No worries. I edited the above post
And even if we disagree on something, it’s just an open door for a friendly debate. 
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Has anyone used Azithromycin as a senolytic and if so, how did you determine dose?
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Not really, but was looking at it a while ago. The study was done in vitro and in vivo the senolityc concentration is almost unattainable in humas since it could be potentially fatal (8-10g or somethig like this).
There are two interesting things I found that might be worth something. Did not really go into depth but maybe someone here would be interested in studying more.
In the examples of anti-aging embodiments, treatment with this approach was directed over a repeating cycle. The compositions include azithromycin as a first antibiotic that inhibits large mitochondrial ribosomes, doxycycline as a second antibiotic that inhibits small mitochondrial ribosomes, and vitamin C as an oxidation promoter to induce mitochondrial oxidative stress. Including. For 5 weeks, azithromycin was administered at 250 mg twice weekly, doxycycline at 100 mg twice daily, and vitamin C at 500 mg once daily. A 77-year-old man of interest had hair growth, mental cognition and agility, strength and stamina, and increased libido, as well as visual acuity, hearing, conversation, coordination and balance, overall well-being and vitality. Reported improvement. The recipient also reported the disappearance of clinically palpable prostate nodules after treatment with this approach, with no other medications, diet, exercise, and changes in daily life.
This is google translated from a japanese patent application for drug combination. Link to application.
And this study:
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I just googled it now once more and found this link that suggest a much lower dose.
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If senescent cells include those which have failed to differentiate correctly because of a problem with mRNA transcription (which appears likely) then getting them to differentiate correctly should resolve the problem in the main.
This can be measured by the average lowest level of hsCRP (when someone has not been recently infected) which is why that is a guide to mortality.
IMO increasing acetyl-CoA levels (and the best approach I think is exogenous citrate) is the most effective way of getting these cells to function properly.
The alternative and potential additional route is through the use of HDAC inhibitors (such as quercetin, curcumin and rosmarinic acid).
I tend to approach this in both directions at once as well as increasing RNA substrate availability.
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This is a no brainier to do.
“For 5 weeks, azithromycin was administered at 250 mg twice weekly, doxycycline at 100 mg twice daily, and vitamin C at 500 mg once daily”
Will be doing this as quickly as I can get to a local pharmacy to pick up the azithromycin and doxycycline.
I will be using a much larger amount of Vitamin C.
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Keep in mind, you’re taking an antibiotic which has potential adverse effects, including C. Diff diarrhea which you really don’t want.
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I am low on the learning curve on this stuff, but from what I’ve read, most senescent cells come from the natural lifecycle of all cells…most cells begin life, reproduce as appropriate, and are then programmed by their DNA to either 1) kill themselves, or 2) go into the “zombie” state where they stop reproducing, but they don’t die. So, killing themselves makes sense, because you can only replicate for so long before mutations become too likely. Going senescent may make sense if the body needs a certain amount of these to aid in wound healing, etc. However an accumulation of senescent cells over time causes problems, the biggest of which is perhaps too much additional/sterile inflammation.
All this being said, I am wondering if trying to turn a senescent cell back into normal operating mode, which would include additional replication, might increase mutations, and perhaps resulting cancers? I’m sure I’m exposing my limited knowledge of the process. This is just something I might worry about, maybe without reason.
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Nah, my take is kill the bastards/senescent cells. They are no good. lol. some of the stuff you hear in some circles of the longevity ban wagon is just fiction man, so much so that i don’t even pay attention to. Another stupid thing is Davis Sinclair of reversing the clock hahaa, I mean sure I’d like to experiment with things I feel have some beneficial effect, in this case RAPA in slowing down the process, which to me is not even slowing down anything. It is rather allowing our bodies to do the right thing so tha we can live our max biological life span (about 110-130). Anyone that believes they can reverse aging, or make humans live to 300 years, or any of that crazy stuff has been snorted way too much white powder(and I don’t mean rapa powder lol).
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If I had told you 50 years ago you could hold a little rectangular phone in your hand and see and talk to another person on the other side of the world with another phone plus find the answer to any question in the world on a global internet, plus watch movies on your phone, you’d be saying it’d be easier to live to 1,000! Yet here we are.
Never discount human ingenuity.
We’re not living to 300 because we haven’t really tried. Now we are starting to. I’d like to join all of you at your 300th!
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Move along, nothing to see here.
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This is very incorrect. There is a reason they are there in the first place. They do have a purpose. Senescent cells are proven to be very important for wound healing and probably for healing of various other things in the body. Think of them like inflammation. Inflammation is bad if it’s high and chronic, but it’s also necessary for various things and without it you would die.
We can’t right now, but we will be able to reverse aging. I’m not talking in the next few decades or something overly optimistics. But eventually we will. If you don’t think so then you likely haven’t read many studies on cellular reprogramming, which will be one key aspect of doing it.
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My view is that a proportion of senescent cells are cells which are stuck having failed to differentiate (through a shortage of acetyl-CoA). The solution IMO is to enable them to progress from this stage.
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IMHO, senomorphics prevent the formation of non-essential senescent cells. Yes, we need some for wound healing and keeping cancer in check, but the majority of senescent cells can and should be kept healthy and functioning in a non-senescent state. This can be done through Rapamycin, taurine, and other senomorphics.
A good round of senolytics is also handy when your senescent burden gets too high.
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@RapAdmin @DeStrider and @Agetron I’m just back from some summer travels and catching up on these potential senolytics, particularly taurine. I’ve generally been tracking a similar, but smaller, stack and protocol to you all, although senolytics is an area that I’ve found little success, other than potential minor positives from Fisetin.
I’m interested in your views on how long after Rapa, you take Taurine and at what dose and duration? Or perhaps you are taking Taurine daily, if so at what level?
BTW: Alan Green posted a very enthusiastic entry in his blog, https://rapamycintherapy.com/ Just search Taurine! Amongst his views, were these statements.
- The Taurine pro-Aging pathway is now busted. We just need to replace Taurine.
- …regardless of why you think Taurine levels decrease with Age; supplementation with Taurine is beneficial.
- At a later time will have a more detailed section on Taurine; as for now buy Taurine before it flies off the shelf. Taurine is very cheap and very safe.
Alan is a very good bloke but clearly likes a little hyperbole when he’s excited.
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Taurine is a senomorphic which is better than a Senolytic because it prevents cells from becoming senescent. Mouse studies have shown taurine supplementation much more effective than dasatanib+ quercetin in mice.
I take 6g of Taurine daily in my afternoon coffee. Based on the research, it’s a no brainer for those 45+ yo.
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GREAT… been talking taurine… 6 grams in my morning coffee.
Definitely feel great… gym recovery fast… within hours.
Best.
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I’ve had too many changes to know the cause but I am recovering faster from resistance training since starting taurine. I don’t find any sleep benefit however.
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The more I read about Senolytics the less enthusiastic I am about killing scenescent cells. I think it best to restore the immune system function to let it work the way it is supposed to work. It knows what to do better than I do. I’m happy to be using rapamycin (and fasting, protein cycling, etc) to restore my on/off cycles of growth/autophagy. The immune system is one of the areas known to be improved by rapamycin.
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It is the same process, you try to slow down senescence with autophagy stimulation (e.g. fasting, rapamycin etc.) and reduce senescence burden with senolytics. It is a much better approach from both sides. One is preventative and the other is “curative”. Some senescence is necessary, too much senescence drives your sterile inflammation which is driving autoimmune and age related diseases.
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