Mendelian randomization studies found no causal link between genes that raise or lower HDL cholesterol and atherosclerotic cardiovascular disease.

“well even using pharmacologic trials and mendelian randomization you're going the concept you're going to come across with is lower is better”

“the evidence from mendelian randomizing like the newer technologies mendelian randomization they've just been slam dunk for apob”

“well even using pharmacologic trials and mendelium randomization you're going the concept you're going to come across with is lower is better”

“and it turns out as we know now at least from the CTP Inhibitors that you can't manipulate HDL and change outcomes and that's one of the elements of demonstrating an overall causal relationship and the mendelian randomization show HDL is not causal whereas they show apob is and cholesterol is too by the way”

“what a number of mendelian randomizations have shown is that APO B includes all the information in triglycerides LDL cholesterol and even HDL cholesterol it sums them which in the sense of vldl and LDL makes perfect sense”

“the 2019 guidelines were very pro-ableb the evidence from mendelian randomizing like the newer Technologies mendelian randomization they've just been slam dunk for apob”

“and I think we would only go on afterwards to see two mendelian randomizations one looking at genes that raised HDL cholesterol one looking at genes that lowered HDL cholesterol neither were found to be causally linked to ascvd”

“By the way HDL cholesterol turns out to be not causally related in the inverse nevertheless.”

“so so it turns out apob and ldlc are highly genetic which is what has allowed us to do the mandelian randomization studies that act as one of the you know there are basically three cornerstones of data that make it unambiguously clear of the relationship between LDL or apob and ascvd”