No, it's completely fair. We have objective criteria for evaluating "best", and expert opinion is Grade C evidence (different groups use different lettering conventions, but suffice it to say that expert opinion is not regarded highly since it is, in fact, not evidence).
LDL is not VLDL. LDL-C is different from VLDL measures. Since this isn't that popularly known, let me explain a bit: people rarely measure LDL-C directly. Instead, they assume that virtually all serum TG is carried by VLDL; they measure HDL; and then they infer LDL-C. It turns out that this inferred LDL-C correlates well enough with directly measured LDL-C for the vast majority of people that it hasn't been worth the cost of implementing a direct test except for research purposes (Canadians will differ on this).
I'm not exactly sure where you are going with the VLDL vs LDL discussion, however, since VLDL is the precursor to LDL. It is always a formal possibility that a confounder is modifying or even inverting the relationship between X and Y, but typically one would expect some evidence in support of that. The LDL-MI association holds up in every population tested - so unless this postulated confounder is present in every population, it's not likely. Plus, most people expect that both VLDL and LDL will correlate with MI risk, though the best studied one is LDL.
>You did not address the Agatston score point, which iirc was the main rebuttal I'd made to your earlier comment. As this discussion is threatening to run off on another tangent, I will end here.
My point isn't that the Agatston score is bad; it's that you're rejecting the intermediate endpoint with the best evidence (LDL-C, which has prospective randomized trials supporting it) and then endorsing an intermediate endpoint that's far less accepted (coronary calcification). I rebutted your Agatston score comment in a couple of ways previously and without actual evidence supporting its importance in the causal chain for MI, I see it merely as a biomarker (unlike LDL-C, which is causal).
>Perhaps GCBC may itself be compelling?
No. Since the GCBC is a book that expresses its author's expert opinion, I do not find it to be evidence. When I hear "evidence," I expect data, not opinion.
No, it's completely fair. We have objective criteria for evaluating "best", and expert opinion is Grade C evidence (different groups use different lettering conventions, but suffice it to say that expert opinion is not regarded highly since it is, in fact, not evidence).
>Citation?
Looking at only those without CVD at time of enrollment, see http://www.ncbi.nlm.nih.gov/sites/pubmed (70,000 participants in that meta-analysis alone).
LDL is not VLDL. LDL-C is different from VLDL measures. Since this isn't that popularly known, let me explain a bit: people rarely measure LDL-C directly. Instead, they assume that virtually all serum TG is carried by VLDL; they measure HDL; and then they infer LDL-C. It turns out that this inferred LDL-C correlates well enough with directly measured LDL-C for the vast majority of people that it hasn't been worth the cost of implementing a direct test except for research purposes (Canadians will differ on this).
I'm not exactly sure where you are going with the VLDL vs LDL discussion, however, since VLDL is the precursor to LDL. It is always a formal possibility that a confounder is modifying or even inverting the relationship between X and Y, but typically one would expect some evidence in support of that. The LDL-MI association holds up in every population tested - so unless this postulated confounder is present in every population, it's not likely. Plus, most people expect that both VLDL and LDL will correlate with MI risk, though the best studied one is LDL.
>You did not address the Agatston score point, which iirc was the main rebuttal I'd made to your earlier comment. As this discussion is threatening to run off on another tangent, I will end here.
My point isn't that the Agatston score is bad; it's that you're rejecting the intermediate endpoint with the best evidence (LDL-C, which has prospective randomized trials supporting it) and then endorsing an intermediate endpoint that's far less accepted (coronary calcification). I rebutted your Agatston score comment in a couple of ways previously and without actual evidence supporting its importance in the causal chain for MI, I see it merely as a biomarker (unlike LDL-C, which is causal).
>Perhaps GCBC may itself be compelling?
No. Since the GCBC is a book that expresses its author's expert opinion, I do not find it to be evidence. When I hear "evidence," I expect data, not opinion.