Yes: professor emeritus (that is, no longer a professor) in the Division of Endocrinology (that is, not a cardiologist). There is a very strong scientific consensus that apoB/LDL-cholesterol is the core driver of atherosclerosis.
Low-density lipoproteins cause atherosclerotic cardiovascular disease.
Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel | European Heart Journal | Oxford Academic]
I think it’s pointless to debate the LDL topic further, at this point it is beating a dead horse. The LDL denialist wackos are going to stick to their positions no matter the evidence. I’ve seen it too much, the repeating ad nauseam of the same flawed arguments that have been debunked and destroyed over and over by superior evidence. The human mind is fascinating, the debate is not.
You’re conflating two different things. When people say that apoB/LDL-C drive “heart disease,” they mean atherosclerotic cardiovascular disease (ASCVD) — the single greatest killer on the planet.
The kind of “heart disease” that involves cardiac fibrosis is heart failure, which is a different kind of cardiovascular problem entirely with different drivers.
True, but don’t jump to the converse. You can have all those other risk factors under control and still be killed by ASCVD if your apoB is high enough: this is exactly what happens in even fairly young people with familial hypercholesterolemia.
Would you please link said discussion?
A good presentation by Joan Mannick on mTOR and rapalogs/rapamycin:
