ABSTRACT
In heterozygotes for FH, the half-life of circulating LDL is prolonged by about 2 days as a result of the receptor defect. Consistent with this, the FCR is approximately half of that in normal people,9,26 and one-fifth or less of LDL catabolism is due to receptors.11 There is an even lower FCR25 and receptormediated clearance in homozygotes.28
