocopherol (RRR-alpha-tocopherol) daily with a meal may help protect adults from chronic diseases like heart disease, stroke, neurodegenerative diseases, and some types of cancer. The amount of alpha-tocopherol required for such beneficial effects appears to be much greater than that which could be achieved through diet alone (see Sources). Since supplements containing 200 IU of d-alpha-tocopherol are often as expensive as supplements containing 400 IU of d-alpha-tocopherol, a less expensive alternative may be to take 400 IU of d-alpha-tocopherol every other day. Alpha-tocopherol supplements are unlikely to be absorbed unless taken with food.

Older adults (65 years and older)

The Linus Pauling Institute's recommendation of a supplement providing 200 IU of natural source d-alpha-tocopherol daily (or 400 IU of d-alpha-tocopherol every other day) with a meal is also appropriate for generally healthy older adults.

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http://lpi.oregonstate.edu/infocenter/vitamins/vitaminE/


What can high-vitamin E foods do for you?
Protect your skin from ultraviolet light
Prevent cell damage from free radicals
Allow your cells to communicate effectively
Help protect against prostate cancer and Alzheimer's disease
What events can indicate a need for more high-vitamin E foods?

Digestive system problems, especially malabsorption
Tingling or loss of sensation in the arms, hands, legs, or feet
Liver or gallbladder problems
Excellent sources of vitamin E include: mustard greens, chard, sunflower seeds, and turnip greens. Very good sources include almonds and spinach.

Description

What is vitamin E?

Even though its name makes it sound like a single substance, vitamin E is actually a family of fat-soluble vitamins that are active throughout the body. Some members of the vitamin E family are called tocopherols. These members include alpha tocopherol, beta tocopherol, gamma tocopherol, and delta tocopherol.

Other members of the vitamin E family are called tocotrienols. These members include alpha, beta, gamma, and delta tocotrienol. As increasing information has become available about these forms of vitamin E, more and more of them are understood to have unique functions.

How it Functions

What is the function of vitamin E?

Prevention of oxidative stress

Although humans must breathe oxygen to stay alive, oxygen is a risky substance inside the body because it can make molecules overly reactive. When oxygen-containing molecules become too reactive, they can start damaging the cell structures around them. In chemistry, this imbalanced situation involving oxygen is called oxidative stress.

Vitamin E helps prevent oxidative stress by working together with a group of nutrients that prevent oxygen molecules from becoming too reactive. This group of nutrients includes vitamin C, glutathione, selenium, and vitamin B3. Some researchers believe that vitamin E is the most important member of this oxidative stress-preventing group.

Supporting healthy skin

Vitamin E has sometimes been described as the "lightening rod" of the cell, allowing reactive molecules to strike the cell, like lightening, without causing damage. This "lightening rod" function of vitamin E is particularly apparent in the case of the skin, since vitamin E directly protects the skin from ultraviolet radiation (also called UV light). In numerous research studies, vitamin E applied topically to the skin has been shown to prevent UV damage. When the diet contains vitamin E-rich foods, vitamin E can travel to the skin cell membranes and exert this same protective effect.

Protection against Bladder Cancer

One of the benefits of making foods rich in vitamin E-nuts, seeds, spinach, mustard greens, peppers and olive oil-a part of your healthy way of eating is an up to 50% reduction in risk of developing bladder cancer, according to research presented at the annual meeting of the American Association of Cancer Research, Orlando, FL, May 23, 2004.

Bladder cancer, which kills 12,500 Americans annually, is the fourth leading cancer killer among men, and is four times more common in men than women. The study, which included 468 bladder cancer patients and 534 cancer-free controls drawn from residents of Houston, TX, collected data using eating habits questionnaires. Those whose vitamin E intake was in the top 25% had half as much bladder cancer as those in the lowest 25%.

Increasing vitamin E intake to the amount consumed by those in the top group would not be difficult since the actually difference in the amount of vitamin E-rich foods the two extremes consumed was small-the equivalent of a single daily serving of spinach or a handful of almonds.

The research team looked at the two most common forms of vitamin E, alpha- and gamma-tocopherol, and found that only alpha-tocopherol was associated with lower bladder cancer risk. Also, whether study participants got their vitamin E from food alone or from vitamin pills, the reduction in risk was roughly the same. Those with the highest intake of alpha-tocopherol from food had a 42% reduced risk of bladder cancer, and those with a vitamin E rich diet who also took vitamin E supplements had a 44% reduced risk.

Vitamin E from Foods, but not Supplements Offers Protection against Prostate Cancer and Alzheimer's Disease

While the type of vitamin E usually used in supplements is alpha-tocopherol, research published in the December 2004 issue of the Proceedings of the National Academy of Sciences indicates another form of vitamin E, gamma-tocopherol, but not alpha-tocopherol, inhibits prostate cancer cell proliferation, without affecting healthy prostate cells.

