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THE VALUE OF ANTIOXIDANTS: Vitamin E
By Dr. Michael G. Kurilla, M.D.
SUMMARY
Oxidation is a chemical process where something reacts with oxygen.
For example, rusted metal and a slice of an apple that turns brown if left
out are common results of the oxidation process. In the human body, oxidation
is a frequent occurrence because we rely on oxygen (which is carried throughout
our bodies by blood) for life. To combat the unwanted effects of oxidation,
nature has evolved a diverse array of antioxidants (agents that either
prevent or repair unwanted oxidation) to counteract the adverse effects
of oxidation.
With an increasing appreciation of the involvement of oxidation in the
initial stages and progression of several major disease processes, particularly
cardiovascular disease, the use of dietary antioxidants is being more critically
evaluated. While not definitively proven at this time, the evidence accumulated
to date is showing vitamin E to play a significant role in slowing or even
reversing major disease processes. Investigators in this area are encouraged
by the findings that the presumed mechanisms underlying the action of vitamin
E are reasonably well understood as well as results of human studies in
general, supporting predictions based on these presumed mechanisms. Equally
encouraging to potential users of vitamin E is the extremely low toxicity.
This article discusses the functions of vitamin E and the results of various
studies that suggest its role in disease reduction, particularly cardiovascular
diseases. Finally, some general guidelines for supplementation with vitamin
E are presented.
VITAMIN E BASICS
The recognition of vitamin E's requirement in our diet goes back 75
years, when Evan and Bishop identified this substance as required for reproduction
in the rat3. The name tocopherol was applied
with tokos (for childbirth) and pherein (to bring forth)
combined with ol (to denote its phenolic chemical nature). What
is referred to as vitamin E is in reality a mixture of at least 8 related
substances that can be divided into two groups, the tocopherols
(alpha, beta, gamma, and delta forms) and the tocotrienols (alpha,
beta, gamma, and delta forms)6. The two
groups have different sources. The tocopherols are most plentiful in oil
seeds, leaves, and other green parts of plants, while the tocotrienols
are found mainly in the bran and germ portions of seeds and cereals. In
humans, alpha-tocopherol appears to be the most important due to its high
biological activity, or usability within the human body.
The major activity of vitamin E is the ability to function as an antioxidant,
particularly for the preservation of polyunsaturated fats14;
it is this group of fatty acids that is most susceptible to oxidative damage.
In addition, there is an increasing recognition among cardiovascular disease
investigators that lipid (fat) oxidation, especially the lipid contained
in LDL (low density lipoprotein), accelerates the process of atherosclerosis13.
Since vitamin E dissolves in fat, and is therefore said to be fat soluble,
it is uniquely suited to functioning as an antioxidant in this environment.
In addition, there is some evidence that other antioxidants may work with
vitamin E to potentiate, or increase the effectiveness of, its antioxidant
activity15.
VITAMIN E AND CARDIOVASCULAR DISEASE
Several lines of evidence have accumulated over the last two decades
that suggest cholesterol levels are crucial for the progression of atherosclerosis9.
Atherosclerosis is a disease process whereby cholesterol is deposited into
the walls of blood vessels resulting in a gradual narrowing of the vessel
along with reduced flexibility ("hardening of the arteries"). The reduction
in the vessel's diameter not only reduces blood flow, but also makes a
blood clot formation more common, and more likely to completely obstruct
blood flow to downstream tissues. In the heart, where alternate blood flow
is limited, this occurrence can precipitate a myocardial infarction ("heart
attack").
LDL cholesterol (known as "bad" cholesterol), rather than total cholesterol
appears to be the major source of cholesterol for starting this process.
Experiments in animals have demonstrated that providing additional LDL
to the blood accelerates this process13.
Those same studies have shown that prior oxidation of LDL (which damages
the LDL) increases the rate that cholesterol gets deposited in vessel walls.
Studies in humans have also revealed that individuals can make antibodies
against their own oxidized LDL and that levels of these antibodies correlate
with risk for myocardial infarction10.
LDL is a tiny particle consisting of cholesterol, proteins, fatty acids,
triglycerides, and an assortment of several types of antioxidants with
alpha-tocopherol being dominant. Therefore, vitamin E is uniquely suited
for the job of preventing LDL from becoming oxidized. To evaluate this
possibility, various lines of investigations have been initiated to study
this possibility15.
EPIDEMIOLOGICAL DATA
A number of studies have reported an inverse correlation between plasma
concentrations of vitamin E and coronary mortality (death due to coronary
artery disease), although this has not been consistently found. What these
studies reveal is that the lowest risk for cardiovascular disease is found
in those people with the highest levels of vitamin E in their blood The
best studies to date have been prospective ones that have followed individuals
who begin the study without cardiac disease and compared disease incidence
with vitamin E intake. The Health Professionals Follow-up Study has followed
nearly 40,000 men age 40 - 75 who started without cardiac disease11.
