The Effect of Vitamin E on Cardiovascular
Diseases
Introduction
Cardiovascular diseases (CVDs) are the
number one killer in the world today which causes close to 18 million deaths
every year. Hypertension, hyperlipidemia, diabetes, and oxidative stress are
some of the risk factors that play a significant role in the development of the
atherosclerosis, myocardial infarction, and stroke. Antioxidants such as
vitamin E have received some attention in the past years as being useful in the
prevention and treatment of CVDs.
Vitamin E is a fat-soluble antioxidant
that is instrumental in neutralization of free radicals, lessening of oxidative
stress, and amelioration of the endothelial function. Nevertheless, its
cardiovascular protection is controversial, and some studies indicate that it
is effective, and others indicate that it has little or no effect. This paper
examines the processes through which vitamin E affects cardiovascular health,
the clinical evidence and the possible impacts and drawbacks.
Understanding
Vitamin E
Vitamin E is a combination of eight
compounds that occur naturally, which are categorized into two groups:
1. Tocopherols
o
Alpha (alpha)
-tocopherol (most biologically active form)
o
Beta
(β)-tocopherol
o
Gamma
(γ)-tocopherol
o
Delta
(δ)-tocopherol
2. Tocotrienols
o
Alpha, beta,
gamma and delta tocotrienols
Of these, α-tocopherol is the most
investigated and supplemented form, because it is very bioavailable in human
beings.
Sources of
Vitamin E
Vitamin E is acquired by food and
supplements. It is found commonly in food:
·
Oils: sunflower oil, olive oil, soybean oil
·
Nuts and
seeds: almonds, hazelnut, sunflower seeds
·
Spinach,
broccoli (Green Vegetables)
·
Foods Adding
Fortification: Cereals,
margarine
Mechanisms of
Vitamin E in Cardiovascular Protection
Vitamin E can produce its
cardioprotective actions in a number of ways:
1. Antioxidant
Properties
·
Inhibits
Free Radicals: Reactive oxygen
species (ROS) are known to cause LDL oxidation that is a major process in
atherosclerosis. Vitamin E transfers electrons to free radicals and stops
oxidative damage.
·
Decreases
Lipid Peroxidation: Vitamin E slows
down the formation of lipid-peroxidation in arteries by preventing the
oxidation of LDL cholesterol.
2.
Anti-Inflammatory Effects
·
Regulates
Cytokines: Vitamin E reduces pro inflammatory
cytokines, such as TNF-a and IL-6, associated with endothelial dysfunction.
·
Inhibits
NF-kB Pathway: This dampens
down vascular inflammation which is a major consideration in the development of
atherosclerosis.
3. Improves
Endothelial Function
·
Increases
Nitric Oxide (NO) Bioavailability:
Nitric Oxide (NO) is necessary in vasodilation. Vitamin E is beneficial in
preserving the activity of endothelial NO synthase (eNOS) enhancing blood
circulation.
·
Lowers the
Apoptosis of Endothelial Cells:
Prevents oxidative damage of blood vessels and preserves the integrity of blood
vessels.
4. Antiplatelet
and Antithrombotic Effects
·
Lowers
Platelet Aggregation: Vitamin E acts
to prevent platelet adhesion that reduces the chances of thrombus formation.
·
Regulates
Prostaglandins: Influences the
thromboxane A2 (a vasoconstrictor), which allows a healthier circulation of
blood.
5. Cholesterol
Regulation
·
Block
HMG-CoA Reductase: Research
indicates that vitamin E has a small effect of reducing LDL cholesterol.
·
Increases
HDL Function: Increases the
function of HDL to clear the cholesterol off the arterial walls.
Vitamin D: Functions and Effects
Clinical Evidence
on Vitamin E and Cardiovascular Diseases
A number of large trials have also
explored the effect of vitamin E supplementation on the outcome of CVD with
variable results.
Supportive
Studies
·
Cambridge
Heart Antioxidant Study (CHAOS, 1996):
o
Discovered that
vitamin E (400 800 IU/day) decreased non-fatal myocardial infarction by a
factor of 77 percent.
o
Nonetheless,
there was no notable outcome on total mortality.
·
Women’s
Health Study (WHS, 2005):
o
Documented a 24
percent decrease in cardiovascular mortalities in women above 45 years who were
taking vitamin E supplements.
·
Secondary
Prevention Studies:
o
According to some
meta-analyses, vitamin E is potentially useful with high-risk groups
(diabetics, smokers, elderly) by lowering the oxidative stress.
Contradictory or
Neutral Studies
·
Heart
Outcomes Prevention Evaluation (HOPE, 2000):
o
Vitamin E (400
IU/day) did not reduce the major cardiovascular events in high-risk patients
significantly.
·
GISSI-Prevenzione
Trial (1999):
o
Did not find any
cardiovascular advantage of vitamin E in patients with post-MI.
·
SELECT Trial
(2011):
o
The supplement
(400 IU/day) of vitamin E had no effect on preventing prostate cancer or CVD
and had the additional effect of increasing hemorrhagic stroke by a small
amount.
Possible Reasons
for Discrepancies
·
Variation in
dosage: When used in high doses it can be
pro-oxidant.
·
Population
Differences: The benefits may
be more in individuals who have an increased oxidative stress (e.g. diabetics).
·
Vitamin E
form: 75 percent of trials were with
3-tocopherol; 3-tocopherol and tocotrienol supplements have some extra perks.
Potential Risks
and Limitations of Vitamin E Supplementation
Vitamin E is otherwise safe but too
much of it (more than 1,000 IU/day) can be dangerous:
·
Risk of
increased Bleeding: high doses have
the ability to inhibit platelet aggregation, which increases risk of
hemorrhage.
·
Pro-Oxidant
Effects: At extremely high doses, the substance
can actually reify the oxidative harm.
·
Drug
Interactions: Can interact
with anticoagulants (warfarin) and statins.
·
Mixed
Results on Meta-Analyses: Other
studies depict no substantial CVD benefits, and it is questionable whether to
be widely supplemented.
Recommendations
for Vitamin E Intake in Cardiovascular Health
Considering the contradictory evidence,
it is possible to make the following recommendations:
·
Preferred
Dietary Intake: Vitamin E should
be derived naturally, in food, and not supplements.
·
Risk
Population Supplementation: Diabetics
and smokers as well as individuals with proven deficiencies may be supplemented
under medical supervision.
·
Do not take
Mega-Doses: Take only the
recommended daily allowance (RDA: 15 mg/day in adults).
·
Combination
Therapy: Vitamin E might be more effective in
combination with other antioxidants (vitamin C, selenium).
Conclusion
Vitamin E has a potential of
cardiovascular protection because of its anti-oxidant, anti-inflammatory and
endothelial-enhancing activities. But the clinical trials have had mixed
results and it is possible that its advantages are dose-dependent,
population-specific, and health-condition dependent. Although dietary vitamin E
is good, supplementation without regard is not advised everywhere. It should be
determined how various forms of vitamin E work synergistically and how those
can be used in an individual approach to cardiovascular prevention in the
future.
In the meantime, the most sensible
strategy in limiting the risk of cardiovascular complications is a diet high in
natural forms of vitamin E, along with heart-friendly lifestyle.
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