Vitamin E, also known as tocopherol, is a fat-soluble vitamin. One of theroles fat plays in the diet is to transport fat-soluble vitamins. SoVitamin E is carried through the body attached to fat. The body storesvitamin E in fat deposits and in the liver.
The best sources ofvitamin E are vegetable oils, including sunflower, safflower, canola,corn, olive, and wheat germ oil; and products made from these oils, suchas margarine, nuts, seeds, wheat germ, mustard greens, broccoli, andunprocessed cereal grains. Leafy-green vegetables also contain Vitamin E,but in smaller amounts. Refined grains, such as white flour, have had thegerm removed. Since the germ of the seed is where vitamin E is located,foods made from refined flours are not good sources. Whole-wheat flourcontains much of the original germ and is a much better source of vitaminE.
Vitamin E may function as an antioxidant. This means it may helpprotect the body cells from oxidation. Oxidation is a chemical reaction inthe body that can lead to cell damage. It is also a natural part of aging.Many scientists believe that this cell damage can lead to chronic healthproblems such as heart disease. Vitamin E supplementation, in addition todiet and lifestyle factors, can contribute to reducing the risk of heartdisease and improving overall health.
Because disorders such as heart disease, stroke and cancer are associated
with free-radical damage, vitamin E is particularly useful for preventing
them. D-alpha-tocopherol and all its forms of acetates or succinate esters
are candidates for the classical anti-oxidation associated with vitamin E.
The purpose of acetate or succinate esters of the tocopherol
alcohol is to impart greater stability or shelf life, but the esters are
not important to the antioxidant role. The acid moiety is removed once
absorbed.(3) The succinate ester is a powder and used for tablets
containing vitamin E. The most common vitamin E product on pharmacy
shelves is the alpha-tocopheryl acetate stereoisomer. Less is known about
the other stereoisomers, but gamma-tocopherol is considered to possess
particular biological importance in the prevention of cancer and heart
disease, and seems to be particularly important to lung cancer risk
reduction in smokers.(1) Gamma-tocopherol also appears to be a precursor
for an endogenous diuretic.(1) Its use may assist in managing high blood
pressure.
In an extended epidemiological study, low levels of
vitamin E were found to be a greater risk for heart attack and stroke than
cholesterol. In 29 percent of the studied cases, there was a causal
correlation between high cholesterol and heart attack, and only in 25
percet of the cases, high blood pressure presented a causal correlation.
However, in 70 percent of cases, low vitamin E levels were
predictive.(10)
Because it is an antioxidant, vitamin E, used in
optimal daily dose correlates with reduced risk for cancer. Therefore, in
some studies it was revealed that a low level of vitamin E, correlated
with a low level of selenium, increases the risk for certain types of
cancer.(11)
Also, vitamin E is very important in reducing or
holding back complications of diabetes. Diabetics have an increased need
of vitamin E, and like vitamin C, it is critical to reducing or holding at
bay the complications of Type I or Type II diabetes.(3)
Those who do not absorb fat well are at risk of
developing a vitamin E deficiency. True deficiency of vitamin E leads to
serious neurological damage and erythrocyte fragility. Malabsorption of
fat should be suspected in those who have "fatty" diarrhea regularly.(7)
Biliary obstruction seriously impairs vitamin E
absorption.(8)
Contraindications
Vitamin E is
contraindicated in anti-coagulation therapy, unless prescribed by a
physician. Because vitamin E can interfere with vitamin K uptake, it can
confound control of anticoagulant medications that lower vitamin K like
Coumadin, unless prescribed by a physician.(5)
Vitamin E is also involved in the production of prostacyclin, which is an
intrinsic anti-aggregation factor. As well, vitamin E facilitates
fibrinolytic activity.(3)
High intake levels of vitamin E reduce the intestinal absorption of
vitamin K, and can confound the management of effective anticoagulant drug
therapy based on vitamin K manipulation, as with Coumadin. Apart from
anticoagulant drug therapy, vitamin E has not been found to produce
coagulation abnormalities in those who are not vitamin K deficient.(5)
Ferrous iron destroys vitamin E. They should be taken at different
times sufficiently separated to avoid interaction.
