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Vitamin E --- How Much Is Enough
The term “vitamin E” refers to a family of eight related, lipid-soluble,
antioxidant compounds widely distributed in plants. The tocopherol and
tocotrienol subfamilies are each composed of alpha, beta, gamma and delta
vitamers having unique biological effects. Different ratios of these compounds
are found in anatomically different parts of a plant. For example, the green
parts of a plant contain mostly alpha tocopherol and the seed germ and bran
contain mostly tocotrienols.
When this family of compounds was first discovered and determined to be
essential for health, a standardized test for its activity was devised for which
the members of the family were rated for their biological activity. In one test,
alpha tocopherol scored highest and was rated 100% with all others having lower
ratings. In accordance with this rating, alpha tocopherol was deemed to be the
essential compound and was called vitamin E. One International Unit (IU) of
vitamin E activity is the activity under this rating of 1 mg of the
plant-derived form of alpha tocopherol.
Since the original rating method was established, many additional important
biological effects of these compounds have been discovered and many nutritional
scientists now consider that rating method to be incomplete. For example, by the
original rating, gamma tocopherol was only 10 to 30% as strong as alpha
tocopherol, yet recent studies have shown it to be essential for maintaining the
health of cell membranes, especially if alpha tocopherol is being supplemented.
New studies continue to elucidate the unique benefits of individual members of
the vitamin E family. For example, tocotrienols have been shown to lower
cholesterol, prevent LDL oxidation, and reduce atherosclerotic plaque formation
more effectively than tocopherols. For these and other reasons, the original
definition of vitamin E has been enhanced to include all eight family members
and the related compounds that convert to them in the body.
Vitamin E compounds are usually produced and made available in esterified form
as alpha tocopheryl acetate or alpha tocopheryl succinate. Neither of these
forms has any antioxidant activity until converted to alpha tocopherol in the
body, but they are much more stable with respect to storage time and temperature
than the unesterified forms. Moreover, while the acetate form is rapidly
activated within the body, activation of the succinate form is slower. The
succinate form appears to access and benefit areas of the tissues that are
unavailable to the other forms. For this reason, there is a tendency to regard
alpha tocopherol succinate (VES) as a distinctly different and beneficial
compound. VES appears to have longer half-life in the body, less effect on blood
clotting, and does not interfere with vitamin A and K absorption. It is also
more beneficial for cancer therapy according to several published studies.
Serious vitamin takers prefer cold-water dispersible dry powder vitamin E
supplements in the form of alpha tocopheryl succinate or acetate because the
cold-water dispersible forms are efficiently absorbed even when taken on an
empty stomach or with a low-fat meal. The non-cold water dispersible (oil) forms
of vitamin E may be poorly absorbed unless taken with several grams of fats or
oils.
Cold-water dispersible vitamin E is twice as expensive as soybean oil E-acetate,
but the cold-water dispersible forms are more efficiently absorbed. Both
“acetate” and “succinate” vitamin E can come from natural sources. The
importance to the consumer is how well the vitamin E absorbs into the
bloodstream. Cold-water dispersible vitamin E, whether in a succinate or acetate
form, always comes in a white dry powder, while noncold-water dispersible
natural and synthetic acetate forms of vitamin E are always in a thick brown
oil.
While 100 IU or more of supplemental vitamin E a day has been shown to reduce
the risk of heart attacks in healthy people, those with pre-existing coronary
artery disease often take 800 to 1600 IU a day based on the pioneering work of
the Shute brothers in the mid 1940s.
One or more members of the vitamin E family may also:
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Maintain cell membrane integrity and reduce cellular aging |
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Inhibit the potentially damaging peroxynitrite radical |
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Inhibit melanoma cell growth in mice |
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Prevent abnormal blood clotting |
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Synergize with vitamin A to protect the lungs against pollutants |
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Protect nervous system and retina |
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Lower the risk of ischemic and coronary heart disease |
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Lower the risk of certain kinds of cancer |
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Protect immune function |
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Reduce the risk of Alzheimer’s disease |
Caution:
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If you are taking anti-clotting medication, consult with your doctor before taking this product. |
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Ingestion of total vitamin E products in excess of 1200 IU daily may interfere with absorption and metabolism of vitamins A and K. |
Dosage and use
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One 400 IU capsule daily is suggested for healthy people. |
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One to five 400 IU capsules daily are suggested for therapeutic use. |
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This product is most effectively utilized when taken with fat-containing, low fiber meals. |
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Vitamin E
Supplementation and Cardiovascular Events in High-Risk Patients
The Heart Outcomes Prevention Evaluation Study Investigators
[Karl Note: This study purports to show that Vitamin E is not helpful to a heart disease patient. You have to learn how to read these fraudulent studies. The key is in the use of "400 IU of natural source Vitamin E. This is so difficult to get -- from so-called "natural sources" that no results could have been expected. Then, this "authoritative study" is cited in hundreds of other papers as "proving" that Vitamin E is useless in treating heart patients. And thus does false information get published and spread! Just below this study is another, showing that vitamin E intake makes arteries healthier!]
