Complementary Alternative Cardiovascular Medicine

Chapter 5 / Vitamin Therapy and CVD 61
CONCLUSION STATEMENT
There is no established evidence for the use of vitamin C supplementation
in CVD prevention.
Vitamin E
Alpha-tocopherol is the predominant lipophilic antioxidant in plasma
membranes and tissue and is the most abundant antioxidant in LDL. On
average, there are six molecules of α-tocopherol per LDL particle; they
can function as antioxidants by trapping free radicals. In prospective
studies (11,13), α-tocopherol supplementation reduced the risk of coronary
events in both men and women. In the female Nurses’ Health Study,
with a cohort of 87,000 women, there was an inverse association between
CAD events and vitamin E intake (13). Reduced risk was seen with a
vitamin E consumption of at least 100 IU/d. In a randomized, placebocontrolled
study in men, the LDL oxidation kinetics in a group supplemented
with 800 IU was similar to the group that received combined
supplementation with 1.0 g ascorbate, 30 mg beta-carotene, and 800 IU
α-tocopherol. There was a 40% decrease in the oxidation rate after 3 mo
of supplementation. Plasma vitamin E levels are significantly lower in
patients (both men and women) with active variant angina than in patients
without coronary spasm (14). In a cohort of 34,486 postmenopausal
women (10), dietary vitamin E was protective in women in the
highest quintile of dietary vitamin E intake. Randomized clinical trials
investigating the effect of antioxidant intake on CAD have shown mixed
results. In the alpha-tocopherol, beta carotene (ATBC) Cancer Prevention
Study (15,16), there was no benefit with respect to CAD for αtocopherol
or β-carotene. This trial was conducted in more than 29,000
Finnish male smokers. However, the dose of α-tocopherol (50 mg/d)
was below the protective range suggested by the Nurses’ Health Study.
In the Cambridge Heart Antioxidant Study (CHAOS), in which 2002
British men and women with angiographically proved CAD were included,
there was a 77% reduction in nonfatal myocardial infarction in subjects
who were taking vitamin E, compared with those on placebo (17), but
there was an increase in cardiovascular and overall mortality.
Among the large trials, the Heart Outcomes Prevention Evaluation
(HOPE) study (with 2545 women and 6996 men ≥ 55 yr) was designed
to test the hypotheses that two preventive intervention strategies, namely
angiotensin-converting enzyme (ACE) inhibition or vitamin E (400 IU),
would improve morbidity and mortality in patients at high risk of cardiovascular
events, compared with placebo for 4–6 yr. There were no significant
differences between vitamin E and placebo in myocardial