If we want to argue about appeal to authority, the side that says “LDL bad” has more MDs and scientists behind it.

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Didn’t Attia once claim that HDL can do all the functions that LDL also does?

I don’t remember this particular claim from Attia or his guests, but if so, that might explain LMHR folks not running out of energy on statins, assuming the lipid energy model they hypothesize is correct.

The original lyrics to that song would have worked equally as well

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Does he actually share his ldl level before and after?

Yes. The Lean Mass Hyper-Responder study includes scanning for plaque and so far shows no increase in plaque with these high LDL-C levels. This is the point. Although @AnUser and @Virilius love ridiculing these people and implying that they are idiots, if you actually look at what they are saying and doing, it’s clear that they are smart, well-educated and believe in the principles of lipidology. Their point is that LMHR is a little niche that lipidology can’t explain and needs further study. In my post here, it shows that lipidologists agree -
https://spotify.localizer.co/t/the-ldl-kingpin-theory-one-ring-to-rule-them-all-lmhr/15982/15?u=ng0rge

***And both Thomas Dayspring and William Cromwell said that they have their doubts but will look at results of any new studies on LMHRs. That’s more than I can say for @AnUser and @Virilius who are so locked in to their own dogma that all they can do is ridicule.

***Both Nick Norwitz and Dave Feldman are open to the possibility that plaque may develop. They are curious, like I am, to scientifically explore exactly what the mechanisms are because it doesn’t seem like the widely accepted medical view of just viewing CVD through the narrow lens of LDL-C/ApoB is the whole answer. Yes, it’s simple and great for public messaging and PR but you’d think that at least on this forum that people could deal with a more complicated truth. I’m not, nor are they, saying that LDL-C isn’t important or that statins don’t work, only that there is more to the story.

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I don’t, I just think they are risking their lives when they could just eat their keto diet while on a statin. One year long studies showing no plaque progression in certain individuals do not prove that LHMR is safe. There is also the issue with selection bias, similar to how some morbidly obese people on a candy diet never develop diabetes.

it’s clear that they are smart, well-educated and believe in the principles of lipidology.

Being smart and well-educated hasn’t stopped other scammers before. And the LMHR hypothesis is taken by the keto diet as the “proof” that they can somehow stuff their faces with butter.

That’s more than I can say for @AnUser and @Virilius who are so locked in to their own dogma that all they can do is ridicule.

My stance is pretty clear.
Statins/ezetimibe/PCSK9i: reduce events, reduce acm, signs of plaque regression
Diet low in sat. fat: reduce events

Until you can show that the supposed effect the LHMR is having actually reduces events and can regress or at least stabilize plaque (over a period longer than one year) then I remain doubtful.

because it doesn’t seem like the widely accepted medical view of just viewing CVD through the narrow lens of LDL-C/ApoB is the whole answer.

The evidence speaks for itself. Other risk factors can matter when your apoB levels are not sufficiently low but I’d love to see someone with a very low apoB count develop plaque.
It’s not a bad idea to explore other targets but you’re arguing like lipidologists got it all wrong and LDL-C is actually good because you distrust “the establishment”.

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I clearly stated that I am not arguing that. But also stated that I am willing to question authority…they aren’t always right.

They are not risking their lives if their plaque is zero to very low - that puts them in the healthiest bracket, even if their LDL-C is high. Most people on Keto are not in this bracket. No one is saying that LMHR is “proven” safe. That is what is being studied. Selection bias? Well, the criterion to be LMHR are already pretty strict so if you’re saying that they are only looking at the healthiest LMHRs, I think that’s unlikely…they’re hard enough to find already.

True. But if you look at “the Proof” podcast with Dave Feldman and William Cromwell, you’ll see that Feldman is being very careful not to encourage this and repeats it several times. Any theory can be used as justification for bad behavior, it doesn’t mean the theory is wrong.
The rest of your post I didn’t disagree with.

Exactly!

