In order to explain why squirrel monkeys on some experimental diets develop cholesterol gallstones, we made a number of measurements on bile acid kinetics and on bile secretion and composition. The pool size of cholic acid was much greater in monkeys on a commercial diet than in any group on a semipurified diet. It was also greater in squirrel monkeys on a lithogenic diet but without gallstones than in monkeys from the same diet group with gallstones. The half-lives of cholic acid tended to be proportional to pool size, and absolute rates of cholic acid synthesis were, therefore, not much affected by diet. Diet did not affect the pool sizes and half-lives of chenodeoxycholic acid as much as those of cholic acid. Dietary cholesterol increased concentrations of cholesterol relative to bile acids and phospholipids in hepatic bile as well as absolute secretory rates of all three components. Interruption of the enterohepatic circulation of bile in fasted monkeys with gallstones resulted in a more rapid and marked increase in the relative cholesterol concentration and decline in the absolute concentration of bile acids in hepatic bile than occurred for monkeys without gallstones. This was due to the low proportion of the bile acid pool outside the gallbladder and the low rate of new bile acid synthesis of the monkeys with gallstones during fasting.