Aging & Longevity News and Discussions

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wjfox
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Ken_J
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That charles guy is a bit insufferable. He came in with the premise that he's getting to call BS on Flim Flam artists, and never even lets anyone talk about the points he brings up.

he's so hung up on the idea of doing things that any interventions have to use the bodies own means to change itself. He doesn't even seem to grasp that one doesn't have to change the beta cells in a type one diabetic to produce insulin again in order to help a type one diabetic to survive years and decades more than they would without medications and insulin injections.
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wjfox wrote: Wed May 11, 2022 8:32 am
Def will have to watch at a later time. At laaaast life extension tech is making its debut! :D
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wjfox wrote: Tue May 17, 2022 5:25 pm
While I admire those who live at long, I'm thinking it can't be fun as the same time, sitting on a wheelchair all day not being able to do much, let alone probably feeling pain everywhere. :?

If they still lived few decades from now and thanks to burgeoning anti-aging rejuvenations, we wouldn't be able to distinguish them from that of a person in their 70s or even younger.
To know is essentially the same as not knowing. The only thing that occurs is the rearrangement of atoms in your brain.
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The secret to a longer lifespan? Gene regulation holds a clue
https://phys.org/news/2022-05-secret-lo ... -clue.html
by University of Rochester

Natural selection has produced mammals that age at dramatically different rates. Take, for example, naked mole rats and mice; the former can live up to 41 years, nearly ten times as long as similar-size rodents such as mice.

What accounts for longer lifespan? According to new research from biologists at the University of Rochester, a key piece of the puzzle lies in the mechanisms that regulate gene expression.

In a paper published in Cell Metabolism, the researchers, including Vera Gorbunova, the Doris Johns Cherry professor of biology and medicine; Andrei Seluanov, professor of biology and medicine; and Jinlong Lu, a postdoctoral research associate in Gorbunova's lab and the first author of the paper, investigated genes connected to lifespan. Their research uncovered specific characteristics of these genes and revealed that two regulatory systems controlling gene expression—circadian and pluripotency networks—are critical to longevity. The findings have implications both in understanding how longevity evolves and in providing new targets to combat aging and age-related diseases.
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Research may reveal why people can suddenly become frail in their 70s

Wed 1 Jun 2022 16.00 BST

A groundbreaking theory of ageing that explains why people can suddenly become frail after reaching their 70s has raised the prospect of new therapies for the decline and diseases of old age.

Researchers in Cambridge discovered a process that drives a “catastrophic” change in the composition of blood in older age, increasing the risk of blood cancers and anaemia, and impairing the effectiveness of white blood cells to fight infection.

The scientists believe similar changes occur in organs throughout the body, from the skin to the brain, potentially underpinning why people often age healthily for decades before experiencing a more rapid decline in their 70s and 80s.

“What’s exciting about this work is there may be a common set of processes at work,” said Dr Peter Campbell, a senior author on the study and head of the cancer, ageing and somatic mutation programme at the Sanger Institute in Cambridge. “Ultimately the goal would be slowing or intervening in the ageing process, but at the very least we see an option to use this to measure biological age.”

https://www.theguardian.com/science/202 ... -their-70s
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Study confirms benefit of supplements for slowing age-related macular degeneration
https://medicalxpress.com/news/2022-06- ... ation.html
by National Eye Institute
The Age-Related Eye Disease Studies (AREDS and AREDS2) established that dietary supplements can slow progression of age-related macular degeneration (AMD), the most common cause of blindness in older Americans. In a new report, scientists analyzed 10 years of AREDS2 data. They show that the AREDS2 formula, which substituted antioxidants lutein and zeaxanthin for beta-carotene, not only reduces risk of lung cancer due to beta-carotene, but is also more effective at reducing risk of AMD progression, compared to the original formula. A report on the study, funded by the National Institutes of Health, published in JAMA Ophthalmology.

"Because beta-carotene increased the risk of lung cancer for current smokers in two NIH-supported studies, our goal with AREDS2 was to create an equally effective supplement formula that could be used by anyone, whether or not they smoke," said Emily Chew, M.D., director of the Division of Epidemiology and Clinical Application at the National Eye Institute (NEI), and lead author of the study report. "This 10-year data confirms that not only is the new formula safer, it's actually better at slowing AMD progression."

AMD is a degenerative disease of the retina, the light-sensitive tissue at the back of the eye. Progressive death of retinal cells in the macula, the part of the retina that provides clear central vision, eventually leads to blindness. Treatment can slow or reverse vision loss; however, no cure for AMD exists.

The original AREDS study, launched in 1996, showed that a dietary supplement formulation (500 mg vitamin C, 400 international units vitamin E, 2 mg copper, 80 mg zinc, and 15 mg beta-carotene) could significantly slow the progression of AMD from moderate to late disease. However, two concurrent studies also revealed that people who smoked and took beta-carotene had a significantly higher risk of lung cancer than expected.

In AREDS2, begun in 2006, Chew and colleagues compared the beta-carotene formulation to one with 10 mg lutein and 2 mg zeaxanthin instead. Like beta-carotene, lutein and zeaxanthin are antioxidants with activity in the retina. The beta-carotene-containing formation was only given to participants who had never smoked or who had quit smoking.
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Saudi Arabia plans to spend $1 billion a year discovering treatments to slow aging

The oil kingdom fears that its population is aging at an accelerated rate and hopes to test drugs to reverse the problem. First up might be the diabetes drug metformin.

June 7, 2022

Anyone who has more money than they know what to do with eventually tries to cure aging. Google founder Larry Page has tried it. Jeff Bezos has tried it. Tech billionaires Larry Ellison and Peter Thiel have tried it.

Now the kingdom of Saudi Arabia, which has about as much money as all of them put together, is going to try it.

The Saudi royal family has started a not-for-profit organization called the Hevolution Foundation that plans to spend up to $1 billion a year of its oil wealth supporting basic research on the biology of aging and finding ways to extend the number of years people live in good health, a concept known as “health span.”

The sum, if the Saudis can spend it, could make the Gulf state the largest single sponsor of researchers attempting to understand the underlying causes of aging—and how it might be slowed down with drugs.

https://www.technologyreview.com/2022/0 ... metformin/
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