Recently, a friend of mine told me he had started taking selenium supplements after being diagnosed with Hashimoto thyroiditis. Intrigued by the idea that a selenium pill could curb such a common disease, I started to dig into the scientific literature regarding this topic. What I discovered is that, since 2002, several trials have investigated the effect of selenium supplements on thyroid autoantibodies in patients suffering from autoimmune thyroiditis, which is currently treated with levothyroxine (LT-4).
According to a recent systematic review and meta-analysis, selenium supplementation effectively reduces Thyroid Peroxidase Antibodies (TPOAb) levels at 3, 6, and 12 months as well as Thyroglobulin autoantibodies (TgAb) at 12 months in LT4-treated populations. Notably, in subjects not receiving thyroid hormone, there was a decrease in TPOAb and TgAb levels at very short-term (3 months) only, but not after 6 or 12 months of supplementation. In particular, in LT-4-treated subjects, a significant drop in TPOAb at three months was observed only in subjects receiving supplementation in the form of selenomethionine and not in those receiving sodium selenite. This might simply be due to the lower absorption rates of selenite compared to selenomethionine.
Although the idea that selenium supplementation could be a valid treatment for subjects suffering from autoimmune thyroiditis is an intriguing idea, there is no sufficient evidence to recommend this treatment as a valid alternative to LT-4. In addition, TPOAb reduction does not necessarily mean a better disease prognosis, since their role in the development of hypothyroidism is not completely clear.
This is not good news especially considering that women of reproductive age are often TPOAb-positive, and this is associated with an increased risk of infertility, pregnancy complications, and preterm delivery,. Selenium supplementation does not seem to have any role in terms of either improved thyroid function or fertility rates in women planning pregnancy.
In conclusion, although supplementing selenium does not seem to solve the problems related to autoimmune thyroid diseases, it is still a good idea to have adequate intakes of this mineral. In another post I have described in more detail how to get enough selenium and which other nutrients are relevant for thyroid function.
For those who want more science
Hashimoto’s thyroiditis (HT), also called chronic lymphocytic or autoimmune thyroiditis (AITD), is a chronic and autoimmune thyroid disease associated with thyroid hypofunction and thyroid autoantibodies production, the most common ones being: thyroid peroxidase antibodies (TPO-Ab) and thyroglobulin antibodies (Tg-Ab). Lymphocytic infiltration is also common,,,,. HT prevalence is highest between 45-55 years, and it is between 4 to 10 times more frequent in women than in men. Curiously, smoking decreases the risk for HT, whereas alcohol, stress, pregnancy and use of some medications can initiate the development of the disease in genetically-predisposed individuals,. Although its exact mechanisms are not clear, HT is considered as a disorder of T cell-mediated immunity, caused by an interaction between susceptibility genes and environmental factors10. In most HT patients, lifelong levothyroxine substitution is required9,13,. HT co-existance with both organ-specific and non-specific diseases should be evaluated together with other non-endocrine autoimmune diseases,.
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 Mazokopakis E, Papadakis JA, Papadomanolaki MG et al. Effects of 12 months treatment with L-selenomethionine on serum anti-TPO levels in patients with Hashimoto’s thyroiditis. Thyroid 2007; 17: 609-12.
 Mazokopakis EE, Tzortzinis AA, Dalieraki-Ott EI et al. Coexistence of Hashimoto’s thyroiditis with papillary thyroid carcinoma. A retros- pective study. Hormones (Athens) 2010; 9: 312-7.
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 Such as iodine, interferon-gamma, immunomodulatory agents such as ipilimumab, pembrolizumab, nivolumab, and the humanised monoclonal antibody to CD52 alemtuzumab.
 E raimidis G, Wiersinga WM. Mechanisms in endocrinology: auto- immune thyroid disease: old and new players. Eur J Endocrinol 2014; 170: R241-52.
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 Pearce SH, Brabant G, Duntas LH et al. 2013 ETA guideline: manage- ment of subclinical hypothyroidism. Eur Thyroid J 2013; 2: 215-28.
 Such as pernicious anemia, vitiligo, celiac disease (CD), type 1 diabetes mellitus, autoimmune liver disease, primary biliary cirrhosis, myasthenia gravis, alopecia areata, sclerosis multiplex, Addison’s disease.
 Such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Sjögren syndrome, systemic sclerosis, mixed connective tissue disease
 Dilas LT, Icin T, Paro JN, Bajkin I. Autoimmune thyroid disease and other non-endocrine autoimmune diseases. Med Pregl 2011; 64: 183-7.
 Boelaert K, Newby PR, Simmonds MJ et al. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. Am J Med 2010; 123: 183.e1-9.