A number of antioxidants in food have been shown to reduce the risk of cardiovascular disease. At present it is unclear as to why dietary antioxidants are protective, but evidence suggests that it may result from a decrease in oxidative stress. Free radicals can cause oxidation of low density lipoprotein (LDL) cholesterol particles, which may be a necessary prerequisite for their binding to the endothelium, which is associated with the subsequent accumulation of macrophages to cause foam cells. Oxidative stress caused by free radicals has also been shown to interfere with nitric oxide synthesis in endothelial cells, and this may have deleterious effects on endothelial function and arterial flow. Green tea shows inverse associations with cardiovascular disease in epidemiological studies and in vitro studies have reported decreases in the susceptibility of LDL to undergo oxidation. However, the effects of green tea in vivo have been less conclusive.
Some clinical studies in humans have demonstrated that green tea is be beneficial at improving vascular function and decreasing LDL oxidation. For example, research published in the American Journal of Clinical Nutrition1 investigated the short and medium term effects of a green tea extract on the vascular function of 14 healthy women. Four capsules of green tea (Camellia sinensis) extract containing a total of 150mg caffeine and 375mg of catechols (270mg as epigallocatechin gallate) or a placebo were administered to the subjects in divided doses before breakfast and lunch. Following green tea administration, the mean diameter of the brachial artery increased significantly in response to post-compression hyperaemia. The flow mediated dilation was 5.68% following the placebo, but was significantly higher (11.98%) following the green tea treatment. In addition, significant reductions in oxidised LDL (37.4%) and anti-oxidised LDL IgM were reported following green tea consumption.
Green tea therefore results in significant physiological changes to brachial artery flow that could be interpreted as an improvement in vascular function. In addition, green tea reduces the susceptibility of LDL cholesterol to oxidation (as measured through a TBARS assay), suggesting that results of in vitro work might be applicable to humans. Interestingly, methodological differences might explain some of the inconsistent results seen between human studies. Methods where the LDL particles are isolated may not produce inhibition of oxidation because flavonoids may not accumulate in the particles as anticipated. Because flavonoids are water soluble, they likely work on the surface of LDL particles to inhibit oxidation. The LDL particles were not isolated in this study, which may have allowed the aqueous containing flavonoids to inhibit the oxidation of the particles when exposed to pro-oxidants, as has been reported in other non-isolation studies.
This study also reported that green tea consumption significantly reduced the levels of anti-oxidised LDL IgM antibodies. However, green tea failed to decrease levels of anti-oxidised LDL IgG antibodies. The measurement of antibodies directed against oxidised LDL particles in this study was performed because the oxidation of LDL particles may increase immunogenicity. Once oxidised, LDL may express proteins that cause the formation of antibodies directed against the particles. However, these immune changes are not fully understood and results from studies are still controversial. Some authors have found no correlation between oxidised LDL and antibody levels in blood, whereas others have reported an inverse association between free oxidised LDL IgM antibodies and cardiovascular disease. A general inverse association has been reported between plasma cholesterol levels and anti-oxidised LDL IgG antibodies in the general population but more work is needed in this area to draw definitive conclusions.
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