Most people not on a statin will end up developing plaque at some point of their life. Statins have not only shown to prevent events but also to actually slow progression and even regress plaque. We don’t need studies for everything when extrapolating from existing research. It’s like arguing against installing guard rails at dangerous locations because studies have only shown them to reduce falls in workers but not for the general population yet. The potential and highly likely benefit far outweighs the potential and unlikely unlikely side effects.
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So weird that neither the American College of Cardiology (ACC) and American Heart Association (AHA), nor the European Society of Cardiology (ESC) recommend statins for seemingly healthy 18 year old women. These guys must not understand your guard rail analogies. You should talk to them.
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Another step to lower LDL -c
FDA Approves Enlicitide, First Oral PCSK9 for High Cholesterol | AJMC
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So proud my LDL-C is 81mg/dl. Its top tier 15-19 yo. While i have twice this age 
No statin nor medication for that.
Also, my T level, Free T, are above the limit top range 
and no im not on TRT or things like that
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Every time I see controversy, the cause can always be traced back to the science not being definitive.
Yes, all cause mortality is decreased in large population studies by lowering LDL, with no known lower limit. No disagreement with this fact, but I do disagree with the way that fact gets interpreted.
Just as important is how we know CVD is a comorbidity issue. LDL shows correlation, triglyceride/hdl ratio is stronger correlation, blood pressure, endothelial health, metabolic health, inflammaging, etc., etc.
In short, it’s a complex topic. Science and limited human ability to interpret data loves to isolate single factors for complex human biology. It’s a necessity to make science experiments functional, even if our bodies don’t work that way.
The reality is more is not known right now than known. The science is not definitive. That’s why we argue so much with polarizing viewpoints. We’re all clamoring in partial ignorance.
We have people walking around with chronically high LDL and no CVD versus people with low LDL and CVD. Science doesn’t have the answer… yet.
There’s no clear cause and effect that understands the full systemic effects to provide definitive prescriptive knowledge, just correlations. So we get controversy as one person attaches to one set of facts and another attaches to a different set. One person sees the data and concludes preventive lowering in their personal situation is smart, other people interpret the same data differently.
For my situation, I’ve run chronically elevated LDL (according to general population standards) my entire life (age 65), but everything else is super-healthy (according to general population standards).
A CTCA shows zero soft plaque and a mere 9 on the hard plaque score (down from 16 in prior test). Despite all the general population derived data and statistical tendencies, what’s clear is my system is working just fine the way it is with no specific interventions (and definitely no statins… yet).
My point is to check first, get a CTCA, and determine if your system operating without outside intervention is on a path of CVD? If no, then it might make sense to trust that your system is operating with a healthy balance, and to distrust the current state of the science as not sufficiently definitive to motivate monkeying with it.
It’s entirely possible in the face of partial science and so much unknown that doing nothing may be the healthiest thing you can do.
Finally, before you take me apart as a Luddite, I have a tall stack of supplements because aging absolutely is a “disease” that causes problems without treatment. I’m a huge fan of Rapamycin and many other things.
I just think we have to be careful and critically think this through. Large population studies may have limited applicability to your personal situation.
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Hmm. I think not. I think the evidence that high LDL/ApoB causes ASCVD is overwhelming. In the face of overwhelming evidence, doing nothing because there are, say, 1% unknowns is not “the healthiest thing you can do”.
Yes, there are people who despite sky high lifelong LDL (including from FHC!) experience no MACE.
But a decision to therefore do nothing when you have high LDL, because you might be the 1-10% who is the exception is not the optimal choice in game theory in information constrained environments. You are playing Russian roulette, with a gun with 100 chambers only one of which (1%) is empty - and you say “spin it, here’s my temple”.
Look, historically every year many people were dying by leaping off the Golden Gate Bridge. Once in a blue moon, once every few years, someone would leap off and survive. We don’t know why exactly - maybe wind combined with clothing, body position, angle of impact or some other factors, but that 1% would survive. Yet the authorities didn’t say “gee until we know exactly why that 1% survive, the healthiest thing we can do for the jumpers is to do nothing”. Instead, they installed protective nets and barriers… and the deaths stopped - as prospective jumpers lives were saved.
