Milk is a rich source of sphingolipids, particularly sphingomyelin (SM). SM represents about one third of total milk phospholipids (52). Traditionally, there has been interest In SM as an anticarcinogenic agent acting in the intestinal tract. But since it was discovered that SM (and more generally sphingolipid) derivatives are cellular signalling substances with possibly important implications for human health, there is a renewed and growing interest and research in this field. This is highlighted by a number of excellent reviews in recent years (2, 7, 23, 25, 36, 38, 40, 51). Dietary SM probably exert a beneficial effect in the gastrointestinal tract, protecting against cancer and bacterial infection. Furthermore, it is reported that the SM content of intestinal cells may regulate cholesterol absorption. But far less is known about the impact of dietary SM and sphingolipids in general on endogenous sphingolipid metabolism. SM is degraded in the intestinal tract, but SM digestive capacity is limited and neither SM nor its metabolites are transported very efficiently from the intestine to other organs. Therefore, it is questionable whether dietary sphingolipids interfere directly with endogenous regulatory mechanisms. But nevertheless, several dietary measures may affect SM levels in lipoproteins and cells, including intestinal cells, and thus SM metabolism. Furthermore, the closely coordinated regulation of cholesterol and SM metabolism deserves attention. It may well be that modifications of cholesterol metabolism, brought about by dietary measures, causes indirectly changes in cell signalling, with potentially important implications for health.