Cardiovascular disease (CVD) is the leading cause of human death in the US. Despite decades of intensive research, the formation of atherosclerotic lesions is not fully understood. Aggregation of low density lipoprotein (LDL) is believed to enhance the initiation of atherosclerosis. We are interested in sphingomyelinase (Smase)-induced aggregation of LDL - as it relates to uptake by macrophages – which we demonstrated previously abides by colloidal principles of mass action. Here we address the relative rates (kinetics of enzyme hydrolysis versus particle aggregation dynamics) to suppress time as an independent variable and view LDL aggregation in ceramide space. Ceramide formation was measured as a function of time for enzyme concentrations in the range 0-0.24 units Smase/mL at a fixed substrate concentration 0.33 mg LDL/mL. LDL aggregate sizes were measured (dynamic light scattering, method of cumulants) as a function of time for the same enzyme concentrations. Trends are shown between ceramide concentrations and resulting aggregate sizes, giving more information on the relationships between these two values both during and after completion of the enzymatic reaction and the aggregation process. We will present our results and discuss the findings from a colloidal perspective. This work demonstrates the role that colloidal science can play in better understanding human disease.