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I didn't misrepresent your findings. I quoted your findings that statins didn't reduce sdLDL, which is consistent with other work showing that sdLDL doesn't bind to LDL-r and must be removed by macrophages, which is independent of statin mechanisms. I didn't say you consider
statin effects to be weak - that's my interpretation of how your findings fit with the literature.
You, as well as @kevinnbass , would benefit from seeing the work of @KenSikaris who covers this topic so well:
@DrPaulMason also covers sdLDL beautifully.
You, as well as @kevinnbass , would benefit from seeing the work of @KenSikaris who covers this topic so well:
@DrPaulMason also covers sdLDL beautifully.
When you say statins "work", yes, statins reduce LDL but they do a whole lot more, including reducing inflammation and coagulation. Since the lit is so clear on sdLDL being the atherogenic form of LDL and not large buoyant LDL, it is reasonable to speculate that the pleiotropic
effects of statins are the likely mechanisms that provides some CHD benefit.
As to statins and primary prevention, the benefits are barely greater than placebo, which is why I say they are anemic, a common conclusion reached by ppl who are highly respected,e.g., Dr. Rita Redberg.
As to statins and primary prevention, the benefits are barely greater than placebo, which is why I say they are anemic, a common conclusion reached by ppl who are highly respected,e.g., Dr. Rita Redberg.
Although many ppl are impressed by statins in sec prev, the ARR is in low single digits compared to placebo. The best effect was 4S, which showed about a 4% mortality benefit, but that was only in ppl who had ⬆️TGs and⬇️HDL. There was no benefit in ppl w/ ⬇️TGs and⬆️HDL.
In closing, I find it remarkable you're unaware of the vast lit on sdLDL related to CHD. I find it telling that since statins didn't lower sdLDL, you dismiss it as relevant to CHD. You have an important finding but you're forcing it to fit your LDL-centric view of CHD.
