What was your weekly dose before? Also what do you mean when you say your kidney function recovered? Thanks!
Rmun
#82
I used to take 6-8 mg a week (I even went up to 20 mg). My creatinine had suddenly risen by 40%, and is now almost back to my initial value.
Creatinine is affected by lots of things as well as kidney function.
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Rmun
#84
I also had oliguria and other signs of AKI.That said, my kidneys were already weakened
40% is a lot. That said rapamycin appears to raise blood serum creatinine levels by 20%.
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As John Hemming says “Creatinine is affected by lots of things”.
I have taken many blood tests over the past 2+ years I have been taking rapamycin.
There is no discernable correlation between my rapamycin intake and my creatine readings.
I’ve been taking Rapamycin for over a year, and my creatinine levels have dropped to just below the lowest point in the normal range. If your creatinine went up, there’s probably confounding factors involved.
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LaraPo
#88
My creatinine was .92, which is a very good number for me. However, it just jumped up a lot, without any changes in rapamycin dose. I blame viral infection and antibiotic that I took.
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There is a relevant discussion here:
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I am glad this thread was started because I’d heard people talking about cycling but I didn’t know why they were doing it.
I had a break from rapa from January through March because I was having trouble ordering online. I restarted in March and have been taking 8mg once a week. I’ve felt no side effects.
However, I just got some blood work done. A1c is 5.2 which was unchanged since the previous test in September 2023. That’s good. Insulin, however, was at 7.0, glucose at 105, total cholesterol at 210, LDL P at 1104, LDL C at 107, all of which represented a significant increase since September 2023. HOMA-IR was up to 1.8 from 0.6 previously. For some reason, HDL C, HDL P, and Trig were unchanged. Haven’t had the opportunity to discuss the results with my doctor yet.
As my diet hasn’t really changed since 2023, I think these changes were probably due to the rapa. And from what I’m reading here, this may indicate mTORC2 inhibition.
As I’ve had 7 weeks on as of last Sunday, perhaps I should do 8 weeks off and then retest my lipids and a1c.
I don’t believe there’s a downside to cycling - we believe this still preserves the longevity benefit, correct?
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KarlT
#91
Maybe another question for Matt K. I doubt anyone knows for sure. Some have certainly questioned the need for chronic use. Who knows maybe a couple times a year is all we need?
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LOL. Who is the control? I remain unconvinced regarding the value of case studies. My dad is alive and riding a bike at 99 (although he is unsure where he is going). If he started Rapa at 90, he might, erroneously, attribute his longevity to this intervention.
This old-school evidence-based MD continues to believe that RCT’s are the only way to demonstrate efficacy. We keep making the same mistakes in medicine.
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KarlT
#93
@SteveRoedde1 Great point. Too much trust in n of 1 here. We should change our thinking to causation vs correlation vs total coincidence.
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The key is always replicability. N=1 becomes reliable if there is enough replication. As far as I personally am concerned I try out things to see first if there is any harm and then I try to identify any effect - given that I am doing a lot of testing.
In the broader sphere of things my objective is improved health. If some of the interventions are having no effect I am not particularly concerned although over time I intend dropping some interventions to find out the effect of such a change where sensible.
Because the choice of an intervention is in the end binary (intervene or don’t) although there are choices as to timing, dosing, cycling etc the final test is in the round.
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@KarlT I agree. My thinking is continuing to shift to using a few fundamental interventions that will have big downstream benefits. At the same time I am moving way from a swarm of barely understood in isolation (and not at all in aggregate) interventions that address symptoms.
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IMO: Your dad has good genes and didn’t do anything lifestyle-wise to shorten his lifespan.
For instance, I would like to know if your father has a genetically low APO A.
These conditions are major contributors to mortality rates, and a lower risk could potentially contribute to increased longevity.
“Studies have shown that individuals with low APO A levels and, consequently, lower HDL cholesterol levels may have a reduced risk of developing cardiovascular diseases, such as heart attacks and strokes. These conditions are major contributors to mortality rates, and a lower risk could potentially contribute to increased longevity.”
Has your father always been on the slim side, indicating a caloric restriction impact on lifespan?
Yes, genes are the major contributor to lifespan, You can do things to enhance this or do things that FIU.
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Your post made me laugh. “although he is unsure where he is going” at 99 years old. Your conjecture, “if he started Rapa at 90”, could also be interpreted as maybe he would know where he is going at 99.
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Hey @SteveRoedde1
I would concur that rapamycin use can improve memory. I was just with my GP physician… today for a 6 month check up. He was very curious about my memory improvement himself.
I don’t know if Alzheimer’s runs in his family or something, but he double checked me when in for my blood panel follow-up at my physical today. Asked ne how the rapamycin was doing on my memory? He said physically my body Is killing it… health and fitness. Told him Rapamycin has really increased my memory and capacity for a lot of things.
Why not start your dad at 90’s with rapamycin and see what happens.
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Possibly. However, that is conjecture, and my point was that case studies (and essentially all “lived experience”), is worthless when it comes to determining causality.
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That’s where I disagree. Enough case studies can give some indication of causality with sufficiently good records.
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