Why doesn’t it reduce cardiovascular death? If it reduces all the other things you would think it would reduce death. Also I didn’t see anything about all cause mortality.
But I’ve been taking it every day and I had tinnitis years ago, it went away, then since the explosion it has been driving me crazy. After just a few weeks it seems to be gone. It does something.
How many weeks of colchicine use resulted in relief from tinnitus?
This would seem to suggest that rapamycin, with its strong effect on systemic inflammation, would also likely reduce risk for cardiovascular disease…
From the Eric Topol substack article:
“We have known for many years that inflammation is a major driver of atherosclerosis and atherothrombosis (plaque + clot). There are now simple ways to measure body-wide inflammation, coronary artery inflammation, and many ways to reduce inflammation, including lifestyle modifications and inexpensive medications. But none of this has yet been incorporated in routine medical practice. In this issue of Ground Truths, I am going to review the body of evidence for taking inflammation seriously and what ought to amount to a rebooting of our approach to heart and vascular disease”
It looks like 4 weeks, but I noticed relief after 2. I skip a couple doses around Rapa because GFJ, though I doubt it’s necessary.
I’ve always thought it was from years of driving open top tractors without any PPE. When earplugs came out it was amazing how they cut down fatigue. Fatigue just caused by the constant noise…
Last week you shared a link to a study about inflammation. I ran it down and looked at a table that showed the importance compared to several other things. It was a marker I hadn’t seen. Started with O maybe. I can’t find it with the search, do you have any Idea what I’m rambling on about?
Are you talking about this post? The Anti-Rapamycin: Increasing mTORC1 Accelerates aging and inflammation
without clinical studies I don’t think you know.
A given therapeutic can likely do multiple things, some of which are helpful, some of which are unhelpful, and without clinical trials you can’t tell whether it all balances out to be a net positive or net negative.
That was an excellent read! Thx for sharing.
Has anyone seen anywhere one can do this test:
Besides the blood marker hs-CRP which costs less than $30, a new, large study using CT coronary angiograms (CCTA) shed light on another means that is more direct. The fat surrounding each of the 3 coronary arteries (a fat attenuation index, FAI) can be used to determine the presence or absence of inflammation
Well it depends. If the rise in LDL is small but inflammation is strongly reduced as is the case with the various SGLT2 inhibitors, it probably doesn’t matter. If LDL is very significantly raised though, that is an issue.
It would also depend on the curve of the raised LDL - if its only raised during a specific/short period after dosing that is one thing, if its continual thats another… lots of variables. I think @AnUser tends to oversimplify things sometimes. These are not simple black and white issues. As with many things… it depends…
Good article, but unfortunately no. I know I had to click on a link, run it through sci hub and the study was really good, but I was in a hurry and lost it. Getting old is a bitch, but no worries. Thanks,
@AnUser But we can control Apo B well
So someone aggressively controlling
Apo B may be better of lowering inflammation via rapa - as long as they offset any change in Apo B and stay highly Apo B controlled
@RapAdmin - having said above, there are different types of inflammation, have you seen data or anecdotes on rapa lowering hs-CRP (marker in the cvsd inflammation trials) - I think it was not lowered in the marmosets
Define “best drug”…
For the 65% of the people that didn’t get hypercholesterolemia - are you saying its a bad drug for them also?
And given in this clinical study it was for daily dosing, what exactly was the curve of increase in LDL in the group that did see increased lipids? I couldn’t see much information on this in the study.
It wasn’t lowered in the marmosets, but Adam said they have a tough time getting measures for marmosets that are equivalent to human measures (its not like they can just take the marmoset blood to LabCorp and do a typical HsCRP test on it). So he didn’t put much value in that measure. He’s reviewing the interview audio recording now and I’ll post it again when he’s finished.
I have no idea - I’ve not seen any clinical trials on this. I wouldn’t ignore it, but I wouldn’t assume its automatically a “net negative” at all doses of rapamycin, in all people, in all situations.
@RapAdmin do you have any sense from anecdotes or from any of the human rapa trials if hs-CRP goes down, such an easy and common test that perhaps we know the answer on that part in humans
I would argue that we are not trying to give recommendation to people here, we are each trying to find the best solutions for our bodies. We can test LDL and inflammation, and many things and adjust course as need be.
Nobody here is suggesting rapamycin, or any drug, is good for everyone. What were are looking to do is to identify good potential therapeutics for ourselves, and then we must test and validate that it is in fact working; this goes for statins, rapamycin, or any other drug.
I think it is highly likely that someone has sub-optimal Apo B levels will get CSVD - whether on Rapa or not
I’m not sure how much s small bump in Apo B can be offset by large bump down in inflammation but would expect some form of exchange rate for anyone who is not at the very extreme low end of Apo B levels
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Do you agree with my statement
So someone aggressively controlling
Apo B may be better off lowering inflammation via rapa - as long as they offset any change in Apo B and stay highly Apo B controlled
I’ve not looked at this at all. It would be interesting to see - and I think you need to look at a wide variety of inflammatory markers, not just hs-CRP.
A broad battery could be good and better, but do not at all think it’s necessarily needed
For instance, for the sake of CSVD hs-CRP seems to have been the main marker in the trials (see the Eric Topol write up on the most recent of the now six choline trials).
And importantly, since hs-CRP is cheap and part of the Levine Age calculator if I recall correct a lot of healthy people on rapa probably have hs-CRP data even if they do not have IL-6 are other inflammatory measures.