How Do Lipoproteins Influence Atherosclerosis? | Cromwell & Feldman | The Proof Clips EP
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- Опубликовано: 21 окт 2024
- Cholesterol isn't just about 'good' or 'bad' labels; it's part of a more complex system involving lipoproteins. Dr Cromwell explains magnificently how our understanding of cholesterol has evolved. He explains that heart disease links to lipoproteins-particles that transport cholesterol through the blood-not simply cholesterol itself.
This discussion covers:
• The history of cholesterol research.
• The role of different lipoproteins.
• How genetics affect cholesterol levels.
• The influence of lifestyle on heart health.
Discover why the simplistic view of cholesterol is outdated and learn about the factors that truly influence cardiovascular risk.
Stream the full episode on RUclips: • High LDL Cholesterol o...
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Dr. Cromwell is so compelling that I (a LMHR) am working on slowly reintroducing carbs to lower my high ApoB (174) even though I am so used to the ketogenic diet that by now carbs are scary. But he is that compelling. He often refers to a study that showed that high ApoB is an independent risk factor for atherosclerosis. What is the name of that study?
Have a research on insulin resistance in relation to LDL and APOB
Why Dave's face is not in the cover image?
Guess because he was not speaking in this part and his face is the whole video thumbnail?
Have I got this right? Dietary fats are transported from the gut in chylomicrons. Carbs are broken down in the gut into glucose and released into the blood stream. Excess glucose in the blood is converted by the liver into triglycerides and packaged into LDL/ApoB lipoproteins. So if triglycerides come from carbs, the problem is carbs?
carbs have always been the problem.
If you are metabolically healthy and you are not taking in excess calories, glucose coming in via food is always picked up by your muscle cells and other organs such as the brain, and be converted to energy for activities, or glycogen for storage first.
If your glycogen storage is full, excess energy that your body doesn’t need at the moment (both carbs and protein) can be converted to fats for further storage. Excess fats you take in can be stored without any needs for the transformation.
@@MT-sq3jo So excess carbs are the reason that triglycerides are raised, and hence LDL/ApoB? Not dietary fats? Is that correct?
The problem is that there are more problems.
It would be wonderful if just excess carbs are the problem, but human bodies are not that simple.
You got some right! Some carbs are broken down in the smal intestine, but most are broken down in the liver!
ApoB by itself is not harmful without the environment. It's the blood pressure that makes it atherogenic. We have a tremendous amount of scientific evidence to suggest that, firstly, it does not form plaque in veins. Secondly, the plaque only forms in places with arteries fork or strong shifts. Thirdly, we have mendelian randomisation studies showing that the higher the blood pressure, the higher the ASCVD progression, Fourthly, patients taking blood pressure medication having fewer events than untreated patients. With that bieng said, it doesn't mean ApoB is not atherogenic in normal blood pressure of 110/70, and it doesn't mean lowering ApoB is not useful. It's just a nuance that bothered me.
I would love to see a more in depth discussion on these points!
“if the serum total cholesterol is 90 to 140 mg/dL, there is no evidence that cigarette smoking, systemic hypertension, diabetes mellitus, inactivity, or obesity produces atherosclerotic plaques.”
William C Roberts (heart arteries cholesterol researcher over 60 years)
@@doddsalfa Yes. In other words, the high concentration of LDL particles (ApoB) over time is causal, necessary & sufficient in the development of ASCVD.
@@kazoz3520 meaning?
@@doddsalfa Roberts was 100% wrong just like Harvard health expert Frederick J. Stare who told the country that sugary sodas and snacks were good for kids and would not cause any health problems. Esselstyn was also 100% wrong.
He is saying that high apoB is not only necessary but sufficient to cause atherosclerosis? Sounds dubious given the recent comparison in the study by Dave Feldman in which people with on average 4 years of high apoB didn't have a more plaques than a similar population with "normal" apoB.
Either lean mass hyper responder are somehow immune to the effects of high apoB or this guy's model is wrong/incomplete.
Or time/lifetime exposure matters ?
@@TheProofWithSimonHill according to the standard plaque progression charts in 4 years of what would be considered sky high apoB we should be able to see significantly higher plaque presence than the control, it doesn't make sense to me, I guess more time and studies will get us closer to the truth.
@@Gengh13 it takes decades for this chronic disease to form most likely, that's what these studies always get wrong. Smoking probably won't give you lung cancer in 4 years either
You know water is bad for you as well? If you drink 10 liters of water in one go...
What is this comparison in regard to?
@@MichaelHorstmann that everything can be a bad thing
When advocating for statins why not be truthful and mention the risks v rewards? Yes maybe the rewards are worth it but to not mention the risks is disingenuous.
The risks were discussed. Point is to not overestimate them and generate unnecessary fear
IDK, I don't think one can or should overestimate the harm that can come from taking any chemicals into the body that will be altering the natural physiology. People put way too much thoughtless trust in the drug peddling doctors and their suppliers.
Thank you for this excellent podcast, gentlemen. ❤
You realize there is a host of meds that are not statins to lower ApoB right?
- cholesterol is a neutral fat. LDL and other apo-b particles are what's atherogenic.
- there are many examples of people with very well-managed apo-b who still get events, but maybe it's because their apo-b has been low for only a relatively short time.
Colesterol has nothing to do with fat! Colesterol is a sterol. Please read for yourself, don't follow thoose numheads here on youtube.
“High apoB was never defined.”
Maybe they define it in the full episode that is linked in description
ApoB is almost the same as LDL it is just to sell more tests. ApoA1 is almost the same as HDL it is just to sell more tests. The tests that matter much more that they hide from the public are MPO, Lp-PLA2, ADMA, F2-IsoP and OxLDL.
Anything below 60 makes it practically impossible for plaque to develop.
Bart Kay, Anthony Chaffee, and Ken Berry for the win.
Yes, they are the absolute winners in the keto clown show.
Yes they are
@@robertusgaThis. I used to believe a couple of those clowns until the set came crashing down. Plant chompers totally destroyed them with simple logic and not name-calling and made up information from people that didn't read the studies. I'm not vegan, but I'm certainly not downing bacon anymore.. might have an animal product a few times a week now. Trying for balance and looking at what's kept the great-great grandma in my family still living alone and driving.
You mean the people who are as from the science as any grocery store cashier?
Think it’s time to speak to the big boys like William c Roberts Caldwell Esselstyn and such
Esselstyn has been on before
@@TheProofWithSimonHill but William c Roberts?
I think a little chat with Bart Kay would be entertaining.
@@HobzyMcRuse ok and Charles Manson?
@@HobzyMcRuse Nah Bart Kay just rambles on about mechanistic shit for hours and when that fails jumps to ad homs