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Stem cell self-renewal with C60

c60 stem cells mitochondria fusion stearic acid aging hydroxytyrosol olive oil mct oil proliferation

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#871 Andey

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Posted 25 March 2019 - 10:17 AM

Reading over "Stem cell aging: mechanisms, regulators and therapeutic opportunities" brings to mind Hector Zenil's work on complex systems modeling.  Specifically, there are systematic approaches facilitating rapid convergence toward predictive models opened up by advances in the application of algorithmic information theory based on sparse datasets.

A simple example would be compiling a dataset of longitudinal measures and experimental outcomes, and constructing stock and flow diagrams to represent various models.  Model selection then consists of measuring the degree to which the models losslessly compress the dataset -- including the models themselves as aspects of the respective decompression programs.  I know this seems alien to most scientists but it is entirely justified as a model selection criterion.  If you think the dataset is impoverished in some way, do the appropriate measurements and add the data to the dataset.

 

 Some seriously smart people amongst us))

 

  If I caught the gist of it, its the same as neural network works - it linearly regresses with training to the most suitable yet the most simple model. I would not say its THE correct way thought as models often fail with new data coming, but its simple and practical, that's for sure.

 

To avoid complete offtopic:

I think there is some synergy with the protocol and hydrogen water. Usually, my HRV plummet the night after leg exercise day. If it coincides with C60 than fall is less pronounced, but when its C60 + hydrogen water than my Oura ring shows completely normal HRV during the night.


Edited by Andey, 25 March 2019 - 10:51 AM.

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#872 bosharpe

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Posted 26 March 2019 - 03:30 PM

 

Proliferation is obtained by symmetric division, whereas differentiation is asymmetric. When I began using C60 back in 2012, I didn't appreciate C60's mode of action, that C60 was stimulating stem cells. If you don't take care to proliferate them, however, you can use them up. In fact, that is the normal situation with aging--

 

 
 
 
There are many causes of aging, but in my view the most central one is the Hayflick crisis that occurs with everyone. Large numbers of somatic cells reach senescence, apoptosis mechanisms get behind, and replacement is limited by depletion of the stem cell pools. So the goal here is to increase both the stem cells pools and apoptosis.

 

 

Yeah, same here. I was too hasty and foolish when I tried C60oo for a short period a few years ago, without this knowledge. 



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#873 jabowery

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Posted 26 March 2019 - 04:04 PM

...
  If I caught the gist of it, its the same as neural network works - it linearly regresses with training to the most suitable yet the most simple model. I would not say its THE correct way thought as models often fail with new data coming, but its simple and practical, that's for sure.

Well, its more general than NNs in that NNs -- particularly recurrent (feedback loops) NNs -- can represent stock and flow diagrams, and vise versa. You can avoid recurrence to first order by resorting to path analysis but that's just to get started toward a recurrent model. You can't really model dynamical systems without recurrence (feedback loops).  

As for new data coming in, data compression operates by prediction. If you can predict the next bit in a bit stream, you don't need to store it. If the next bit is not what the algorithm predicted, then it is stored. That's how you measure how "predictive" your model is with lossless compression.

To avoid complete offtopic:...


My apologies for "derailing" the current thread with a meta issue. Where does this belong?

Edited by jabowery, 26 March 2019 - 04:07 PM.


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#874 Fafner55

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Posted 30 March 2019 - 01:10 AM

Guarente found success in proliferating stem cells and regenerating the gut in aged mice with large doses of NR over 6 weeks. 

 

“Biologists find a way to boost intestinal stem cell populations" (2019) https://medicalxpres...-stem-cell.html
Cells that line the intestinal tract are replaced every few days, a high rate of turnover that relies on a healthy population of intestinal stem cells. MIT and University of Tokyo biologists have now found that aging takes a toll on intestinal stem cells and may contribute to increased susceptibility to disorders of the gastrointestinal tract.
The researchers also showed that they could reverse this effect in aged mice by treating them with a compound that helps boost the population of intestinal stem cells. The findings suggest that this compound, which appears to stimulate a pathway that involves longevity-linked proteins known as sirtuins, could help protect the gut from age-related damage, the researchers say.
"One of the issues with aging is organ dysfunction, accompanied by a decline in the activity of the stem cells that nurture and replenish that organ, so this is a potentially very useful intervention point to either slow or reverse aging," says Leonard Guarente, the Novartis Professor of Biology at MIT.
 
"NAD+ supplementation rejuvenates aged gut adult stem cells" (2018) https://onlinelibrar...111/acel.12935 
The tissue decline due to aging is associated with the deterioration of adult stem cell function. Here we show the number and proliferative activity of intestinal stem cells (ISCs) but not Paneth cells decline during aging, as does ISC function assessed ex vivo. Levels of SIRT1 and activity of mTORC1 also decline with aging. The treatment with the NAD(+) precursor nicotinamide riboside (NR) rejuvenates ISCs from aged mice and reverses an impaired ability to repair gut damage. The effect of NR is blocked by the mTORC1 inhibitor rapamycin or the SIRT1 inhibitor EX527. These findings demonstrate that small molecules affecting the NAD/SIRT1/mTORC1 axis may guide a translational path for maintenance of the intestine during aging.
 

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#875 Turnbuckle

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Posted 30 March 2019 - 08:45 AM

 

Guarente found success in proliferating stem cells and regenerating the gut in aged mice with large doses of NR over 6 weeks. 

