Can statins be pro-healthspan/longevity even if they don't increase mice lifespan? How do they interact with metformin/rapamycin/other geroprotectors?

Mice just don’t die of heart disease like humans - this is why ITP went negative on them (even though, like, they were harmless). Humans uniquely have high LDL levels… My impression (I’ve seen a lot) is that statins are on the marginal pro-longevity, but with very small effect size in the ultra-healthy

The main concern is that statins reduce Coenzyme Q10


My intuition is that the effect size becomes larger the longer you live & the length of statin use.
It’s a given that everyone develops advanced ASCVD in older age, you can search for statistics on positive CAC scans. It’s above 90% for those above 70, which means ASCVD has been developing for decades.

Since that is a given, increasing the time to positive CAC means delaying ASCVD. If you do not delay ASCVD, it will bottleneck your longevity. So it is synergistic with other longevity drugs.

If 30 mg/dl apoB is hypothetically the cut off point, you will never develop ASCVD, so you don’t have to worry about the bottleneck. If it’s below 60 almost likewise.


Do mice die of cardiovascular disease? If not, then longevity studies don’t apply to statins.

Statins can also cause calcification, which is not favorable for longevity

I take Policosanol before bed and it seems to improve nighttime cortisol issues - although this is based on observed symptoms not any actual testing. It’s my “statin” and I then supplement with COQ10.

Interesting, that might be the mechanism of plaque stabilization, after all events reduce and all cause mortality decreases in people with a high chronological age who take statins. I’m not sure what that would do in people without ASCVD (positive CAC), yet.

However I don’t think those types of studies showing calcification is based on study designs which can assess causal relationships, “cause” is a very strong word. Unless you have one that does?

I thought this was interesting

Thanks, I’m not sure how that applies for people without lesions, and for those that do, is it really a bad thing?

I would rather reduce plaque and prevent calcification - I think Zetia + PCSK9i is going to turn out to be a superior treatment path over statins

They still reduce events, etc similarly as any other treatment IIRC, so I’m not really certain it is a large problem. Outcomes > mechanisms. Since outcomes are positive, and similarly to other treatments, correct me if I am wrong, then it suggest it is a beneficial effect if it exists (stabilization of plaques).