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Properties and
Uses
In recent years, consumers have been
advised to use polyunsaturated fats instead of saturated fats in order to
reduce the risk of heart disease. Some preliminary data suggest that this
advice is having a favorable impact in reducing the risk of heart disease. It
has been reported that in animals, the dietary need for vitamin E increases
when the intake of polyunsaturated fatty acids becomes greater. Nutrition
scientists have established that cellular membranes containing polyunsaturated
fats are more easily damaged by free radicals than those which contain
saturated fats. In order to protect membranes which contain high levels of
polyunsaturated fats, the increased consumption of vitamin E is not only
justified but essential.
In chickens, selenium deficiency causes
poor absorption of vitamin E from the digestive tract. Vitamin E enhances the
cancer preventive effect of selenium on chemical-induced breast cancer in rats.
The relevance of this observation in humans has not been evaluated as yet.
Both vitamin E and zinc act as a
stabilizer of cellular membranes. Red blood cells from zinc - or vitamin
E-deficient animals are easily broken by free radicals. Supplementation of
diets with either vitamin E or zinc makes these membranes more resistant to
free radical attack. Zinc-deficient diets cause skin and joint damage in the
chicken. Dietary supplementation with high vitamin E doses prevents the above
harmful effects of zinc deficiency. These studies suggest that some effects of
vitamin E and zinc on cells are similar.
The exposure of vitamin E to iron and
copper enhances the destruction of vitamin E. It has been reported that in low
birth weight infants, administration of iron may cause the development of
vitamin E deficiency anemia, particularly in those infants who were fed formula
containing higher levels of polyunsaturated fatty acids.
Vitamin C protects vitamin E from the
harmful effects of iron and copper as well as helps to regenerate vitamin E
immediately after it has been destroyed by free radicals. During vitamin E
deficiency, the levels of vitamin A (retinol and retinyl esters) in liver and
retinol in plasma decrease. These levels are increased during alpha tocopherol
supplementation. The consumption of higher levels of dietary vitamin A increase
the need for vitamin E in the body. Most human studies suggest that the
consumption of vitamin E is essential for efficient vitamin A utilization and
liver storage. Vitamin E deficiency may also cause deficiency of vitamin B-12.
Thus the alterations in the level of vitamin E may effect the levels of other
vitamins such as vitamins A, C and B-12.
Vitamin E has been shown to interact with
some pollutants which are present in the environment and diet. The primary
atmospheric pollutants are ozone and nitric oxide which are capable of
generating free radicals in the body. Vitamin E has been shown to protect
against the harmful effect of ozone and nitric oxide. The major food pollutants
are nitrites which are present in fresh fruits and vegetables as well as in
bacon, sausage and cured meat. Nitrites by themselves are not harmful to
adults, but they can combine with amines in the stomach to form nitrosamine.
Nitrosamines are among the most potent cancer causing agents for both animals
and human beings. The presence of vitamin C or vitamin E in the stomach may
prevent the formation of or reduce the levels of nitrosamines. Taking vitamin C
or E before eating fresh fruits and vegetables that contain high levels of
nitrites is not needed, because they contain another group of chemicals called
phenolics, which, like vitamin E, act as an antioxidant and can prevent the
formation of nitrosamines. However, it is important to take vitamin E just
before eating bacon, sausage, or cured meat in order to prevent the formation
of nitrosamines.
In addition to nitrosamines, many other
mutagenic substances (agents which cause genetic changes) are formed in the
digestive tract. All mutations do not cause cancer, but all cancers are
preceded by mutations. It has been shown that the levels of mutagenic
substances in the feces are higher for persons who are meat eaters than for
those who are vegetarians. The presence of higher levels of fecal mutagenic
substances may increase the risk of some cancers. It has been reported that
taking vitamin E or vitamin C reduces the mutagenic substances in the feces.
Furthermore, reports indicate that taking both vitamin E and C is more
effective than taking either individually.
Many chemicals are not carcinogenic until
they are converted to an active form in the body. In some cases vitamin E can
prevent the conversion of inactive forms of such cancer causing substances to
active forms. Vitamin E also prevents the action of tumor promoting and tumor
initiating agents which are present in the environment and diet.
