Longevity InTime: Autonomous AI Institute. Anti-Aging Digital Health Immortality Transhumanist AI Channel
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Last post from David Sinclair in LinkedIn presenting the Paper *"Loss of Epigenetic Information a cause of mammalian aging"*

“I am delighted to share the latest paper from our lab at Harvard Medical School and from our collaborators around the world.”
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“If we are correct, it means that cancer, diabetes and Alzheimer's might have the same underlying cause that can be reversed to treat or cure age-related conditions with a single treatment. Experiments in the lab are testing this.”
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“Genetic information is the hardware and the epigenome is the software. We think aging is due to corrupted software, that can be rebooted to restore youth.”
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“This week Davidsohn and colleagues showed our exact system extends lifespan in very old mice, when initiated at the human equivalent age of 70-80! I suspect the rejuvenation process exists in salamanders and reptiles but we have lost this ability (for now)”
https://www.linkedin.com/posts/sinclairda_medical-healthcare-work-activity-7019789833485078528-wgXq
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Dear friends: I am organizing a special AMA (Ask Me Anything) session with Aubrey de Grey and his new LEV (Longevity Escape Velocity) Foundation this coming Sunday January at 8:00am (PT), 11:00am (ET) and 5:00pm (CET). Kindly join our live YouTube streaming and ask Aubrey anything you wanted to know. The live session will be in English with Spanish translation as well, so kindly share with your English- and Spanish-speaking friends, please: https://www.youtube.com/watch?v=H9ozWUMGG1E
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Dear friends
I want to draw your attention to the conference:
*Longevity Nation –
Enhancing research development and education for healthy longevity*

March 26-27, 2023

Bar Ilan University, Nanotechnology Bldg 206, Ramat Gan, Israel

This conference will explore the interdisciplinary interrelations of science, technology and society in addressing the challenges of population aging. By bringing together leading voices in the longevity space and public figures, the Longevity Nation conference will strongly contribute to increasing the synergy of science, technology and aging society, and help advance ethical scientific and technological solutions for healthy longevity for the benefit of the entire society. Building on national and international strengths in this area, this conference will help build the supportive national longevity ecosystems and enhance international cooperation in the Longevity Field.

http://www.longevitynation.org/

The registration is at the link below (the attendance is free, but registration is required). The page also includes information for possible support for Vetek (Seniority) Association – the Movement for Longevity and Quality of Life, Israel, the chief organizer of this conference.

http://www.longevitynation.org/register-free-and-donate/

Looking forward to seeing you and jointly promoting research, development and education for healthy longevity!

(And thanks for spreading the word!)

Ilia Stambler
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“Adding 40 Active Years to Each Guest of Yas in Abu Dhabi. Pitch video competition”:

https://youtu.be/zamg8IGcCak

Longevity InTime Founder & co producer of Chef Oleg Teterin applied to Abu Dhabi’s Yas Island competition for a “World’s Best Job” - Brand Ambassador of Yas Island in Abu Dhabi, UAE.

Oleg introduced, as he thinks, the “World’s Best Concept” to make Yas Island the first land where active living 120+ is possible for any of 8 Billion inhabitants!

If you agree that active living 120+ is the most important, please share this message through your network and add this hashtag. We believe that only UAE and especially Yas island can make the dream of all people who want to live as long as possible come true!

May The Longevity Be With You, Yas!

#YasIslandAmbassador
Here is an article that could hang on the banner of immortalists along with, say, SENS:
https://pubmed.ncbi.nlm.nih.gov/23805382/ (2013, 625 citations).
The authors tell how to beat cancer.
What's the problem now? modern detection methods detect cancer when it has ~10^8 cells and 64mm3 volume (well, that's what they say).
Their mathematical model shows that in such a large volume of cells there should be cells whose individual mutations make them resistant to several therapies at once. After treatment, they survive, multiply, and the tumor becomes resistant to the therapy.

