Iodine is a raw material for the thyroid production of hormone which i
s on the major external control of TSH. The thyroid adaptation to iodi
ne deficiency consists in an increasing iodine concentration from the
circulation, an enhancing iodination of the tyrosyl residues in thyrog
lobulin, a decreasing iodine storage associated to a better recycling
of non hormonal iodine and thyroid hyperplasia to provide more synthet
ic possibilities. Genetic variation and environmental factors explain
the wide variation of individuals response to iodine deficiency result
ing in a high prevalence of goiter, a mild TSH level increase or overt
hypothyroidism. At long term iodine deficiency may have severe pathol
ogical consequences and induce neuropsychological deficits in school-c
hildren. A policy of iodine supplementation mainly by iodized salt mus
t be undertaken in many areas in the world. Effects of an iodine exces
s on thyroid function are variable depending upon the underlying thyro
id disorder and ambient iodine intake. The most subjects remain euthyr
oid by mechanisms of autoregulation based on an inhibition of thyroid
hormone synthesis and a decrease in the thyroide iodide trap. Euthyroi
d individuals from high iodine intake areas or those with a history of
lymphocytic thyroiditis, treated Graves' disease or subtotal thyroide
ctomy develop hypothyroidism. On the other hand iodine induced hyperth
yroidism is more common in areas of iodine deficiency and in older pat
ients with nodular goiter.