1/ Retweeting for balance from my good friend and colleague, @DrNadolsky
To be sure, I agree large LDL particles can be participants in atherogenesis.
The real question is whether they are independently initiating and/or accelerating atherosclerosis (regardless of context).
To be sure, I agree large LDL particles can be participants in atherogenesis.
The real question is whether they are independently initiating and/or accelerating atherosclerosis (regardless of context).
https://twitter.com/DrNadolsky/status/1275472325127794689
2/ Existing medical consensus is that yes, regardless of context, more LDL=more risk of CVD, full stop.
Myself, I believe context does indeed matter. Which is why I suspect we haven’t yet gotten a study to meet the #LCCholesterolChallenge
cholesterolcode.com/lccholesterolc…
Myself, I believe context does indeed matter. Which is why I suspect we haven’t yet gotten a study to meet the #LCCholesterolChallenge
cholesterolcode.com/lccholesterolc…
3/ In short, I think the context of why we get particular lipid patterns (such as atherogenic dyslipidemia) helps to expose the underlying root cause of atherogenesis.
I often refer to this as “lipid profile centric” thinking vs “lipoprotein centric” thinking.
I often refer to this as “lipid profile centric” thinking vs “lipoprotein centric” thinking.
4/ This is why I’m happy to be teaming up with @DrNadolsky and @DrRagnar to test these differing hypotheses directly with #LMHRs, a population with many who have excellent CVD risk markers save the one of interest: #LDL
Help us make it happen-> CitizenScienceFoundation.org 501(c)(3)
Help us make it happen-> CitizenScienceFoundation.org 501(c)(3)
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