Sure, I totally agree we don’t know everything about lipids and ASCVD. In fact, I’m in a very similar situation. Lifelong high TC (240-270 mg/dL) and LDL (145-185). At age 60, I went on a statin (atorvastatin 10mg/day) and it dropped my TC and LDL nicely… the first year. But every year after, it kept climbing until three years later I was right back to where I started - despite taking the statin religiously. At age 65, I had a CAC done - score ZERO. My PCP refused to give me a higher dose or other LLT. But instead of saying “I don’t know why I have no apparent calcified plaque, I better do nothing as that’s likely healthiest”, I decided to self-prescribe pitavastatin 4mg/day + bempedoic acid 180mg/day + ezetimibe 10mg/day. Why? Because even though my CAC was zero (I have as yet not done CT angio, so no idea about soft plaque), atherosclerosis builds up in folks who show NO plaque in their 60’s and suddenly they DO get plaque in their 70’s. If you plan on living to 90+ and beyond, do you take a chance and do nothing, or do you take measures? I take measures. Furthermore, even if I were to have also zero soft plaque (unknown), and I were guaranteed no MACE I’d still want to lower my ApoB/LDL, because high values are also associated with higher cancer rates and other morbidities. The list of high LDL/ApoB negatives apart from CVD is long, while the list of positives short (some protection from bacterial infections?). Statins lower ACM apart from lowering lipids - but inclusive of CVD also see UK Biobank 8% ACM benefit from statins (atorvastatin). There are pleiotropic advantages (including lower inflammation), and I chose pitavastatin as having the best profile with lowest rates of side effects commonly associated with statins. As luck would have it, my LLT brought my ApoB/LDL down, but not as much as I’d like - so when Lp(a) lowering drugs come out I’ll jump on those (my Lp(a) is sky high), and on new ApoB lowering drugs too.
But that’s my approach - and the reasoning behind it. Someone else may reach a different conclusion and that’s their responsibility and choice in turn. We all see things differently - and I for one like hearing views different from mine… in fact, I love it, because nobody learns just by listening to themselves - questioning is highly appreciated… that’s the biggest reason why I make posts like this, hoping to hear a different perspective. YMMV.
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Well, the way I see this high/low LDL-c thing comes down to basically one thing. Having insurance against the silent killer. There is a reason it is called so, and it comes in very sneaky. It is nearly impossible to get ACVD if your LDL-c is low, whereas there is no guarantee that one will be alive at any given time if their LDL-c is high. Some people will be totally fine even with high LDL-c levels, I knew a couple, but all people (not just some) will be fine if their LDL-c is low. The only beef I have is, I’m not 100% sure we may know all the side effects of statins/low LDL-c. I read some reports that it might affect hormones, but I’m not very well versed on the issue. If that were true, I’d be in favor of trying to find a balance between finding a LDL-c level that is protective of ACVD at the 95% interval, while maybe not going low enough to affect the hormones. As an example, a 60-70 level I think was protective for about 95% of people (based on some study/chart someone had posted a while back) while maybe not being low enough for possible known or unknown side effects. And that is the level I’m looking for. So, I’m not in the camp the lower the better. In my opinion there comes a point where you may be trying too hard to fix something that does not need fixing.
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How about this anecdote.
My father is 80 and new to memory care.
He had chronically elevated LDL. His bp is 110/70 on no meds today. He played tennis until a year ago. He was a runner at different points in his life. Always very active. Didn’t like the idea of taking a statin given his otherwise healthy status.
He ate things like wheatgrass 40 years ago. Never ate much red meat. Lived at Esalen for a few years which was basically vegetarian by memory although he did eat meat when he left there for trips. Certainly didn’t eat SAD. No processed foods, dinner often big salad with mushrooms.
Never a cardiac event. Never had need for a stress test (to my knowledge).
A PhD that worked until 73.
LDL is a risk factor for Alzheimer’s disease.
My FIL had the same story except a banker and not as California in lifestyle (still top 5% diet). He died in memory care at 81. LDL mid 150s on no statin. Tennis stopped at mid 70s because he had a slower dementia decline.
Both wealthy enough, graduate school education (Duke and Stanford), top 5% diet, tennis players even after 70.
Anecdotes aren’t science. Both the good and the bad.
You are right - biology isn’t simple and you should not think about one marker or one outcome. Your post failed to consider dementia.
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You’re right, I failed to address dementia in my post, but not my analysis. Sorry, in the interest of brevity, I didn’t list all the tests. My bad.
I also did a full body MRI with Neuroquant analysis for the exact reason you listed. I have zero white matter on my blood brain barrier. So that issue is fully addressable in testing as well. The BBB will begin showing signs of damage at minimum a full decade before any dementia/Parkinson’s symptoms appear. The bonus for this test is that it also pulled cancer risk off the table for the immediate future.
