the pellagra diet, and this vitamin may be 

 responsible for the skin complications that 

 are almost always observed in clinical pella- 

 gra. 



Six other B-complex vitamins can only be 

 mentioned. Vitamin B 12 (APA), the anti- 

 pernicious anemia factor, has recently been 

 crystallized from liver concentrates, and this 

 crystalline product displays great potency in 

 maintaining the activity of the erythrocyte- 

 forming tissues of the body. Likewise folic 

 acid is now recognized as an important factor 

 in normal red-cell formation, and most cases 

 of pernicious anemia respond completely to 

 the administration of APA in combination 

 with folic acid. Inositol and para-aminoben- 

 zoic acid, respectively, are reported to pre- 

 vent the falling and the graying of the hair 

 of rats; and a deficiency of pantothenic acid 

 is associated with certain nerve and skin dis- 

 orders. However, deficiencies of these last 

 three vitamins have not been demonstrated 

 in man, perhaps because the very small re- 

 quirements are almost inevitably provided in 

 almost any diet — or because inositol and 

 para-aminobenzoic acid, at least, like certain 

 other B-complex components are synthesized 

 in significant quantities by the bacteria of 

 the intestinal tract. Finally there is biotin, a 

 vitamin that initially was shown to be essen- 

 tial for the growth of yeast. This compound 

 also seems necessary, in very minute amounts, 

 in many mammals, including man. Biotin is 

 widely distributed in natural foods, although 

 molasses, egg yolk, and liver have an espe- 

 cially high content. Raw egg white, on the 

 other hand, contains a specific protein, avi- 

 din, which interferes with the absorption of 

 biotin. One of the few human cases in which 

 a biotin deficiency has been demonstrated 

 was that of a man whose diet consisted al- 

 most entirely of raw eggs and wine. 



Both biotin and pantothenic acid are now 

 known to serve as coenzymes in cellular me- 

 tabolism. Biotin is active in reactions leading 

 to the synthesis of certain purines (p. 89) 

 and in reactions involving the fixation or 

 transfer of C0 2 ; whereas pantothenic acid 



Absorption, Metabolism, and the Diet - 353 



is a constituent of the very important coen- 

 zyme A (p. 154). 



Rickets— which is caused by a deficiency 

 of vitamin D — was fairly prevalent some 

 fifty years ago, but the spindly, crooked legs 

 of the rachitic child are seldom seen today. 

 In rickets, the deposition of calcium and 

 phosphorus compounds in the growing bones 

 is faulty; and consequently the bones are 

 weak and malformed. 



Vitamin D, or calciferol, is derived from 

 ergosterol — a closely related steroid com- 

 pound — when the latter is irradiated by ul- 

 traviolet light. The body accomplishes this 

 transformation in the skin, provided there 

 is an adequate exposure to direct sunlight, 

 or to some other source of ultraviolet radia- 

 tion. Ergosterol, which is called the provita- 

 min, is present in many animal fats such as 

 butter; and in summer vitamin D deficien- 

 cies are relatively rare. But in winter — and 

 under other conditions of reduced sunlight 

 — supplementary concentrates of vitamin D 

 should be added to the diet of children and 

 of women during pregnancy and lactation. 

 Great excesses of vitamin D are to be 

 avoided, however, since they may lead to 

 malformations of the limbs. 



Vitamins E and K have been identified 

 also. A deficiency of vitamin E (a-tocopherol) 

 induces sterility, at least in some animals, 

 such as the rat. Female rats abort their young 

 long before the normal time of birth; and 

 males become sterile, due to degenerative 

 changes in the testes. At present it has not 

 been shown that a vitamin E deficiency is 

 responsible for any kind of sterility in man, 

 although this possibility has not been ruled 

 out completely. Certain types of muscular 

 paralysis and of heart disease, on the other 

 hand, have responded well to the administra- 

 tion of vitamin E, although the relation be- 

 tween these diseases and a lack of a-tocoph- 

 erol remains obscure. 



With a deficiency of vitamin K, the liver 

 fails to synthesize adequate quantities of 

 prothrombase; and consequently the coagu- 

 lating capacity of the blood becomes im- 



