How Endothelial Dysfunction Causes Atherosclerosis | Dr Thomas Dayspring | The Proof Clips EP

[@davidzip8841]

This is a really useful video. If this was taken from your longer series with Mr. Dayspring I need to go watch them for a third time. If you haven’t watched those videos, do yourself a favor and watch them.

[@TheProofWithSimonHill]

Yes it is!

[@lotembenatar7163]

8 minutes of great explanation that makes so much sense

[@megavegan5791]

There is not a better explanation of this on the Internet. I know, I've searched for 7 years. But, there are plenty of "don't blame the firemen for being at the scene of the fire" LDL-denier rants.

[@johng9382]

I never did like the firemen/arsonists analogy. In a fire scenario, it seems like LDL is more like kindling, not causing the fire or putting out the fire, but adding to the fire (inflammation) by just hanging around.

[@MT-sq3jo]

People feel a need to invent stories to justify why their high blood cholesterol levels is a non-issue, or even good for them. No need to argue with these folks, let cardiovascular diseases catch up with them eventually.

[@jamesalles139]

I don't see any mention of the glycocalyx?

[@nickytaylor6338]

Potentially silly question but as I understand the first part of the video, its a combination of the ApoB particle crossing the endothelium and the monocyte crossing the endothelium, then the macrophage that forms engulfing the ApoB particles, which over time builds into foam cells and thereafter leads to atherosclerosis. I understand that ApoB passes naturally through the endothelium. Thats part 1 in the process. But Part 2 - why do the monocytes cross the endothelium (and then become macrophages which engulf the ApoB)? Because there is inflammation? But later in the video, it states that this process happens even when there is no inflammation? Help!

[@jimdandy8996]

Which causes which?

[@megavegan5791]

LDL is the only *required* risk marker. All other risk factors are only contributory.

[@jimdandy8996]

@@megavegan5791 Isn't inflammation or some other mechanism also required in order to disrupt the endothelial lining for the LDL to pass inward?

[@ScottSummerill]

Would it be correct to say that high cholesterol is actual a liver and/or gallbladder dysfunction? Why not put our focus there? Maintaining a healthy liver and gut microbiome.

[@CharlieFader]

Maintaining a healthy microbiome is easier said than done, especially if you don’t start with a healthy one.

[@MT-sq3jo]

Genetics, aging, lifestyle and diets have a lot to do with elevated cholesterol, without the pre-requisites of any internal organ disease.

[@But1non]

Glycocalyx thins out with sugar

[@HakuCell]

6:44+

[@daviddubois2476]

Seems simple. You need to manage your endothelial health, ApoB, AND any chronic inflammation that you have. Dr. Dayspring is awesome, but he is a statin guy, so he focuses on ApoB. Focus on all three. Why not?

[@jimdandy8996]

Add Rapamycin. It may suppress macrophage activity.

[@MT-sq3jo]

Topic of the discussion was cardiovascular diseases prevention via management of blood lipids. So obviously management of APO B was the main focus. Statins are the first line of meds for high APO B, and he also covered other alternatives including ezetimibe and PCSK9 inhibitors. By the way, statins do exhibit anti-inflammatory effects.

[@jimdandy8996]

@@MT-sq3jo Also anti-mitochondrial effects too unfortunately.

[@k.h.6991]

Of course. Follow the whole foods plants based diet Simon advises, and you will do all three. Medication may still be necessary, depending on circumstances (genes, current health status), but food should be the first line of defense.

[@CliveWebber]

Dr. Dayspring is a lipidologist; I would fully expect him to be a “statin guy” who focuses on lipoproteins! As far as I know, there aren’t ways to quantify someone’s endothelial health, and there may not be medications to address endothelial dysfunction. Your endothelium can be damaged by a ton of different things; even a viral infection, which you wouldn’t have much (or any) control over. And regarding inflammation, you need some inflammation or else you’re dead. Generally those who already have heart disease are on an anti-inflammatory med… aspirin! But until we have meds that can specifically target the inflammatory response that create foam cells, it probably isn’t wise to dramatically lower inflammation throughout your body. You need an immune system after all. Obviously if you have chronic inflammation from an autoimmune disorder, that should be addressed. But again, Dr. Dayspring is a lipidologist, so that’s not in his wheelhouse.

[@ccamire]

You are a very good host but he is not able to present his theory on how the plaque buIld up. He did not speak about blood clotting factors which are the main ingredients of the plaque morphology. He did not talk about blood flow or viscosity. How come we have a plaque or blood cloting issue called called stroke and ther are no cholesterol and endothelial cells. Quite confusing to following him, he is all over the place