They have two conclusions on how to avoid this.
1) fig.3 - the extreme importance of progress in the early detection of cancer. If you reduce the detection threshold from 5mm to 1mm, even modern methods can cure. If there are fewer cells, then most likely there will not be among them resistant to several types of therapy at once. (well, these are approximate arguments on a specific mathematical model, but in general something like this)
2) increase the number (and quality) of therapies in combination so that there are no cells resistant to all of them.

Both conclusions are not just quite mainstream, but probably the main directions in NIH / etc research in general, and receive a lot of funding.

Maybe one of the hottest topics of discussion among immortalists should be how to detect tumors with a diameter of 1mm?
By the way, Batin has a post about defeating cancer - defeating aging https://www.facebook.com/MikhailBatin/posts/4971748182845046 (December 2021).

P.S. it is clear that their model is simplified, and there are all sorts of other theories out there, for example, cancer stem cells, but still, in my opinion, it is more than worthy of being on the banner. Or maybe there are newer interesting works on this topic.

Vladimir Shakirov
💬 Misha Batin

Such strange things with aging

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The problems start from the very beginning. There is no definition for human aging. The most common definition is that aging is something that increases the likelihood of death. It is also incorrect, since it does not say anything about what actually happens to a person.

Intuitively, aging is what makes a young person old. But what?

Some scientists will name the reason - by-products of metabolic reactions. Such a definition does not explain the enormous difference in life expectancy between species. Actually, the theory of aging should explain the difference in life expectancy between species.

It would be nice like this: you load the data of the DNA sequencing of an animal into a computer, at the output the neural network says what is the average duration of the species. Also not a theory yet, but it will become easier to look for a cure for old age.

Here we are faced with the problem of the minimum sufficient information to create a life extension technology. How much more do we need to learn? Is one global transcriptome analysis sufficient?

Any omics research is limited. The transcriptome does not tell us about the functionality of proteins. The proteome does not speak of the compartmentalization of proteins.

Of the dozens of types of post-translational modifications, we have studied in detail the effects of only phosphorylation and acetylation. Ubiquitination, carbonylation, sumonylation, nitrosylation, methylation, butyration, and many others have been studied only on the example of individual proteins.

Let's add microRNAs here, each of which binds and degrades the transcripts of dozens of genes. Thousands, perhaps tens of thousands, of these miRNAs have already been discovered. Finally, there are thousands of genes whose proteins we do not know. We can predict their primary structure, but we have never looked at their function in experiments.

Having finished with proteins, we move on to lipidoma. This is a huge area and also directly related to aging. There is even a lipid theory of aging. Further, the ocean of uncertainty is the metabolome.

That is, now it is completely unpredictable for us: is it enough for us to know about some three effects on mice with a 50% increase in lifespan (for example, a safe epio-rollback) or do we need a metabolic model to create a cure for old age. There are a million intermediate options between these statements.

The difficulty with the aging of living things is that organisms can repair themselves. Aging just consists in second-order errors - repair mechanisms break down. Or they don’t even break, and they have a predetermined expiration date.

That's not all the complexity. The genome itself is immortal. Every cell in our body carries the information of how to be young, can be reprogrammed and create a new organism.

In general, it is a mystery: how can two old organisms create a very young one? This happens for two billion years in a row, and errors do not accumulate.

If the theory of the accumulation of errors were comprehensive, life would cease to exist on earth.

There is no agreement among experts on the relationship between major (age-related) diseases and aging. Is disease a continuation of aging or a separate process? It is logical to think that the continuation. At first we imperceptibly deteriorate, and when it becomes noticeable, we call it a disease.

The question then becomes, why are the R&D departments of pharmaceutical giants looking at different targets than aging researchers? The best specialists are involved in the company, they do not eat their bread for nothing.

That is, most scientists, in fact, believe that aging is a separate process and acts as a risk factor in relation to diseases (I emphasize that we are talking about 18 major diseases of age).

And some researchers say that this is a quasi-process. That is, there is no general aging in itself, but there is aging of organs, and together we see it as aging.
Somewhere in the mid-10s, scientists gave up on the definition of aging, well, they study what they see. It's pretty clear what it's about.

A paradoxical situation has arisen. At any conference on aging, there are 50 reports on various topics, and not a single one, how exactly all processes are connected.