Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, December 18, 2013

Tea, flavonoids, and cardiovascular health: endothelial protection

Would this have prevented the plaque buildup in  my arteries?

Tea, flavonoids, and cardiovascular health: endothelial protection

  1. Claudio Ferri
+ Author Affiliations
  1. 1From the Department of Life, Health, and Environmental Sciences, University of L'Aquila, L'Aquila, Italy (DG, GD, PDG, MDF, EF, PC, and CF); and University “Sapienza”–II Faculty of Medicine, Rome, Italy (LF).
+ Author Notes
  • 2 Presented at the conference “Fifth International Scientific Symposium on Tea and Human Health,” held at the US Department of Agriculture, Washington, DC, 19 September 2012. The conference was organized by Jeffrey Blumberg, Tufts University, Boston, MA, and a Steering Committee including representatives from each of the symposium cosponsors: the American Cancer Society, the American College of Nutrition, the American Institute for Cancer Research, the American Medical Women's Association, the American Society for Nutrition, and the Linus Pauling Institute. The symposium was underwritten by the Tea Council of the USA. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the Tea Council of the USA or the cosponsoring organizations.
  • 3 This symposium was supported by the American Cancer Society, the American College of Nutrition, the American Institute for Cancer Research, the American Medical Women's Association, the American Society for Nutrition, the Linus Pauling Institute, the University of Western Australia, and the Unilever Food and Health Research Institute.
  • 4 Address correspondence to D Grassi, University of L'Aquila, Department of Life, Health, and Environmental Sciences, Viale S Salvatore, Delta, 6 Medicina, 67100 Coppito, L'Aquila, Italy. E-mail: davide.grassi@cc.univaq.it.

Abstract

Several studies have suggested that tea consumption might protect against the development and progression of cardiovascular disease, one of the leading causes of morbidity and mortality worldwide. The endothelium plays a pivotal role in arterial homeostasis. Reduced nitric oxide (NO) bioavailability with endothelial dysfunction is considered the earliest step in the pathogenesis of atherosclerosis. Endothelial dysfunction has been considered an important and independent predictor of future development of cardiovascular risk and events. The association between brachial NO-dependent flow-mediated dilation (FMD) and cardiovascular disease risk has been investigated in several prospective studies, suggesting that FMD is inversely associated with future cardiovascular events. Dietary flavonoids and tea consumption have been described to improve endothelial function and FMD. A proposed mechanism by which dietary flavonoids could affect FMD is that they improve the bioactivity of the endothelium-derived vasodilator NO by enhancing NO synthesis or by decreasing superoxide-mediated NO breakdown. This could be of clinical relevance and may suggest a mechanistic explanation for the reduced risk of cardiovascular events and stroke observed among tea drinkers in the different studies. The purpose of this article is to provide an overview of the relation between tea consumption and cardiovascular disease, with a focus on clinical implications resulting from the beneficial effects of tea consumption on endothelial function.

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