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.

Sunday, March 8, 2015

Popular antioxidant likely ineffective, study finds - CoQ10

Does this research contradict the use of CoQ10 as necessary for the side effects of statin use? What does your doctor have to say?

Clinical Studies Show That Cholesterol Lowering Drugs Reduce The Level of CoQ10 To A Critical Level




Popular antioxidant likely ineffective, study finds - CoQ10

The popular dietary supplement ubiquinone, also known as Coenzyme Q10, is widely believed to function as an antioxidant, protecting cells against damage from free radicals. But a new study by scientists at McGill University finds that ubiquinone is not a crucial antioxidant -- and that consuming it is unlikely to provide any benefit.
The findings, by a team led by Professor Siegfried Hekimi in McGill’s Department of Biology, are published today (March 6) in Nature Communications.
Ubiquinone is a lipid-like substance found naturally in all cells of the body. Cells need it to produce energy from nutrients and oxygen – a function performed by tiny structures, known as mitochondria, within cells. Because it was also thought to function as an antioxidant, ubiquinone has been recommended for a variety of ills and as an anti-aging supplement; global sales of the substance are estimated to amount to hundreds of millions of dollars a year.
“Our findings show that one of the major anti-aging antioxidant supplements used by people can’t possibly act as previously believed,” Hekimi says. “Dietary supplements cost a lot of money to patients throughout the world – money that would be better spent on healthy food. What’s more, the hope for a quick fix makes people less motivated to undertake appropriate lifestyle changes.”
In order to study how energy metabolism affects aging, the McGill researchers created the first strain of mice in which scientists are able to gradually eliminate ubiquinone – and then to restore it at will to normal levels. Because of ubiquinone’s role in energy production, loss of the substance in the mice led to severe sickness and early death. But the researchers were surprised to find no signs of elevated oxidative damage to cell membranes or DNA from free radicals, the sometimes-harmful molecules created by the oxygen chemistry during metabolism. The team also determined that this unexpected lack of damage didn’t stem from deployment of some other antioxidant strategies by the animals.
At the same time, the research yielded new insights into the importance of ubiquinone in helping mitochondria produce energy. “Many patients are sick because their mitochondria don’t work properly, including because they don’t contain enough ubiquinone,” Hekimi says. “We’ll be using the results of this study to devise ways, and possibly new drugs, to boost ubiquinone levels or help residual ubiquinone to function effectively in defective mitochondria.” To that end, his research team recently received a grant from MitoCanada, a charity that seeks to help patients with mitochondrial diseases.
The published research was supported by the Canadian Institutes of Health Research.

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