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Selenium for thyroid diseases.

Selenium is an essential trace mineral that functions as an antioxidant, enhances immune function, and has antiviral activity. Selenium also plays a role in the conversion of thyroxine to triiodothyronine (the active form of thyroid hormone). Previous research has demonstrated that selenium supplementation (usually 200 mcg per day) can decrease the severity of autoimmune (Hashimoto's) thyroiditis. Recent research has confirmed that observation, and has found that selenium treatment can resolve autoimmune thyroiditis completely in a small proportion of patients. In addition, a new study demonstrated that selenium supplementation (200 mcg per day) can slow the progression of eye disease and improve quality of life in patients with Graves' disease with mild ocular involvement (Graves' ophthalmopathy; also called Graves' orbitopathy).


Selenium and Graves' Orbitopathy

Approximately half of patients with Graves' disease have ocular involvement. Moderately severe and active forms of Graves' orbitopathy can be effectively treated with glucocorticoids, orbital irradiation, or both. Milder forms may improve spontaneously and generally require only local measures (such as artificial tears) to control symptoms. it is has been suggested that oxygen free radicals and inflammatory mediators (cytokines) may play a role in the pathogenesis of Graves' orbitopathy.

One hundred fifty-nine patients with mild Graves' orbitopathy were randomly assigned to receive, in double-blind fashion, selenium (an antioxidant) at a dose of 100 mcg twice a day, pentoxifylline (an anti inflammatory agent) at a dose of 600 mg twice a day, or placebo for 6 months, and were then followed for an additional 6 months.(1) All patients were euthyroid (as demonstrated by thyroid function tests) during the study. After 6 months, compared with placebo, selenium treatment (but not pentoxifylline) was associated with an improved Graves' orbitopathy-specific quality-of-life score (p < 0.001), less eye involvement (p = 0.01), and less progression of Graves' orbitopathy (p = 0.01). The proportion of patients who showed a clinically significant improvement in the quality-of life score was significantly greater in the selenium group than in the placebo group (74% vs. 24%; p < 0.001). Exploratory evaluations at 12 months confirmed the results seen at 6 months. The results of this study indicate that selenium supplementation improved quality of life, reduced ocular involvement, and slowed disease progression in patients with mild Graves' orbitopathy.

Selenium and Autoimmune Thyroiditis

Seventy-six patients (aged 15-75 years) with autoimmune thyroiditis, with a normal or slightly elevated TSH level and a free-T4 level within the normal range, were randomly assigned to receive 80 mcg per day of sodium selenite or no sodium selenite for 12 months. It was not clear whether the dosage referred to elemental selenium or to sodium selenite. After 12 months, the mean serum thyroperoxidase (TPO) antibody concentration fell by 30% (p = 0.001) in the selenium group, but did not change in the control group. No change was seen in this parameter after 6 months of treatment. Five patients receiving selenium became TPO-negative, whereas no patient in the control group became TPO negative. TSH and free-T4 levels did not differ between groups. These results indicate that administration of selenium for 12 months decreased TPO antibody levels in patients with autoimmune thyroiditis, and resolved the disease completely in about 1 of 8 patients.(2)


One of the recurring clinical observations by practitioners of nutritional medicine is that combinations of nutrients often work better than single nutrients.(3) Additional research should therefore focus on the use of a comprehensive nutritional program, rather than selenium by itself. Nutrients that have anti-inflammatory activity and/or may be beneficial in the treatment of autoimmune conditions include fish oil, magnesium, vitamin E, vitamin C, vitamin D, zinc, and copper.

Graves' ophthalmopathy (also known as thyroid eye disease [TED], dysthyroid/thyroid-associated orbitopathy [TAO], Graves' orbitopathy) is an autoimmune inflammatory disorder affecting the orbit around the eye, characterized by upper eyelid retraction, swelling (edema), redness (erythema), conjunctivitis, and bulging eyes (proptosis).(1)

It is part of a systemic process with variable expression in the eyes, thyroid, and skin, caused by autoantibodies that bind to tissues in those organs, and generally occurs with hyperthyroidism.(1) The most common form of hyperthyroidism is Graves' disease. About 10% of cases do not have Graves' disease, but do have autoantibodies.

The autoantibodies target the fibroblasts in the eye muscles, and those fibroblasts can differentiate into fat cells (adipocytes). Fat cells and muscles expand and become inflamed. Veins become compressed, and are unable to drain fluid, causing edema.(1)

Annual incidence is 16/100,000 in women, 3/100,000 in men. About 3% to 5% have severe disease with intense pain, and sight-threatening corneal ulceration or compression of the optic nerve. Cigarette smoking, which is associated with many autoimmune diseases, raises the incidence 7.7 fold.(1)

Mild disease will often resolve and merely requires measures to reduce discomfort and dryness, such as artificial tears and smoking cessation if possible. Severe cases are a medical emergency, and are treated with glucocorticoids (steroids), and sometimes cyclosporine.(2) Many antiinflammatory biological mediators, such as infliximab, etanercept, and anakinra are being tried, but there are no randomized controlled trials demonstrating effectiveness.(1)


(1.) Marcocci C, et al. Selenium and the course of mild Graves' orbitopathy. N Engl J Med. 2011;364:1920-1931.

(2.) Nacamulli D, et al. Influence of physiological dietary selenium supplementation on the natural course of autoimmune thyroiditis. Clin Endocrinol. 2010;73:535-539.

(3.) Gaby AR. Nutritional Medicine, 2011.

Alan R. Gaby, MD
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Author:Gaby, Alan R.
Publication:Townsend Letter
Article Type:Editorial
Geographic Code:1USA
Date:Oct 1, 2011
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