Malabsorption of bile acid increases cholesterol synthesis and activates hepatic LDL receptors which leads to enhanced elimination of cholesterol from the body. Interruption of enterohepatic circulation of bile acids may lead to a smaller bile acid pool, which, in turn, impairs cholesterol and fat absorption by reduced micellar solubilization. Together with reduced cholesterol absorption, the increased cholesterol loss as bile acids also reduces plasma cholesterol concentrations and the biliary cholesterol excretion, too. Diminished biliary cholesterol in bile acid malabsorption may contribute to the increased incidence of gallstones associated with ileal dysfunction. Malabsorption of bile acid leads to a fall in LDL-cholesterol concentration, and an increase of HDL-cholesterol concentration has been reported. VLDL-triglyceride concentrations are almost invariably raised. Enhanced cholesterol and bile acid synthesis in ileal dysfunction is reflected by raised concentrations of plasma cholesterol precursors, especially lathosterols, which can be used as an indicator of increased bile acid loss to faeces. Cholesterol absorption, in turn, correlates positively with plasma plant sterol concentrations levels and the ratio of lathosterols to campesterols can be used as a screening measurement for ileal dysfunction. Plasma fatty acid composition is also altered as a response to fat malabsorption associated with ileal dysfunction. The proportion of essential fatty acids is inversely correlated with faecal fat excretion and endogenous fatty acid synthesis is activated.