#268

What is surrealistic is your behavior. We all know people who smoke a lot and yet never had lung cancer. Is that a reason not to stop smoking? That was the point of my question above: one counter example cannot guide our decision making process.

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#269

There is a 50% probability of having a CAC score of 0 at age 45 for men.

image

Do you see the error in assuming the apoB didn’t cause disease?

ApoB can at the same time cause disease, but still not cause disease in a specific individual. It’s considered the necessary cause.

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#270

@adssx
I wasn’t trying to make a general argument for advising people but for this specific individual (why I jokingly mentioned divorce) isn’t it true that his wife @medaura doesn’t need to pressure him?

#271

For ppl who regularly smoke, isn’t it just a matter of time (re getting cancer) or can it happen that some of them would never get lung cancer even if they smoke?

#272

I agree. This should be an individual decision. But in a couple if you believe (and you may be wrong) that your partner isn’t taking care of their health it can frighten you (“what if they die soon/before me?”).

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#273

I don’t know. I would assume you have a baseline risk based on your genes that increases over time with exposure to cigarette smoke and pollution until it reaches a certain threshold (and maybe some interventions can also decrease the risk). So maybe with time, if they live long enough, all smokers get lung cancer :man_shrugging:

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#274

Ha, if we ever get a divorce it won’t be over this, trust me. I second guess myself for pressuring him — my concern is there’s always a chance there’s a peripheral artery that wasn’t checked by ultrasound and might be thickened so the disease could have started and wasn’t properly caught. That does seem unlikely though. He even got a brain MRI for an unrelated reason and no problems there. But he’s got one apoe4 allele, like me, which is an independent risk factor. The European cardiologist seemed surprised at finding nothing but said with those numbers, any US / Canadian cardiologist would have put him on a statin stat…. Yet is it possible that’s just close minded? Is it possible that he has some sort of unique phenotype / genotype that’s not yet been identified, for whom cholesterol and high TG are somehow protective? His dad is very obese, has been for decades and eats like a pig and walks / moves very little but on a fairly low dose of statin he’s got no stroke / heart problems in his 70s. His mother who’s pretty trim and active (and also on a statin) had a little stroke recently. I would have never have guessed based on their looks and lifestyle that she’d have a stroke before him. There’s so much we don’t know. This past year my intervention for hubby has been to insist he eat better, add a lot more fiber to his diet, avocado toast and broccoli sprouts galore, fuck me even got a sauna so Rhonda Patrick would be proud, and he takes rapa which he claims gives him an insane burst of energy when he plays pick up basketball or indoor soccer with other guys roughly his age. He’s also lost weight from eating better (not that he was fat but the gut area was starting to thicken too much for my liking and his) so he feels better from that. I also prepare him a shitload of supplements primarily aimed at lipid regulation and he takes them about half the time — the other half he forgets. So we’ll see at his upcoming physical how his numbers look but he feels better in general. For my peace of mind primarily he seems resigned to trying a statin if his bloodwork is still all over the place but much as I can be a hypochondriac on behalf of those I love, I’m not losing any sleep over his lipids because so far they seem to have done diddly squat to hurt him. Why? Who knows… is it guaranteed to stay that way in the future? Again, who knows.

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#275

Heart disease is the number one killer for most of the population so I always enjoy these conversations and I always learn a bit more and see a paper I had missed, so this is all good. Better to have too much than to little, and if you are not interested just skip the thread. :smiley:

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#276

There are people who are obese and eat candy all day yet never go on to develop t2 diabetes. Then there are health-conscious people in their 20s and 30s who are learn, exercise daily and only eat keto or vegan and still go on to develop t2 diabetes. Genetics can play a huge role regarding disease development but nethertheless, high blood sugar is not good nor is high sugar consumption.

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#277

I know. So I don’t eat candy all day. My FIL does and yes, no diabetes for the fat bastard either. My husband is more or less doing all the right things in terms of lifestyle. The question is what if that’s just his normal and healthy baseline in terms of lipids and that pharma intervention could be counterproductive? There are fat tails in the distribution of cardiac events for high TG / LDL.

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#278

My intention was in no way to minimize the importance of learning more about heart disease, it’s causes and potential solutions. My point was only that these threads sometimes seem to get bogged down in a loop, like a wheel spinning in the mud. I am still learning more (like how you can still have plaque buildup with a CAC score of zero) but want to use my time efficiently (it is limited, after all, for all of us).

