Yes, that’s the big issue with eze, in that the big benefit is only seen in hyperabsorbers, pretty limited group.

Not so much:

High cholesterol absorption is relatively frequent in humans. In a general population, about one third were found to be high cholesterol absorbers (>60% cholesterol absorption).

High cholesterol absorption: A risk factor of atherosclerotic cardiovascular diseases? 2023

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Right, a minority. Of course 30% is better than 5%, but eze is still a much narrower applicability drug compared to statins which work for all except the small minority who are intolerant.

I can attest that the triple therapy of Atorvastatin 5 mg + Bempedoic Acid + Ezetemibe lowered my father’s ApoB from 130 to 34. It lowered mine from 120 to 48. That’s a 74% reduction for my father and a 60% reduction for myself. We now both have the cholesterol levels of little children.

I literally feel young at heart. :wink:

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Bempedoic acid seems to have a reasonable safety profile, at least in the short term (new drug), but gout is a problem:

So maybe SGLT2i to the rescue:

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Congrats, DeStrider, to both you and your father! Because I’m getting ready to hop on the BA+eze train (I’m already on 10mg/day of atorvastatin), I want to know whether the lowering of LDL achieved by BA results in lowering of CV events, hence my questions and PubMed research. Because it’s all well and good to lower LDL, but that by itself doesn’t guarantee benefits - see niacin.

We need to know that BA is at least as safe, and at least as effective per LDL unit lowered as statins. So far, at least according to the studies I cited above, BA seems safe and effective - short term, because as a newish drug, it doesn’t have the clinical track record. Early evidence is cautiously encouraging, although perhaps it’s not as powerful as some statins. I continue to be intrigued by pitavastatin.

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I believe that Bempedoic Acid and Ezetemibe will be just as effective as statins with fewer side effects. Of course we need time to prove it, but I have enough evidence to convince me to continue taking them.

Here is a rather interesting Nick Norwitz yt video, wherein he reports on the results of his consuming an epic amount of eggs (two cartons a day!). Obviously a giant amount of cholesterol taken in. He explains how the body blocks the endogenous production of cholesterol (through cholesin) when in the presence of dietary (exogenous) cholesterol to maintain a balance.

He claims his LDL levels declined by 2%, and when he added 60g a day of fruit (banana, blueberries, cherries etc.), his LDL levels plunged consistent with the LMHR model hypothesis.

All, very interesting, but I wonder how does a drug like ezetimibe fit into this?

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Short Biography

Nicholas G. Norwitz, PhD, MHP. Dr. Norwitz is pursuing his MD at Harvard Medical School. He received his bachelor’s degree in cellular biology from Dartmouth College in 2018, from where he graduated Valedictorian. He received the Goldwater Scholarship in 2016 as well as the Keasbey Memorial Scholarship in 2018, a merit scholarship that provided funding for his DPhil (PhD) at Oxford University in the UK. He completed his PhD in 2020 on the topic of ketogenics and neurodegenerative disease. He is also a certified metabolic health practitioner (MHP) with the Society of Metabolic Health practitioners. He is published on the topics of Alzheimer’s disease, Parkinson’s disease, ketogenic diets, diabetes, lipidology, inflammatory bowel diseases, osteology, exercise sciences, nutrition sciences, and metabolic health. His primary clinical and research interest is in using lifestyle interventions to prevent or improve chronic metabolic diseases.

And your credentials are? Or maybe you’d rather just post your facial expression.

He explains in the video what’s necessary to get the public’s attention.

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That is why I wondered how ezetimibe fits into this, and I was hoping he would address this. The other thing I always wandered about the LMHR hypothesis, is if LDL in this model represents a lipid energy transport substitution for triglycerides, what happens if you lower LDL through statins or BA or eze, etc. Do you just run out of energy, and your athletic energy output is lowered? Has he ever addressed this?

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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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