To discover the mechanism by which oral contraceptives increase the level of cholesterol saturation of human bile, we measured biliary lipid secretion rates, gallbladder and hepatic bile lipid composition, bile acid pool size, bile acid composition, and plasma lipoprotein levels in five healthy women during routine oral contraceptive treatment and again during normal menstrual cycles on no medication. The molar percent cholesterol in both gallbladder and hepatic bile was higher in every subject while taking oral contraceptives (p less than .02). Oral contraceptive usage was accompanied by a significant enhancement of biliary cholesterol secretion (65 versus 46 mg/hr, p less than .01), but there was no significant change in bile acid or phospholipid secretion, total bile acid pool size, or bile acid composition. These findings indicate that oral contraceptive usage increases biliary cholesterol secretion, thereby raising the level of cholesterol saturation of bile and predisposing to cholesterol precipitation and gallstone formation.
PIP: To discover the mechanism by which OC (oral contraception) increases the cholesterol saturation of human bile, the authors measured biliary secretion rates of cholesterol, bile acids, and phospholipids in 5 normal women, both during OC usage and during cycles on no medicaltion. In the same subjects bile acid pool size, bile acid composion, and plasma lipoproteins were also measured. Data showed that the molar percent cholesterol was higher during OC usage in both gallbladder and in hepatic bile. The lipid secretion data showed that this increase in the relative cholesterol content of bile was due to highly significant enhancement of cholesterol secretion into bile, rather than to a decrease in bile acid or phospholipid secretion. Bile acid and phospholipid secretion, bile acid composition, and total bile acid pool size did not change. These results indicate that the mechanism responsible for increased saturation of bile with OC usage is an increase of biliary cholesterol secretion, independent of any change in bile acid or phospholipid output.