106 INANITION AND MALNUTRITION 



McCollum and Simmonds (McCollum '22) found that rats, kept at an early- 

 age upon diets in which the inorganic content is unsatisfactory, develop abnormal 

 forms and become permanently stunted. They become stocky, owing to failure 

 to grow in length. This permanent suppression of growth is contrasted with the 

 successful recuperation after retardation by vitamin deficiency, likewise after 

 inadequate protein diet (Osborne and Mendel) and resembles the results of 

 general underfeeding (Jackson and Stewart). 



The effects of phosphorus deficiency upon growth have likewise been demon- 

 strated. Hart, McCollum and Fuller ('09, '09a) found that pigs at 40-50 

 pounds made normal gain in body weight up to 75-100 pounds on low phosphorus 

 grain diets. Then followed loss of weight, weakness and collapse (presumably 

 due to exhaustion of the available phosphates stored in the skeleton). Good 

 results followed upon the addition of calcium phosphate to the diet. 



Lipschutz ('10, '11) obtained continued though subnormal growth in puppies 

 on a phosphorus-poor diet of rice and egg albumin, supplemented by salt mix- 

 tures. The skeletal lesions resembled those of scurvy (vitamin deficiency). 

 Heubner ('11) similarly observed that puppies continued to grow for 7 weeks on 

 rice diet, which is poor in phosphorus (also otherwise deficient), with subsequent 

 decline. On a tapioca diet, growth ceased in 3 or 4 weeks, and marked emacia- 

 tion followed. On refeeding with rich mixed diet, normal appearance and 

 health were rapidly restored, but in body size and weight the dog remained 

 permanently dwarfed, corresponding to a puppy of 3 months. Masslow ('13) 

 also found that puppies on phosphorus-poor diet continue nearly normal 

 growth for about one month, but later lose weight, become emaciated and die. 

 Sherman ('n) concluded from a study of typical American dietaries that 

 human malnutrition is frequently due to phosphorus deficiency. Further data 

 on calcium and phosphorus deficiency will be mentioned later in connection 

 with the discussion of rickets. 



Emmett, Allen and Sturtevant ('20) and Swingle ('22) cite evidence that 

 iodin is effective in causing the metamorphosis of amphibia, which recalls the 

 well-known experiments of Gudernatsch, showing acceleration of metamorpho- 

 sis by thyroid feeding. The question of iodin deficiency will be considered later 

 in the chapter on the thyroid gland. Smith ('17) concluded that iodin deficiency 

 in the diet during gestation in sows results in the birth of weak, hairless pigs of 

 full size but with edematous skin and other abnormalities, ascribed to disturbance 

 of function in the fetal thyroid gland. There may be a similar occurrence in 

 sheep and other domestic animals. 



Fetzer ('13) found that, on diets deficient in iron pregnant rabbits can supply 

 from their own bodies the iron necessary for fetal growth only up to a certain 

 limit, beyond which fetal death occurs. Hess (,'22) cites evidence indicating 

 that in some cases a lack of iron in the diet of infants may lead not only to anemia 

 but also to marked retardation in growth, with prompt recovery upon addition of 

 spinach. 



Rachitis. — While the lesions in rickets appear most prominent in the skeleton 

 (to be considered in a later chapter), it is nevertheless a general metabolic dis- 

 order with certain broader aspects which may be briefly mentioned here. The 



