“…[18][19][20] CGPS participants were also nonfasting, which may have influenced the assessed lipoprotein profile. Although it is likely that VLDL and triglyceride-rich particles represent causal effectors (rather than merely biomarkers) of increased cardiovascular risk based on genetic epidemiology, mendelian randomization, and clinical trial data of triglyceride-lowering therapies, 7,16,[21][22][23] future randomized trials will be required to definitively establish the therapeutic potential of targeting these subfractions. More broadly, these results are consistent with mendelian randomization studies which have prioritized apoB as the causal lipoprotein risk factor for atherosclerosis, 6,16,24 but future studies will be needed to delineate the causal roles of the specific components of each lipoprotein fraction and subfraction.…”