Previous findings of increased production of large VLDL particles by estrogen have been confirmed in a trial using estrogen-dominant oral contraceptives. Estrogen has been found to have LDL subclass-specific effects and to shift the distribution of apolipoprotein (apo)E from HDL to VLDL. Several recent studies document decreases in lipoprotein (a) [Lp(a)] levels, but the metabolic mechanism is yet unknown. The effects of progestational agents on lipoprotein metabolism remain unclear in view of conflicting reports.