During the study period, the group with the highest intake of vitamin E
had a 40% reduction in cardiovascular disease incidence compared to the
lowest group. This risk reduction held up even after controlling for a
wide array of other known risk factors. The study was also able to separate
contributions from dietary sources and supplements. Only vitamin E supplements
(>100 IU/day) had a significant effect.
The Nurses' Health Study followed over 87,000 women, age 34 - 59 for
eight years and correlated vitamin E intake with cardiovascular disease
incidence12. A similar reduction in cardiac
disease was noted at 34%. In addition, the investigators were able to show
that only supplementation of greater than 100 IU/day of vitamin E was associated
with the reduced risk. Another key finding was that at least 2 years of
supplementation was necessary before risk reduction was found. This is
particularly relevant because the proposed way that vitamin E works is
by preventing LDL oxidation. Since the oxidized LDL deposit process is
slow and gradual, occurring over many years, a reduction in oxidized LDL
would be expected to only show up after some period of time of vitamin
E use.
Finally, there have been studies assessing the progression of disease
(which is different from disease induction, or cause). One such study was
addressing atherosclerosis reversal by cholesterol lowering drugs with
antioxidants5. In this case, supplementers
who took >100 IU/day of vitamin E had less progression of their vessel
narrowing compared to non-supplementers. In the group taking cholesterol
lowering therapy and vitamin E, there was even partial regression (an improvement
in the degree of narrowing) of the lesions. Other smaller trials have specifically
examined vitamin E therapy in the case of angioplasty (surgery to repair
obstructed blood vessels) to reduce restenosis (stenosis means obstruction
to flow; restenosis is the process whereby the vessel becomes obstructed
again in a rapid fashion after repair) rates2.
While the trends are in favor of vitamin E, these trials have been too
small to detect statistically significant differences.
CO-ANTIOXIDANTS WORKING WITH VITAMIN E
The study of LDL oxidation has led investigators to examine the mechanism
of how vitamin E protects polyunsaturated fats. Appreciation of other antioxidants
has developed the notion that while vitamin E protects lipid, there must
be other antioxidants present to recycle vitamin E. The other major antioxidants
with substantial activity are coenzyme Q10 and vitamin C15.
The possibility of additional factors (these so called co-antioxidants)
may provide an explanation for failing to detect a significant vitamin
E effect in earlier studies where the additional antioxidants were not
taken into account. This scenario has been evaluated in a study similar
to the above designs, but utilizing an elderly population (ages 67 - 105)
over a period of nine years7. In this group
all the vitamin E users experienced a reduction in cardiac mortality (deaths
due to cardiac disease) of 41%, but vitamin E use alone produced only a
31% reduction, whereas a combined vitamin E and C use produced a 48% reduction.
This is strong evidence that antioxidants can work together to reduce risk
of disease due to oxidative processes.
OTHER USES OF VITAMIN E
Certainly, cardiovascular diseases are by no means the sole province
of vitamin E. The role of vitamin E in protecting the skin from UV (by
the sun) damage is well appreciated. There are well established uses in
specific pediatric diseases and at least one genetic disorder14.
Improvement in immune system function is also plausible. There is some
interest in possible cancer reduction (possibly related to immune system
augmentation). One study has found a 23% reduction in cancer deaths, although
the results were too weak to be considered conclusive evidence7.
SAFETY CONCERNS
A number of studies have addressed the safety of oral vitamin E supplementation1,8.
In some cases, doses were very high (2000 IU/day). In general, there have
been little to no adverse effects reported. Most of the few side effects
that appear in the literature are largely either anecdotal reports where
vitamin E was presumed to be the cause or they are incidental findings
in toxicity studies that have not been replicated by other studies. Also
of comfort are animal studies where high doses have been used to look for
mutagenic (the ability to damage DNA), carcinogenic (the ability to cause
cancer), or teratogenic (the ability to cause birth defects when ingested
by pregnant women) effects. None of these effects were found.
LIMITATIONS AND LACK OF PUBLIC POLICY RECOMMENDATIONS
In spite of the above data, there has been no official declaration on
the use of supplemental vitamin E. There are several reasons for this situation.
In the first place, there are no prospective, randomized, double blind
studies that have unequivocally demonstrated the ability of vitamin E for
reducing cardiovascular disease. This type of study is regarded as the
"gold standard", particularly for public policy. The only study that has
come close is the infamous Finnish beta-carotene study which was looking
at lung cancer4. Lost in the press reports
were the facts that vitamin E was also included and that cardiovascular
diseases were also evaluated. No effect of vitamin E was noted; however,
this study actually validates earlier studies since only 50 IU/day of vitamin
E was supplied and based on the previous studies, at least 100 IU/day are
required for an effect.
