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OVER a hundred years ago Prevost (1830) suggested that a deficiency of iodine was responsible for goiter. This hypothesis has since been supported by the following pieces of evidence: 1) in many areas where the incidence of goiter is high, the iodine content of the soil, food and drinking water is low3; 2) the daity output of iodine in the urine of individuals residing in such areas is also low and, since these people may be considered to be in balance with their environment as regards iodine, it follows that their iodine intake also is low (von Fellenberg, 1923–1930; Lunde, 1928; Stanbuiy et al., 1952); 3) the thyroid glands of individuals in goiter districts usually have a low iodine concentration4 and an increased avidity for iodine (Stanbury et al., 1952); 4) the administration of iodine in small amounts reduces the incidence of endemic goiter in men and animals.5
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Axelrad et al. (1955) studied this question.
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