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
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.
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?
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).
I meant only to suggest caution and not contradict any position of the medical profession. Read articles and draw your own conclusions. The fifth article below states “…those participants who took higher doses of statins were 34 percent more likely to be hospitalized for acute kidney injury during the first 120 days of treatment, compared to their counterparts who were taking lower doses. This risk remained elevated two years after starting treatment. The findings appeared online March 19 in the journal BMJ.”
Here’s the relevant part of the article, if we focus on cause-and-effect, which ultimately, all research aim to discover. And what’s relevant in our lives.
The new research does not establish a cause-and-effect relationship between high-dose statins and acute kidney damage, another expert pointed out.
The study is observational, but randomized controlled trials, which are considered the gold standard of research, do not show any uptick in kidney injury among people who take statins, said Dr. Sripal Bangalore, a cardiologist at NYU Langone Medical Center in New York City.
Although the results are surprising, Bangalore said, the reason behind them may have more to do with why these individuals needed such high doses of the statins in the first place. “They may have been in worse shape compared to people who take low doses,” he said.
I think that is right. Personally I think the statin in Red Yeast Rice caused me some issues with memory function so I stopped taking it. My LDL-C is below 3 mmol/L (UK) most weeks anyway.
I think it is clear that the burden of senescence combined with cellular inefficiency has an effect on the function of cells. Personally I think these are the key two things that stop longer genes from functioning as a consequence of the stalling and termination of RNA Pol II. However, more broadly I think there is a consensus that these things matter.
Senescence has an effect on other cells in the body. Hence if one part of the body is starting to function badly enough to warrant an attempt at correction via the use of medication then other parts are likely to have difficulties.
Hence if you select a group of people who are particularly ill they will have a wide range of different medical problems.
There is an interesting question as to whether the changes to cytosolic metabolism caused by statins in itself is pro longevity. I think it is more likely the case that this increases the availability of cytosolic (and therefore nuclear) Acetyl-CoA (to me a key objective of pro healthspan interventions). However, I personally would prefer not to disrupt my cellular metabolism in the way that statins do.
“Yet most physicians and cardiology experts would still insist that one’s thirties are too young to begin to focus on primary prevention of cardiac disease. This viewpoint is directly challenged by a 2018 JAMA Cardiology paper coauthored by Allan Sniderman, comparing ten-year versus thirty-year risk horizons in terms of prevention. Sniderman and colleagues’ analysis found that looking at a thirty-year time frame rather than the standard ten years and taking aggressive precautionary measures early—like beginning statin treatment earlier in certain patients—could prevent hundreds of thousands more cardiac events, and by implication could save many lives.
For context, most studies of statins used in primary prevention (that is, prevention of a first cardiac event) last about five years and typically find a “number needed to treat” (or NNT, the number of patients who need to take a drug in order for it to save one life) of between about 33 and 130, depending on the baseline risk profile of the patients. (Amazingly, the longest statin trials to date have lasted just seven years.) But looking at their risk reduction potential over a thirty-year time frame, as the Sniderman study did, reduces the NNT down to less than 7: For every seven people who are put on a statin at this early stage, we could potentially save one life. The reason for this is simple math: risk is proportional to apoB exposure over time. The sooner we lower apoB exposure, thus lowering risk, the more the benefits compound over time—and the greater our overall risk reduction.”