Vitamin E influences the effectiveness of
many drugs which are currently used in cancer treatment. The above concept has
been demonstrated on cancer cells in vitro. For example, vitamin E acetate in
combination with vincristine, 5-fluorouracil, adriamycin, or cholorozotocin
produced a synergistic effect, whereas vitamin E in combination with bleomycin,
1-2-cholrethyl)-3-cyclohexyl-1-triazeno-imidazole-4-carboxamide (DIIC),
mutamycin or cis-diamine) dichloro-platiumn 11 (cis-platiumn 11) produces an
additive effect on the inhibition of growth of neuroblastoma cells in vitro. In
glioma cell cultures, vitamin E acetate in combination with vincristine or CCNU
produced a synergistic effect whereas vitamin E in combination with bleomycin,
5-fluoracil, adriamycin, DTIC, mutamycin and cis-platinum produced an additive
effect on the inhibition of growth. These studies suggest that the
effectiveness of the interaction of vitamin E with cancer chemotherapeutic
drugs depends upon tumor form and type of drug. Vitamin E succinate also
enhances the effect of some naturally occurring substance such as
prostaglandins and sodium butyrate on neuroblastoma cells in vitro. The
relevance of the above results in humans is not known at this time.
Several experimental studies have been
reported that vitamin E protects normal tissue against radiation damage;
however, higher doses of vitamin E succinate enhance the effect of radiation on
cancer cells in vitro. In addition, vitamin E succinate markedly reduces the
occurrence of radiation induced cancer in vitro. High doses of vitamin E
succinate also enhance the effect of heat on cancer cells in vitro. The above
effects of vitamins have not been tested on humans as yet.
Vitamin E protects cells from the toxicity
of certain heavy metals. For example, organic mercury is known to cause
neurological diseases because of damage to the brain cells. The administration
of vitamin E immediately before treatment of animals with organic mercury
markedly reduces the symptoms of brain damage in rats, mice and quail. Vitamin
E succinate also protects glia cells, one of the cell types present in brain,
in vitro against organic mercury-induced toxicity.
Only selenium appears to enhance the
effect of vitamin E on the prevention of chemical-induced cancer in vitro.
Vitamin E administration has been useful
in the treatment of those disease in humans which are due to vitamin E
deficiency. Vitamin E acetate (400 IU) has been shown to be useful in the
treatment of cystic mastitis, the most common cancerous growth of the breast in
females. Vitamin E acetate (1600 IU/day) before the administration of
adriamycin reduces its toxic effect in patients with cancer. This is consistent
with the animal studies in which vitamin E has been shown to reduce the toxic
effects of adriamycin on heart and skin. Vitamin E also protects against lung
damage in animals produced by bleomycin, a commonly used drug in the treatment
of cancer. One study reports that vitamin E therapy reduces some of the
symptoms of premenstrual syndrome.
Several animal and a few human studies
have suggested that vitamin E may be useful in the prevention of some human
cancer. Currently, the effect of oral intake of vitamin E (400 to 800 IU/day)
in the form of alpha tocopherol, alpha tocopheryl acetate or alpha tocopheryl
succinate on the risk of developing some forms of cancer among the high risk
human populations is being studies.
Vitamin E may reduce lung damage produced
by cigarette smoke. There is increasing evidence that free radicals are
generated in the lung by the substances which are present in the cigarette
smoke. These free radicals are responsible for increasing the risk of lung
cancer well as of emphysema (a chronic lung disease in which breathing becomes
difficult). The level of vitamin E in the fluid surrounding lung tissue is six
times less among smokers in comparison to those who do not smoke. The presence
of higher levels of vitamin E in these fluids or in lung tissue may protect
lungs from the attack of free radicals.
Vitamin E may have a role in the
management of some neurological diseases. A group of neurologists are
initiating a new clinical study using vitamin E in combination with deprenyl in
order to slow down the progression of disease in patients with Parkinsonism. It
is believed that free radicals are generated by degradation products of
dopamine (a chemical which is essential for brain function) and by drugs used
in the treatment of Parkinson's Disease.
There are very limited animal studies
regarding the use of vitamin E in the management of cancer. One clinical study
has utilized high intravenous doses (up to 2 grams per day) of alpha tocopherol
in the treatment of 1V Stage metastic neuroblastomas. The objective regression
was observed in 50% of treated patients. Preliminary data suggest that vitamin
E can help in the management of cancer in more than one way. It can kill tumor
cells, enhance the effect of tumor therapeutic agents (drug, radiation and
heat), reduce their toxic effect and enhance the immune functions. Numerous
animal and one human study suggest that high doses of vitamin may enhance the
body's immune defense system. More human studies are needed to evaluate the
rate of vitamin E in the treatment of cancer.
Free radicals have been implicated in
accelerating the aging processes of organisms as well as individual organs in
the body. Therefore, the supplemental use of vitamins on a regular basis should
slow down aging processes. This hypothesis has not been adequately tested in
humans or animals. In vitro data show that the addition of vitamin E increases
the survival of nerve cells. |