Plus, the anti-cancer effect of gamma-tocopherol, when combined with other forms of vitamin E such as delta-tocopherol, appears to be additive.

As noted above, Vitamin E is a generic term for a family of at least eight structurally related molecules. When the first research was conducted on vitamin E by the Shute brothers early in the 19th century, in rats, one fraction of vitamin E, alpha tocopherol, appeared more potent since it was necessary for successful pregnancy and production of offspring. For this reason, the Shutes named the vitamin "tocopherol," from the Greek word meaning "to give birth."

More recent research has revealed that, in humans, other vitamin E fractions may be even more beneficial. Gamma-tocopherol has been found to exhibit anti-inflammatory effects, which has led researchers to think this fraction may be more cardioprotective than the alpha-tocopherol found in most supplements. Not only is gamma-tocopherol anti-inflammatory, but it is also highly attracted to the nucleus in cells-the site where mutations in the genetic code can promote the development of cancer.

When Dr. Jiang and his team investigated the anti-carcinogenic potential of various forms of vitamin E, they found that gamma-tocopherol, particularly in combination with other forms of vitamin E such as delta-tocopherol, induced apoptosis (cell death) in androgen-sensitive prostate cancer cells within 3 days of treatment. Alpha-tocopherol alone did not have this effect.

The gamma and delta E fractions appear to induce apoptosis by interrupting the synthesis of sphingolipid, a fatty molecule in cell membranes that acts as a signaling messenger to modulate events inside the cell. In the cell membranes of human prostate cancer cells, the interruption of sphingolipid's synthesis by gamma and delta tocopherols causes the cancerous cells to self-destruct, while leaving healthy cells unaffected. Both fractions, as well as alpha tocopherol, are naturally present in foods rich in vitamin E, which include a number of greens (mustard greens, turnip greens, spinach, collard greens, and kale), sunflower seeds and almonds.

A high intake of vitamin E from food, but not from supplements (which usually contain just alpha-tocopherol) is also inversely associated with Alzheimer's disease. Rush University's Martha Clare Morris, Sc.D., lead nutrition researcher for CHAP, the Chicago Health and Aging Project, found a 67% lower risk of Alzheimer's in subjects with the highest intakes of vitamin E from food and concluded: "various tocopherol forms rather than alpha-tocopherol alone may be important in the vitamin E protective association with Alzheimer's disease."

Other roles for vitamin E

While most of the research on vitamin E has focused on its role in prevention of oxidative stress, a variety of new roles have recently been suggested. Most of these new roles involve the transfer of chemical information from one cell to another, or across different structures inside of a cell. This transfer of chemical information is referred to as "cell signaling," and many researchers believe that cell signaling cannot accurately take place without the help of vitamin E.

Deficiency Symptoms

What are deficiency symptoms for vitamin E?

Deficiency symptoms for vitamin E are difficult to pinpoint and controversial in the research literature. The area of broadest agreement involves malabsorption. In many research studies, low levels of vitamin E are associated with digestive system problems where nutrients are poorly absorbed from the digestive tract. These problems include pancreatic disease, gallbladder disease, liver disease, and celiac disease.

A second area of focus for vitamin E deficiency symptoms is called peripheral neuropathy. This area focuses on nervous system problems in the arms, hands, legs, and feet. Pain, tingling, and loss of sensation in these extremities have been associated with vitamin E deficiency. Although many healthcare practitioners report that skin problems appear closely linked to vitamin E deficiency, there are limited human research studies to support this view.

Toxicity Symptoms

What are toxicity symptoms for vitamin E?

When obtained from food sources alone, vitamin E has no documented research of toxicity. Vitamin E supplements, when taken in very high doses of 3000 IU or more, have been shown to have toxic effects. These effects include intestinal cramps and diarrhea, fatigue, double vision, and muscle weakness. Below the 3000 IU level, the research on vitamin E toxicity is inconsistent, but the majority of studies do not demonstrate toxic effects.

An exception to the generally low risk of toxicity associated with vitamin E involves simultaneous vitamin K deficiency. For persons with vitamin K deficiency, high intake of vitamin E can prolong bleeding time and interfere with clotting. In 2000, the National Academy of Sciences set a Tolerable Upper Intake Level (UL) for vitamin E of 1,000mg (or 1,500 IU of vitamin E in the form of alpha-tocopherol). This daily limit applies to supplemental vitamin E only, and is intended to apply to all individuals age 19 and older.

Impact of Cooking, Storage and Processing

How do cooking, storage, or processing affect vitamin E?

