Putting this up for argument rather than for agreement. I have read it twice and I am still not certain what it supports.
ApoB is the more informative number and it is cheap. LDL-C estimates cholesterol mass in atherogenic particles; ApoB counts the particles, and it is particle count that tracks risk — which is why the two can disagree and why the disagreement is the clinically interesting case. Triglycerides fall substantially with weight loss and improved insulin sensitivity, HDL moves modestly, and LDL-C often barely moves at all, which surprises people who expected everything to improve together.
Where I think it is weakest: the follow-up is short relative to how long people actually take these drugs, so durability is an assumption here rather than a finding.
The question I want answered is whether an unchanged LDL-C alongside a large triglyceride fall is a good result or a bad one, because ApoB and LDL-C seem to be telling different stories. Happy to be told the question itself is wrong.
wei_SG said:ApoB is the more informative number and it is cheap.
Agreed on the mechanism, with the caveat that the head-to-head used semaglutide 1mg, not 2.4mg. It is still the best direct evidence available, but it is not the comparison most people think they are citing.
wei_SG said:ApoB is the more informative number and it is cheap.
Careful with treating an unchanged LDL-C as a failure. If ApoB and triglycerides both fell, the particle picture improved regardless of what the calculated LDL says.
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Browse GL BiochemShort answer first, then the reasoning. Steady state is faster than people expect: half-life about five days, so you are at plateau in roughly three to four weeks rather than five. That matters when you are deciding whether a dose step has finished expressing itself.
LarryQC_SD said:Agreed on the mechanism, with the caveat that the head-to-head used semaglutide 1mg, not 2.4mg.
Mine went the same way, slower.