ApoB-containing lipoproteins deliver lipids for growth or repair, and excessive deposition without removal leads to atherosclerosis.

“the body of evidence implicating the causal role of a poby and LDL P is so overwhelming”

“but again i think the causal relationship between apob and atherosclerosis is as strong as virtually anything we see in medicine for which you can't do the perfect experiment where you have to rely on natural experiments nevertheless maybe it's not entirely clear what the dose response looks like”

“when you prospectively follow a cohort the way the Framingham cohort was followed or the Framingham Offspring or the Mesa cohort or any of these cohorts have been followed you can take a bunch of people and you could measure their APO b or their ldlc or whatever metric it is that you're trying to determine if it in fact has a causal relationship to the disease of interest you can follow them over decades and you would demonstrate as has been demonstrated that the people with higher B higher ldlc higher non-hdlc and lower HDL all have a higher risk of developing atherosclerosis over time but it's hard to say that that's causal just based on that information because over the ensuing 20 years that you follow them they are free to make other choices that may impact those variables of interest and other variables”

“but again I think the causal relationship between apob and atherosclerosis is as strong as virtually anything we see in medicine for which you can't do the perfect experiment where you have to rely on natural experiments nevertheless maybe it's not entirely clear what the dose response looks like”

“there are these range of HDL particle sizes if they're large it means that reverse cholesterol transport is occurring when there's inflammation that is driving cardiovascular disease that reverse cholesterol cholesterol transport is not occurring and the HDL particle remains small in in general”