By use of exact balance studies Aub, Bauer, Heath and Ropes (1) demonstrated that calcium and phosphorus excretion are markedly increased in patients with hyperthyroidism, and that the same phenomena could be induced by feeding thyroid to normal individuals. This excessive excretion of calcium in hyperthyroid states has been reported in other clinical and experimental studies (2,3,4,5,6). In order to account for these findings and for the osteoporosis observed in hyperthyroidism by themselves and others (4,7,8,9,10), Aub, et al. (1,11) postulated that thyroid has a specific stimulating catabolic effect on the calcium deposits in the bones. They pointed out that most of the other necessary body elements are not readily excreted to the degree of producing comparable negative balances. Parhon, Derevici and Derevici (12) reported slightly lower calcium content in the bones of the treated animals after feeding thyroid to 12 dogs over a period of 3 weeks. The considerable variation among the controls renders their results of doubtful significance. Hoskins (13) noted that the bones from rats fed thyroid appeared slightly heavier than those of the controls in the wet and dry state. Thompson (14) reported a decrease in bone ash from rats in which hyperthyroidism was induced by high calcium-low iodine diets.The studies here reported were undertaken in an effort to determine, by chemical and histological observation, whether a specific effect of thyroid upon the calcification of the bones of rats could be demonstrated. The study led to the observation of the effect of thyroid upon growth at the epiphyseal junction of the long bones, which is also reported.Bircher (15) fed young rats with thyroid for 4 months and, by means of x-ray and histological examination, demonstrated a retardation of growth with almost complete closure of the epiphyses of the long bones. Dott (16) noted by x-ray study a 28 per cent increase in the rate of growth of femurs from 2 puppies fed thyroid. The final bone length and stature were fixed at a subnormal limit because of premature epiphyseal ossification, observed histologically. Gudernatsch (17) fed thyroid to tadpoles and found that the treated animals underwent metamorphoses earlier than the controls, but always remained much smaller in si2e. Hoskins (18) found that injection of the monoacetyl derivative of thyroxin into rats inhibited growth in length and weight, but reported that x-rays showed an acceleration of 'epiphyseal activity,' without closure of the epiphyses.