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That’s an answer to a different question. I don’t disagree that CVD risk is multi factorial - having T2DM massively increases the risk, for example. But this be
by KempyKolibri 2y ago
That’s an answer to a different question. I don’t disagree that CVD risk is multi factorial - having T2DM massively increases the risk, for example. But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk.
CAC scores (which it sounds like what you’re referring to) only look at calcified plaque, but not soft plaques. So there’s a whole category of risk that is missed by them. People’s CAC only tends to go up when they’re in a very late stage of atherosclerosis, and calcified plaques also tend to be more stable than soft plaques, so if two individuals had the same mass of plaque, but one’s was soft and the other’s one’s hard (sorry for the “carry on cardiology”) then we’d actually expect the individual with the CAC score of zero to be at greater risk of a CVD event.
It’s my interlocutor’s burden to show that arterial wall damage and/or an individual’s inability to repair damage is required for ASCVD to take hold, and so far they’ve yet to meet it. That’s what I’m looking for, basically.
- jodrellblank 2y agoSounds like CAC scores are the same thing. I can only link some other doctor's article[1] which says that the CAC does only measures hard plaque, but that a score of 0 has been studied and goes with a very low risk of heart attack (1-2%) over the next ten years. When you say soft plaques are a whole category of risk, that suggests they are not a significant risk factor. So something doesn't add up here. From what I could gain in the paper you linked in another comment, they write that apoB with less LDL in it goes more easily into the arterial wall, apoB with more LDL in it causes more damage once in the arterial wall, and those two effects cancel out, so overal more LDL is worse. These things don't add up to a coherent picture. If eating less fat reduced LDL, that should reduces plaque buildup (by your claims and your study's claims) and that should reduces heart disease risk, and that should show up in the CAC scans. And apparently it doesn't. If eating more fat increases LDL and that increases heart disease risk, that should show up in Dr Davis' CAC scans and he should think that worsens heart disease risk, and he doesn't. > "But this being the case does not serve as evidence that arterial wall injury or an inability to repair damage is required in order for high serum cholesterol to be a risk." It doesn't, and I don't make that claim. So I have no more comment. Agree that it's multifactorial (or appears that way). [1] https://myheart.net/articles/ct-coronary-artery-calcium-heart-scan-the-facts/ https://myheart.net/articles/ct-coronary-artery-calcium-hear...
- KempyKolibri 2y agoDepends on your age. In this study, in those under 40 with obstructive coronary artery disease, 58% had a CAC of zero. So it can be a dreadful risk marker in some scenarios: https://jamanetwork.com/journals/jamacardiology/fullarticle/2785586 https://jamanetwork.com/journals/jamacardiology/fullarticle/... Your Dr Davis just appears to be one person saying something is the case, without providing any evidence for it. I don’t see why we should believe his claims that serum cholesterol is irrelevant over the incredibly robust evidence I’ve brought to the table. I agree that the two things don’t add up, but why wouldn’t we then just favour the higher quality evidence? Seems like Davis is a quack with historical form for just making things up without any evidence in order to sell a product: https://www.healthyeating.org/blog/detail/rdn-s-book-review-wheat-belly https://www.healthyeating.org/blog/detail/rdn-s-book-review-...
- jodrellblank 2y agoThat is another interesting link; I don't discount that link or try to refute it, although I do note that you present it as "58% had a CAC of zero" which sounds very bad, but they're talking of 23,759 sympotmatic patients, 1278 are under 40, and 39-68 of them (the numbers aren't clear[1]) actually do have CAD, and half of those have zero CAC score. That's 1.5% of people under fourty with symptoms have disease and have zero score. If there are any other causes of obstructive CAD other than fats getting into the artery walls, those cause would all have to be in that group as well (I don't know of any but I can speculate several). I don't think Dr Davis has said serum cholesterol is irrelevant, the statement I linked is that dietary fat removal doesn't stop CAC score increasing. Why we should believe him is that he's got a feedback loop with a measuring machine. Science is about settling abstract arguments by testing them against the real world, right? So you can dismiss Paul Mason by saying he's an idiot, he can't read, he's looking at old studies, and he's a sports medicine doctor so he's not treating heart disease anyway, but Dr Davis is actually a cardiologist and he gets a patient with a heart problem, he takes actual measurements (CAC score) then gives advice to change their life, then sees them again for followup over years and years, measures again and sees the results. The measurement is not based on whether he is smart or stupid, it's not affected by which studies he's citing. He's a quack selling a book? The US Bureau of Labour says Cardiologist is the highest paying job in the USA[2]. He could just as easily be shilling low-fat books instead of low-carb books so that makes no sense that he would be shilling a book which goes against his findings instead of one which goes with his findings. Why does he need to shill any product - his financial incentive is do do more treatments, more stents, more bypass surgery, prescribe more statins for pharma kickbacks. Could he be totally wrong, and his patients are dying en-masse, and others are leaving him to go to another cardiologist for bypasses, and other patients are eating something different and lying to him - I'd actually believe it, yes, but who knows. If we go with that he appears to have found something which reduces his patients' need for surgical intervention over years and decades, then it seems that the biggest things to affect heart disease risk are metabolic syndrome et al, and they appear to have far more effect on serum fats than dietary fat intake does, and far more effect on fats-causing-plaque-buildup than dietary fat does. Less fat in the blood is better, is something your links claimed, and that can also be something Dr Davis would agree with through insulin resistance improvements; as I asked in my other comment, I have no idea what the link there actually is. At this point serum LDL seems important, dietary fat intake might be but it seems less important/effective as a way to modulate serum levels than fixing other diesease processes does? [1] It says: "Results A total of 23 759 symptomatic patients, of whom 12 771 (54%) had a CAC score of 0, were included. Overall, the prevalence of obstructive CAD was relatively low across all age groups, ranging from 3% (39 of 1278 patients) in those who were younger than 40 years [..] In patients with obstructive CAD, 14% (725 of 5043) had a CAC score of 0, and the prevalence varied across age groups from 58% (39 of 68) among those who were younger than 40 years" - how can there be 39 people with CAD under fourty in total and also (__ of 68) under fourty with CAD and zero score? Where did the 68 come from? [2] https://cardiovascularbusiness.com/topics/healthcare-management/cardiologist-salary/cardiologist-officially-highest-paying-job-us https://cardiovascularbusiness.com/topics/healthcare-managem... (I don't know why they don't say "CEO" but whatever, it's a high paying job, he doesn't need to be shilling anything).