Lean mass hyper-responders might possess a protective genetic component against accelerated atherosclerosis despite high LDL.

“i would argue given given how the hypothesis is stated as stated actually it should be the other way around you paul you should actually develop atherosclerosis faster than the homozygous fh toddler because you have an existing lifetime burden of several decades 43 years yeah 43 years so you actually have unless you had optimal ldl levels for the last four decades but even then i think what they would consider to be optimal levels to where it's regress regression level i think is something like in the 30 to 50 milligrams per deciliter or something like that i'm not even sure if it's that um but if you have 100 or above for sure you should have already have accumulated a lot of quote unquote ldl burden that is now part of the balance sheet and therefore if you're adding to it”

“and if they don't there's going to be some really interesting questions about if the paradigm around ldl slash apob is complete or we really need to contextualize it and i would argue for the latter”

“and if they don't then it's really going to shake the foundations of ldl as a primary mover or apob which is essentially synonymous with ldl”