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First, consider some studies:
Effect of iodine and thyroid hormones in the induction and therapy of Hashimoto’s thyroiditis
To lower the incidence of autoimmune thyroid diseases in predisposed subjects, a daily iodine supplementation seems to be superior to high-dose weekly administrations
Effect of small doses of iodine on thyroid function in patients with Hashimoto’s thyroiditis residing in an area of mild iodine deficiency.
Small amounts of supplementary iodine (250 microg) cause slight but significant changes in thyroid hormone function in predisposed individuals
I consider these studies reflective of the model wherein
- the immune system will downregulate antibodies to self antigens if the antigens are constantly present
- the immune system will upregulate antibodies to self antigens when there is a spike in self antigens
If the thyroid is inflamed, for a number of potential reasons, there is a higher chance, due to the higher presence of white blood cells, that autoimmunity will develop and progress.
Potential reasons for inflammation:
- insufficent selenium
Selenium and Thyroid Disease: From Pathophysiology to Treatment
In fact, it was found that selenium deficiency decreases the synthesis of thyroid hormones, as it decreases the function of selenoproteins, in particular iodothyronine deiodinases (DIOs), which are responsible for the conversion of T4 to T3. This decreased production of thyroid hormones leads to the stimulation of the hypothalamic-pituitary axis due to the lack of negative feedback control, increasing TSH production. TSH stimulates the DIOs to convert T4 to T3 , with consequent production of hydrogen peroxide, which is not adequately removed by less active glutathione peroxidases (GPx) and accumulates itself in the thyroid tissue causing thyrocyte damage with subsequent fibrosis. The thyroid gland is characterized by a high tissue concentration of selenium (0.2–2 μg/g), being the organ with the highest amount of selenium per gram of tissue, because it contains most of the selenoproteins [1, 13]. Since it is incorporated into selenoproteins, which have an important antioxidant activity, selenium contributes to the antioxidant defense in the thyroid, by removing oxygen free radicals generated during the production of thyroid hormones [14, 15]. Being incorporated into iodothyronine deiodinases, selenium plays also an essential role in the metabolism of thyroid hormones [1, 16]. So far, about 25 selenoproteins were described . Table Table33 depicts selenoproteins which play a major role in thyroid homeostasis. The iodothyronine deiodinases control the thyroid hormone turnover and catalyze the conversion of T4 to its biologically active form, T3, through the removal of an iodine atom from the external ring . They can also inactivate thyroid hormones by the removal of an iodine atom of the inner ring, with the conversion of T4 to reverse T3 (rT3), the inactive metabolite. Glutathione peroxidases are responsible for glandular protection, since they remove the excess of oxygen free radicals produced during normal synthesis of the thyroid hormones [19, 20].
- insufficient glutathione (to react with glutathione peroxidase)
- insufficient tyrosine (to react with the oxidized iodide (TPO catalyzed reaction))
- insufficent Na or Cl (salt) (see thyroid)
- lifestyle factors for inflammation
Taking a relatively large amount of iodine (relative to a person’s normal consumption) will exacerbate or cause inflammation because:
- if there is already and autoimmunity, the furtherance of hormone production will provide even more antigen to be recognized (in the form of Tg and TPO)
- if there is not already autoimmunity, but if there already inflammation, the furtherance of hormone production will provide more antigens for the potential self antibody creation
- if there is not autoimmunity or inflammation present, the increased production will result in increased metabolites (radicals) that the thyroid may not be capable of handling (just like a muscle, strain increase has to be gradual to let the muscle adapt), and inflammation will result from the
My theory according to my model is, if you decrease the causes of inflammation and autoimmunity (spikes in antigen via spikes in hormone production), you can decrease autoimmunity by slowly increasing thyroid hormone production (by slowly increasing iodide consumption). Like many other organs, use determines size and capacity, and expanding use slowly will increase size and capacity, whereas suddenly expanding use may cause damage.