Resveratrol is still considered to be a very new founding in scientific study but its already getting a lot of attention, and the main limelight is pointed to Resveratrol because Dr.Oz gave a special highlight on Oprah show. Important focus ACAI BERRY has a very high substantial content which could help in many ways.
Resveratrol is a chemical compound found in certain plants. It is called a phytoalexin because plants naturally produce it as an antibiotic substance to fight both bacteria and fungi. Plants containing resveratrol include the grapes and skins of grapes that produce wine, raspberries, mulberries, blueberries and cranberries. Resveratrol can also be found in peanuts, certain pine trees and in Japanese knotweed. Wine has been identified as the rich source Resveratrol which is why Wine is thick and bold RED in colour.
what is the use of Resveratrol?
The groups of Howitz and Sinclair reported in 2003 in the journal Nature that resveratrol significantly extends the lifespan of the yeast Saccharomyces cerevisiae. Later studies conducted by Sinclair showed that resveratrol also prolongs the lifespan of the worm Caenorhabditis elegans and the fruit fly Drosophila melanogaster. In 2007, a different group of researchers were able to reproduce Sinclair's results with Caenorhabditis elegans, but a third group could not achieve consistent increases in lifespan of D. melanogaster or C. elegans.
In 2006, Italian scientists obtained the first positive result of resveratrol supplementation in a vertebrate. Using a short-lived fish, Nothobranchius furzeri, with a median life span of nine weeks, they found that a maximal dose of resveratrol increased the median lifespan by 56%. Compared with the control fish at nine weeks, that is by the end of control fish's life, the fish supplemented with resveratrol showed significantly higher general swimming activity and better learning to avoid an unpleasant stimulus. The authors noted a slight increase of mortality in young fish caused by resveratrol and hypothesized that it is its weak toxic action that stimulated the defense mechanisms and resulted in the life span extension.
Later the same year, Sinclair reported that resveratrol counteracted the detrimental effects of a high-fat diet in mice. The high fat diet was compounded by adding hydrogenated coconut oil to the standard diet; it provided 60% of energy from fat, and the mice on it consumed about 30% more calories than the mice on standard diet. Both the mice fed the standard diet and the high-fat diet plus 22 mg/kg resveratrol had a 30% lower risk of death than the mice on the high-fat diet. Gene expression analysis indicated the addition of resveratrol opposed the alteration of 144 out of 153 gene pathways changed by the high-fat diet. Insulin and glucose levels in mice on the high-fat+resveratrol diet were closer to the mice on standard diet than to the mice on the high-fat diet. However, addition of resveratrol to the high-fat diet did not change the levels of free fatty acids and cholesterol, which were much higher than in the mice on standard diet.
A further study by a group of scientists, which included Sinclair, indicated that resveratrol treatment had a range of beneficial effects in elderly mice but did not increase the longevity of ad libitum–fed mice when started midlife.
In 1997, Jang reported that topical resveratrol applications prevented skin cancer development in mice treated with a carcinogen.
There have since been dozens of studies of the anti-cancer activity of resveratrol in animal models. No results of human clinical trials for cancer have been reported.
However, clinical trials to investigate the effects on colon cancer and melanoma (skin cancer) are currently recruiting patients.
In vitro resveratrol interacts with multiple molecular targets (see the mechanisms of action), and damaged cells of breast, skin, gastric, colon, esophageal, prostate, and pancreatic cancer, and leukemia.
However, the study of pharmacokinetics of resveratrol in humans concluded that even high doses of resveratrol might be insufficient to achieve resveratrol concentrations required for the systemic prevention of cancer.
This is consistent with the results from the animal cancer models, which indicate that the in vivo effectiveness of resveratrol is limited by its poor systemic bioavailability.
The strongest evidence of anti-cancer action of resveratrol exists for tumors it can come into direct contact with, such as skin and gastrointestinal tract tumors. For other cancers, the evidence is uncertain, even if massive doses of resveratrol are used.
Thus, topical application of resveratrol in mice, both before and after the UVB exposure, inhibited the skin damage and decreased skin cancer incidence. However, oral resveratrol was ineffective in treating mice inoculated with melanoma cells. Resveratrol given orally also had no effect on leukemia and lung cancer; however, injected intraperitoneally, 2.5 or 10 mg/kg of resveratrol slowed the growth of metastatic Lewis lung carcinomas in mice.
Resveratrol (1 mg/kg orally) reduced the number and size of the esophageal tumors in rats treated with a carcinogen.
In several studies, small doses (0.02–8 mg/kg) of resveratrol, given prophylactically, reduced or prevented the development of intestinal and colon tumors in rats given different carcinogens.
Resveratrol treatment appeared to prevent the development of mammary tumors in animal models; however, it had no effect on the growth of existing tumors. Paradoxically, treatment of pre-pubertal mice with high doses of resveratrol enhanced formation of tumors. Injected in high doses into mice, resveratrol slowed the growth of neuroblastomas.
All the information above can be found at WIKIPEDIA