So you are absolutely correct about LDL and the dementia/Alzheimer’s risk factor. Thank you for pointing that out.
And I stand by the point of my post, which is that it’s wise to first get tested before loading your system up with a bunch of meds producing unknowable risk profiles based on large population study conclusions. Your biology is an N=1. You’re situation isn’t random, so large population studies may - or may not - apply, but the unknown risk factors associated with all of those meds absolutely, positively apply to any person choosing to ingest them.
There are tests to extract your actual risk profile from the large population studies to determine relevance. That’s the key. You don’t have to accept the random distribution conclusions nor the unknowable risk profile of the meds.
Stated another way, there are risks no matter which path you choose. Loading your system up with a bunch of lipid-lowering meds doesn’t necessarily lower risk for each person. In certain situations, it likely raises your risk (but of course, that risk is unknowable). In my case, it would be exchanging a known risk of close to zero (because of testing) for unknown risks that could potentially be massive caused by all those meds. The known risk of close to zero is the obvious choice because today’s “science” is tomorrow’s fiction.
I prefer to trust the elegance of biology when it is proven working well. Don’t fix it if it aint broken. There’s WAY MORE unknown about human biology than known. The knowledge of today will appear laughably pathetic in the future.
That’s why it makes sense to test first to determine the relevance of the large population statistics to your personal situation. It’s just prudent risk management.
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You either didn’t read my post, or you didn’t understand it.
You’re reply completely misses the point without any understanding about conditional probabilities, expectancy analysis, and risk management principles.
You’re treating the exceptions to the LDL/CVD analysis as random. At our age, it’s not random because you can determine your risk profile through testing. That’s the point. I’m not challenging the little bit that science has figured out. The facts are the facts for large populations. I’m trying to find my way through all that remains unknown in that research by adding a testing step to convert N=1 into knowable facts that determine my personal risk profile.
Testing completely changes the distribution of returns. Using your Russian Roulette example, you can know with confidence if the chamber pointing at your head is loaded, or not. Once you have the information, the prudent risk management path is reasonably knowable with confidence (but never deterministic).
If testing shows the chamber is loaded, then meds likely lower risk.
If the testing shows the chamber is not loaded, then the decision to load your system with meds resulting in unknowable risk profile is exchanging a known (nearly zero) risk profile for an unknowable, possibly large risk profile. That decision doesn’t make any sense.
And of course, your Golden Gate Bridge analogy is completely inapplicable. We’re talking conditional probabilities based on testing, not random unknowns. The point is to lower risk for any decision by using testing first to change the distribution from random to conditional.
Your final analysis where you chose to load up with lipid lowering drugs despite no CAC at age 60 instead of choosing to take additional tests to determine soft plaque and blood brain barrier health is clear evidence where our analytical thought processes diverge.
You and I were in very similar situations, and I chose testing to determine risk profile. I chose to convert unknowns into knowns to change the distribution of returns.
You chose to accept the risk profile of the large population samples, and further accept the unknowable risk profile of loading your system up with a bunch of meds when it may have been working perfectly. In my mind, you raised your risk to some unknowable degree, when you had the chance to lower it to near zero.
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Just to debate a bit.
The risk profile of statins is about as well known as anything can be. Yes we don’t know a lot of things but when it comes to this, we actually know a lot.
Now, show me the study on this full MRI and 10 year follow up and dementia rates. And do you not care about the 11th year?
Or the 20th year?
All the unproven testing in the world is also playing with unknowns. They are more expensive unknowns.
My background is surgery and I my am so primed to believe the mantra “X-rays lie” which of course means “imaging lies” by extension. Not super fond of medicines either but I would argue a statin is better studied than imaging - particularly MRIs predicting dementia. But happy to be proven wrong. What I see is lots of chatter, relatively short term data and usually only good with combined with other markers including cognitive testing etc.
Lots of money to be made with special MRis and none with statins so you know where the investments are going. Especially since AI can get worked in there too…
No one’s brain is ideal beyond about 30. Heck, even at 30 learning is impaired. Biology is never ideal when it comes to brain aging - just lesser degrees of bad. At least that is one way of looking at it.
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BTW is it established (through studies) that high LDL-c is the cause (or one of the causes) of dementia? Maybe it was discussed earlier and sorry if I missed it.
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Yes - made it to the 2024 Lancet risk factor list.
A full 7% of modifiable risk tied for number 1 with hearing loss.
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Fabulous. I’m always eager to learn.
So let me try to lay out your argument and correct me if I misunderstood.
