Hemolysis -> increased erythropoiesis -> increased cholesterol consumption for RBC membrane synthesis -> decreased serum LDL.
This is an association with hemolytic anemia, not a direct effect of unconjugated bilirubin itself. The mechanism is not fully settled, but increased erythropoietic demand is the traditional explanation. A
review of anemia and cholesterol discusses this proposed marrow consumption; in sickle-cell disease, lower LDL also tracks more closely with the severity of anemia than hemolysis alone in
this cohort study.