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.
More apoB particles floating through your blood, there's more risk that they're going to interact with endothelium, and more likely some of them will get stuck in the endothelium and you know, trigger a cascade, which could build up to a fatty plaque and later a plaque.
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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the question now becomes as you put it tom how iron-clad is the story that it's the apo b-bearing particle in the presence of injured endothelium that is the trojan horse that begins this destructive trajectory of taking that cholesterol into the sub-endothelial space becoming retained undergoing this chemical oxidation process which then kicks off an inflammatory response that paradoxically as an attempt to repair the damage results in what can be a fatal injury
atherosclerosis atherogenesis is a multi-complex multifactorial disease and that's why even when peter and i if we consult on a case and we realize in this person we have to beat up apo b and get their particle numbers to a more physiologic range we don't stop once we do that we examine in great detail for other things that might be injuring the endothelium or the arterial wall and see are any of those treatable or so so we're getting a little bit smarter on lipoproteins but there certainly is more to it than just particle number
but it doesn't seem to bother many of my friends you walked through the pathophysiology of how the APO B bearing particle wreaks havoc in the artery wall many many years before we see clinical events
the question now becomes as you put it Tom how Ironclad is the story that it's the APO B bearing particle in the presence of injured endothelium that is the Trojan Horse that begins this destructive trajectory of taking that cholesterol into the sub-endothelial space becoming retained undergoing this chemical oxidation process which then kicks off an inflammatory response that paradoxically as an attempt to repair the damage results in what can be a fatal injury
but the Lipo proteins that have apobs on them can enter the artery wall when the endothelium uh is intact but they do so more prevalently and more easily when the endothelium is damaged
if those um apob wrapped lipoproteins get trapped inside the endothelial layer a chemical process known as oxidation takes place and that leads to inflammation
so so we already talked about how we get into this process where uh you know you you have the the apob uh carrying lipoprotein let's again just simplify it and call it the the LDL in this situation although as we'll talk about I'm sure they can also be an LP little a it it's it's it's enters that subendothelial space and its presence alone uh makes it susceptible to have its contents oxidized