We are all n=1 and therefore no population study can fully describe (and prescribe!) our medical path. Agreed 100% - I’ve been a relentless advocate of personalized/precision medicine.
Since we are all n=1, before you take a med based on a population study, you should make sure the study (studies) apply to your unique situation - you do this by testing yourself.
TEST —> if applies, you take the med, if not, you don’t.
Agreed. But. Like in any logical proposition “if-then” you must make sure the “if” value ‘true’ or ‘false’. IF your test is valid THEN - your conclusion. And I’m disputing the value of the ‘if’ - I don’t assign it as ‘true’.
You claim the fact that your plaque scores (soft) is zero (calcified insignificant) means you have no atherosclerosis and therefore will not benefit from LLT, for example statins.
I dispute that. I don’t think that’s a given at all.
(1) the fact that you have calcified plaque indicates that you are capable of forming plaque. Given high ApoB/LDL over time is capable of forming plaque means given time you are still in danger. There are people who have zero scores in their 60’s only to develop plaque in their 70’s - look at MESA graphs. I run at night along the autobahn in black clothing and have not been struck by a car - I think it’s still safer for me to get off the autobahn than to keep running in the belief that I’m immune to being struck just because I have not been struck so far.
But let’s say you have zero plaque of any kind including calcified (for the sake of argument). Your biology is not plaque forming - fine. You are assuming that your present biological factors which allow for minimal/zero plaque despite high LDL will be stable. That’s a risky assumption. It’s like the “obese but metabolically healthy” who in time are shown to in the long run not be healthy. You age. Your physiology changes. And one day, your biology may become plaque forming.
Decision tree:
Your high LDL is a risk factor with unknown factors offsetting. You don’t know if those factors will change. Crushing LDL has been shown to virtually eliminate atherosclerosis regardless of time frame and aging. What is safer? It is safer to crush the LDL (I’ll get to risks of LLT factoring in, later), than hope your biology holds… especially that you/we don’t know what factors allow you at present not to form plaque.
(2)You are assuming that no atherosclerosis means no CVD. Pathologies associated with atherosclerosis are only part - although a very large part - of vascular diseases (including strokes). Meanwhile, studies show that crushing LDL results in vanishingly small CVD outcomes. The focus here is outcomes. With LLTs we have outcomes - I’ll take outcomes over hopes and prayers any day. You are not testing for all CVD causes by looking at plaque - you might be in danger. Crushing ApoB takes care of all causes (because: outcomes) and so I don’t have to worry about what I have not tested for. You have to worry about what you didn’t test for that will still result in CVD.
Decision tree: there are other causes of CVD than atherosclerosis. Regardless of what those causes are, LLTs (crushing ApoB) show exceptional outcomes. I’ll take LLTs (where I do know outcomes) over the unknowns of other factors which might cause CVD and which my “no atherosclerosis” test does not account for.
(3)You are not accounting for other risks associated with high ApoB/LDL. You addressed demential somewhat)
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Sorry, I accidentally posted before I finished.
(3)Other dangers of high ApoB. Dementia is hardly the only one. Yes, you tried to test for cancer. But I’d rather remove the risk factors for cancer, dementia etc., instead of having to keep hunting/testing for when cancers might appear. Prevention.
Here we need to talk about ACM. Statins show ACM advantage apart from CVD. Your test for atherosclerosis is narrowly focused on CVD. But if a statin can lower my risk of death in addition to lowering my risk of MACE then even if it does nothing for you vs CVD, it still does something for other causes of death.
Decision tree: additional ACM lowering beyond CVD means take LLT even if your CVD risk is zero.
(4)LLTs present unknown risks. Agreed. There are known and unknown risks. For known risks, you can attempt to ameliorate (T2DM - if at risk, pick pitavastatin or a non-statin LLT). But that still leaves unknown risks. How to think about it? Well, through ACM. ACM essentially aggregates risks and tells you the net - lower or higher. Since statins improve ACM, it means the unknown risks net out to my advantage.
Decision tree: there are unknown risks of LLTs. A statin might be particularly damaging to my n=1 - I might be the outlier. Here it’s a probability - there is no way ahead of time to test yourself for ACM (all possible risks!), so all you can do is look at the odds. If the odds say the majority of people benefit from statins (ACM lower), then I’m going with the better odds. I might be wrong, but that’s genuinely unknowable and so going with the better odds is the rational decision here. YMMV.
