1 year anniversary - time for some objectivity?

Hahaha… damn you are like a dog with a bone Maveric. Won’t let go. Youth. Lol.

However, was on TRT with only muscle growth… function for a full year plus .There was ample time for TRT to do more… it leveled at 6 months…

Functional decline issues started improving only 3 months after starting with rapamycin. And, has continued. Probably my N=1 gets a meh… not gobsmacked! Hahaha.

Those 50 or older get it.

The combo of Rapamycin/Acarbose/Cypionate seems to be great for 60+.

Just might end up dancing on your grave… lol.

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One positive effect that I have experienced that is not subjective is the dramatic reduction of actinic keratoses. This is probably due to the anti-cancerous effects of rapamycin.
I haven’t had to see my dermatologist in almost two years. Previously I was seeing my dermatologist every few months for treatment.

The complete elimination of age-related “essential tremors” is hardly subjective and was not the result I was expecting.

The other could be considered subjective, but I don’t think so, the complete reduction in arthritic pain. Honestly, I wake up in the morning and go about my business, and think “What the f*ck! How can I be 81+ years old and be pain-free?”.

As you can see my “results” are mainly concerning age-related problems.
Rapamycin isn’t going to fix anything that’s not wrong.
I think younger people just have to have faith that it will certainly increase their health span, if not their life span.

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We could all show our objective lab values but it would mean little as we are not interested in improving lab values but in living healthier and longer and there is no data that rapamycin will make humans live longer but even if we accepted lab data as some sign that rapamycin is working(*), we are just to uncontrolled to draw any conclusions

(*)and even in the lab animals if we were to look at their blood results we would not be impressed, they appeared to be unhealthier like us (higher blood glucose, triglycerides and ldl) yet they lived longer. One of the more remarkable objective findings in mice was that older mice started on rapamycin actually improved their cardiac function significantly, their heart was in a better condition when they died than when they started rapamycin. Something we maybe could test (with the polar or other wearable fitness tests?)

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I agree with this generally, but one of the difficult things we face right now is what are the “right” measures, and what are “good” results? What is the “wrong direction”?

I think we need to talk with researchers more. For example - from what I’ve read, it seems that mice live up to 28 % longer on rapamycin despite glucose and lipid disregulation. Does this mean that these numbers are less important than some other factor in terms of the longevity increase? If we looked only at the mouse lipid and glucose measures we might conclude that it is “failing” to improve things, while at the same time the mice are living healthier and longer, with fewer diseases.

Talking with Matt Kaeberlein at the Longevity Summit the other week, he thinks that any increase in blood glucose level responsiveness to carbs is a good thing… it probably shows that the system is functioning well, just like what you see in people who are fasting or eat carbs after caloric restriction (he puts himself in the Blaggosklonny camp in this area).

I also talked with Tim Peterson who studied MTOR in the Sabatini lab and is now running a Washington University lab (and helping run VitaDAO), and his opinion was that high glucose levels might be a good proxy for mTOR2 inhibition (so a CGM might be a good way to track potential immune system depression). Matt K. disagreed with this.

So while I’m all for measuring outcomes… its really unclear to me right now what the optimal measures are. Its something that I think we and the researchers really need to figure out.

I was recently talking with the National University of Singapore medical team that is starting a rapamycin trial in early 2023 in people as part of their new longevity clinic. They also are struggling with these issues… their IRB is asking questions like "what do you do if blood glucose levels or lipid levels rise above recommended clinical levels? What are the cuttoff points for changes in these levels for excluding someone from the trial? Do you add metformin, or lipid reduction agents? … How does that impact the interpretation of the trial? Nobody has great data-based responses to these types of questions yet.

Everyone is grappling with these issues right now.

So - I wouldn’t get too critical on any of the users here about their approach or interpretations. Everyone is all over the map still.

That said, I do encourage everyone to measure blood results frequently so we at least understand what is going on in our bodies. Over time we’ll figure out what the right measures are.

And if results are not to what you think they should be, take a break from rapamycin.

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No rapamycin studies in identical twins that I’ve ever heard of. But an interesting idea!

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Just following on from Arhu, in another post I spoke about an echocardiogram I had earlier this year. It showed slightly reduced systolic function in the left ventricle. At that time I was not taking Rapamycin.

I’ve been on Rapa now for three months and intend getting another echo at some stage early 2023. It will be interesting to see if there is any improvement.

Either way, I will share the results with this community.

I also use InsideTracker and will get my first ‘on Rapa’ blood draw in a few months time. Will share some before and after data…….

Echo Post - Echocardiogram before and after Rapa

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Lab reports show marked improvement.
I have taken rapamycin for the last fourteen months. I agree with the comments re. the paucity of measurable markers for physical changes. However,I have had several lipid panels done since I started taking rapamycin and my results are remarkably better than they’ve ever been. My doctors are amazed that a 78yo male is in great condition. Many variables can affect these outcomes including diet and exercise, both of which I am diligent about on a daily basis.

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Since there isn’t really good evidence for rapamycin, that uncertainty plays a role in your risk vs. reward analysis. The downside risk at dosages weekly seem minimal to me as @Arhu says, mostly possible immune suppressant effects, so the other factor is cost of treatment.

You can calculate how much rapamycin will cost you for many decades, and guess what the chance is for a healthspan or longevity benefit, your own based on your own uncertainty and because of that the expected value. For example, a 20% chance of 15 yr longevity increase is an expected increase of 3 years. Will rapa cost you more than 3 years of wages? Of course this doesn’t measure healthspan, you can do a similar calculation for this.

It’s a start, and maybe I’m going about this the wrong way, and you might think differently.

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The question with dosing frequency is the proportion of time for which mTOR is inhibited, because of the 60 hour half life it is quite a high proportion of time.

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I agree with MK here. The increase in glucose probably just shows that the rapamycin is working as it should.
As far as cardiovascular disease, we have the rabbit study showing prevention despite lipid elevation.
I haven’t seen evidence linking blood glucose to immune suppression with rapamycin. In fact, it’s becoming difficult referring to rapamycin as an immune suppressant.

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This is from Dudley Lamming, et al, the hypothesis that many of these effects (blood glucose/lipid disregulation and immune suppression) are due to mTORC2 inhibition.

I was talking with Tim Peterson about trying to identify an easy proxy for immune suppression that we can identify to minimize risk. His thought was blood glucose disregulation, but Matt K. didn’t agree.

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5 1/2 years ago I started off at just 2 mg’s per week and almost immediately my glucose went up by about 10% and hasn’t changed since.
Hard to believe that it was from TOR 2 inhibition at that dose and such a short time interval .

Equally hard to believe that I was immunosuppressed at 2 mg’s per week.

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Hey, I saw you were Dutch because you posted a link of farmaceutisch kompas in an older post. I was wondering how you got rapamycin. Via the GP?

If you could tell me how you did it I’d appreciate it.

via een vriend maar ik zou het zelfs aan mezelf mogen voorschrijven

Hoe bedoel je ook aan jezelf voorschrijven? Via die online artsen die je een recept sturen? Ik probeer het namelijk hier te verkrijgen, vandaar dat ik doorvraag. :slight_smile: Maar anders even op vakantie in Turkije proberen.

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Ik ben arts in ruste en praktiserend tandarts dus mag zelf voorschrijven…

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Are these just random letters? :laughing:

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Just plop them into google translate and find out.

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Dutch is quite close to English anyway so one can make reasoned guesses as to the meanings.

I would like to start Rapam again since my glucose level is back to around 100 but I’m wondering if Acarbose would be more effective than Metformin to maintain reasonable glucose levels. I am pre diabetic , testing around 100/110 fasting

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