Tea is rich in antioxidant polyphenols (catechins, flavonols, theaflavins a
nd thearubigins). Epidemiological evidence relating regular consumption of
tea or related polyphenols to CHD is equivocal, Catechins are absorbed from
tea, but low plasma concentrations are attained. The bioavailability of th
eaflavins and thearubigins is unknown. Tea does not reduce blood pressure o
r plasma lipids in well-controlled human trials. Tea polyphenols inhibit LD
L lipid peroxidation in vitro, but the effect ex vivo is small. The plasma
antioxidant potential increases after drinking green but not black tea. Tea
consumption tended to reduce the development of aortic atherosclerosis in
rabbits. Tea polyphenols exert marked effects on cells, and inhibit neutrop
hil migration and inflammatory responses, sometimes at low concentrations.
These diverging results suggest potential beneficial effects, but emphasize
the need for good human trials of tea using early markers of CHD before fi
rm conclusions can be drawn.