Peter Attia· MD
I call this loosely lipid cellular lipid malabsorption or I just generally shorten it to lipid malabsorption basically here's here's the issue that I have with the existing Mendelian randomization for that matter almost all of the gene based studies is what we're trying to get is as much as we can the isolation of just a higher gradient of LDL particle count right and that's what we all secretly we want your wand when you're talking about where we can waive it and then there's just magically more LDL particles in some people or for that matter less LDL particles right without touching any other parts of the process the problem is that I believe of I'm keeping a list of my own s in peas of those genes that are either resulting in higher or lower LDL C and unfortunately of the ones that I find in the Mendelian randomization 's they don't just result in the higher LDL cnl the LP they also come to be that way because there's a lack of lipids or liberal protein uptake by the cells therefore particularly with endothelial cells you've got to be concerned that that could cause dysfunction and therefore could be a reason for why you would have higher levels of atherosclerosis