{"id":2721,"date":"2022-07-15T08:57:50","date_gmt":"2022-07-15T08:57:50","guid":{"rendered":"https:\/\/seleniumfacts.com\/?p=2721"},"modified":"2022-06-29T09:21:13","modified_gmt":"2022-06-29T09:21:13","slug":"selenium-supplementation-and-hashimotos-disease","status":"publish","type":"post","link":"https:\/\/seleniumfacts.com\/index.php\/selenium-supplementation-and-hashimotos-disease","title":{"rendered":"Hashimoto’s Disease Patients Benefit from Selenium Supplementation"},"content":{"rendered":"

Hypothyroidism is the medical condition caused by an underactive thyroid gland that is not producing sufficient quantities of thyroid hormones. It is the failure of the thyroid gland to function normally.<\/strong><\/p>\n

\"Jan
Endocrinologist Jan Aaseth, M.D., Ph. D., ERT, explains that, in Norway, the diagnosis of Hashimoto\u2019s disease is made after a clinical examination that involves determination of the patient\u2019s circulating levels of the thyroid hormone thyroxine (T4), thyroid stimulating hormone, and thyroperoxidase antibodies [Aaseth 2022].<\/strong><\/figcaption><\/figure>The most common form of hypothyroidism is related to Hashimoto\u2019s disease. Hashimoto’s disease is an autoimmune disorder most common among middle-aged women. Symptoms include anxiety, dry skin, fatigue and lethargy, muscle aches and muscle stiffness, negative mood, sensitivity to cold, slow thinking and poor memory.<\/strong><\/p>\n

The standard treatment for Hashimoto\u2019s disease is twofold:<\/strong><\/p>\n

1) treatment with a synthetic hormone called levothyroxine, which works like the T4 hormone that is naturally produced by the thyroid gland<\/strong><\/p>\n

2) monitoring of thyroid stimulating hormone levels<\/strong><\/p>\n

Lack of Focus on Selenium Status in Hashimoto’s Disease<\/h5>\n

However, more than 10% of Hashimoto\u2019s disease patients have symptoms of hypothyroidism in spite of this levothyroxine treatment. In this context, there is generally a lack of focus on the patients\u2019 selenium status, selenoprotein P status, and the status of the two deiodinase selenoenzymes<\/em><\/strong> that are involved in the activation of thyroid hormones and the conversion of the biologically inactive T4 hormone thyroxine to the biologically active T3 triiodothyronine hormone [Aaseth 2022].<\/p>\n

The selenium containing DIO1 and DIO2 deiodinase enzymes are necessary to catalyze the release of iodine (i.e., deiodinate) from T4 to increase the quantity of circulating T3 [Aaseth 2022].<\/p>\n

 <\/p>\n

\"Thyroid<\/p>\n

Attribution: Claire Moore, Public domain, via Wikimedia Commons.<\/span><\/p>\n

A Role for Selenium Supplementation in Hashimoto\u2019s Disease<\/h5>\n

As early as 2010, there was clinical evidence that suggested that selenium supplementation could be useful as an adjunctive therapy to levothyroxine (LT4) in the treatment of Hashimoto’s thyroiditis<\/em><\/strong><\/a>. A systematic review of studies involving patients diagnosed with Hashimoto\u2019s thyroiditis and undergoing levothyroxine (LT4) treatment showed that selenium supplementation for 3 months was associated with significantly lower concentrations of thyroid peroxidase auto-antibodies (TPOAb) and with a significantly higher chance of improvement in well-being and mood<\/em><\/strong> when compared with controls [Toulis 2010].<\/p>\n

Clinical Evidence for Selenium Supplementation of Hashimoto\u2019s Disease Patients<\/h5>\n
Selenium yeast supplement<\/h6>\n

In a six-month randomized controlled trial (RCT) with a selenium yeast-treated group (n = 43) and no treatment in control group (n = 47), Hu et al. found that the selenium yeast treatment significantly decreased thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb), and thyroid stimulating hormone (TSH) levels<\/strong><\/em><\/a>. The selenium yeast treatment \u2013 200 mcg\/day \u2013 significantly increased selenium, glutathione peroxidase 3 (GPx3), and selenoprotein P concentrations, compared with the control group [Hu 2021].<\/p>\n

Moreover, the percentage of activated regulatory T cells was significantly higher in the selenium-treated group than in the control group. The selenium yeast supplementation had a beneficial effect on thyroid auto-antibodies and thyroid function by increasing the antioxidant activity and upregulating the activated regulatory T cells [Hu 2021].<\/p>\n

In an open-label clinical study, researchers administered 200 mcg\/day selenium yeast supplements to 100 Hashimoto\u2019s disease patients with known selenium deficiency. After three and six months of supplementation, the patients\u2019 serum selenium levels increased to moderate levels [Wang 2021].<\/p>\n

The patients\u2019 concentrations of thyroglobulin antibodies (TGAb) decreased significantly after six months of selenium supplementation<\/em><\/strong><\/a>. In the high antibody group, the thyroid peroxidase antibodies (TPOAb) decreased significantly after 3 and 6 months of selenium supplementation.<\/p>\n

The researchers concluded that, in patients with autoimmune thyroiditis and normal thyroid reference range, there was a general selenium deficiency<\/em><\/strong>. After six months of treatment with selenium yeast, there were significant reductions in the concentrations of TGAb and TPOAb antibodies.<\/p>\n

Sodium selenite supplement<\/h6>\n

In a an open-label clinical trial, researchers administered selenium in the form of sodium selenite at a dose of 100 mcg\/day for 6 months to newly diagnosed and previously untreated Hashimoto’s thyroiditis with either normal production of thyroid hormone or sub-clinical hypothyroidism. 29 women completed the study.<\/p>\n

The selenium supplementation increased the concentrations of selenium and selenoprotein P in the serum and decreased significantly the level of anti-thyroid peroxidase antibodies<\/strong><\/em><\/a>, thus limiting the development of overt hypothyroidism [Kryczyk-Kozio\u0142 2021].<\/p>\n

Autoimmunity to Selenoprotein P in Hashimoto\u2019s Disease<\/h5>\n

Selenium is needed for the synthesis of the protective antioxidant glutathione peroxidase selenoenzymes. Selenoprotein P is the primary transporter of selenium in the body.<\/p>\n

In 2021, Sun and a team of researchers reported finding natural auto-antibodies to selenoprotein P in patients with thyroid disorders<\/em><\/strong><\/a> (ca. 6-7 % of patients). The autoimmunity to selenoprotein P impairs selenium transport and negatively affects the biosynthesis of the glutathione peroxidases [Sun 2021].<\/p>\n

It may be that, in cases of selenoprotein P deficiency, selenium supplementation will be needed to compensate.<\/p>\n

Clinical Evidence for Selenium Supplementation of Elderly Citizens with Normal Thyroid Function<\/h5>\n

In the Danish PRECISE pilot study (PRECISE = PREvention of Cancer by Intervention with Selenium), a randomized, double-blind, placebo-controlled trial, researchers administered selenium yeast supplements to 491 males and females aged 60\u201374 years as follows [Winther 2015]:<\/p>\n