Exactly. This tracks with the impact of CR on fertility. It suppresses it, but preserves it longer. The net effect is slower aging and longer lifespan. Which is why I was wondering if calling this suppressive effect “aging” is accurate.

The analogy is to a candle. You need a big flame for it to throw enough light to see - being fertile. When the candle is at the end close to burning out - aging - the light level drops and it’s too low to see - infertile.

But now you find a way to keep the flame low - CR, rapa - even though it’s still the middle of the candle - too low flame to see - infertile. It seems/looks just like the low light at the end of the candle, old age, so it looks like “hey, it’s made it age faster!”. But really what is happening, is that by keeping the flame low - slowing down ageing - the candle lasts a lot longer - longer life - than a candle that is burning fully and so burning out quicker. And so it preserves the potential of going full flame - fertile for much longer, and when you want a bigger flame - fertility - you STOP the CR, rapamycin and now there’s enough light to see, long after the other candle has burned out. CR and rapamycin might preserve fertility longer this way, but of course if you want to reproduce, you must stop the CR, rapamycin.

CR prolongs life, preserves fertility longer, but to achieve reproduction must be stopped at that moment. Which is why we say that CR slows down aging and prolongs life by trading off reproduction. But it would be factually incorrect to say that CR accelerates aging of any tissue - it does the opposite, it slows down the aging, including reproductive capability.

If rapamycin is a CR mimetic in this respect, it’s possible that exactly the same thing is true of the effects of rapamycin on fertility. One way to test this is to see if fertility bounces back after stopping CR/rapamycin. We know it does for CR in animals. Does stopping rapamycin bounce back all the biomarkers associated with fertility in humans? That could be a big clue. Keeping in mind that as we saw in mice, the effects of rapamycin persist for quite some time after stopping use. So it needs time.

That’s the hypothesis. It might be wrong. It might be that in fact rapamycin hastens aging in humans. We don’t know, because unlike in animals, we have no adequate studies. That means we are gambling. Looking at the totality of the evidence and arguments, some of us walk away from rapamycin, and some take it. I’m gambling that it’s slowing aging, so I take it, but I might be wrong. Which is why I have never advised anyone, nor would I advise anyone that they take rapamycin - it’s a gamble. All I can do is explain why I take it. What you do is 100% your decision.

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Thats a fair position to take. I have my own views as to what aging/development is. Obviously I think I am right, but I have to accept I may be wrong.

Hence I come to conclusions as to how best to act in the circumstances. Anyone else can take a different view.

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I was in the Ageless RX Pearl trial that ended last year. To be considered for a candidate you had to be within a certain age group. I’m 77 so was maybe 75 when I first took part in the trial. The idea of taking low dose Rapamycin is to keep a person healthier as they age. Someone at your age wouldn’t have been allowed in the trial. I was taking 15MG of the compounded form of Rapa and was just offered a chance to increase it to 20MG starting next month. I bike ride, and hit Planet Fitness at least five times a week. I do have Arthritis but overall my health is good.

Video of the trial results. It appears to have benefited women a little more then men.

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Hi! I believe 6mg/week of Rapamune is a very substantial dose. Late Dr Green recommended only 2mg/week to people around the age of 40. You might be better off with 1-2 mg every 2-4 weeks in my opinion. At this low dose, you’ll still experience rejuvenation, but won’t necessarily get permanently supressed cell division.

As rapa has ~3-4 day half life, 6mg/week results in very sigificant growth supression. According to a study conducted in Iran, people who’ve had organ transplant only use 8.4mg/week of Rapa on average (spread out daily – Sirolimus Dose Requirement in Kidney Transplant Recipients in Iran - PubMed). People are fooling themselves when they call 6mg/week enteric coated tablets “low dose” – it is not.

We have studies that suggest Rapamycin can interfere with testicular function; naturally it should! But only at high doses.

Same with Brian Johsonson’s experience, he used too high a dose, and stacked too many mTor inhibiting interventions on top of each other (intermetting fasting, vegan diet, CR, Rapa, numerous supplements…). In the end he was looking like a sick cancer patient for the longest time!

So, 1) don’t stack 2) go low dose if you decide to take it at all. Best of luck!!

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ChatGPT also said it will make AMH higher, also you have to keep in mind it also shortened my cycle length which is a typical sign of ovarian age.

I’d be allowed to a trial for ovarian aging, because ovaries die very fast after my age.

Based on your AMH, I understand that you were not in “menopausal transition stage -3a” which was the criterion to be allowed to the ovarian aging trial.

ChatGPT is quite useful at summarising things, but it tends to provide the conventional wisdom. It is probably worth investing some time to find using ChatGPT or a more traditional search engine or another LLM a list of the papers that study this and analyse those.

Just heard from AgelessRX. I didn’t realize at the time how little Rapamycin I was taking. 15MG compounded was maybe 3 to 5 mg. They finally said I can move to 20mg compounded formula which should put me up to about 6mg a week, which is about what the average user is taking. At such a low dose during the trial, I wonder if that was part of the reason there was little movement or results especially for men.

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The trial basically proved that if you don’t take that much rapamycin not a lot happens. The low dosing is almost certainly why not much of an effect was seen.

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