Groundbreaking TAME trial, which directly targets aging as an endpoint, finally begins this November, reveals lead clinician Dr Nir Barzilai.
Back in 2015, when his revolutionary anti-aging trial TAME finally received FDA approval, it would have been forgivable to think that Dr Barzilai had, at last, got past the hard part. But TAME went into financial limbo, with many wondering if it would ever be able to escape. “We wasted valuable time negotiating,” said Dr Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine,“but we’re finally on track.” His trial TAME (Targeting Aging with Metformin) had been stalled for four years while he and his colleagues engaged in funding negotiations with the US NIH (National Institute of Health).
https://www.longevity.technology/worlds ... een-light/
Longevity ⇒ World’s first anti-aging trial is happening! Using metformin to “TAME” aging
World’s first anti-aging trial is happening! Using metformin to “TAME” aging
Ph.D. student at Harvard Medical School, doing research on aging
Re: World’s first anti-aging trial is happening! Using metformin to “TAME” aging
Interesting stuff!
In the article, it says, "As for who provided the $40m funding, Barzilai remains coy, “I can’t tell you who gave us it, but it will be a great story one day!” I wonder who the private donor was?!
In the article, it says, "As for who provided the $40m funding, Barzilai remains coy, “I can’t tell you who gave us it, but it will be a great story one day!” I wonder who the private donor was?!
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Vandevalk1
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Fred
Re: World’s first anti-aging trial is happening! Using metformin to “TAME” aging
Also on the same site a good NEW interview with the lead researcher and designer of the TAME-trial, Dr Nir Barzilai. In the excerpt below is one of the best explanations of how metformin may protect against disease and enhance longevity that I´ve seen:
"Q: You’re best known for your work with Metformin, a diabetes drug that many researchers believe could also prove to be beneficial for Longevity. In a nutshell, how does it regulate aging?
A: We haven’t fully understood and mapped out the mechanisms by which metformin acts upon aging, but here’s the best summary I can give. Metformin gets into the cell by a transporter called OCT-1 and it binds to complex 1 of the mitochondria, which are the energy generators of our cells. This binding causes two major changes in how the mitochondria work.
First there’s the metabolic part: you have a change in the energy sensing of the cell. It activates a hormone that senses for nutrient deprivation, called AMP Kinase, which normally goes up when you haven’t eaten for a while. When AMP Kinase goes up, it triggers a decrease in another signaling pathway called M-TOR. M-TOR is a major pathway of aging. This is a very simplified explanation, but when it is reduced, cells conserve more energy, they don’t synthesise as much fat and cholesterol, and they focus on burning their reserves.
Secondly, metformin acts like very weak cyanide. This means it disrupts slightly (not totally, like cyanide does) the process by which we break down nutrients with oxygen for energy. With this, there’s less Reactive Oxygen Species being released, less inflammation, and less DNA damage.
It also has a number of non-mitochondrial effects, not all of which we understand in terms of how they may contribute to aging. But it improves loads of things, and pushes back the onset of age-related diseases."
https://www.longevity.technology/dr-nir ... echnology/
"Q: You’re best known for your work with Metformin, a diabetes drug that many researchers believe could also prove to be beneficial for Longevity. In a nutshell, how does it regulate aging?
A: We haven’t fully understood and mapped out the mechanisms by which metformin acts upon aging, but here’s the best summary I can give. Metformin gets into the cell by a transporter called OCT-1 and it binds to complex 1 of the mitochondria, which are the energy generators of our cells. This binding causes two major changes in how the mitochondria work.
First there’s the metabolic part: you have a change in the energy sensing of the cell. It activates a hormone that senses for nutrient deprivation, called AMP Kinase, which normally goes up when you haven’t eaten for a while. When AMP Kinase goes up, it triggers a decrease in another signaling pathway called M-TOR. M-TOR is a major pathway of aging. This is a very simplified explanation, but when it is reduced, cells conserve more energy, they don’t synthesise as much fat and cholesterol, and they focus on burning their reserves.
Secondly, metformin acts like very weak cyanide. This means it disrupts slightly (not totally, like cyanide does) the process by which we break down nutrients with oxygen for energy. With this, there’s less Reactive Oxygen Species being released, less inflammation, and less DNA damage.
It also has a number of non-mitochondrial effects, not all of which we understand in terms of how they may contribute to aging. But it improves loads of things, and pushes back the onset of age-related diseases."
https://www.longevity.technology/dr-nir ... echnology/