 

 

 

Have these effects been noted systemically? If not, it is yet more evidence that NR is digested prior to absorption. As for the 6 week time frame, C60 looked good over the lifetime of rats, but seemed to fade in humans over a period of years, for the reasons that have been discussed from the opening post. So let's please not have NR intruding into this thread. It's a false hope, driven by marketing.


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#876 Fafner55

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Posted 30 March 2019 - 11:24 AM

At the minimum, Guarente's publication shows that significant regeneration is possible and possible pathways involved. But while he mentions the relationship between NAD+ and mitochondrial defects, it is surprising that he doesn't mention mitophagy. Also, there is no discussion of inflammation that may be related to leaky gut. I don't know Guarente's reasons for keeping the scope of this research narrowly focused, but it does raise questions.

 

Contrast Guarente's publication with the impressive regeneration of the gut demonstrated in a recent publication by Longo. With high turnover tissues like the gut, promoting proliferation alone appears to be sufficient to achieve regeneration.

"Fasting-Mimicking Diet Modulates Microbiota and Promotes Intestinal Regeneration to Reduce Inflammatory Bowel Disease Pathology" (2019) https://www.cell.com...1247(19)30181-0  



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#877 Fafner55

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Posted 30 March 2019 - 07:00 PM

Turnbuckle, regarding your post #720, is there evidence that the Hayflick limit can be extended in a meaningful way by eliminating senescent cells? It seems reasonable but I haven't seen published results.



#878 Turnbuckle

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Posted 30 March 2019 - 07:11 PM

Turnbuckle, regarding your post #720, is there evidence that the Hayflick limit can be extended in a meaningful way by eliminating senescent cells? It seems reasonable but I haven't seen published results.

 

The Hayflick limit refers to individual cells. The cellular Hayflick limit can be exceeded by telomerase activators, but I believe it’s generally unwise to do so, as this allows cells to grow epigenetically older than would otherwise be possible. Better to kill and replace.



#879 mkutsen

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Posted 31 March 2019 - 04:01 AM

The Hayflick limit refers to individual cells. The cellular Hayflick limit can be exceeded by telomerase activators, but I believe it’s generally unwise to do so, as this allows cells to grow epigenetically older than would otherwise be possible. Better to kill and replace.

It should be noted that in adults even stem cells have shorter telomers.  Thus they are not capable of as many divisions as embryonic stem cells.  

When inducing pluripotent stem cells the telomers revert  back to the original length.


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#880 mkutsen

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Posted 06 April 2019 - 03:10 AM

It should be noted that in adults even stem cells have shorter telomers.  Thus they are not capable of as many divisions as embryonic stem cells.  

When inducing pluripotent stem cells the telomers revert  back to the original length.

Here are some references:

1. https://www.ncbi.nlm...pubmed/21222203

 

2. https://www.ncbi.nlm...les/PMC2360127/


Edited by mkutsen, 06 April 2019 - 03:10 AM.


#881 Turnbuckle

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Posted 06 April 2019 - 10:54 AM

It should be noted that in adults even stem cells have shorter telomers.  Thus they are not capable of as many divisions as embryonic stem cells.  

When inducing pluripotent stem cells the telomers revert  back to the original length.

 

Embryonic stem cells are the key. The typical progression goes from embryonic SCs Þ adult SCs Þ transit amplifying cells Þ somatic cells.

 

Embryonic (pluripotent) cells weren't known to exist in the adult until a few years ago, and apparently escaped detection due to their small size, and thus they are called Very Small Embryonic-Like Stem Cells (VSELs).

 

This evidence supports that VSELs are pluripotent stem cells that most likely serve as precursors of both mesenchymal and hematopoietic compartments of stem and progenitor cells. 

https://www.ncbi.nlm...les/PMC3159118/

 

Pluripotent VSELs ... were first reported by Ratajczak and group in adult mice tissues ... These are diploid cells with high telomerase activity...

https://www.ncbi.nlm...cles/PMC3586435

 

 

Thus I made these cells the primary target of this protocol, using threonine because that is their primary nutrition--

 

Embryonic stem cells (ESCs) undergo unlimited self-renewal while maintaining a pluripotency, which is defined as the ability to develop into cells of all three embryonic germ layers. ESC self-renewal is characterized by special proliferative and epigenetic properties and a unique metabolic profile. One of the key features of this specialized nutritional metabolism is a stringent requirement for the amino acid threonine.

https://www.ncbi.nlm...pubmed/24232288

 

Mouse embryonic stem (mES) cell proliferation depends exclusively on the nutritionally essential amino acid, L-threonine, in the medium. Other essential and non-essential amino acids need not be added to the medium for mES cell proliferation. 

https://www.ncbi.nlm...les/PMC4206991/

 

 

One could, of course, take telomerase enhancers to lengthen the telomeres of adult stem cells, but they also lengthen the telomeres of transit amplifying cells, and that blocks the turnover you need to reverse epigenetic age as it allows those transit amplifying cells to get epigenetically older than they would normally. Early on I worried about telomere shortening of adult stem cells and added a telomerase enhancer to the protocol, only to see my initial drop in epigenetic age begin to rise again. It was then I realized that you don't want to mess with telomeres in a global sense, as they are the sell-by dates by which potentially old and dysfunctional cells are eliminated.


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#882 Vany

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Posted 17 April 2019 - 07:06 PM

 

2. It is intended as a geriatric treatment, not for young people.

 

 

Hi Turnbuckle,

 

Thank for your great contributions here and for this protocol. After reading this thread I still don't understand why this protocol would not be beneficial for young people (~30-40 yo). Wouldn't it prevent aging by preserving a good stem cell pool ? Can you elaborate on this please ? Thank you !


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