Using HBA1C and LDL to Determine Ideal Rapamycin Dosage

Care to link to those “5 excellent studies”?

I hope you find this entertaining, because it’s never going to stop. :rofl:

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It’s just sad because those people are here in order not to die, yet they keep killing themselves by believing in misinformation about cholesterol. It doesn’t matter if rapamycin increases their theoretical maximum lifespan to 120-130 if they die in their 60s from a stroke or a heart attack.

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I believe that you guys are half right. I believe you need high cholesterol AND inflammation most likely caused by senescent cells to lead to arteriosclerosis. Rapamycin helps get rid of the inflammation although it increases the cholesterol.

Why do I believe this? In Japan they did a study of arteriosclerosis prone mice. Those with senescent cell inflammation had clogged arteries. Those that had no senescent cell burden due to a special vaccine had no arteriosclerosis.

So, if you don’t have the inflammation but have cholesterol or vice versa, you appear to be safe from CVD. However lowering both factors is desirable IMHO.

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I’d expand the biomarker list beyond HDL, LDL and HbA1c to include albumin, CRP, and creatinine:

Albumin, CRP, and Creatinine: Better Markers Of Longevity Than Lipoproteins And Glycemic Status

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Interesting choices. My creatinine went down after taking Rapamycin from about 10% above the lower bounds to just below the lower bounds (67.1 umol/L to 0.75 mg/DL)
Sorry for the different units but they were done in different countries. Would this be the result you would expect?

As for Albumin, it went from 43 g/L to 49 g/L. This is a marked increase although both values are within normal bounds. Would this also be what you expect?

Unfortunately I did not measure CRP, but I will at the next blood draw.

Thank you for your thoughts and insights.

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This is a great study but I wonder if it mostly tells us about markers of longevity for 85+yo people. I left a question on the youtube video asking for clarification (see below). I’m mostly confused about the hba1c marker being a poor indicator of longevity.

“For clarification, is this study evaluating markers for longevity between 85+ yo people? Meaning, if people with high hba1c had already died before 85yo and so were excluded from this study, could hba1c scores stop being a clear marker of poor longevity because those people are not in the study? Otherwise, I’m surprised at the hba1c result in this study.”

When considering that the average lifespan is < 80y for men and women, and that only people > 85y were included in this study (to > 110y), by definition, it’s evaluating biomarkers that may be related to longevity.

Whether these would be the best predictors up to 85y is another story…

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I am glad that my creatinine and albumin levels are moving in the right directions after taking Rapamycin. I believe CRP should too. I have some older data that I can compare with after my next blood draw. Thanks for the informative video! :slight_smile:

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It’s just not statistically significant. Absence of evidence isn’t evidence of absence.

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@DeStrider be sure to keep looking for disconfirming evidence on this point. I think we all need to act on what we think is best but always be looking for more information on the biggest bets. When you go against (regarding inflammation being necessary) what some leading lipidologists are saying on a topic that is the leading cause of death, it’s a big bet. Maybe you are right. What’s the upside and the downside? For me. I’m acting very aggressively on ASCVD, perhaps more than needed. My CRP is 0.19. I hope you are right.

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Statins lower both LDL and inflammation so there’s zero reason not to take them.

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Possible increase negatively in liver markers. And possible increase in Alzheimer’s risk for APOE4 allele carriers.

For PCSK9 inhibitors I would agree however.

And increase the risk of diabetes.

Today is a rainy day and maybe I should have read a good book but instead I was reading 2019 Guidelines on Dyslipidaemias (yeah, I must lead a really sad life, I must do something about that :rofl:) but was in a way negatively surprised that while there are several class of drugs intended to lower LDL-C or TC the only class of drugs that has (strong) evidence for ASCVD prevention are statins. I know this is nothing new, but reading it again in that structured way poses a question. If LDL-C is the main culprit of ASCVD why is not every lipid lowering strategy the same?

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Source?

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The increase in risk is moderate and heavily outweighed by the risk reduction of ASCVD.

Couldn’t someone check for diabetes risk anyway, that’s very measurable? If A1C increases, for example

True, maybe you’re saving someone if you post info about cholesterol.

I wouldn’t take metformin nor Rosuvastatin even if you put a gun to my head :smile:

@Joseph_Lavelle I do believe that keeping both HBA1C and LDL levels in normal ranges is the best bet. Even though I think you need senescent cells and LDL cholesterol to get ASCVD, I’m not willing to bet my life on it.

Also it’s just a hypothesis right now posited by a Japanese university cardiologist. The data on mice he experimented on with his team is incredibly promising. Although I think the reduction of senescent cells as a treatment is still too fringe for mainstream doctors to embrace.

Unfortunately statins don’t work for me. So, I’ve got to find another way to lower my LDL.

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