Fat-Soluble Vitamins

Volume 30 of the series Subcellular Biochemistry pp 455-488

Vitamin K Metabolism

  • Paul NewmanAffiliated withVitamin K Laboratory, The Haemophilia Centre, St. Thomas’s Hospital
  • , Martin J. ShearerAffiliated withVitamin K Laboratory, The Haemophilia Centre, St. Thomas’s Hospital

* Final gross prices may vary according to local VAT.

Get Access


The discovery of vitamin K can be largely attributed to the Danish scientist Henrik Dam, whose work on sterol metabolism in chicks required the feeding of carefully controlled diets, some of which were depleted in lipids (Dam, 1929). This often caused internal hemorrhages and other symptoms similar to scurvy, but which Dam showed to be incurable by large doses of vitamin C. The finding of the lack of influence of cod liver oil concentrates (as a source of vitamins A and D), but the protective effect of cereals and seeds, prompted Dam to suggest that the bleeding syndrome was caused by a lack of an essential dietary component that was different from vitamins A, D, and C (Dam and Schoenheyder, 1934; Dam, 1934). Further work by Dam with experimental diets showed the factor was fat soluble, heat stable and occurred in various animal and plant tissues, hog liver fat being one of the best sources. In 1935, after ruling out vitamin E (hog liver fat was many times as active as wheat-germ oil), Dam proposed that the antihemorrhagic factor was a new fat-soluble vitamin that he called “Koagulations vitamin” or vitamin K (Dam, 1935a,b). Other rich sources of vitamin K were found to be green leaves such as alfalfa. Another surprisingly rich souce was bran or fishmeal which had become putrifled by the action of bacteria (Almquist and Stokstad, 1935; Almquist et al., 1938), suggesting that microbial action as well as plant biosynthesis is capable of producing the factor. Improvements in the assay method based on the restoration of normal clotting time in hemorrhagic chicks led to the proposal that a lack of vitamin K caused a deficiency in prothrombin activity and that vitamin K might be some kind of coenzyme or prosthetic group required for active prothrombin (Schoenheyder, 1936). However, subsequent work showed that prothrombin precipitates were active after all lipids had been removed and that vitamin K concentrates could not induce blood to clot (Dam et al., 1936).