High
simultaneous intake of vitamin A may interfere with vitamin E absorption.
Some anticonvulsants including phenobarbital, phenytoin, and carbamazepine
significantly
lower plasma vitamin E levels by altering absorption, distribution and
metabolism.(9)
Vitamin E and vitamin C interact beneficially with C regenerating
E, making it again active as a membrane radical chain-breaking
antioxidant. However, there is evidence that vitamin C can act as a
pro-oxidant, especially in the presence of iron, if adequate levels of
vitamin E are not present.(6) The optimal dose range of vitamin C should
be encouraged, but with equal attention to an optimal dose range of
vitamin E, which many experts in natural medicine would say is 200 to 800
IUs per day.
Selenium interacts with vitamin E beneficially,
enhancing its action. The daily recommended dosage of selenium is 200
micrograms. This interaction stems from its role in glutathione
regeneration of vitamin E in conjunction with the enzyme glutathione
peroxidase, which incorporates four atoms of selenium. Selenium is also
involved in the production of thioredoxin, which regenerates vitamin C,
which in turn regenerates vitamin E.(1)
Human studies and experience show that adverse side effects from vitamin E
is virtually nonexistent when used in a dosage range up to 720 mg per
day.(2) At doses above 720 milligrams, and particularly doses of 1600 to
3000 mg/day, side effects can occur with prolonged use, and documented
side effects include gastrointestinal complaints, creatinuria, and
impaired blood coagulation, which subside rapidly with dose
reduction.(2)
In large studies with oral use of Vitamin E and also
in human studies with double-blind protocols, few adverse side effects
have been reported, even with doses as high as 3200 IU/day (natural
vitamin E), or when use of vitamin E has been long term.(2) Tests for
mutagenicity, carcinogenicity and teratogenicity have proved negative.(2)
The Recommended Dietary Allowances (RDA) are listed
below.(3)
Age/Years
International Units/Day
Up to 1
4.5 to 6.0
1 to 10
9.0 to 10.5
Males
11 + 15
Females
11 +
12
Pregnant
15
Nursing
18
These values
represent the conventionally accepted amounts of vitamin E required to
avoid symptomatic deficiency states, which result in obvious pathology,
particularly neurological damage due to oxidative stress. However, a
concept of optimal dosing recognizes a greater daily need in order to
optimally accomplish the central antioxidation role vitamin E plays in
preventing membrane phospholipid peroxidation, including HDL, LDL, and
other blood borne lipid particles, thus maintaining membrane integrity.
Since biological membranes provide the framework for life and health,
vitamin E antioxidation efforts should be optimal.
The recommended
optimal amount of vitamin E accepted by a broad range of health care
professionals is 400 to 800 IU per day, preferably in divided amounts in
the case of 800 IU per day, and with meals.(3)
A daily amount of
400 IU is quite acceptable if vitamin C is also supplemented.(1,3) See
Interactions below.
Natural Versus Synthetic Vitamin
E
Synthetic vitamin E (dl-alpha tocopherol), and its acetate
ester, has been shown to have lower biological activity than naturally
occurring d-alpha tocopherol and its acetate ester.
The table
below shows the commonly understood activity relationships between the
various d-alpha and dl-alpha stereoisomers.(3)
Vitamin E Isomer
Biological Activity
MG Per 400 IUs
d-alpha tocopherol
1.49
268
d-alpha tocopheryl acetate
1.36
249
dl-alpha tocopherol
1.1
364
dl-alpha tocopheryl acetate
1.0
400
d-beta tocopherol
0.60
-
d-gama tocopherol
0.15 - 0.45
-
d-alpha tocotrienol
0.3
-
d-delta tocopherol
0.015
-
From the table it can be seen that 400 mg of dl-alpha tocopheryl
acetate defines 400 IU. Fewer milligrams of d-alpha tocopherol or d-alpha
tocopheryl acetate are required to equal the biological activity of 400 IU
dl-alpha tocopheryl acetate. The two d-alpha versions respectively present
49% and 36% greater biological activity. The listed activities are the
accepted ratios of how the different stereoisomers performed biologically
in conventional standardized animal testing comparing each stereoisomer to
dl-alpha tocopheryl acetate, which standardized testing includes
absorption and retention considerations. However, in the April 1998 issue
of the American Journal of Clinical Nutrition, study results were
published that indicated that the more realistic biological activity ratio
of the natural to the synthetic versions of alpha-tocopherol in humans is
essentially 2.0.