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Most of your post I don’t disagree with, because it’s says that there are a lot of uneducated people out there (some doing Keto) that are just using this info to justify being in poor health.
What I’m saying is that shouldn’t mean that these people (Norwitz, Feldman, et al) should be treated as entertainers (gladiators as you put it) with nothing significant to say. I think that’s obvious enough…if some idiot likes you on social media, does that mean you’re an idiot?

***Now, to where I quoted you above…It DOES matter if the LMHR study group doesn’t progress in plaque (and they are monitoring so that if they do, they can take corrective action BEFORE damage is done) because that contributes to our scientific knowledge of what’s happening. That it might annoy someone (like you) DOESN’T matter. “terrible and irresponsible messaging”? They are not saying that just being on Keto will save you. They are saying that the amount of plaque is what matters.
Yes, Norwitz stated that he thinks the case of Lean Mass Hyper Responders deserves attention and the studies need funding (like rapamycin), That’s why he is hamming it up (and the facial expression). If some idiot used us for justification to just sit in a recliner in front of the TV while gulping coke and eating doritos - but it was OK because he was on rapamycin - would that condemn us all to being “entertainers”?

Here’s another item to consider. My mother had arterial scans two years in a row. Both times the scans (or should I say shams?) reported no plaque and no blockages (done by LifeLine Screening whom I will never use again). Within a year after the second ‘all clear’ scan, she had 3 stents, a heart attack and a stroke because the scans somehow missed the plaque (or they spontaneously occurred within 9 months?). In retrospect, she should have had proper scans done at a hospital. However, I want to bring it to your attention that scans are not perfect and can give false results.

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How common is this? My reading online indicates that doctors/cardiologists consider CCTA, CAC and CIMT to be reliable tests - of course when done by reliable providers (and CIMT takes some skill). I wouldn’t spread doubts about the tests unless you have good reason to do so. But certainly saying that you should take a look at the provider is always good advice in medicine.

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Do you know specifically what modality of scan they used?

I know they used ultrasound to examine the carotid arteries. I did the scans through them myself and got the same results - no problems! Next year I am going to get a CAC from the hospital.

This is the provider. I don’t trust their results.

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I got scammed by LifeLine Screening one year based on an add claiming they do CIMT. After getting their scan and reading the results, they revealed that they only do a simplified version of CIMT that only measures the speed of blood flow in the carotid artery, which only shows signs of plaque after there is 50% or more stenosis. So you can have 50% plaque stenosis and still get an all clear from LifeLine Screening. Next time I got a real CIMT (for $275 in San Diego), which gives you actual Carotid Intima Media Thickness for left and right carotid arteries, plus estimates of plaque stenosis level (if there is significant plaque).

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3 blood biomarkers may be key to predicting cardiovascular risk

For this study, researchers analyzed data from the Women’s Health Study (WHS), funded by the National Institutes of Health (NIH). Since 1993, the study has followed female health professionals ages 45 years and older.

The primary endpoint of the Women’s Health Study was a participant having their first major cardiovascular event, such as a heart attack, stroke, or death from heart-related issues.

All study participants had their blood samples tested for certain biomarkers, including high-sensitivity C-reactive protein (hsCRP), low density lipoprotein cholesterol (LDL-C) — also known as “bad cholesterol” — and lipoprotein(a), or Lp(a), for short.

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Here’s an interesting CAD Risk Calculator. My 10 year risk is 2.1%. Yet, if I change my age to 80 and leave all else equal, it becomes 16.8%. Why would this be?

http://reference.medscape.com/calculator/192/reynolds-cad-risk

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Because more plaque has accumulated.

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Yes, but I have an ApoB and LDL of 48. Would there be that much more plaque? Those values are taken into account. I hear of people saying that below 50, you can avoid CVD. 16.8% doesn’t seem like avoiding CVD.

I think that calculator is based on if you hadn’t done any lipid lowering treatment the previous decades.

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