Except it isn’t. Dayspring argued with me over this that Daniel Steinberg’s seminal research showing oxidation of the polyunsaturated fatty acids in the LDL particle membrane is *the* central mechanism driving its accumulation in atherosclerotic plaque is “outdated” because “LDL aggregability” is an independent driver of macrophage uptake. Steinberg died a few years ago. But he was #3 just below Brown and Goldstein in LDL receptor fame and he chaired the 1984 NIH Consensus Conference that solidified the consensus that LDL-C “causes” heart disease, and his lab’s work laid out the central mechanism by which LDL particles wind up in plaque. The problem with Dayspring’s argument is that a) oxidation itself is a major driver of LDL aggregability and b) the other major driver is the ratio of choline to saturated fat, which just happens to also be a major determinant of fatty liver disease. The reality is every mechanism through which LDL particles wind up in plaques is completely separable from their concentration. There are zero drugs and zero clinical trials that can distinguish between the impact of concentration versus the impact of oxidation. This is a MECHANISTIC claim, not an “outcomes” claim so you MUST rely on mechanistic research to answer the question. On this mechanistic claim about concentration being the driver, Steinberg’s graph from 1983 remains undefeated, shown below. The range at which macrophage uptake of non-oxidized particles (bottom line) plateaus is massively below the physiological range, below an ApoB of 5 or an LDL-C of 7. Meanwhile, oxidation (top line) causes a 5-fold increase. So at physiological concentrations, concentration is irrelevant and oxidation is paramount.