EFFECTS ON THE THYROID AND PARATHYROID GLANDS 443 



produced by calcium deficiency, and were prevented by the addition of cod 

 liver oil to the diet. 



The importance of iodin deficiency in the hyperplasia of the thyroid gland 

 in dogs was demonstrated by Marine ('07). He found that canine goiters 

 improve rapidly upon the administration of iodin, with (1) reduced prominence 

 of the fibrous stroma; (2) nearly complete disappearance of the columnar epi- 

 thelium, with return to the normal, low cubical type; (3) nuclear change from 

 large, pale, vesicular type to small and deeply staining; (4) increase in the 

 amount of stainable colloid. 



Smith ('17) concluded that an iodin deficiency in the diet of pregnant swine 

 causes hyperplasia and hypofunction of the fetal thyroid gland. This results 

 in maldevelopment of the fetus, the affected pigs being born full sized, but weak, 

 and hairless, with poorly developed hoofs, edematous skin, etc. The thyroid 

 gland in these pigs appeared "dark red, sometimes almost black, and presents 

 a constant enlargement which varies only in proportion to the acuteness of 

 the malady. A histological examination of the thyroid shows a uniform hyper- 

 plasia and a distension of the blood-vessels." The iodin content of these 

 glands was found very low, and the disease was prevented by the addition of 

 iodin to the diet of the pregnant sows. Similar cases occur frequently in sheep, 

 and occasionally in cattle and horses. Smith also cited Fenger's observation 

 that the fetal thyroid (in slaughtered animals) is often found hypertrophied, 

 with low iodin content. Hart and Steenbock ('18a) likewise concluded that 

 hairless pigs are caused by fetal goiter due to deficient intake of iodin. 



Marine and Kimball ('21) emphasized the lack of iodin as the cause of 

 simple goiter, small doses of iodin being effective in prevention or cure. "Ana- 

 tomically a wide range of changes may be present, depending on the species of 

 animal and on the stage (duration) of the disease. It always begins with a 

 decrease in the colloid material and a hypertrophy of the epithelial cells, at 

 first cubical, later columnar, with infoldings and plicatures. In man 

 and fowls, the stage most commonly observed is characterized by an 

 abundance of colloid material — the so-called cystic or colloid goiter of the older 

 writers — while in dogs, cattle, sheep, pigs, fish, etc., the accumulation of colloid 

 is seen only in the late regressive or quiescent stages." Hayden, Wenner and 

 Rucker ('24) produced goiter in rats by restricted iodin in the diet. 



McClendon ('22) and McClendon and Williams ('23) studied the relation of 

 the incidence of human goiter among the drafted men in the recent war to 

 the amount of iodin in the drinking water of the corresponding districts of the 

 United States. The evidence indicates that the prevalence of goiter is inversely 

 proportional to the supply of iodin. They state that Chatin (C. R. Acad. 

 Sc, Par., 1850) advanced the hypothesis that simple goiter is correlated with a 

 low iodin-content of the drinking water. 



McCarrison ('22) likewise concludes that "The factors which give rise to 

 goiter center around the supply of iodin and the needs of the thyroid gland for 

 iodin," but he points out that there are various factors which may bring about 

 the insufficiency of iodin. Mellanby ('22) states that while a deficiency of 

 iodin causes a thyroid enlargement in animals (dogs), this deficiency does not 



