SELENIUM AND HASHIMOTO’S
Nutrient depletions are very common in Hashimoto’s. One particular nutrient that is depleted in Hashimoto’s is Selenium. A dosage of 200 mcg per day has been found to reduce thyroid antibodies in clinical trials, in some studies Selenium cut the antibodies in half within three months….Curious about the science behind it? Read on
In normal thyroid function, iodide from food sources will trigger the production of hydrogen peroxide so that the iodide can be converted to its usable iodine form. The reactive hydrogen peroxide causes oxidative damage that is neutralized by the antioxidant selenium, which is also a necessary building block in thyroid synthesis.
However, in the presence of excess iodide intake, more hydrogen peroxide will be produced, requiring more selenium for neutralization. Hydrogen peroxide is a reactive oxygen species that can cause tissue damage. Coupled with selenium deficiency, one can understand that excessive iodine intake can lead to dangerous levels of hydrogen peroxide production. When the reactive hydrogen peroxide causes oxidative damage and inflammation of the surrounding thyroid tissues, this inflammation triggers lymphocytes or white blood cells (WBCs), to converge and clean up.
As the WBCs are converging, small amounts of antibodies will be formed to help mark the damaged cells that need to be cleaned up. Mouse models have been found to have spontaneously occurring low levels of circulating TPO antibodies, which may serve a clean-up function. In instances of higher turnover of cells seen with excess oxidative damage due to iodine excess and selenium deficiency, more antibodies are produced and an immune system shift can be induced, resulting in the failure to recognize self from non-self. This is how autoimmunity perpetuates. Thus, selenium deficiency has also been recognized as a risk factor for Hashimoto’s.
More iodine–>More H2O2–>Not enough selenium/glutathione to neutralize–>Lots of cells with oxidative damage–>Inflammation and convergence of WBCs–>Excessive amount of antibodies form to mark damaged cells –>Immune shift–>Self-recognition impaired (autoimmunity)
According to the National Institutes of Health, most cases of selenium deficiency are associated with severe gastrointestinal problems such as Crohn’s disease or surgical removal of the stomach, however, selenium deficiency may also occur in celiac disease and other inflammatory bowel disorders due to the malabsorption from damage to the small intestine.
The co-occurrence of Hashimoto’s and celiac has been clearly established. I would even venture to say that one does not need to have full-blown celiac to have an impaired absorption of selenium.
Selenium plays a very important role in thyroid function:
Acting as catalyst to convert the inactive T4 to the biologically active T3 and protecting thyroid cells from oxidative damage from hydrogen peroxide by forming selenoproteins
Three specific diseases have been associated with selenium deficiency:
Keshan disease is found in selenium-deficient children and is associated with an enlarged and malfunctioning heart.
Kashin-Beck disease, which causes bone malformation, is found when iodine and selenium are both deficient.
Myxedematous Endemic Cretinism results in intellectual disability. Scar tissue is seen in place of the thyroid.
Note: Myexedema: mucin and edema. Mucin is a substance that accumulates in hypothyroidism.
Studies have proposed that supplemental selenium could alleviate toxic effect of excessive iodine intake on the thyroid.
Selenium is a trace mineral that is incorporated into proteins to make antioxidants like glutathione peroxidase. This type of protein is known as a selenoprotein, and prevents damage from hydrogen peroxide generated from the conversion of iodide to iodine by breaking down the hydrogen peroxide into water particles. This allows for the removal of the cells affected by oxidative damage, leads to the preservation of tissue integrity and prevents the convergence of white blood cells. (Xu)
H2O2+ Glutathione Peroxidase à H2O (water)
However, in the presence of excessive iodine, a relative selenium deficiency occurs. Since glutathione peroxidase is made of selenium, the enzyme activity will be compromised when selenium is depleted. According to Xu, et. al., “Selenium supplements alleviate damage of TPO that results from iodine excess.” The scar tissue seen in the selenium-deficient children affected with myxedematous endemic cretinism further supports the notion that a lack of the antioxidant selenium leads to the destruction of thyroid tissue due to inability to neutralize the hydrogen peroxide.
In a study done with mice that developed autoimmune thyroiditis induced by iodine, this development was prevented when selenium was given. Selenium reduced the TgAb titers and increased the number of circulating T regulatory cells that help the immune system recognize itself and prevent the lymphocytic (WBC) infiltration of the thyroid cells that is present in autoimmune thyroiditis.
A study in Africa showed that two months of selenium supplementation restored the glutathione peroxidase activity, and improved thyroid function through increased conversion of T4 to the active T3.
A similar study found that selenium intake protects against thyroid autoimmunity by acting as an antioxidant, and also has an effect on HLA-DR gene expression, further preventing autoimmunity. Furthermore, ultrasounds of the thyroid following selenium supplementation showed reduced lesions in the thyroid gland.
The RDA (Recommended Daily Allowance) for selenium has been defined as 55 mcg in the United States, and an upper limit of 400 mcg has been suggested. A study done in South Dakota did not find any signs of toxicity at levels as high as 724 mcg, however, changes in nail structure, a sign of toxicity, were reported with selenium intake of 900 mcg per day in China. Most reported toxicity cases have been associated with industrial accidents and manufacturing errors. Some symptoms of selenium toxicity that have been reported include GI disturbances, hair loss, changes in hair and nails, peripheral neuropathy, fatigue, irritability, garlic-smelling breath, and a jaundice-like yellow tint to the skin.
While it may be tempting to increase selenium intake by increasing consumption of selenium-rich foods such as Brazil nuts, it is important to realize that selenium content varies widely for foods grown in different soils. While the Dakotas have selenium-rich soils, other areas such as Russia and China have deficient levels of selenium.
Again, importation of foods further complicates these issues. The amounts of selenium in a single Brazil nut have been reported to range tenfold depending on where the nut was grown. This means there could be anywhere from 55 mcg to 550 mcg per ounce of nuts. Additionally, absorption issues due to GI problems may limit the availability of selenium from food sources.
While the RDA of selenium may often be found in multivitamin/mineral combinations, that will not be sufficient for TPOAb reduction. Studies have been done to test the minimal dose of selenium for TPO antibody reduction, and that dose was established to be 200 mcg daily, even a 100 mcg dose did not produce a statistically significant TPO antibody reduction. The bioavailability of minerals is very delicate and can be greatly affected by food or the presence of other substances.
Multivitamin supplements also have so many different ingredients that the absorption of this important mineral may be reduced. I recommend taking the selenium on an empty stomach with vitamin E, which works in synergy with selenium, to ensure proper absorption.