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.
any cholesterol in the artery only got there within an apob particle it doesn't just float in it gets there within an apob particle either vld or ldl that gets into the arterial wall and gets stuck there that's the cause of atherosclerosis
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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 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
APOB is necessary but not sufficient for atherosclerosis uh you have to have it but by itself it's not enough you also have to have inflammation and endothelial damage or dysfunction for the apob particle to get in there and cause damage
that's so critical because the particle that can leave plasma enter the artery wall and start off this atherogenic process are the apob family