Apart from biliary cholesterol supersaturation, crystallization-promoting proteins and impaired postprandial gallbladder motility, the intestine may be an important factor in the pathogenesis of cholesterol gallstones. Prolonged intestinal transit could increase gallstone risk by enhancing formation in the intestinal lumen of the secondary hydrophobic and pro-lithogenic bile salt deoxycholate. Furthermore, in normal subjects there is an intimate relationship between gallbladder and intestinal motility in the fasting (interdigestive) state. In gallstone patients we found disordered intestinal motility, absent gallbladder contraction and abnormal release of the hormone motilin in the interdigestive state. These disturbances could contribute to gallstone formation.