|
| |
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.
|
|