|The Prevention and Control of Iodine Deficiency Disorders - Nutrition policy discussion paper No. 3 (UNSSCN, 1988, 130 p.)|
A mild increase in Incidence of thyrotoxicosis has been described following iodized salt programmes in Europe and South America and following the Introduction of Iodized bread in Holland and Tasmania (Watanabe et al., 1974; Stewart et al., 1971; Ramzin et al., 1973). A few cases have been noted following iodized oil administration in South America (Watanabe et al., 1974). No cases have yet been described in New Guinea, India or Zaire. This is probably due to the scattered nature of the population in small villages and limited opportunities for observation (Kavishe et al., 1981). The condition is largely confined to those over 40 years of age.
Detailed observations are available from Tasmania, where in 1966 physicians in Launceston and Hobart first noticed an increase in the number of patients with thyrotoxicosis. Each of these cities had a thyroid clinic serving a population of the order of 180,000, Launceston covering the northern half of the island and Hobart the southern (Vidor et al., 1973).
It was apparent that the rise in incidence of thyrotoxicosis had occurred in association with a rise in iodine intake from below normal to normal levels (Stewart et al., 1971) due to iodized bread consumption which was introduced in April 1966.
Scrutiny of records in northern Tasmania revealed a rise in the incidence of thyrotoxicosis as early as 1964, associated with rise in food imports and the introduction of iodophors to the dairy industry during 1963. There was a much larger rise in thyrotoxicosis incidence from 1966 following the iodization of bread. Analysis of the cases by age revealed the predominance of patients over the age of 40, although a rise had occurred also in those under this age.
A cohort effect was demonstrated because the peak passed - the peak being composed mainly of those over the age of 40 with life-long iodine deficiency and autonomous thyroid glands which continued the rapid turnover of iodine after the increase in iodine intake.
It was clear that the increase in thyrotoxicosis was caused mainly by these patients with toxic autonomous goitre and not Graves' disease. The findings support the old view of two types of thyrotoxicosis - Graves' disease and Plummer's disease (Vidor et al., 1973).
The condition can be readily controlled with antithyroid drugs or radio-iodine. It seems likely that spontaneous remission occurs in many cases. In general iodization should be minimized for those over the age of 40 because of the risk of thyrotoxicosis.
Apart from thyrotoxicosis the risk of iodism or iodide goitre seems to be small. An increase in lymphocytic thyroiditis (Hashimoto's disease) has been claimed following iodization but this is still disputed (Stanbury et al., 1974).