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Do the coronary scans look at plaque in the arteries around the brain? If not, then one can in the unlikely scenario where one doesn’t have plaque at a certain age, still have it around the brain and presumably increase the risk of stroke and maybe dementia. I don’t mean to scare anyone but there’s other places where plaque can develop and it might not necessarily be correlated with other areas that are clear. Perhaps high LDL levels can also increase risk of something past BBB if it’s from genes.
I don’t know much about atherosclerosis effect on events, except that it increases risk, or drugs on plaque. But we know that LLT and genes that target the same mechanism lowers events. The only person who had an event with PCSK9 loss of function in the Cohen 2006 study was an obese male smoker, with very high BP and a high Lp(a). That most didn’t even if there plenty of smokers etc is what some people claim metabolic health with insulin sensitivity can do. Targeting both might be wise.
Simon Hill got rid of his calcified plaque if we believe it was accurate over 1 yr and reduced his soft plaque with serial CCTA. I don’t remember how he did it, except diet changes to lower lipids. He’s going on a monthly PCSK9i drug now because of family history and detected plaque.
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Effect of Statins on All-Cause Mortality in Adults: A Systematic Review and Meta-Analysis of Propensity Score-Matched Studies
“In conclusion, statin use was associated with a significantly reduced risk of all-cause mortality in real-world cohorts with CVD and non-CVD.”
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I have to laugh…
Chiming into a thread filled with people committed to extreme statin use, then proclaiming “test first,” is like walking into a Baptist church filled with devout zealots and questioning the relevance of religion.
My bad. I know better, but I wanted to introduce an idea that might help many who would be unduly swayed by the pro-statin crowd.
I’ll make one more comment, and then I’ll bow out and get back to work…
The arguments made by you and David Cary since my last reply are easily solved by one thing - periodic, continued testing. Retest every few years to see if enough changed to merit intervention.
CVD isn’t something that rolls over you like a tidal wave. It’s progressive over many years, so periodic testing should pick it up in the early stages of development.
Again, I’m not against using statins. However, I am against using statins without testing first to see if they apply to your situation. It’s not wise to introduce unknown risks that could be large from aggressive med stacks when the risk your trying to control is monitored and not a problem.
If you have evidence of CVD or related problems, then by all means follow the best protocol available given our limited scientific knowledge. No argument.
However, if it’s not broken, don’t fix it. If testing shows no evidence of a problem, then adding a pile of meds that mess with your system is exchanging an unknown - and potentially large risk - for a known, carefully managed risk. Do that often enough with enough meds, and serious consequences approach certainty.
My point in chiming in was not to tell the pro-statin crowd that God doesn’t exist. For the right situation, they make sense. Instead, I was trying to balance a thread that’s overwhelmingly “pro-statin for everyone” and “crush it” with the idea that it would be smart to test first to determine your actual risk.
The truth is there’s a risk to everything you do, including the risk of doing nothing at all. The only question remaining is what risks make the most sense for your personal situation, and that can only be assessed by testing first. Until then, you’re reliant on applying large population studies to your personal situation, and I’ve already had so many run-ins proving that line of analysis is wrong that I’d be a fool to accept it as reasonable.
As Mark Twain wisely said, “It ain’t what you don’t know that gets you into trouble. It’s what you know for sure that just ain’t so.” Beware of acting on false certainties from limited research.
The science of lipids and CVD is barely in it’s infancy. The cutting edge protocol for today will look ridiculous in a few years. Today’s scientific fact is tomorrows fiction. If you can safely kick the can down the road for years at a time as science continues to improve, then that’s just smart risk management.
Hope that helps!
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I must admit, I’m somewhat downcast by this response. I thought we were having a respectful and illuminating exchange. I certainly don’t recognize myself as someone who holds onto beliefs with religious fervor. I’ve regularly declared in multiple threads that I am willing to change my opinion on a dime if the evidence justifies it. Evidence and argument - that’s the whole point of my posting here too.
I am by no means opposed to testing. I do it all the time. But I try to clearly understand the limitations and the data what does the test measure and what does it tell me, what conclusions can I draw.
Testing for one aspect of CVD (plaque) even repeated is not going to tell me anything about non-plaque related CVD morbidities. Not to mention the rest of non-CVD morbidities.
And you cannot test for everything, since such tests don’t exist. ACM encompases all causes, and you can’t test for all causes preventatively.
But outcomes tell me odds. I can take - or not - some steps (meds, interventions) and expect a given % chance of getting that outcome. If with statin use ACM is lower apart from CVD, then it makes sense to spring for them as the ACM number also incorporates the risk of the statin or other LLT - if this is significant in the cohort, then it’s just playing the odds. Of course, I might pull out the wrong card and be one of the outliers for whom it’s a disaster - but as you say, there is also risk associated with doing nothing. But which is the bigger risk. Comparing those risks I go with the better odds.
