A new hypothesis: iodine and gastric cancer

Eur J Cancer Prev. 1993 Jan;2(1):17-23.


The authors have hypothesized that iodine-deficiency (I-def) or in some cases iodine-excess (I-excess) is associated with the development of gastric cancer. They report a short review of their own work and general literature on this subject in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-def (or I-excess) endemic goitre and high GC-death rate are reported; (2) immunology, where the possible correlations between I-def, immune-deficiency and GC are reported; and (3) thyroid gland and stomach correlations, both being embryologically derived from primitive gut and able to concentrate iodine. This ability is impaired by nitrates, thiocyanate, salt and by I-excess, which in fact can cause goitre. In our study I-def goitrous people have shown more atrophic gastritis than normal subjects. These data enable us to hypothesize that I-def or I-excess might constitute a new risk factor for gastric cancer, both by regulating gastric trophism and by antagonizing the action of those I-inhibitors (such as nitrates, thiocyanate and salt) previously studied as risk factors for gastric cancer.

MeSH terms

  • Female
  • Gastritis, Atrophic / complications
  • Gastritis, Atrophic / metabolism*
  • Goiter / complications
  • Goiter / metabolism*
  • Humans
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin G / drug effects
  • Iodine / analysis
  • Iodine / deficiency*
  • Iodine / pharmacology
  • Male
  • Risk Factors
  • Stomach Neoplasms / epidemiology
  • Stomach Neoplasms / etiology*
  • Stomach Neoplasms / immunology


  • Immunoglobulin G
  • Iodine