The available experimental data suggests that the
greater biological activity of natural relative to synthetic
alpha-tocopherol is due to the preferential enrichment of VLDL by
stereo-selectivity of the natural d-stereoisomer, via a liver tocopherol
transfer protein (TTP), and subsequently involving other circulating
lipoproteins, with an ultimate selective delivery of the natural
stereoisomer to the tissues by these lipoproteins. Furthermore, the
research found that over time the l-stereoisomer that was initially
distributed to the tissues was poorly retained and was selectively and
over time eliminated in the bile due to natural vitamin E cycling, with a
tissue retention of predominately the natural
d-alphatocopherol.(4)
This research calls into question the
practice of equating the natural and the synthetic retail versions simply
because the respective softgel capsules are filled gravimetrically in such
a way that each delivers 400 IU irrespective of the source. The
conventional basis of international units stems from animal comparisons,
that appears to not represent human conditions. And consumers who chose
synthetic vitamin E, ultimately obtain less biological value for their
money, simply because the stereoselectivity of the liver transfer protein
"ignores" the bulk of the l-alpha isomer, and selectively fails to retain
it. Over time (approximately 1 to 2 years and beyond), using synthetic
vitamin E delivers about half the antioxidation value of using the
natural. Since using vitamin E for all-body health enhancement is a life
long matter, this difference can be considered to be of practical
significance.
1. Packer, Lester, Colman, Carol, The Antioxidant Miracle, John Wiley &
Sons, New York, 1999 2. Kappus, H., Diplock, A.T., "Tolerance and
safety of vitamin E: A toxicological position report", Free Radical
Biology & Medicine, 13: 55-74, 1992 3. Murray, Michael T., Encyclopedia
of Nutritional Supplements, Prima Publishing, Rocklin, CA, 1996 4.
Burton, Graham W., et al, "Human plasma and tissue alpha-tocopherol
concentrations in response to supplementation with deuterated natural
and synthetic vitamin E", American Journal of Clinical Nutrition, 67:
669-684, 1998 5. Bendich, A., Machlin, L.J., "Safety of oral intake of
vitamin E", American Journal of Clinical Nutrition, 48: 612-619,
1988 6. Wefers, H, Sies, H, "The protection by ascorbate and
glutathione against microsomal lipid peroxidation is dependent on vitamin
E", European
Journal of Biochemistry, 174: 353-357, 1988 7. Sokol, R.J., "Vitamin E
deficiency and neurological disease", Ann Rev Nutr, 8: 351-373, 1988 8.
Bjorneboe, A., et al, "Absorption, transport and distribution of vitamin
E", European Journal of Nutrition, 120: 233-242, 1990 9. Kataoka, K.,
et al, "Vitamin E status in pediatric patients receiving antiepilepic
drugs", Developments in Pharmacological Therapy, 14: 96-101, 1990 10.
Gey, K.F., "Inverse correlation between plasma vitamin E and mortality
from ischemic heart disease in cross-cultural epidemiology", American
Journal of Clinical Nutrition, 53 (suppl): 326s-334s, 1991 11. Knecht,
P., "Vitamin E in cancer prevention", American Journal of Clinical
Nutrition, 53(suppl): 283s-286s, 1991 12. Paolisso, G., et al,
"Pharmacologic doses of vitamin E improve insulin action in healthy
subjects and non-insulin-dependent diabetic patients",
American Journal of Clinical Nutrition, 57:650-656,1993
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