Paul Saladino· MD
and I think that something that I've and you and I have talked about offline but that I have pushed back on consistently is that not every elevation not every increase in apob containing lipoproteins carries the same increase of cardiovascular risk and I'm speaking for myself I'm not speaking for Dave I'll let him give his thoughts on this kind of stuff if he if he would like but Dave tries to stay kind of agnostic with all this as he's researching this but my perspective is that not every elevation of apov containing the proteins carries the same cardiovascular risk and for the mainstream to suggest something like the lipid hypothesis in published papers like the 2017 European atherosclerosis Society paper in which the title is LDL cholesterol causes atherosclerosis I think those things are confusing to people predominantly in settings where people are ketogenic or low carb or just eating more saturated fat from animal foods like butter and less seed oils and they inevitably or I should say often see an increase in LDL and AAL B containing with proteins and in that situation if these people are not insulin resistant and have normal thyroid metabolism and normal macrophages and genetics that don't align with monogenic or even polygenetic FH I don't think that there's an easy case to make I think it's much harder to make the case and we should question this much more carefully about the potential increase or lack there of cardiovascular risk aob B anything you want to add to that statement or asterisk or anything Dave I'm not saying that's your position I'm just kind of giving context to all the things we're talking about