An alternative criterion for evaluating a senolytic.
I apologize in advance for my bad English!
Quantifying the effectiveness of senolytics is a task for which methodologies are still being developed. Throughout the years, I have always been tormented by the question of what are the correct criteria for confirming the effect of therapy. I started doing self-experimentation at the age of 37. At that time I had a disease, as a result of which my morphologically healthy sperm were estimated at 0.5 percent according to Kruger. I have tried almost everything known without any real measurable effect for about 3 years. Eventually I resigned myself, and stopped working on the subject. Over the next 9 years, I tried many medications and supplements that are considered promising in terms of prolonging life. I do a lot of lab tests and even have my own equipment. I have improvements in some physiological indicators, but nothing drastic.
The interesting thing happened to me when I started taking imatinib and semaglutide. Along with the subjective feeling that my health was improving, I began to observe things that should not be possible.
Imatinib is a powerful immunomodulator, thanks to which I no longer suffer from rheumatic pain. I haven't thought about its senolitic possibilities. For senolytics I used D + Q + Azithromycin. I use semaglutide instead of metformin because with it glucose control is stricter.
Now my morphologically healthy sperm are estimated at 7% according to Kruger, after 2 years of imatinib 100 mg / day and semaglutide 0.5 mg / week. Such an improvement can be explained by the removal of the defective cells from which the sperm are formed.
Based on this, I think that the Kruger spermogram can be used to quantify the action of senolytics.
I'm not sure what the role of semaglutide is, but I've noticed that the chi effect only works when used together. Unfortunately, I used other things during this period, so the claim about the action of I + S is not scientifically substantiated. Now I have stopped everything but lithium. I will monitor the progress and report to you :)
With respect, Boyan Spasov.
Spasov Why do you say imatinib is acting as a senolytic? I did some light research and found some research papers that says it isnt a senolytic. Dasatanib is of course though, did you mean that?
"Unlike other tyrosine kinase inhibitors such as imatinib, which have been shown to be non-senolytic, dasatinib induces apoptosis caused by addiction receptors such as ephrins by partially inhibiting Src kinase. Fisetin, on the other hand, is another natural avonoid that is considered senolytic with similar effects like dasatinib and quercetin "
Hello Fred! Like you, I did not expect imatinib to be a senolytic.
I started using it for rheumatic pains. I had read many articles about tyrosine kinase inhibitors and nowhere in them did I claim that imatinib could be a senolytic. In several places, the authors almost come to this conclusion, but since aging is considered an irreversible process by modern medicine, some are afraid that their authority may suffer if they make such a statement :)
The reversal of imatinib type 1 diabetes is very similar to that of a senolitic inducer.
Another even more interesting is the farnesyltransferase inhibitor lonafarnib, which has shown the potential to reverse progeria.
I agree that selectively induced apoptosis in the defective cells from which sperm develop does not necessarily mean senolytic activity.
But for now, this hypothesis seems very likely to me.
In this forum, someone had said that they would believe in rejuvenation when they see a 60-year-old who looks like a 20-year-old :) Well, I already believe!
Best regards, Boyan Spasov.