Iodine and
selenium (Se) are both essential elements to
thyroid hormone economy, while they represent key players in the development of
autoimmune thyroiditis.Chronic high
iodine intake has been associated in various studies with increased frequency of
autoimmune thyroiditis. In susceptible individuals,
iodine excess increases intra-thyroid infiltrating Th17 cells and inhibits T regulatory (TREG) cells development, while it triggers an abnormal expression of
tumor necrosis factor-related apoptosis-inducing
ligand (TRAIL) in thyrocytes, thus inducing apoptosis and parenchymal destruction. As was shown in a mouse model, high
iodine supply leads to changes in the immunogenicity of the
thyroglobulin molecule, upregulation of vascular
intercellular adhesion molecule-1 (ICAM-1), and
reactive oxygen species (ROS) generation in the thyrocytes. Serum Se levels were found decreased in
Hashimoto thyroiditis and especially in
Graves' disease as well as in
thyroid-associated ophthalmopathy patients, the levels being related to the pathogenesis and outcome.
Selenium is strongly involved, via the variable
selenoproteins, in
antioxidant, redox, and anti-inflammatory processes.
Selenium enhances CD4+/CD25 FOXP3 and T regulatory cells activity while suppressing
cytokine secretion, thus preventing apoptosis of the follicular cells and providing protection from
thyroiditis.
Selenium supplementation may be useful in autoimmune
thyroid diseases, though, while usually well-tolerated, it should not be universally recommended, and it is also likely to be helpful for those with low Se status and autoimmunity. Broadly speaking, the achievement and maintenance of "selenostasis" as well as adequate urinary
iodine excretion are mandatory to control disease, while, putatively, they may additionally be critical to preventing disease.