Since lipids (sterols, phospholipids and triacylglycerols or triglycerides) are oils (hydrophobic) they are transported in plasma in protein wrapped vehicles called lipoproteins. The surface proteins which convey solubility and structure to lipoproteins are called apoproteins or apolipoproteins. Thus, the only way sterols get into the artery wall is as passengers in the lipoprotein particles transporting or trafficking them. The particles are driven into the arterial intima by concentration gradients. Quantitating atherogenic lipoproteins is the best determinant of CV risk and thus particle concentrations are not only the best way to predict risk, but are also the best goals of therapy. Historically, for a variety of logistic reasons, few clinicians have performed lipoprotein testing. But this is changing and in April 2008, the ADA and ACC issued a consensus statement on LipoProtein Management mandating particle quantification in patients with moderate, high or very high risk; if you are basing CV risk and goals of therapy using lipid profiles, you are simply using lipid concentrations as surrogates or proxies of lipoprotein concentrations. You are guessing! Previously we have assumed that if LDL-C is elevated LDL-P (LDL particle concentration) is also elevated. Unfortunately, in an insulin resistant world, where small LDL particles predominate, that is not always true and very often the least useful surrogate of LDL-P is LDL-C! In these patients there is a major disconnect between LDL cholesterol and LDL particle concentrations. Lipid profiles report lipid concentrations: how much cholesterol is within all of the LDL, HDL or VLDL particles that exist in a deciliter of plasma. Never confuse LDL- C or HDL-C with LDL-OP or HDL-P.