Conclusions

Overall, changes in how goiter was defined progressed erratically. As theories and techniques employed in anatomy and pathology were developed, the concept of "goiter" shifted from the simplistic idea of a swollen neck, to an enlarged thyroid of several types, to a range of different thyroid diseases. However, early taxonomies did not disappear but persisted along with the new.

Along with these changes in taxonomy came parallel changes in purported causes and the possibilities of prevention. Focusing for the moment only on iodine, one can demonstrate a continuous link from the Chinese use of seaweed through the European Middle Ages and folk medicine, to the discovery and use of the element in the nineteenth and twentieth centuries. In actuality, however, although empirical "folk" medicines containing iodine were effective against goiter, they were used along with many others that seem to have had no benefit. Nineteenth-century French physicians may have been "right" in proposing iodine as a treatment for endemic goiter, but they did not convince their colleagues. That iodine deficiency might cause goiter was confounded by iodine's use in goiter treatment and prophylaxis; furthermore, the technical inability to measure consistently and accurately small amounts of iodine led to persistent and valid controversy. Improvements in the iodine assay in the late nineteenth and early twentieth centuries provided a solid basis for resurrecting earlier beliefs in its effectiveness; moreover, because it was thought that iodine ought to prevent endemic goiter, the studies were done that proved it. But the pendulum then swung to the other extreme, with many researchers believing that iodine was the answer to all endemic goiter. It was not, however, and we now face the scientific challenge of teasing out several probable factors in addition to iodine deficiency that can produce endemic goiter, as well as the political challenge involved in iodine prophylaxis on a worldwide basis.

In conclusion, sporadic goiter is usually not due to iodine deficiency but is mainly the result of an intrinsic thyroid disease, often related to genetic, immunologic, or enzymatic factors; it is apparently influenced by gender, as it is more common in women. Sporadic cretinism (or neonatal hypothyroidism) is almost never caused by iodine deficiency, but is usually the result of failure of the thyroid gland to develop; thus there is no goiter. For this condition, a public health approach, with testing of all newborns, is mandatory to prevent irreversible brain damage.

On the other hand, endemic goiter and cretinism are usually related to a low dietary iodine, although goitrogens, genetic, and immunologic factors may be operative in some locales. Taking iodine cures some and prevents almost all; again a public health approach is essential.

Clark T. Sawin

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