The guy behind novos who I respect seems to think well of rapamycin when it comes to immune system
Why Rapamycin Actually Improves Immune Health and Function
interesting…
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The “daily” dosing would definitely lower your immune system, thats exactly the dosing for organ transplant patients for lowering rejection risk. 8mg/week might also do it a little I suspect. and 8mg may be too high for you, especially if you’re lighter in weight or if, as you are, frequently in less pathogen-free environments (remember, all the mouse lifespan studies are using mice in pathogen-free environments, which is basically the opposite of backpacking and traveling in lesser developed countries and eating street food).
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Oh, I’m not saying he’s wrong. Its just as they say “the dose makes the poison”. It all depends on your dosing (and body weight, individual variations, etc.). At lower doses, pulsed dosing, rapamycin has been shown to improve immune system function. At higher or daily dosing it does function as an immune suppressant.
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Is this based on any human study or just mechanistic speculation on your part because you don’t like statins and are on a keto diet?
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Thanks. Actually, I’m on the bigger side. 6’3 210. I saw a lot of folks taking 6-7 and thought with my weight id top it off. But I agree about the pathogen part. Do you think that its also possible that some of the large stack I’m taking could also assisting in clamping the mtor so I might need less as well?
Ah, yes, some of your other supplements also are on the list of things that might impact your body’s absoption of rapamycin. Also foods… like citrus fruits, can greatly impact the bioavailability. See these posts:
Here: Rapamycin Interactions with Other Food, Drinks, Supplements and Drugs
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Wouldn’t taking rapamycin with olive oil only be best for absorption?
Taking with olive oil (or any fatty meal) should increase absorption by about 30%. “best” is whatever your goal is. If your goal is 3X, then grapefruit is best.
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What biomarkers are you guys recommending?
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I heard that Dr Green tells his rapa patients to keep antibiotics on hand for infections. I haven’t had any infections of any sort.
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That is what all we heard. That is why it is difficult to be really objective about rapamycin. It was used for immunosuppression in transplant recipients and it has remained an “immunosuppressant” ever since. But most studies show that it actually improves immune function (even in healthy humans), but immunosuppressive reputation remains. Matt Kaeberlein said on multiple occasions it should be called immune modulator instead.
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I’m not on a keto diet but rather on Mediterranean diet as I like it and it works for me. Further I’m not against statins for some people in some situations. Every medical intervention is a game of trade offs including statins. The link to the study discussing a role Ldl-c plays in this case of the Covid outcomes with the links to the other studies as well Cholesterol-lowering treatment may worsen the outcome of a Covid-19 infection. | The BMJ
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Hard to get excited about a study that uses the word “may” in the title.
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documented in human studies as well. In a meta-analysis of 19 cohort studies including almost 70,000 deaths, Jacobs et al. found an inverse association between serum cholesterol and mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin (4).
It’s another (bad) association study with the typical U-curve mortality. As always, we have better evidence in the form of intervention trials which show that statins lower all cause mortality.
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There is another meta analysis debating statins and overall impact on the cvd and all cause mortality. The finding is that overall benefits of statins are modest, may not be strongly mediated through reduction in Ldl-c. Perhaps this is due to off the target action of statins? Anyway may is used in the article again as the subject is very controversial. some people are getting on the bandwagon of ldl-c reduction as low as you can go but perhaps some caution should be exercised here as well? contro
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The more important view IMO is not whether statins work or not (and I believe they are almost worthless in primary prevention strategies for a low risk individuals or may even cause harm) but something we all forget about, but has been proven in case of ASCVD and probably other areas as well, that most of damage accumulation happens before many people get interested in longevity, before midlife crisis. If your lifestyle choices were not pro longevity and for that matter LDL-C, BP, blood glucose were elevated trough your adult life up to age 50 you have a really poor chance of undoing this damage and living long healthy life.
The absence of established risk factors at 50 years of age is associated with very low lifetime risk for CVD and markedly longer survival. These results should promote efforts aimed at preventing development of risk factors in young individuals. Given the high lifetime risks and lower survival in those with intermediate or high risk factor burden at 50 years of age, these data may be useful in communicating risks and supporting intensive preventive therapy.
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I believe they are certainly indicated for those with some ckd though right? I have low level kidney disease - IGA nepropathy. But yeah, I also follow attia/stanfield.
Also do the statins differ in the longevity regard? Novos isnt a fan of statin but thought simvastatin in particular extended mice lifespan which is why I choose this one The Anti-Aging Supplements David Sinclair Takes | 2023 Scientific Review.
and fluvastatin may hav a sirt 6 link
If they cause harm, how come they reduce all cause mortality in the trials?
If your lifestyle choices were not pro longevity and for that matter LDL-C, BP, blood glucose were elevated trough your adult life up to age 50 you have a really poor chance of undoing this damage and living long healthy life.
I agree on that at least. If you already have a high calcium score, chances are not even the most radical apoB lowering medication will protect you from heart disease.
There is some statistical reduction in ACM but it is very weak and by that you may need to read my sentence again, since I was mentioning just low risk individuals and primary prevention.
But at least we agree on something!
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low risk individuals and primary prevention.
I would argue the opposite. Statins lower all cause mortality better in those with moderate CVD risk than in patients at high risk.
Among those with moderate CKD, rosuvastatin was associated with a 45% reduction in risk of myocardial infarction, stroke, hospital stay for unstable angina, arterial revascularization, or confirmed cardiovascular death (HR: 0.55, 95% CI: 0.38 to 0.82, p = 0.002) and a 44% reduction in all-cause mortality (HR: 0.56, 95% CI: 0.37 to 0.85, p = 0.005).
The use of statins in this high-risk primary prevention setting was not associated with a statistically significant reduction (risk ratio, 0.91; 95% confidence interval, 0.83-1.01) in the risk of all-cause mortality. There was no statistical evidence of heterogeneity among studies (I 2 = 23%; 95% confidence interval, 0%-61% [P = .23]).
Those results are in line with your “start early” approach. Once you’ve developed heart disease, diabetes etc. it’s hard an uphill battle for longevity even on radical interventions.