It comes down to the question as to where they come from. I think a lot are stem cells that are stuck in partial differentiation.
1 Like
J0hn
#24
I wonder if you could measure beta-galactosidase in plasma and whether that be a surrogate marker for the number of senescent cells in the human body ?
1 Like
Go for the non infected level of CRP.
1 Like
nym
#26
thank you
Current senolytic approaches are not supported by data in humans and a cause for scepticism
i thinks it’s too early to say that rapamycin is a senolytic. there is some evidence that it may block establishment of senescent phenotype but obviously that’s a hard thing to prove in humans. my bet is that it will have an indirect effect on senescence by rebalancing the immune system and allowing clearance. in my case, however, my immune system is already optimised so i need to work on lessening induction of senescence rather than improving clearance.
4 Likes
This comes back to the mechanism question. Apart from replication senescence what causes senescence? I think most is cells failing to differentiate.
1 Like
@nym Could you expand on your top methods for preventing senescence (supplements/medications/therapies)? This is an incredibly interesting topic and we are all very thankful for your expert opinions.
3 Likes
Here’s an interesting paper on the causes of senescence:
“Senescence can be triggered by oxidative stress, telomere damage/shortening, DNA damage, mitochondrial dysfunction, chromatin disruption, inflammation, epigenetic dysregulation, and oncogene activation…”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610675/#:~:text=Factors%20leading%20to%20senescence,17%2C%2025-27).
1 Like
@nym Thank you. In particular, thanks for the reminder that this is a two part process: improving the immune system to support clearance and reducing creation of senescent cells.
How did you “optimize” your immune system? I recall you used rapamycin. Anything else you think useful besides the basics: gut health, staying below a personal fat threshold, solving nutritional deficiencies, etc.?
Since senescent cells can cause other cells to become senescent, there’s a compounding effect that goes both ways. Making fewer while taking out the trash should make a big difference. What are the biggest levers in the long list of causes of senescence? Reducing oxidative stress / mitochondrial dysfunction (I hope since this is what I’m working on for myself)?
1 Like