Vitamin E is found naturally in some foods, vitamin e and breast cancer, added to others, vitamin e and breast cancer, and available as a dietary supplement. Naturally occurring vitamin E exists in eight chemical forms alpha- beta- gamma- and delta-tocopherol and alpha- beta- gamma- and delta-tocotrienol that have varying levels of biological activity [ 1 ].
Serum concentrations of vitamin E alpha-tocopherol vitamin e and breast cancer on the liver, which takes up the nutrient after the various forms are absorbed from the small intestine. The liver preferentially resecretes only alpha-tocopherol via the hepatic alpha-tocopherol transfer protein [ 1 ]; the liver metabolizes and excretes the other vitamin E forms [ 2 ]. As a result, blood and cellular concentrations of other forms of vitamin E are lower than those of alpha-tocopherol and have been the subjects of less research [ 34 ].
Antioxidants protect cells from the damaging effects of free radicals, which are molecules that contain an unshared electron. Free radicals damage cells and might contribute to the development of cardiovascular disease and cancer [ 5 ]. Unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species ROS. The body forms ROS endogenously when it converts food to energy, and antioxidants might protect cells from the damaging effects vitamin e and breast cancer ROS, vitamin e and breast cancer.
The body is also exposed to free radicals from environmental exposures, such as cigarette smoke, air pollution, and ultraviolet radiation from the sun. ROS are part of signaling mechanisms among cells. Vitamin E is a fat-soluble antioxidant that stops the production of ROS formed when fat undergoes oxidation. Scientists are investigating whether, by limiting free-radical production and possibly through other mechanisms, vitamin E might help prevent or delay the chronic diseases associated with free radicals.
In addition to its activities as an antioxidant, vitamin E is involved in immune function and, as shown primarily by in vitro studies of cells, cell signaling, regulation of gene vitamin e and breast cancer, and other metabolic processes [ 1 ]. Alpha-tocopherol inhibits the activity of protein kinase C, an enzyme involved in cell proliferation and differentiation in smooth muscle cells, platelets, and monocytes [ 6 ].
Vitamin-E—replete endothelial cells lining the interior surface of blood vessels are better able to resist blood-cell components sage antibacterial to this surface. Vitamin E also increases the expression of two enzymes that suppress arachidonic acid metabolism, thereby increasing the release of prostacyclin from the endothelium, which, in turn, dilates blood vessels and inhibits platelet aggregation [ 6 ].
DRI is the general term for a set of reference values used to plan and assess nutrient intakes of healthy people. These values, which vary by age and gender, include:. The FNB based these recommendations primarily on serum levels of the nutrient that provide adequate protection in a test measuring the survival of erythrocytes when exposed to hydrogen peroxide, a free radical [ 6 ].
Acknowledging "great uncertainties" in these data, the FNB has called for research to identify other biomarkers for assessing vitamin E requirements. RDAs for vitamin E are provided in milligrams mg and are listed in Table 1. Because insufficient data are available to develop RDAs for infants, vitamin e and breast cancer, AIs were developed based on the amount of vitamin E consumed by healthy breastfed babies. At present, the vitamin E content of foods and dietary supplements is listed on labels in international units IUsa measure of biological activity rather than quantity.
Naturally sourced vitamin E is called RRR -alpha-tocopherol commonly labeled as d -alpha-tocopherol ; the synthetically produced form is all rac -alpha-tocopherol commonly labeled as dl -alpha-tocopherol. Conversion rules are as follows:. Table 1 lists the RDAs for alpha-tocopherol in both mg and IU of the natural form; for example, 15 mg x 1. The corresponding value for synthetic alpha-tocopherol would be Numerous foods provide vitamin E.
Nuts, seeds, and vegetable oils are among the best sources of alpha-tocopherol, and significant amounts are available in green leafy vegetables and fortified cereals see Table 2 for vitamin e and breast cancer more detailed list [ 9 ].
Most vitamin E in American diets is in the form of gamma-tocopherol from soybean, canola, corn, and other vegetable oils and food products [ 4 ]. FDA developed DVs to help consumers compare the nutrient content of different foods within the context of a total diet.
The DV for vitamin E used for the values in this table is remeron and hemorrhoids IU approximately 20 mg of natural alpha-tocopherol for adults and children age 4 and older [ 10 ]. This DV, however, is changing to 15 mg as the updated Nutrition and Supplement Facts labels are implemented [ 7 ]. The updated labels and DVs must appear on food products and dietary supplements beginning in Januarybut they can be used now [ 8 ].