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#279

Thanks for the summary. There are some things I’d frame and explain differently for those three buckets (especially how MR in the context of CVD is stronger than in other areas*), but at a meta level if think the following might be more important to add:

  • while those three groups have some strengths and weaknesses there is a scientific consensus of a hierarchy of how valuable the data is from different types of studies and they are not ranked the same - in general association studies are massively weaker than MR and controlled clinical trials

  • perhaps even more important is that there is a massive wealth of mechanistic understanding of the cardiovascular disease process. CVD is one of the areas in medicine that we understand the most and the best. It’s not like Alzheimer’s or cancer. This includes all the in vivo animal studies and in vitro studies. While we don’t know everything the consensus is that we really do know that Apo B is causally involved and virtually a necessary conciliation for CVD. Yes, we also know that inflammation plays a role. That glucose plays a role etc. and decreasing each of those is valuable too.

I’m not saying people in general should make medical decisions based on mechanistic understanding and logic without data. Rather this is a case where the mechanistic understanding is stronger than in almost any other part of medicine - and it aligns basically perfectly with randomized trials, MR, animal studies.

The last thing I think might be missing from the framework is what we know about side-effects and risks. In the context of - what is the upside here (avoiding number 1 killer (heart) AND number 1 thing leading to real, severe disability (stroke). Again, Apo B lowering is one of the areas in medicine where we have the most info about that - and the risk/effects profile of the tools available is generally very favorable - especially if one applies @约瑟夫_拉维尔 ’s framework of quickly and broadly evaluating any adoption of a medicine and dial it in/up/down/out. For instance while statins are probably totally find for a majority of people, for some people they won’t be - but for almost of those case that will be clear from what the person experiences over the first days or weeks and/from blood work over the firsts weeks/months. Try and if not optimal move on and try something else.

Finally, while I know that some people don’t like Dr Attia (and I personally strongly disagree with him on some topics like about protein intake protocols, etc), his general framework of how we can and need to move from Medicine 2.0 to 3.0 seems very relevant here.

See for instance The evolution of medicine and the transition to “Medicine 3.0” from round 3min to 11min 45sec in link below

(Better covered in his book if I recall correctly)

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#281

So you’re telling me @Neo that your standard of evidence isn’t one compiled by a Superintelligent Laplace demon?

#282

I used to believe this, but now see it’s impossible. You can’t know both position and momentum of say an electron. You change things when you measure them. It’s not a matter of not being smart enough or not having a computer fast enough. It’s unknowable. I have no idea what’s actually going on but it seems more like a simulation all the time.

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#284

This is the straw man. Recognize that I am saying the MR studies and RCT’s specifically about apoB in context, not the methodology in general. Meaning I am waiting to hear someone question the specific RCT’s or MR studies that have been posted a gazillion times. Different studies have worse or better methodologies. To reject RCT and MR as a whole basically means someone is a quack, psuedoscientist, lysenkoist, whatever label fits.

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#285

All of the above is true and well explained but it seems some people have difficulties grasping stochastic processes and view the curves as deterministic which they are not.

BTW as an example of MR, I’ve posted about an MR study about the causality of APOB for CAD and indeed there is some causality but much less than people think: The causal effect is 0.464 (Model-averaged causal effect 0.392). Better than any other coronary artery disease predictors (LDL, etc.) they looked at though but still rather weak.

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#286

Yes, please! More of this type of language! :star_struck: :star_struck: :star_struck: :ok_hand: :ok_hand: :ok_hand: :clap: :clap: :clap:

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#287

@cl-user do you have any comments on my reply to your post on this?

#288

@AnUser I know you’re honest in defending your views (and I somewhat agree with them) but, as I cannot send you an MP, just to remind you that writing in bold + all caps is like shouting. In addition to being rude, it is counter-productive (assuming that your intent is to convince others): your “opponents” in this debate won’t be convinced by the same arguments (otherwise they would have changed their mind long ago) and “neutral” readers/lurkers (the silent majority) can be repelled (as I was initially) and prefer to “side” with the seemingly more rational and peaceful participants than with the religious zealot yelling at others.

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#289

Who said anything about rejecting them? It is not a black and white world.

1 Like