https://academic.oup.com/jas/article-ab ... 40/4745435
Abstract
Goldemberg (1, 2) has maintained that sodium fluoride was a specific therapeutic agent for depressing the metabolic rate in experimental animals and in human thryotoxicosis. In a previous effort (3) to confirm Goldemberg's work on experimental animals, we found that we could not reduce the basal metabolic rate of the white rat by feeding sodium fluoride, and that sodium fluoride accentuated the stimulatory action of dessicated thyroid. In experiments with chicks (4) it was found that mild doses of dessicated thyroid and effective doses of sodium fluoride not only did not counteract each other, but were additive in action.
An attempt was made to introduce fluorine into dessicated thryoid material by the simple expedient of shaking the two in aqueous solution. A progressive increase in the quantity of fluorine introduced into dessicated thyroid was obtained with concentrations from .25% up to 2.0%. The fluorine content was increased from a very slight trace to .045%. Preliminary analyses showed a loss of iodine which appeared to be a mole for mole replacement of iodine by fluorine. The method used for basal metabolism determination failed to show any measurable difference between the NaF treated and the untreated dessicated thyroid in a thirty-day period, although a daily ingestion of 7 mgs. of the 2% NaF treated sample was equivalent to 11.3 mgs. of the washed dessicated thyroid sample in raising the metabolic rate. The inclusion of .045% F in the fluorinated sample caused a noticeable anorexia.