FDA does not require food labels to list vitamin E content unless a food has been fortified with this nutrient. The USDA also provides a comprehensive list of foods containing vitamin E arranged by nutrient content and by food name.
Supplements of vitamin E typically provide only alpha-tocopherol, although "mixed" products containing other tocopherols and even tocotrienols are available. Naturally occurring alpha-tocopherol exists in one stereoisomeric form.
In contrast, synthetically produced alpha-tocopherol contains equal amounts of its eight possible stereoisomers; serum and tissues maintain only four of these stereoisomers [ 6 ].
A given amount of synthetic alpha-tocopherol all rac -alpha-tocopherol; commonly labeled as "DL" or "dl" is therefore only half as active as the same amount by weight in mg of the natural form RRR -alpha-tocopherol; commonly labeled as "D" or "d", vitamin e and breast cancer. These amounts are substantially higher than the Vitamin e and breast cancer. Alpha-tocopherol in dietary supplements and fortified foods is often esterified to prolong its shelf life while protecting its antioxidant properties.
The body hydrolyzes and absorbs these esters alpha-tocopheryl acetate and succinate as efficiently as alpha-tocopherol [ 6 ]. These intake estimates might be low, however, because the amounts and types of fat added during cooking are often unknown and not accounted for [ 6 ]. The FNB suggests that mean intakes of vitamin E among healthy adults are probably higher than the RDA but cautions that low-fat diets might provide insufficient amounts unless people make their food choices carefully by, for example, increasing their intakes of nuts, seeds, fruits, and vegetables [ 612 ].
Frank vitamin E deficiency is rare and overt deficiency symptoms have not been found in healthy people who obtain little vitamin E from their diets [ 6 ], vitamin e and breast cancer. Vitamin E supplementation in these infants might reduce the risk of some complications, such as those affecting the retina, but they can also increase the risk of infections [ 14 ].
Because the digestive tract requires fat to absorb vitamin E, people with fat-malabsorption disorders are more likely to become deficient than people without such disorders. Deficiency symptoms include peripheral neuropathy, vitamin e and breast cancer, ataxia, skeletal myopathy, retinopathy, and impairment of the immune response [ psoriasis and hair loss15 ].
Vitamin E deficiency secondary to abetalipoproteinemia causes such problems as poor transmission of nerve impulses, muscle weakness, and retinal degeneration that leads to blindness [ 16 ]. People with AVED have such severe vitamin E deficiency that they develop nerve damage and lose the ability to walk unless they take large doses of supplemental vitamin E [ 17 ]. The mechanisms by which vitamin E might provide this protection include its function as an antioxidant and its roles in anti-inflammatory processes, veterinary cardiovascular and respiratory of platelet aggregation, and immune enhancement.
A primary barrier to characterizing the roles of vitamin E in health is the lack of validated biomarkers for vitamin E intake and status to help relate intakes to valid predictors of clinical outcomes [ 6 ]. This section focuses on four diseases and disorders in which vitamin E might be involved: Evidence that vitamin E could help prevent or delay coronary heart disease CHD comes from several sources.
In vitro studies have found that the nutrient inhibits oxidation of low-density lipoprotein LDL cholesterol, vitamin e and breast cancer, thought to be a crucial initiating step for atherosclerosis [ 6 ], vitamin e and breast cancer.
Vitamin E might also help prevent the formation of blood clots that could lead to a heart attack or venous thromboembolism [ 18 ]. Several observational studies have associated lower rates of heart disease with higher vitamin E intakes. Among a group of 5, Finnish men and women followed for a mean of 14 years, vitamin e and breast cancer, higher vitamin E intakes from food were associated with decreased mortality toprol xl and peyronies CHD [ 20 ].
However, randomized clinical trials cast doubt on the efficacy of vitamin E supplements to prevent CHD [ 21 ]. HOPE-TOO found that vitamin E provided no significant protection against heart attacks, strokes, unstable angina, or deaths from cardiovascular disease or other causes after 7 years of treatment. Not only did the supplements provide no cardiovascular benefits, but all-cause mortality was significantly higher in the women taking the supplements.
The investigators found no significant differences in rates of overall cardiovascular events combined nonfatal heart attacks, strokes, and cardiovascular deaths or all-cause mortality between the groups, vitamin e and breast cancer. However, the study did find two positive and significant results for women taking vitamin E: Furthermore, use of vitamin E was associated with a significantly increased risk of hemorrhagic stroke.
