The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
so this is why if you look at the APO b or even the LDL particle count in diabetics it's through the roof or in people with high triglycerides due to mostly decreased clearance and so the ldlp goes up but what's driving the total ldlp it's the small ldlp
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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 HDL particles become so small they break apart apoa1 goes down to the kidney where it can be catabolized into amino acids and excrete it hence explaining why diabetics people with high trigs have such low HDL particle counts and low HDL cholesterol
the liases mostly hepatic lias takes the trigs out and then the LDL particle becomes very small so you have a small LDL particle which per particle can't carry many cholesterol molecules but the major reason apob goes up is an LDL that is small the apob assumes a different confirmation on the surface of the LDL and it is no longer recognized by the LDL receptor so you have marketly delayed clearance of the small LDL