The Biological Relations of the Higher Aliphatic Alcohols to Fatty Acids*

Almost 50 years ago, Munk and Rosenstein (1) reported the feeding of cetyl palmitate, as spermaceti, to a patient suffering from a chronic chyle fistula. Whereas they could recover a good portion of the palmitic acid, as tripahnitin, from the chyle, they were unable to demonstrate the presence of any cetyl alcohol in this material. It has since been shown by Mancke (2) that, even when large amounts of cetyl alcohol were added to the diet, the rise in cetyl alcohol excretion in the feces accounted for but a small fraction of that fed. Even after intensive feeding, however, he was unable to demonstrate any cetyl alcohol in the depot fat, the milk, or the lymph of his experimental animals. He concluded that the alcohol was rapidly destroyed by the animal. Gardner (3) discovered cetyl alcohol to be a normal but minor constituent of mammalian feces, and this finding has been confirmed (4). Schoenheimer and Hilgetag (4) were able to isolate cetyl alcohol, and on occasion small amounts of octadecyl alcohol, not only from normal mammalian feces, but also from the sterile feces of new born infants, the intestinal wall, the feces of dogs with biliary fistulae, and the contents of sterile operative intestinal cysts. Having thus successively eliminated bacterial action, diet, and bile as sources of the cetyl alcohol found, they concluded that