ROLE OF IODINE DEFICIENCY IN THE PRODUCTION OF GOITER BY THE REMINGTON DIET

Abstract

None of the foodstuffs used in the Remington diet, not even NaCl, was essential for the induction of goiter by a diet sufficiently low in I. Prevention of such goiters by a small dose of I completes the demonstration that I deficiency is the essential factor in their production. The Remington diet, which consistently produced thyroid enlargement in rats and mice, was examined systematically in order to determine whether it contained any factor other than its deficiency in I that could be responsible for goiter production. Possible presence of a postive goitrogenic factor in any one of the foodstuffs used in this diet was investigated by comparing the weight, histology and function of the thyroid gland of mice fed the diet free of the foodstuff with those of mice fed the basic control diet. Of all the foodstuffs composing the diet, only NaCl appeared to play an important role in the production of goiter. Relative roles of I deficiency and NaCl ingestion in goiter production were clarified by a study in which both the I and NaCl intake were systematically varied. At the lowest I level (4.1 [mu]g I/100 g diet) goiter developed in the presence or absence of NaCl, but the weights and radio-I uptakes of the glands were increased by this salt. When the I intake was raised to 12.2 or more ug of I/100 g of diet, thyroid enlargement was prevented whether or not the animals received NaCl. Therefore, NaCl ingestion did not produce goiter in the absence of I deficiency.