I think it is useful at times to look at what may be acheived by a particular biological function. I think senescence is a tool the body uses to prevent cells which have bad mitochondria and hence running the risk of being cancerous or otherwise functioning badly from getting fully differentiated and become somatic cells.
I think the fact that senescent cells are found moreso where cells are rapidly dividing means it is quite likely that the proportion of senescent cells in the category I have identified is quite high.
However, we don’t have any information to define the proportion. You, therefore, are welcome to assume it is low and look for other tools. The interesting question with macrophages is to what extent they may solve the issue through and exchange of mitochondria.
However, this remains an area with considerable uncertainty.
I thought I would see what I could find out about IVDD and whether these senescent cells would fall into the category I have identified. A symptom of this is bad mitochondria.
Here is a chatGPT(5.5paid) answer to the question:
when cells are senescent in IVDD what evidence is there that their mitochondria are damaged
Conclusion
The evidence is strong that mitochondrial dysfunction is a major feature and likely driver of nucleus pulposus-cell senescence in IVDD. The best-supported abnormalities are mitochondrial depolarisation, excess mitochondrial ROS, fragmentation or cristae damage, impaired ATP-generating machinery and defective clearance through PINK1–Parkin mitophagy.
The narrower proposition that every naturally senescent cell in a human degenerating disc contains damaged mitochondria remains incompletely demonstrated. The strongest current interpretation is that mitochondrial damage characterises an important subset—probably a large subset—of senescent disc cells and can both initiate and maintain their senescent state.
I’m not fond of your personal senolytic protocol (I think its way too long, bigger then tested protocols, and it includes very questionable substances like EGCG in enormous amount of 3g, when 800mg considered hepatotoxic. Licorice extract can even cause arrhythmias. Other substances also have their downsides. Too noisy, Q + F + EVOO + piperin seems enough). But I am completely agree with your main idea that senescent cells should be eradicated if possible, as if we do not have 100% effective way, then some of them will rest, and it will be enough for their beneficial (possible) effects.
We all have to remember and not forget some general ideas of late M.Blagosklonny and A.Green when they spoke about aging, and about Dawkins idea of genocentric evolution from his book “The selfish gene”. Nothing in biology (including senescens) is oblige to be beneficial for an individual. Maybe some things (including senescens) IS DESIGNED to kill us, to limit our years to give younger people space to live and breed.
So no need to claim every biological process as beneficial “as it exists because this is how evolution works, and every thing has its purpose”.
Maybe this purpose is to kill you right after your fertility is lost.
Interestingly 4 test subjects over a 7 month period had positive results with 3 cycles. I’ve posted those results.
With regard to the EGCG 2,850 mg (depending on body weight) is for 3 days on 4 days off 4 times in 1 month. This is an acute dose, not chronic use. Yes it is very high and pushes the safety limit and that should be taken into consideration. My personal blood work showed zero liver chemistry issues over 4 years of doing this 4 times a year. Same for the 4 test subjects who did 3 cycle’s in 7 months.
The other compounds, high dose for short periods, acute use, not chronic.
This type of high dose cycling is also used with our fav drug Rapamycin. With many pushing their dose to the point where they get immune suppression symptoms like mouth sores.
Also the quercetin dose is based on the fact the initial 2x Phase 1 studies used a liposomal form (Thorne) that is 10 to 20 times more bio-available than regular Q. This fact is often missed when people think 1250mg (as the dose indicated in the studies) is all they need for Q to be a senolytic when the study dose would be 12,500 to 25,000mg of typical Q at 98%
I’ve read many follow on studies by other researchers doing D+Q studies and NONE of them seem to caught on to this nuance. This means their results are compromised by under dosing Quercetin.
Having said all that I’ve moved on to FOX04-DRI as it covers more than just epithelial and adipose derived senescent cells as the D+Q protocol is limited to.