Iodine Deficiency
  Bourdoux et al., Brussels, Belgium, collected 104 salt samples from Europe and 582 samples from elsewhere to test for iodine content. They found in 40% no iodine at all and in another 19% an inadequately low iodine content while only in 11% sufficient iodine was present to meet physiological needs. In 30% iodine content was excessive. The samples originated from 87 countries of which 16 were industrialized and 71 were developing countries. Eighty percent of samples with sufficient or elevated iodine concentrations originated from developing countries with previous iodine deficiency. Furthermore, the data suggest that most European countries have adopted adequate standards for correcting iodine deficiency but the wide range of values from many samples outside Europe indicate that there is a problem with iodination techniques or preservation of the iodine content. Contempré et al., Brussels, Belgium and Madrid, Spain, studied the effect of thiocyanate overload on different groups of rats that were on different intakes of iodine and selenium. These studies were done to investigate further the mechanism of myxoedematous cretinism that is highly prevalent in Central Africa. It has been suggested that iodine and selenium deficiency in combination with thiocyanate overload may contribute to damage of the thyroid in this type of cretinism. In Central Africa thiocyanate overload in combination with iodine and selenium deficiency has been documented. They found that in rats thiocyanate overload has a necrotic effect on the thyroid, especially in the presence of iodine deficiency, and more so if also selenium deficiency is present. These findings underline the dilaterious effect of these factors on the thyroid gland in humans. Iodine deficiency leads to increased thyroidal H2O2 synthesis while selenium deficiency results in decreased inactivation of synthesized H2O2. H2O2 is damaging to the thyroid gland while thiocyanate by itself also promotes follicular cell necrosis.