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Iodine, Helicobacter Pylori, stomach cancer & evolution.
Iodine, Helicobacter Pylori, stomach cancer & evolution.
Venturi S, Grossi L, Marra GA, Venturi A, Venturi M
The Newsletter of the International Center for Studies and Research in Biomedicine, Luxembourg, Vol. 7, No. 2, April 2003, pp 1-7.


The authors have hypothesized that dietary iodine (I) deficiency or excess are associated with the development of atrophic gastritis and gastric cancer (GC). They report a short review of their own work and general literature on this correlation in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-deficiency, endemic goitre and high gastric cancer-death rate are reported; (2) iodine and atrophic gastritis correlations, and (3) immunology, where the correlations between I-deficiency, immune-deficiency and gastric cancer are reported.

Thyroid cells phylogenetically and embryologically, derived from primitive Iodine-concentrating gastric cells which, during evolution, migrated and specialized in uptake and storage of iodine, in order to adapt the organisms from Iodine-rich sea to Iodine-deficient land.

Stomach and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide and so protects the cells from peroxidations. Iodide seems to have an ancestral antioxidant function in all iodide-concentrating organisms from primitive algae to more recent vertebrates. In Italy, gastric cancer is more frequent in farmers and in Iodine-deficient populations, living in mountainous and hilly areas, than in fishermen. In the last two decades, Italian decrease of gastric cancer seems to be correlated more with the higher dietary consumption of Iodine-rich fish rather than with consumption of fruit and vegetables, which indeed has decreased in Italy.

In conclusion, iodine deficiency or excess seem to constitute an important risk factors for atrophic gastritis and gastric cancer, both by antioxidant activity and regulating gastric trophism and by antagonizing the actions of both Helicobacter pylori and of Iodine-inhibitors, such as nitrates, thiocyanate and salt, well-known risk factors for gastric cancer.

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Full Text in European EpiMarker 2003 (Researchgate.net)