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1/ Thanks for the commentary @DaveKeto. Maybe there is some misunderstanding of the point of the article. It wasn't set out to be a "rebuttal of the triad". Rather, it was a mere clarification of points that perhaps were missed during the live discussion. https://twitter.com/DaveKeto/status/1249805679876902914
2/ By all criteria required to assess causality, LDL is independently causal in ASCVD. This vital importance of this was focused on in the article.
If high LDL in context of triad is not an issue, then burden is first on you to demonstrate that LDL is not independently causal.
If high LDL in context of triad is not an issue, then burden is first on you to demonstrate that LDL is not independently causal.
3/ That's why the distinction was made to readers between systems biomarkers/mediating factors and an independent causal factor.
With all the evidence accumulated in this area, LDL is seen to be causal, independent of the influence of other factors (also incl. inflammation).
With all the evidence accumulated in this area, LDL is seen to be causal, independent of the influence of other factors (also incl. inflammation).
4/ Dave, you and I agree there are interesting Q's still unanswered. But point of this article was to clarify why LDL is correctly deemed causal in ASCVD & there's nothing you've pointed to that refutes that. The article is stating what you need to refute, not other way around.
5/ As per our email correspondance, we took care to try to accurately reflect your position. I see some of your followers may not think that. Can you tell me which of the claims attributed to you are not your position? Happy to amend if necessary.