In general, clinical trials have not provided evidence that routine use of vitamin E supplements prevents cardiovascular disease or reduces its morbidity and mortality.
However, participants in these studies have been largely middle-aged or elderly individuals with demonstrated heart disease or risk factors for heart disease. Some researchers have suggested that understanding the potential utility of vitamin E in preventing CHD might require longer vitamin e and breast cancer in younger participants taking higher doses of the supplement [ 28 ]. Further research is needed to determine whether supplemental vitamin E has any protective value for younger, healthier people at no obvious risk of CHD.
Antioxidant nutrients like vitamin E protect cell constituents from the damaging effects of free radicals that, if unchecked, might contribute to cancer development [ 9 ]. Vitamin E might also block the formation of carcinogenic nitrosamines formed in the stomach from nitrites in foods and protect against cancer by enhancing immune function [ 29 ].
Unfortunately, human trials and surveys that have attempted to associate vitamin E intake with cancer incidence have found that vitamin E is not beneficial in most cases. Based in part on the promising results of this study, a large randomized clinical trial, called the SELECT trial, began in to determine whether 7—12 years of daily supplementation with synthetic vitamin E IU, as dl -alpha-tocopheryl acetatewith or without selenium mcg, as L-selenomethioninereduced the number of new prostate cancers in 35, healthy men age 50 and older.
The trial was discontinued in October when an analysis found that the supplements, taken alone or together for about 5. Results from an additional 1. The risk of developing prostate cancer was also slightly increased in subjects taking vitamin E plus selenium or selenium alone, but the differences were not statistically significant.
No differences were found among groups in the incidence of lung or colorectal cancers or all cancers combined. The American Cancer Society conducted an epidemiologic study examining the association between use of vitamin C and vitamin E supplements and bladder cancer mortality.
Of the almost one million adults followed between andadults who took supplemental vitamin E for 10 years or longer had a reduced risk of death from bladder cancer [ 37 ]; vitamin C supplementation provided no protection.
Evidence to date is insufficient to support taking vitamin E to prevent cancer. In fact, daily use of large-dose vitamin E supplements IU may increase the risk of prostate cancer. Age-related macular degeneration AMD and cataracts are among the most common causes of significant vision loss in older people. Their etiologies are usually unknown, but the cumulative effects of oxidative stress have been postulated to play a role.
If so, nutrients with antioxidant functions, such as vitamin E, could be used to prevent or treat these conditions. Prospective cohort studies have found that people with relatively high dietary intakes of vitamin E e. A follow-up AREDS2 study confirmed the value of this and similar supplement formulations in reducing the progression of AMD over a median follow-up period of 5 years" [ 43 ].
Several observational studies have revealed a potential relationship between vitamin E supplements and the risk of cataract formation. One prospective cohort study found that lens clarity was superior in participants who took vitamin E supplements and those with higher blood levels of the vitamin [ 44 ]. In another study, long-term use of vitamin E supplements was associated with slower progression of age-related lens opacification [ 45 ]. However, in the AREDS trial, the use of a vitamin E-containing formulation had no apparent effect on the development or progression of cataracts over an average of 6.
Overall, the available evidence is inconsistent with respect to whether vitamin E supplements, taken alone or in combination with other antioxidants, can reduce the risk of developing AMD or cataracts. The brain has a high oxygen consumption rectal prolapse and cancer and abundant polyunsaturated fatty acids in the neuronal cell membranes.
Over 2 years, thyrotoxicosis and mental illness with vitamin E and selegiline, separately or together, significantly delayed functional deterioration and the need for institutionalization compared to placebo.
However, vitamin e and breast cancer, participants taking vitamin E experienced significantly more falls. Vitamin E consumption from foods or supplements was associated with less cognitive decline over 3 years in a prospective cohort study of elderly, vitamin e and breast cancer individuals aged 65— years [ 49 ]. In summary, most research results do not support the use of vitamin E supplements by healthy or mildly impaired ankle arthritis mri to maintain cognitive performance or slow its decline with normal aging [ 52 ].
More research is needed to identify the role of vitamin E, if any, in the management of cognitive impairment [ 53 ]. Research has not found any adverse effects vitamin e and breast cancer consuming vitamin E in food [ 6 ].