Rapamycin podcast with physician Brad Stanfield

Rapamycin podcast: In this episode of “Rapamycin Master Series” I interview the physician Brad Stanfield from New Zealand. He has quite recently set up a Rapamycin clinical trial. This trial is a first step in investigating the effects of Rapamycin and if it can minimize muscle loss (sarcopenia) in humans when we get older. In this episode you will understand why muscle is important for longevity and strategies to keep it up. Both my mother, 80 years old, and my father, 70 years old, got problems with muscle loss. It was tough to see them become step by step weak and fragile in life but also that they were not able to shower and go to the toilet without help. So keeping muscle health up is one of the important things when it comes to living well for a longer time in life. This is the big key takeaway I hope you take with you from this episode!

Let’s together also help out to fund Brad’s clinical trial and move the Rapamycin longevity needle. On this page you can find more information on the trial and a donate button at the bottom.

Here is the youtube episode


Thanks Krister. Your videos are highly informative. I have learned something new and actionable in each one.

My biggest take away from this one was to start a statin to lower my LDL cholesterol to 60-70 with 5 mg of Crestor.



I agree, the part with LDL cholesterol made me think little bit extra on that and start to see how I can start lowering things. But I also need to understand more about this topic. I know Peter Attia also have quite aggressive approach in lowering cholesterol but I’m not yet convinced that the lowest values are the ones to strive for. When I interview Peter I will dig into this topic but it would be interesting to also talk to some other experts in the field.

This is for example Blagosklonny’s view with increased lipids when taking rapamycin. I will also talk with him about it later this month.

“Noteworthy, statins can prevent rapamycin-induced dyslipidemia [202]. This benevolent dyslipidemia is caused by lipolysis and inhibition of lipoproteins uptake by the tissues (see Figure 2 in [94]). Dyslipidemia is reversible by itself [64]. Yet, it is easier to combine rapamycin and statins than to prove that dyslipidemia is totally harmless. Statins can “mitigate the fear” of this rapamycin-induced “side effect”.”

Source: From rapalogs to anti-aging formula - PubMed

Is there any great researcher or physician how has a balance view in the topic because I think the topic is more complex then viewing high or average values as bad. I wonder if Thomas Dayspring, Gil Carvalho or Andreas Eenfeldt could be interesting ones to discuss about this in the future. The thing that I would like the guest to have about is knowledge about rapamycin so that we can discuss that in the episode. If someone has a good name please let me know :pray: Probably Peter is the guy.


The interview was really interesting. If I understood it correctly, he proposed to take rapamycin on Saturday and start exercising Monday. What’s the purpose of that? Rapamycin always elevates lipids as we know, so doesn’t it make sense to start exercising right away? I was confused about that part.

My interpretation of why he thought it is not good to combine Rapamycin the same day as exercising is the potential risk of blunting effect of exercise. He thought that it’s probably better to exercise during other days to get most of the exercise. So it’s about optimizing the exercise effect but if we take it the same day then we just don’t get the optimized effect of exercise. Is this a big problem? I would argue that if a person is regularly practicing efficient exercise then probably not but that’s my view.

In this timestamp he mentions the reason for the design of the trial:


Great interview. I really like the bullet points as you go through the interview to help imprint the main points. The lower LDL level are commonly advised when there is established heart disease, but getting cholesterol levels too low can be an issue for maintaining healthy hormone levels that need adequate cholesterol levels ( usually total cholesterol above 140).


Brad didn’t really add any additional insights. You also didn’t challenge him on the study design as I proposed in the previous thread.

I think it might be interesting to do shorter interviews with some of the established members from this site. It would be interesting to hear the rationales for different protocols and the associated results/side effects. I don’t see anyone else on Youtube providing these case studies so your channel would be in a unique space.


Great to hear, David, and thanks for sharing your view on cholesterol. Your view is good aligned with my view but when people have a different view than what I have I really want to understand them to check that if I or they have missed something. My guess is that Peter Attia and Brad Stanfield is seeing something that I have missed. Also the rapamycin physician Bradley Rosén points out something similar in this tweet.


I like that you try to push me to the next level! Big thanks for that :pray: It’s little bit like a training partner who coaches and helps out with lifting heavier weights and taking some extra repetition. So continue with that type of feedback!

Regarding case interviews, I have already started planning on potential peoples to interview. Would you be interested in a case interview and share your experiences in the area?

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What hormone levels and do you have links to these studies?
Common sense tells me this is false, that is not listed as a side effect. :thinking:


What did your doctor think of your LDL in January 2021? It was outside the reference range. I think it was above the 99th percentile. It was/is extremely high. 4.6 mmol/L is probably still around 94th percentile.

The reference values differ between USA and Sweden. If I remember it correctly USA is much harder when it comes to keep for example LDL low. I don’t remember the argument why Sweden differ in this view but they have a reason for this.

This is what was said about my values:

"Your blood lipids generally look good. Your LDL cholesterol is slightly elevated, but your Apolipoprotein B value shows that the particles of LDL cholesterol are large, which is associated with a reduced risk of cardiovascular disease.

Your Apo ratio value is slightly elevated, which is because you have fairly high levels of LDL cholesterol and levels of HDL cholesterol that are in the lower range. A high Apo ratio increases the risk of cardiovascular diseases - but needs to be put in relation to other markers and health factors."

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Ha, I think there are smarter people here than me!

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I don’t think they differ in your case, it is too high even for the conservative/medicine 1.0 system. See the following link in Swedish where 5.0 mmol/L LDL speaks for familial hypercholesterolemia: Avancerade lipidrubbningar – utredning och behandlings­rekommendation - Janusinfo.se

You should def have Thomas Dayspring on :pray:

The most important thing is healthspan/lifespan IMO, not solely have to be about rapamycin.


I add you to the list of potential case report guests. I think you can provide good stuff!

Sure. If you refer to any text book that covers basic hormone production you will see that all hormones come from a base of cholesterol. Advanced lipid testing is a better predictor, but more expensive and not as commonly used.

I agree with this, but on your evidence based decision tree, this would be on the low side. No RCT to support this, but where expert opinion has a value!

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Okay, I’ve already looked previously on this question and for example testosterone decreases by around -3% with statin usage. Just because hormones comes from cholesterol doesn’t mean it is a clinical significant effect.


Yes. My understanding is cells make their own cholesterol. The statins merely improve the liver’s ability to mop up the excess in the plasma. The body has an interesting reluctance to waste cholesterol. This must come from a time when the cost of making cholesterol and the scarcity of food made a difference. Not anymore.


I think you make good points and after reviewing the data on minimal change in testosterone levels with statin use see why you are skeptical.

In a world of extremes where the carnivore diet people are pushing messaging and the plant based diet (with better data) are pushing theirs, it can be confusing for the lay public and even medical professionals. I was hoping to give a suggestion that while it is important to get cholesterol low, that there may be levels that create consequences and considered too low. In clinical practice we don’t always have the advantage of RCT support everything we do. The expert opinions offered at many of the conferences I have attended for over 25 years suggest that there may be a too level of cholesterol and often point the basic hormone cascade as a reason we may want to be careful of going too low.

This site has a great combination of people with all back grounds, but the messaging can get muddy. If a LDL of 60 is great then 30 must be better, or if a Rapamycin dose of 6mg is good then 60mg must be better.

That being said, If I have a patient that has total cholesterol of 150, LDL of 60, normal advanced lipid testing and no plaque on a CIMT or calcium score that is on a statin drug, I would not increase their dose.