From a safety standpoint, the doses needed to produce an apparent effect
are well within tolerance limits, although a purist might wish to see more
long term data. Lack of gold standard studies would appear to be one major
reason for reluctance. Another aspect that may be troublesome for public
policy officials is the need for supplementation, rather than mere dietary
recommendations. The doses that appear beneficial are beyond the range
that can be obtained from diet alone. This implies that people will need
to buy supplements and this makes public policy officials more reluctant
to offer this type of advice.
RECOMMENDATIONS
In order to achieve vitamin E levels commensurate with those that appear
to afford some beneficial effects, supplementation is necessary; dietary
sources of vitamin E are not sufficient to reach these amounts. At least
100 IU/day of vitamin should be taken; levels up to 400 IU/day are well
within safety limits and are in the range of what many cardiologists are
cautiously recommending now. In terms of what type of vitamin E to take,
alpha-tocopherol is the most important form for LDL oxidation. On the other
hand, excessive intake of one type may adversely affect other tocopherol
species, so a mixed tocopherol is safer. There has been little or no examination
of the tocotrienols, but their lower levels suggest that while they may
possess some biological activity, the tocopherols are the important players.
Since the preparations are standardized to IUs, there is less concern for
the specific distribution provided that alpha-tocopherol is the major species.
Natural and synthetic tocopherols have the same antioxidation properties,
but the biological properties of the different forms vary, so natural is
likely better.
Netrition recommends taking 400 IU of natural
vitamin E daily for
the best antioxidant benefits along with a balanced diet
and a complete multi-vitamin and mineral supplement.
REFERENCES CITED
1. Bendich A, Machlin LJ: Safety of oral intake of vitamin E. Am
J Clin Nutr 48:612619, 1988
2. DeMaio SJ, King SB, Lembo NJ: Vitamin E supplementation, plasma lipids
and incidence of restenosis after percutaneous transluminal coronary angioplasty
(PTCA). J Am Coll Nutr 11:6873, 1992
3. Evans HM, Bishop KS: On the existence of a hitherto unrecognized
dietary factor essential for reproduction. Science 56:650651,
1922
4. Heinonen OP, Albanes D, The AlphaTocopherol BC: The effect of
vitamin E and beta carotene on the incidence of lung cancer and other cancers
in male smokers. N Engl J Med 330:10291035, 1994
5. Hodis HN, Mack WJ, LaBree L, et al: Serial coronary angiographic
evidence that antioxidant vitamin intake reduces progression of coronary
artery atherosclerosis. JAMA 273:18491854, 1995
6. Kamaleldin A, Appelqvist LA: The chemistry and antioxidant properties
of tocopherols and tocotrienols. Lipids 31:671701, 1996
7. Losonczy KG, Harris TB, Havlik RJ: Vitamin E and vitamin C supplement
use and risk of allcause and coronary heart disease mortality in older
persons: the Established Populations for Epidemiologic Studies of the Elderly.
Am J Clin Nutr 64:190196, 1996
8. Meydani SN, Meydani M, Rall LC, et al: Assessment of the safety of
highdose, shortterm supplementation with vitamin E in healthy
older adults. Am J Clin Nutr 60:704709, 1994
9. Mitchinson MJ: The new face of atherosclerosis. Br J Clin Prac
48:149151, 1994
10. Puurunen M, Manttari M, Manninen V, et al: Antibody against oxidized
lowdensity lipoprotein predicting myocardial infarction. Arch Int
Med 154:26052609, 1994
11. Rimm EB, Stampfer MJ, Ascherio A, et al: Vitamin E consumption and
the risk of coronary heart disease in men. N Engl J Med 328:14501456,
1993
12. Stampfer MJ, Hennekens CH, Manson JE, et al: Vitamin E consumption
and the risk of coronary disease in women. N Engl J Med 328:14441449,
1993
13. Steinberg D, Parthasarathy S, Carew TE, et al: Beyond cholesterol.
Modifications of lowdensity lipoprotein that increase its atherogenicity.
N Engl J Med 320:915924, 1989
14. Thakur ML, Srivastava US: VitaminE metabolism and its application.
Nutr Res 16:17671809, 1996
15. Thomas SR, Neuzil J, Mohr D, et al: Coantioxidants make alphatocopherol
an efficient antioxidant for lowdensity lipoprotein. Am J Clin
Nutr 62:1357S1364S, 1995
Dr. Michael G. Kurilla, M.D. has extensive education, work experience, and
sound reasoning which shows in his articles. He holds an M.D. and Ph.D. in
molecular virology from Duke University. He received Pathology training at the
Brigham & Women's Hospital and performed a postdoctoral fellowship at
Harvard University with the head of infectious diseases at the Brigham &
Women's Hospital. He also worked on the faculty at the University of Virginia in
the departments of Pathology and Microbiology - dividing his time between
clinical duties at the Clinical Microbiology for the University of Virginia hospital
and basic research on viral immunology.
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