Oxidized LDL with an oxidized ApoB100 particle is atherogenic, while native LDL is not.

“negative LDL non oxidized LDL we it probably doesn't do the same thing not exercise LDL doesn't get picked up by macrophages”

“there's something about the ldl particle that matters that i think is so fascinating they basically had a lean mass hyper responder in their practice they didn't treat them thankfully thank god because they didn't need treatment with a statin and they didn't have atherosclerosis they're admitting there's a third or a fourth variable one of these third or fourth variables is the oxidation of ldl right and this idea that maybe not native ldl doesn't seem to cause atherosclerosis but maybe oxidized ldl does or maybe oxidized ldl is a better risk or maybe there are things causing oxidation of ldl that we should be thinking about”

“as far as i'm aware the overwhelming body of evidence in the scientific and medical medical literature is that oxidized ldl is at least required and certainly central to the whole progression of atherosclerosis as far as i'm aware there is no other alternative hypothesis offered right this goes all the way back to the 1980s and brown and goldstein and steinberg in winston looking for how ldl would initiate atherosclerosis and finding that it had to be oxidized in order to do it nobody's ever debunked those findings that i'm aware of i don't think so”

“oxidized LDL is probably the main problem and that's a much better predictor of how many of these plaques how much of this repair that's going on in your arteries is going to lead to actually let's just say long-term projects that are likely to be bad”

“LDL does not cause atherosclerosis because LDL is not enough to cause atherosclerosis”

“the liver clears oxidized LDL pretty quickly so does your immune system so that's not the problem”

“it has to actually be retained it has to aggregate it has to get damaged and oxidized and taken up by macrophages I mean it's a whole long process it's not like we just throw an LDL somewhere and suddenly magic happens”

“at some point you overwhelm the intrinsic mechanisms within an APB particle to maintain that linolic acid as unoxidized right you m you overwhelm the vitamin E and the lipid fraction you overwhelm any coenzyme Q10 and you get oxidized LDL and I think most people would agree oxidize LDL is the real problem that is the atherogenic particle”

“it's the size of the LDL particle really doesn't determine the ease with which it gets through the cell or not or between the cells what's much more important is because most of the LDL that gets into the sub in Mithila space gets right back out and doesn't cause any trouble where the trouble comes is when they get retained and when they get oxidized and when they kick off an inflammatory response”

“So your biggest lever to actually reduce your overall amount of oxidized LDL is just to prevent as much getting into the inima and retained as possible.”

“And do we not believe that an oxidized LDL versus a non oxidized LDL would be more agenic on a per particle basis? Yes. An oxidized LDL is more atherogenic in the periphery.”

“And we do know oxidized LDL is more atherogenic on a per particle basis.”

“And when we look at people who have higher levels of oxidized LDL, it's typically a downstream effect of how much LDL got into their inima in the first place.”

“potentially it would also be more o more arogenic outside because it has a greater probability of becoming retained and ox and remaining oxidized and inciting uh the inflammatory response.”