Green tea is a super weapon?

Many people rely on the health benefits of green tea. The research is interested more and more in to the traditional drink – with encouraging results.Green tea

In Asia green tea is used for relief and healing of various diseases for centuries. And even in Western countries, green tea is now regarded by many people as a wonder weapon against all sorts of ailments. From diabetes to cancer, toward Alzheimer’s and multiple sclerosis – In all of these diseases, green tea is able to exert positive effects by its beneficial properties. However, the study on the subject of situation has been rather thin. Now seems to gradually change. Green tea has become a popular research subject among medical professionals, and current studies allow to take notice.

Epigallocatechin gallate (EGCG) is the substance that gives to green tea its salutary effect. More recently, scientists have discovered that a sufficient amount of EGCG can slow down the growth of tumors. The amount of cancer cells reduced by the administration of the polyphenol in many animals significantly.

Effect of EGCG on inflammatory processes.

Evidence of a beneficial effect of green tea on blood glucose provides another study. Suggest two cups of green tea to stop rise of sugar blood level in twice after a starch containing meal (ie for example with pasta or potatoes). The reason for this is that EGCG inhibits starch digestion, causing the blood sugar increases more slowly after eating.

Other encouraging results show research on cell cultures. So evidence was found that EGCG reduces inflammation and curb misguided immune system. In addition, it can prevent nerve cells from destruction by its own immune system. That could make green tea a valuable partner in the therapy of autoimmune diseases, such as Multiple Sclerosis.

Researchers also investigate whether the extract of green tea is able to overcome in sufficient quantity, the blood-brain barrier to act directly in case of Alzheimer’s. Checks will also show whether EGCG can stop the formation of pathogenic amyloid fibrils at a very early stage in humans.

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