Paul Saladino· MD
I've also read that apoE can interact with the LDL receptor in some spaces
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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.
I've also read that apoE can interact with the LDL receptor in some spaces
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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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apoe4 generated proteins lead to more rapid clearance of LDL but if I understand economically not LDL there's no Foe on LDL yeah yes yet okay sorry sorry yeah so it's all on the remnants and on vldl I see and that's the point so because it's the remnants and the vldl those readily get attracted down regulate the LDL receptor so there's less LDL receptor to get rid of LDL is that the chain of events
the explanation is is that Apple e of course sits on vldl and on vldl remnants and apple E4 actually is a better ligand for the ldr receptor it's an amazing story better ligand than e32 and so especially the chylomicron remnants and the vldl so IDL races into your liver and that will down regulate the ldr receptor and therefore LDL goes up
ApoE4 does not allow cholesterol to be recycled to the liver as readily & thus leads to higher circulating cholesterol levels
loosely speaking, this is an oversimplification, if you're a 3/4 or 4/4, in theory you should have a harder time clearing LDL particles from circulation.