6 ms·

Depends 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 so

• jodrellblank 2y ago
  That 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).
  • KempyKolibri 2y ago
    I probably should never have entertained the Dr Davis derail. The whole bringing up of this character was your attempt to answer my question "What’s the evidence that [atherosclerosis] only takes place in individuals with arterial wall injury or without the ability to repair damage?" Your response was "Some people live a long time with high(er) fat diets and no heart disease". But this is not evidence that atherosclerosis only takes place in individuals with arterial wall injury or without the ability to repair damage. That could equally be evidence that some people are genetically less predisposed to arterial retention, regardless of arterial wall injury, for example. There are plenty of hypotheses that negate your proposed one that are equally likely on the evidence you've provided. So this whole thread is just a tangent that doesn't engage with the core question. That said, here goes: My point on CAC was that your entire argument hinges on being able to look at a CAC score and say "this score is a reliable indicator of whether a person has coronary artery disease". But if you're under 40 and actually have CAD, there's a 58% chance that when you get your test results back, it will show 0 CAC (even though you have CAD!). So demonstrably, CAC is a poor proxy for CAD, and so a lynchpin proposition in your argument is clearly false. Whether the numbers look different when read a different way is irrelevant. The above is true, and demonstrates how CAC is not a reliable metric. > 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. Literally from the article you linked: "Can you look at your cholesterol and say “Oh, my cholesterol is 240. I must have heart disease.”? No, of course not — cholesterol is virtually worthless when it comes to predicting heart disease" So he says exactly that, unless you're willing to quibble over a semantic difference between "virtually worthless" and "irrelevant". > Why we should believe him is that he's got a feedback loop with a measuring machine It's not just "why should we believe him", it's "why should we believe him over meta-analyses of RCTs, and other high quality data?" Look at where "expert opinion" and "case reports" (which is the evidence you're citing, if we're being generous) sits relative to the MAs of RCTs that I'm bringing to the table on the hierarchy of evidence (https://en.wikipedia.org/wiki/Hierarchy_of_evidence https://en.wikipedia.org/wiki/Hierarchy_of_evidence). It's not clear to me why you're throwing out robust evidence with comparatively low risk of systematic bias and relying on bottom-tier evidence instead. Can you please explain to me why this is a superior epistemic framework? > He's a quack selling a book? Yes. I'd take a quack to be anyone wearing the coat of science while violating the standards of modern science. Whether or not he stands to gain (or cares about) the money his book makes isn't relevant to that claim, it's based entirely on the nature of what he has to say/publish. Indeed, going back to the previous point, dismissing the enormous body of high quality evidence showing LDL cholesterol is a causal agent in atherosclerosis by referring to serum cholesterol measurement as "virtually worthless" merely because of his own personal experience, with the plethora of biases that entails, is textbook quackery. The fact that he's published a pop science book that blames many of the ills of the world on wheat with no evidence to back up such an assertion is just the cherry on top. So I don't need to speculate why he's a quack, and his salary doesn't alter my point. Maybe he does it because being a number one bestseller satisfies his ego in a way nothing else can. Maybe having that accolade means he can charge more for his cardiology services, so there's an indirect financial benefit. Maybe he genuinely believes wheat is the devil's food? I don't really care, my point is that his output suggests he's not a sound practitioner of the scientific method. Your entire argument here seems to boil down to "there's this guy who sees patients and he says they're not leaving his practice and they're getting better, how would he have patients if everything he says about heart disease wasn't true?" This is wild, the kind of arguments I see from homeopathy advocates. We should always aim for the evidence base most likely to be free from bias. That is not one clinician's account of how they do things.
• jodrellblank 2y ago
  Splitting this into a separate reply, I said: > "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)." Here's one speculation of lay-person reasoning: - Cosmetics people like Retinol skin creams because it makes skin look better. That's a fact that people recommend it. - One way it does this by making it plumper, which smooths out wrinkles. I think that's a fact. - It does this by increasing skin cell "turnover", i.e. what it does at the epithelial layer is trigger stem cells to split, making more skin cells, making thicker skin. That's a claim I've seen and am not sure if it's a fact, but it's a plausible mechanism of action. - We eat retinol in our food, in the form of Vitamin A, that's a fact. - Vitamin A gets through the guts into the body, that's a fact - it couldn't be a vitamin if it passed straight through us and out. - Vitamin A gets into the blood stream; fact, there are lab tests of serum retinol levels. - Vitamin A in the blood is supposed to be wrapped in Retinol Binding Protein to carry it through the blood, but it isn't always. It's normally captured by the liver, and released from the liver wrapped in RBP, but not all of it is captured by the liver and is free in the blood stream. The more of it in the diet, the more gets past the liver, the more of it is free in the blood stream. I've seen it claimed, have no sources to back it up. - Blood vessels have an epithelial layer on the inside, an internal skin. Claim. - Retinol in the diet -> retinol in the blood -> triggers stem cell split in the blood vessel walls -> thickening of the walls ("youthful!") -> narrowed blood vessels. Speculation. (What do we have in this random link[1] I haven't read? "Until recently, it was thought that the sole important retinoid delivery pathway to tissues involved retinol bound to retinol-binding protein (RBP4). More recent findings, however, indicate that retinoids can be delivered to tissues through multiple overlapping delivery pathways, involving chylomicrons, very low density lipoprotein (VLDL) and low density lipoprotein (LDL)" - retinol is not only able to split stem cells, it's a pretty potent molecule in various forms; "Retinoids and immunotherapy may be used to treat high-risk or recurrent neuroblastoma" says Canadian Cancer Society; there's one bro-science connection for increased total LDL -> increased blood vessel damage which is nothing to do with the LDL per-se, but something it carries along with it. Something we eat a lot of as Vitamin A and carotenoids, something the US and Canada fortify flour and low-fat dairy and margarine with, which is another tie-in to both low-wheat and low-fat diet). [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC4073323/ https://pmc.ncbi.nlm.nih.gov/articles/PMC4073323/