American Journal of Clinical Nutrition, Vol. 80, No. 4, 1088,
October 2004
© 2004 American Society for Clinical Nutrition
Reply to U Kapil and R Prakash
Michael Zimmermann
Laboratory for Human Nutrition
Swiss Federal Institute of Technology
Seestrasse 72/PO Box 474
CH-8803 Rüschlikon
Switzerland
E-mail: michael.zimmermann{at}ilw.agrl.ethz.ch
Dear Sir:
We agree that it is likely that a greater length of time than 5 mo is needed to completely deplete thyroidal iodine stores. However, urinary iodine may decrease to concentrations that indicate iodine deficiency before thyroidal iodine stores are depleted. A central mechanism by which the thyroid gland adapts to a chronically insufficient iodine supply is to sharply increase iodide clearance from the extrathyroidal iodide pool (1). As thyroidal trapping increases, less iodide from the extrathyroidal pool is available for renal clearance. Thus, even if thyroid hormone production and turnover are normal, urinary iodine may decrease to concentrations that indicate iodine deficiency (2). In our study, it is likely that intrathyroidal iodine stores were depleted in the children by 14 mo after iodized salt was discontinued, which resulted in the deterioration of thyroid function described at that time point (3).
REFERENCES
- Stanbury JB, Brownell GL, Riggs DS, et al. In: Perinetti H, Itoiz J, Castillo EBD, eds. Endemic goiter. The adaptation of man to iodine deficiency. Cambridge, MA: Harvard University Press, 1954:1–209.
- Delange F. Iodine deficiency. In: Braverman LE, Utiger RD, eds. Werner & Ingbar's the thyroid: a fundamental and clinical text. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2000:295–316.
- Zimmermann MB, Wegmüller R, Zeder C, Torresani T, Chaouki N. Rapid relapse of thyroid dysfunction and goiter in school-age children after discontinuation of salt iodization. Am J Clin Nutr 2004;79:642–5.[Abstract/Free Full Text]