Again, I myself do tests, I don’t oppose them. Though at the other extreme, yes, there are many cardiologists who tell you there is no point in testing because what do you learn - if you have plaque you should do LLT, if you don’t have plaque you should be on LLT preventatively anyhow - since studies show that even with ideal lipids lowering them keeps improving your odds. I’m not that extreme by any means - I test (soon I’ll do a CT angio) and will continue to test.
If it’s not broken don’t fix it - this saying fails immediately in this case, because odds are, that it’s not broken yet. A huge flaw in your approach (IMO) is underestimating the importance of PREVENTION. You have no health problems despite smoking; or a bad diet; or HIGH ApoB etc. - lung screening, CT angio screening and a colonoscopy show no ill effects of smoking, bad diet and HIGH CHOLESTEROL. I would still prefer not to smoke, eat a good diet and lower my ApoB. Even though I understand that there are centenarians and supercentenarians (Vincent Dransfield) who smoked, ate crap, drank, didn’t exercise and were hale and spry… we don’t know everything about medicine as you say. But we do know enough to look at the evidence and play the odds.
I agree with Mark Twain wrt. what we know and don’t know… except I apply it in the other direction than you - I say you don’t know if you’ll be just fine with your current “no prevention” approach - perhaps you are too certain that these tests tell you all you need to know. You speak of the risk of meds (although as I’ve said, ACM encompases the risks of meds by definition) - but I keep thinking about Bryan Kennedy in his conversation with Matt Kaeberlein, when he mentioned that his team did a data dive on the NHANES and UK Biobank folks. He found people who had healthy biomarkers in the “good range”. He then divided them into two groups. One who came by their “good range” naturally without drugs. The second was a group who got into the “good range” only with the help of the common drugs for BP, LLT, blood sugar. It is the latter group who lived longer and were biologically younger. Food for thought. All those drugs apparently had additional pleiotropic effects to boost their biology and worked synergystically. On another occasion another MK guest observed that fixing one system/organ had a good effect on other organs.
That said, I do agree: gobbling up drugs willy nilly will lead to disaster. The danges of polypharmacy. But in my book that’s not a reason to not practice it, but to embrace it - I am pretty conservative compared to many on this site, and take relatively fewer drugs/supplements. But I do extemely extensive resarch on drug interactions before I select or add a drug to my stack. I don’t shrink from the challenge - I embrace it. Yes, science evolves - and I try to keep up with it as evidence rolls in… which is why my stack is not static, but constantly re-examined.
I think part of why we seem to be at odds here is down to this statement of yours:
I prefer to trust the elegance of biology when it is proven working well. Don’t fix it if it aint broken.
First, note that the heavy lifting - nay, all the lifting is done by the word “proven”. Well of course, if something is proven to work well, only a fool would monkey with it. The trouble is that it’s rarely proven. As in your plaque tests don’t prove you will never have CVD or other problems stemming from a greatly elevated ApoB - a big point of our disagreement. What we are left instead with is playing the odds as best we understand them.
But there is a more global issue with that statement that I am in a radical disagreement with. I don’t believe in “the elegance of biology” - I believe it is the exact opposite of elegant. We are the result of random evolution, a patchwork of solutions “just good enough” tacked on as long as they work at the lowest acceptable level to get us to the time of procreation and assured genetic line preservation (maybe up to grandmother hypothesis if we’re being optimistic). Antagonistic pleiotropy shows that conclusively. It’s all “barely” and “eh, good enough”. It’s a mess of accrued solutions and modifications layering on top of each other like deposits at the bottom of a massive fossilzed garbage dump. We are a grab-bag, a mess, and we regularly fail along all sorts of axis - most definitely not an intelligent design, but a make-do at the lowest possible cost driven by chaos and chance and happenstance. So in my view - I look at our bodies as a deeply, deeply flawed piece of machinery, and the only hope we have is to tinker with it endlessly until such a time when we have the knowedge to actually re-design it with intelligence - genetic engineering. Hence, I ask “how much can I do to be the healthiest” while you ask “what if doing nothing is the healthiest”. Because I see a mass of flaws on the way to failure, while you see a completed elegance best left alone. Opposites. YMMV.
Thank you for sharing your views!
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Well stated. Thank you for your reply.
We agree to disagree.
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