The key to disentangling the divergent views in this discussion - all well reasoned - boil down to perception of risk.
We are all perceiving the different risks in different ways in a situation where there is no “riskless” conclusion. Every choice presents a risk.
As I stated before, I’m not anti-statin. If I had any evidence of progression of CVD based on testing then I would be aligned with your view. Statins/Ezetimide/Bemp Acid are all well-understood meds with solid treatment histories. If you have a KNOWN PROBLEM, then the prudent thing is to treat it given the quality of what’s currently available.
The question is what you should do if you know based on testing that you have no problem, or if you’ve never tested to determine if you have a problem?
Certain members advocate “crushing it” based on results from large population research without first testing to know what’s happening in your N=1. I disagree.
I happen to fall in the camp of having tested with no meaningful CVD - and certainly no progression - since I undertook testing. In fact, my hard plaque has reduced slightly between tests, but the amount is so small to begin with that it could just be a rounding error.
Given no meaningful CVD (possibly even declining) at age 65 based on multiple tests, all with reasonably high accuracy (despite claims in this thread to the contrary), what is the smart path forward??
The answer depends on your perception of risk for each choice, exactly as first stated at the beginning of this answer.
My belief is our current understanding of human biology will look somewhat close to the stone-age in not so many years given the rapid pace of learning. Humans have a peculiar characteristic of believing we know more than we do. Our egos mistake the vastness of our knowledge (particularly when highly educated) as definitive because we’re oblivious to the vastness of our ignorance. We only see what we know. The outliers in research results are constantly showing us how little we understand. FAR, FAR, FAR more remains unknown than is known. And every new breakthrough over time further reduces risk.
So my view is to not monkey with anything that isn’t broken (based on testing) because each treatment has multiple systemic impacts. If my CVD is actually zero to slightly in decline at age 65 based on testing, then it’s reasonable to conclude my risk of death is most likely to come from trauma or cancer, not CVD. I’ve almost died skiing, mountain biking, road cycling, severe heat stroke crossing a desert, and more. It’s almost unbelievable that I’m still alive given how close I’ve come to death multiple times. CVD is low on my totem pole of risks.
To further minimize the already very small CVD risk, I can repeat the CTCA test every three years to monitor any changes, as well as track my blood markers annually for any meaningful change. Again, all the above are improving right now, so there’s no prudence to “treating” a non-problem that’s improving without intervention.
Others in this thread see it differently. They view taking the meds as “preventative,” but what are you actually preventing if there’s no evidence of disease for your personal system?
The next question is what is this preventative protocol doing to other aspects of your biology? Advocates would claim it’s fully tested, and the risks are known. I disagree. I think the risks they currently measure are known, but far more remains unknowable. If the drugs are powerful enough to “crush it” on the lipids, then it’s reasonable to assume there are powerful systemic effects because everything adjusts to this influx of drugs and changed composition. Nothing happens in isolation in a biological system.
My views is shaped by two applicable sources of experience:
(1) My adult lifetime spent developing systematic trading and risk management models for the financial markets (another dynamic, complex, interdependent system). I’ve seen many really smart, well-educated, well-reasoned people (like those in this thread) blow up entire portfolios time and time again because they thought they knew more than they did. They failed to see the risk of all that they don’t know, and all that remains unknowable. My training was unusual because it taught me to always guard against what I don’t know, and treat what I do know as suspect. These failed portfolio managers accepted risks they didn’t understand based on the limited knowledge they had, mistaking that limited knowledge as more comprehensive than it actually was. Again, this is a common human problem that’s positively correlated with education.
(2) I recognize the value and importance - but also the limited applicability - of large population study results to my individual biology. Ultimately, as this field comes out of the dark ages that it’s currently in, the only path forward will be personalized medicine. I’ve shared elsewhere how my A1c numbers have no relevance to conventional A1c analysis based on large population studies. Similarly, if I ended up in an emergency situation, my daughter (an emergency medic) has told me that my resting heart rate around 40 would cause alarm bells based on standard training. How much applicability is there to all the lipid research for my N=1 situation when the study population represents the general population (eating a SAD, metabolic disorder, chronic inflammation, out of shape, blood pressure problems, on and on…)
I"m not going to blind myself by ignoring the research as irrelevant, but I’m also not going to blindly assume it applies to me. I study the research as it’s published to learn what I can, and to understand tendencies. But I’m always careful at pretending that I know more than I do. Inside every one of those studies and average results are massive outliers in the data, and those outliers matter because you might be one of them (quite frequently, I am!).