ABSTRACT
Background Observational and experimental studies suggest that the amount of vitamin E ingested in food and in supplements is associated with a lower risk of coronary heart disease and atherosclerosis.
Methods We enrolled a total of 2545 women and 6996 men 55 years of age or older who were at high risk for cardiovascular events because they had cardiovascular disease or diabetes in addition to one other risk factor. These patients were randomly assigned according to a two-by-two factorial design to receive either 400 IU of vitamin E daily from natural sources or matching placebo and either an angiotensin-converting–enzyme inhibitor (ramipril) or matching placebo for a mean of 4.5 years (the results of the comparison of ramipril and placebo are reported in a companion article). The primary outcome was a composite of myocardial infarction, stroke, and death from cardiovascular causes. The secondary outcomes included unstable angina, congestive heart failure, revascularization or amputation, death from any cause, complications of diabetes, and cancer.
Results A total of 772 of the 4761 patients assigned to vitamin E (16.2 percent) and 739 of the 4780 assigned to placebo (15.5 percent) had a primary outcome event (relative risk, 1.05; 95 percent confidence interval, 0.95 to 1.16; P=0.33). There were no significant differences in the numbers of deaths from cardiovascular causes (342 of those assigned to vitamin E vs. 328 of those assigned to placebo; relative risk, 1.05; 95 percent confidence interval, 0.90 to 1.22), myocardial infarction (532 vs. 524; relative risk, 1.02; 95 percent confidence interval, 0.90 to 1.15), or stroke (209 vs. 180; relative risk, 1.17; 95 percent confidence interval, 0.95 to 1.42). There were also no significant differences in the incidence of secondary cardiovascular outcomes or in death from any cause. There were no significant adverse effects of vitamin E.
Conclusions In patients at high risk for cardiovascular events, treatment with vitamin E for a mean of 4.5 years has no apparent effect on cardiovascular outcomes.
Source Information
The writing group (Salim Yusuf, D.Phil., Gilles Dagenais, M.D., Janice Pogue, M.Sc., Jackie Bosch, M.Sc., and Peter Sleight, D.M.) assumes responsibility for the overall content and integrity of the manuscript.
Address reprint requests to Dr. Salim Yusuf at the Canadian Cardiovascular Collaboration Project Office, Hamilton General Hospital, 237 Barton St. E., Hamilton, ON L8L 2X2, Canada, or at yusufs@fhs.mcmaster.ca.
Related Letters:
Vitamin E Supplementation and
Cardiovascular Events in High-Risk Patients
Jialal I., Devaraj S., Yusuf S.
N Engl J Med 2000; 342:1917-1918, Jun 22, 2000. Correspondence
This article has been cited by other articles:
| Am J Clin Nutr 2002 Sep;76(3):549-55 | SOURCE |
OBJECTIVE: The objective was to determine the effects of vitamin C and vitamin E, alone or in combination, on in vivo lipid peroxidation.
DESIGN: We conducted a placebo-controlled, 2 x 2 factorial trial of vitamin C (500 mg ascorbate/d) and vitamin E (400 IU RRR-alpha-tocopheryl acetate/d) supplementation in 184 nonsmokers. The mean duration of supplementation was 2 mo. The outcome measures were changes from baseline in urinary 8-iso-prostaglandin F(2alpha), urinary malondialdehyde + 4-hydroxyalkenals, and serum oxygen-radical absorbance capacity.
RESULTS: The within-group mean changes (and 95% CIs) in urinary 8-iso-prostaglandin F(2alpha) (pg/mg creatinine) were 9.0 (-125.1, 143.1), -150.0 (-275.4, -24.6), -141.3 (-230.5, -52.1), and -112.5 (-234.8, 9.8) in the placebo, vitamin C alone, vitamin E alone, and vitamins C + E groups, respectively. No synergistic effect of these 2 vitamins on urinary 8-iso-prostaglandin F(2alpha) was observed (P = 0.12). Neither vitamin had an effect on urinary malondialdehyde + 4-hydroxyalkenals. Vitamin C, but not vitamin E, increased serum oxygen-radical absorbance capacity (P = 0.01).
CONCLUSIONS: Supplementation with
vitamin C or vitamin E alone reduced lipid peroxidation
to a similar extent. Supplementation with a combination
of vitamins C and E conferred no benefit beyond that of
either vitamin alone.
Publication Types:
PMID: 12197998 [PubMed - indexed for MEDLINE]
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