I think an implicit assumption in Feldman’s observations, as well as those of other LC advocates who are skeptical of LDL, is that insulin resistance matters more than the LDL numbers.
Consider, that half of the folks who have heart attacks, do not have elevated LDL. The High HDL-Low Tri pattern signals low insulin resistance. The Feldman Challenge that goes out on the Twitter and has yet to be cashed is to provide a non-drug, non-gene study that controls for high HDL, low Tri, and still implicates high LDL.
The short of it is, ketonians have not been studied much for CVD.
My position on statin use for High LDL with high HDL and low Triglycerides is that someone would have to show me the science demonstrating an all cause mortality benefit to statin therapy, not a CVD mortality benefit. All cause, because dead is dead, while CVD is survivable. To date, to my knowledge, the only improvement to ACM from statin use is to men under 50 (check), who have already suffered a heart attack (whoops). As I do not fit that demographic, I will not take statins.
My endocrinologist was very concerned about me having FH. Fine, even if I have the genes for it, let’s look at other risk factors. My dad never really moved beyond pre-diabetes, is 74, has never had any CV event, but is suffering from Alzheimers, despite cholesterol levels that have been elevated for his entire adult life. My dad was put on a statin recently, and NOW, at 74, has been prescribed metformin, as a precaution. Hmmm… It’s known that statins increase your likelihood of developing T2DM. Part of why I don’t want that.
My uncle did have a heart attack or two some time in his late 40s or early 50s. He smoked, had real T2DM, and died of lung cancer before he turned 70.
My dad is a first level relative. My uncle is a second. My uncle engaged in multiple risk factors, my dad fewer (he smoked into his 30s), and me currently, fewer still (no smoking since a couple in high school). So, should I be worried about the FH? If so, should I worry about the LDL or just avoid things that produce chronic inflammation, and will make the LDL more dangerous? I think I’m gonna opt for not worrying about LDL-C, LDL-P, ApoB, Lp(a), or anything but inflammatory markers and insulin resistant measures.