Chapter VIC 



B VITAMIN DEFICIENCY STATES 



General Considerations 



When for some reason the supply of one of the B vitamins to an animal 

 organism is diminished to a level below the nutritional requirement, the 

 B vitamin content of the organism slowly diminishes, as a result of both 

 molecular attrition and excretion. The time required for the shortage to 

 become manifest varies with both of these factors and with the rate at 

 which the nutritional deficit is incurred. Eventually, however, the short- 

 age of vitamin will be felt in the individual metabolizing cells of the 

 body and the cellular function becomes retarded or deranged in some 

 other manner. The various organs and tissues of the body vary in their 

 ability to fend for themselves under such adverse conditions, as evidenced 

 by the fact that deficiencies do not primarily affect all portions of the 

 animal with equal severity, and that death from B vitamin deficiency 

 generally results from the loss of function of some one most susceptible 

 organ or tissue, and seldom from general inanition. 



Since all the B vitamins are required by every living cell, and except 

 for nicotinic acid and choline, animal tissues are apparently incapable 

 of B vitamin synthesis, it would appear that all B vitamin deficiencies 

 might result in largely the same symptoms in any given species of animal. 

 This is generally true, except for those instances where a particular 

 tissue has an unusually high requirement for some one vitamin; 1 in this 

 case the cells of that tissue may suffer disproportionately from the deficit, 

 and the tissue will develop a specific pathology in response. It is there- 

 fore believed that the symptoms of the avitaminoses are generally not 

 due to any particular biochemical effect but rather to a diminished func- 

 tion of the cells of the various body tissues, resulting in a pathological 

 condition of the tissue concerned. 



From the overall standpoint, the progress of an avitaminosis generally 

 follows a rather set pattern, in which the course of the disease is first 

 manifest in general feelings of poor health, accompanied by a decreased 

 fasting urinary vitamin excretion level. As the symptoms progress there 

 is a gradual decrease in tissue vitamin levels until the point is reached 

 where clinical deficiency signs and symptoms occur and macroscopically 

 and microscopically demonstrable pathology results 2 (see Figure 17). 



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