This viral thread from @bschermd is a great read. Veins and arteries see the exact same LDL/ApoB, yet plaque forms almost exclusively in arteries — and a pristine vein grafted into arterial flow rapidly develops atherosclerosis. That points strongly to hemodynamic stress and endothelial injury as the primary trigger (Response to Injury) over a pure Response to Retention model. Our Keto-CTA data in a metabolically healthy cohort with a wide spread of LDL/ApoB (going from under 100 to over 500) show no association with either the presentation or progression of plaque. Which is why we've needed to do this exact research for so long. This central illustration is from our match analysis in JACC Advances (Budoff et al., 2024), where we compared 80 metabolically healthy ketogenic hyper-responders (mean LDL-C 272 mg/dL, HDL-C 90, TG 64, after 4.7 years on keto) to 80 tightly matched controls from the Miami Heart cohort (mean LDL-C 123 mg/dL). Despite the ~149 mg/dL difference in LDL-C, there was no significant difference in coronary plaque burden by CCTA total plaque score, CAC score, or other measures. And crucially, there was no correlation between LDL-C levels and plaque burden in either group. (Full paper: jacc.org/doi/10.1016/j.jacad…)