Short story made too long already, I view the risk/reward of ingesting powerful drugs as unfavorable when there’s no known problem to treat for my N=1. I fully understand that statins have been heavily studied, large populations use them so those risks that are understandable given our current state of the art.
But that doesn’t equate to riskless. The chances of drugs powerful enough to have those powerful lipid-lowering effects carrying no other meaningful risk is highly unlikely. Human biology has so many self-correcting mechanisms and adjustments that aren’t fully understood… yet. I have a hard time buying the idea that I can dramatically lowering my LDL and APOb without causing a variety of systemic adjustments and compensations. Maybe it’s true, but I’d give it low odds and a negative expectancy outcome.
Regarding the cost of each approach, as long as the CTCA test shows zero plaque problem, then the Cleerly analysis is just a waste of money. Not necessary at all. So that means your statin/ezetemide/etc. treatment net-net cost might end up being a smidge more than one CTCA every three years. They’re certainly comparable in cost to where it’s not a meaningful difference in the whole scheme of things.
And regarding the concerns for dementia/Alzheimers raised in this thread, it’s called “type 3” diabetes for a reason. The best science knows now is that disease symptoms are preceded many years by damage to the microvasculature of the blood brain barrier. Some will disagree that the Neuroquant/MRI is a good test for that, but it’s an indication that when clear, aligns with all the comorbidities of blood pressure, metabolic health, chronic inflammation, and general CVD to imply reduced risk. Of course, if I had a family history of demential/AD then I might lean more the other way. However, I’m encouraged by recent research in applying magnetic resonance, Ibogaine, and various other treatments having nothing to do with statins/LDL/etc. to improve brain health. I think it’s reasonable to anticipate a variety of breakthroughs in dementia treatment/prevention over the next several years now that they’re targeting research in productive directions.
Bottom line is I don’t buy the idea that pumping an existing healthy system with powerful medications that cause equally powerful systemic effects qualifies in any way as “preventative” when that individual’s N=1 shows there’s nothing to prevent. My reasoning (based on the vastness of all that’s unknown and unknowable) says that approach is adding unknowable risk, not reducing it.
I get that others disagree. Cronos Tempi has explained that position clearly. We agree to disagree on how to interpret what’s known, unknown, and unknowable from the research provided, and that has led us to different risk/reward analysis.
In my mind, every year that I can safely avoid unnecessary treatments is another year where science improves and potential breakthroughs may occur that are safer and produce superior results. That certainly appears true with the latest developments in isolated branches of dementia research, and I’m confident it will prove true as they disentangle the comorbidity issues clearly demonstrated by the CVD research so that we can get beyond large population, generalized results to conclusions that are personally applicable. Until then, we have testing to determine our N=1 strategy.
Finally, I want to be clear that this logic is somewhat unique to cardiovascular health in its many forms (CVD, dementia, etc.) because of the nature of the data anomalies and comorbidity complications. It does not apply to Mtor/Rapamycin, for example.
In other words, there are many people who live long, full, healthy lives and never experience any CVD or dementia. It’s not a given based on aging, which is why I was suggesting testing first. Some people never develop a problem due to a combination of reasons that the current state of the art in science has yet to disentangle.
Other aging processes are universal enough (aligning with Cronos Tempi’s view about how biology being flawed in the sense of certain aging processes) that “preventative” treatment to control that specific aging process and maintain general health at a high level is prudent. I include Rapamycin and Mtor in this category.
However, I don’t include CVD and statins into that “general preventative” category applying to everyone reading this thread. That’s why I chimed in.
I think the anomalies in the data shows this is far more complex than general population research conclusions will indicate. We are far more ignorant on this topic than certain experts would imply. The proof of the lack of definitive science is both the anomalies in the data and the controversy in this thread. Controversy can only exist in the absence of definitive scientific proof. Therefore, the only prudent path forward is to test first to determine your N=1 situation.
There’s literally no reason not to test first. You have to know your plaque level and stenosis to determine a prudent path of action. You might need an immediate triple-bypass, or you may never need anything at all. The knowledge that comes from testing is what determines the prudent risk/reward analysis for your N=1 situation. The alternative is flying blind.
Hope that clarifies!
