The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
when they are they are ingesting LDO and that it's likely LDL that is oxidized and you like you were tying this all together the oxidative stress the oxidative state of the LDL when they are eating oxidized LDL they become foam cells and the foam cells make up a fatty streak and that is the precursor lesion to atherosclerosis
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
the LDL particle going into the seven feels face getting taken up by the macrophages with the scavenger receptors and forming the beginning of a foam cell in a fatty streak
it's not just moving into the sub endothelial space it's becoming oxidized either in the blood or in the southern athelia space and then being retained in the sub endothelial space this is in the blood vessel wall it has to be retained there in the proteoglycan matrix it has to be seen by a macrophage as an oxidized LDL particle and it has to trigger you know the pathogen associated molecular pattern receptors the toll-like receptor patterns on macrophage and them get taken up as an invader so when our LDL is taken up by a macrophage it becomes a foam cell which is a precursor of a fatty streak and that's what an a thorough sclerotic Legion forms from
I do think that retention of LDL is the key event in the in the initiation of atherosclerosis and what I'm talking about now is the retention of the LDL particle which is a lipoprotein particle that circulates in our bloodstream in the sub endothelial space onto a proteoglycan layer
what we have here is oxidized aldl getting taken up and moving into the subendothelial space what's interesting is that in this diagram at least they're not showing LDL moving into the subendothelial space just oxidized LDL
there is a model of atherosclerosis which posits that part of the thing that's going on is that these LDL particles are becoming either endocytosed or pulled into the submental space and they are binding two proteoglycans there
macrophages will not ingest native LDL LDL must be oxidized to begin the formation of foam cells
macrophages must engulf oxidized LDL particles to make foam cells which are the beginning of a fatty streak and atherosclerosis
macrophages must engulf oxidized LDL particles to make foam cells which are the beginning of a fatty streak and atherosclerosis
for whatever reason arteries like to retain LDL then they aggregate they get oxidized and macrophages attack them it becomes foam cells
these there's so many of these they're going in and out through the 70 nanometer you know Gap Junctions even via transcytosis sometimes all these different ways that these things are getting into your arteries they get oxidized they get damage in there the immune system macrophages forms foam cells and then you get this fibrous plaque
they get oxidized they get damage in there the immune system macrophages forms foam cells and then you get this fibrous plaque and then one day you know the the I think I you know I've showed the model here you've got these plaque and then one day a plaque ruptures you've got you know a thrombus here and then it plugs up your your entire Lumen and that's how you have a heart attack
these things are getting into your arteries they get oxidized they get damage in there the immune system macrophages forms foam cells and then you get this fibrous plaque
The problem occurs when proteoglycans bind to and let's just make math easy and not get into the LP little A's and the VL deals at the moment let's just talk about the LDL since that's the largest burden of this but when these proteoglycans bind to the LDL and it gets retained all of a sudden now you have something that's where it's not supposed to be that's not where we want that thing it's obviously in a high oxygen environment so it's going to undergo a chemical reaction called oxidation because it's carrying a cargo a sterile that and by the way they can be carrying phytosterols and other things like that but these things have ample opportunity to undergo an oxidative reaction it's that oxidative reaction that then kicks off an inflammatory response in the endothelium
an LDL part out truly oxidized LDL particle which is the only type that a macrophage in your arterial wall can internalize is oxidizing the wall of the artery and what is oxidized it's the phospholipids on their surface or maybe some free star rolls beatify toaster or cholesterol that oxidized surface lipids is what the scavenger receptor on a macrophage is gonna pull that particle into it and then you you start accumulating cholesterol and you have a sterile Laden Feltham cell bingo you got the disease
what is true is that ldls themselves as lipoproteins are bad actors because of what they do what they do is they go into artery walls where they get oxidized and they basically dump their oxidized sterile contents into the sub endothelial space which elicits an immune response and a whole bunch of other things that lead to atherosclerosis
ldls themselves as lipoproteins are Bad actors because of what they do what they do is they go into artery walls where they get oxidized and they basically dump their oxidized sterile contents into the sub endothelial space which elicits an immune response and a whole bunch of other things that lead to atherosclosures
it's it's cholesterol is a rich Target for oxidation and as that happens we we once again uh have this example of the immune system which is out there uh basically surveying constantly looking for things that are bad usually in the form of monocytes and they're sensing they're seeing a chemical signal for that oxidation and as they enter that space they become this other type of cell they they they metamorphy into something called a macras and the job of the macras is to literally consume to phagocytose to eat the thing that it is concerned with and when it begins to eat that oxidized cholesterol that produces the foam cell
Ultimately, what's happening in atherosclerosis is that the inflammatory response is being activated by the accumulation of indigestible waste products, specifically oxidized cholesterol, in macrophages in the artery wall, which turn to foam cells, and generally make cells around them angry.
there's been evidence that these small dense ldl particles will insert themselves into the arterial lining the arterial wall and of course the lps is a signal to our immune cells resident macrophages sense the lps signal and it's like oh i've got to get rid of that bacteria because it's a threat so it comes and try to try to engulf through phase phagocytosis what it thinks is a bacteria but which actually is a small dense ldl particle with an lps bound to it through a lipid lipid interaction inserted into the arterial wall and so it phagocytosis that entire lipoprotein and you get the formation of what's called a foam cell sort of a soft plaque and this is stuck in our arterial wall