Peter Attia· MD
the problem it would appear is that very crude metrics like the amount of cholesterol in an HDL or even the number of HDL particles or the size of an HCL particle those are basically the only things we can measure clinically at least those are so crude and so far removed from providing any quantification of the process you just described that I suspect in part that's why we are stuck in a way that we are not on the APO b side of The Ledger because so much of the damage caused by apob is simply captured in the number of them given the stochastic nature with which they enter artery walls and get retained