Exposure to air and factory processing can be particularly damaging to the vitamin E content of food. In wheat, for example, where most of the vitamin E is found in the germ layer, commercial processing removes 50-90% of the food's vitamin E. In 60% extraction wheat flour - the kind that is used to make over 90% of all breads, baked goods, and pastas sold in the U.S., the alpha tocopherol content drops almost 90%, and the beta tocopherol content drops 43%. (Alpha and beta tocopherol are two forms of vitamin E.)

To help protect their vitamin E content, vegetables oils like olive oil, sunflower seed oil, and peanut oil should be kept in tightly capped containers to avoid unnecessary exposure to air.

Factors that Affect Function

What factors might contribute to a deficiency of vitamin E?

Since vitamin E is a fat-soluble vitamin, poor absorption of fat in the digestive tract can contribute to vitamin E deficiency. Some specific health conditions that can cause fat malabsorption include pancreatic disease, celiac disease, and gallbladder disease. Premature birth has also been shown to increase risk of vitamin E deficiency in infants.

Drug-Nutrient Interactions

What medications affect vitamin E?

Use of the following medications can reduce the body's supply of vitamin E: Anticonvulsant drugs (like Dilantin ™) and cholesterol-lowering drugs (like probucol, cholestyramine, clofibrate, colestipol, and gemfibrozil) can significantly reduce the body's supply of vitamin E.

Long-term, regular use of mineral oil (for example, as non-prescription laxative) can also compromise the body's supply of vitamin E.

Nutrient Interactions

How do other nutrients interact with vitamin E?

The recycling of vitamin E in the body is intricately connected to four other nutrients: vitamin C, glutathione, selenium, and vitamin B3.

Vitamin C is required to keep vitamin E in its metabolically active form; glutathione (a very small protein molecule called a tripeptide and consisting of three amino acid building blocks) is required to keep vitamin C in its active form; and selenium (a micromineral) and vitamin B3 (in a special form called NADPH) are required to keep glutathione in its active form.

The fact that vitamin E is so heavily dependent on vitamin C, vitamin B3, selenium, and glutathione means that a diet high in vitamin E cannot have its optimal effect unless it is also rich in foods that provide these other nutrients.

At moderately high levels of 1,000 milligrams or more, vitamin E can interfere with the bodily activities of vitamin K. The potential injury to vitamin K metabolism was largely the reason why the National Academy of Sciences, in the year 2000, set a Tolerable Upper Limit (UL) of 1,000 milligrams per day for vitamin E.

Health Conditions

What health conditions require special emphasis on vitamin E?

Vitamin E may play a role in the prevention and/or treatment of the following health conditions:

Acne
Alzheimer's disease
Angina pectoris
Asthma
Atherosclerosis
Breast cancer
Diabetes
Epilepsy
Fibrocystic breast disease
Gout
Graves' disease
Infertility (male)
Inflammatory bowel disease
Macular degeneration
Menopause
Migraine
Multiple sclerosis
Oral cancers
Osteoarthritis
Parkinson's disease
Peptic ulcers
Peripheral vascular disease
PMS
Pregnancy-induced hypetension
Psoriasis
Rheumatoid arthritis
Senile cataracts
Squamous cancer
Stroke
Tardive dyskinesia
Vaginitis
Form in Dietary Supplements

What forms of vitamin E are found in dietary supplements?

The vast majority of vitamin E supplements contain a single form of the vitamin, alpha-tocopherol. More specifically, most supplements contain a natural form of alpha-tocopherol, called d-alpha tocopherol (or d-alpha tocopheryl acetate). Practitioners often prefer this form of the vitamin over a synthetic version called l-alpha tocopherol.

However, because vitamin E is actually a family of vitamins involving many tocopherols and many tocotrienols, some practitioners recommend vitamin E supplements containing not only d-alpha tocopherol, but other tocopherol and tocotrienol forms of vitamin E.

Supplements containing this wide variety of vitamin E forms are typically referred to as "mixed tocopherol" or "mixed tocotrienol" supplements. Human research studies comparing the effects of different types of vitamin E supplements are too limited to allow definite conclusions, but recent research suggests dietary vitamin E is preferable to supplements containing only one fraction of this nutrient.

What are current public health recommendations for vitamin E?

In 2000, the National Academy of Sciences established the following Adequate Intake (AI) levels for vitamin E:

Males and females, 0-6 months: 4 milligrams
Males and females, 6-12 months: 5 milligrams
In 2000, the National Academy of Sciences established the following Recommended Dietary Allowances (RDAs) for vitamin E:

Males and females, 1-3 years: 6 milligrams
Males and females, 4-8 years: 7 milligrams
Males and females, 9-13 years: 11 milligrams
Males and females, 14 years and older: 15 milligrams
Pregnant females, 18 years and older: 15 milligrams
Lactating females, 18 years and older : 19 milligrams
http://www.whfoods.com/genpage.php?pfriendly=1&tname=nutrient&dbid=111