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Green Tea
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Green Tea Helps Prevent the Development of AtherosclerosisGreen tea has been shown to effectively lower risk of atherosclerosis by lowering LDL cholesterol, triglycerides, lipid peroxides (free radicals that damage LDL cholesterol and other lipids or fats) and fibrinogen (a protein in the blood involved in the formation of blood clots), while improving the ratio of LDL (bad) to HDL (good) cholesterol. |
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In animal studies in which green tea was given in human equivalent doses to hamsters, atherosclerosis was inhibited 26-46% in those receiving the lower dose (equivalent in humans to 3-4 cups per day) , and 48-63% in those receiving the higher dose (10 cups a day in humans). |
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In both atherosclerosis and cancer, cell growth and proliferation is central to the disease process. In atherosclerosis, plaques form in the lining of the arteries, which grow thicker and less elastic, impeding blood flow. In cancer, normal brakes on cells turn off, and they multiply out of control. Green tea can help stop abnormal cell proliferation. Catechins, among the main active compounds in green tea leaves, shut down the primary relay station through which growth factors central to both atherosclerosis and cancer send their messages for growth. These relay stations, called tyrosine kinase receptors, are essential for the transmission of messages sent by platelet derived growth factor, insulin-like growth factor, epidermal growth factor, fibroblast growth factor, and vascular endothelial growth factor. The result is the prevention of or halting of the disease processes that depend upon excessive cellular growth. Two other damaging factors that cause the cells lining our vasculature to proliferate are AGEs (advanced glycation end products) and MAPK (mitogen-activated protein kinase). AGEs form when sugars inappropriately bind to and distort proteins. MAPK activity is normally enhanced in the presence of elevated levels of LDL cholesterol. In laboratory studies, green tea polyphenols were shown to dose-dependently inhibit AGE-stimulated proliferation of vascular smooth muscle cells and to prevent the increase in MAPK normally seen when LDL levels are high.
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