Vitamin E consists of a number of compounds, tocopherols and tocotrienols,
that function as lipid-soluble antioxidants. A hypothesis is that vitamin E
may slow the progression of atherosclerosis by blocking the oxidative modi
fication of low-density lipoprotein cholesterol and thus decrease its uptak
e into the arterial lumen. Basic science and animal studies have generally
supported this hypothesis. Observational studies have primarily assessed pa
tients with no established coronary heart disease (CHD), and results have g
enerally supported a protective role of vitamin E in CHD. Early primary and
secondary prevention clinical trials (Alpha-Tocopherol, Beta-Carotene Canc
er Protection study and Cambridge Heart Antioxidant Study) showed mixed res
ults. Despite years of encouraging evidence from basic science and observat
ional studies, 3 large randomized clinical trials (Gruppo Italiano per In S
tudio della Sopravvivenza nell'Infarto miocardico, Heart Outcomes Preventio
n Evaluation, and Primary Prevention Project) with a combined total of more
than 25,000 patients failed to show a significant benefit with vitamin E t
aken as a dietary supplement for the prevention of CHD. Four large randomiz
ed primary prevention trials currently under way should add to our knowledg
e. The American Heart Association has recommended consumption or a balanced
diet with emphasis on antioxidant-rich fruits and vegetables but has made
no recommendations regarding vitamin E supplementation for the general popu
lation. Although vitamin E supplementation seems to be safe for most people
, recommendations from health care professionals should reflect the uncerta
inty of established benefit as demonstrated in clinical trials.