Monday, January 22, 2007

Selenium treatment for thyroid disorder - Another thank you to Dr. Hames

Yet another "Thank-you" to Dr. Hames for his work on the health benefits of Selenium. He brought this mineral to international attention with research on the positive effects on cardiovascular health.

Today researchers are finding how valuable this mineral is to the treatment of other disorders, namely thyroid autoimmune disorders (see below). The Medical College of Georgia announced recently that in Feb. 2007 it will dedicate a portion of the Robert B. Greenblatt, M.D. Library to house a permanent exhibit of the research manuscripts and articles of the late Dr. Curtis Hames as a memorial to his pioneering work. A fantastic example of an unassuming small country doctor impacting the world of medicine.

Topic: Selenium Treatment in Patients with Autoimmune Thyroiditis
Reference: "Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses," Turker O, Kumanlioglu K, et al, J Endocrinol, 2006; 190(1): 151-6. (Address: Thyroidology Unit, Department of Nuclear Medicine, GATA Haydarpasa, Istanbul, Turkey. E-mail: ).
Summary: In a 9-month study involving 88 women with autoimmune thyroiditis, supplementation with L-selenomethionine in doses higher than 100 microg/d was found to suppress serum concentrations of thyroid peroxidase antibodies (TPOAb), though the rate of suppression was found to decrease over time. All study subjects were receiving L-thyroxine, which kept their TSH levels at or below 2 mIU/l. The study involved 3 stages. In the first stage, which lasted 3 months, subjects were divided into 2 groups - one group (S2) received 200 microg/d L-selenomethionine and the other group received a placebo (C). In the second 3-month stage, 40 subjects from Group S2 were divided into 2 groups. One group (S22) continued to receive 200 microg/d L-selenomethionine, while the other group (S21) received a lower dose of 100 microg/d. In the third 3-month stage, 12 subjects from Group S22 continued to receive 200 microg/d L-selenomethionine (S222), while 12 subjects from Group S21 increased their dos e from 100 microg/d back to 200 microg/d (S212). Results found significant decreases in serum titers of TPOAb and thyroglobulin antibody titers among subjects in Group S2 (those who received 200 microg/d for the first 3 months). Subjects in Groups S22 (those who received 200 microg/d for the first and second 3 month periods), and S212 (those who received 200 microg/d for the first period, 100 microg/d for the second period, and 200 microg/d for the third period) experienced significant reductions in serum titers of TPOAb. Subjects who received placebo experienced no significant changes and subjects who received 200 microg/d for all three stages of the study (S222) also did not experience any significant changes in TPOAb titers. Increases in TPOAb titers were found among subjects who received 200 microg/d for the first stage and then reduced their dose to 100 microg/d for the second stage (S21). The authors of this study conclude that, "L-selenomethionine substitution suppresses serum concentrations of TPOAb in patients with AIT, but suppression requires doses higher than 100 microg/day which is sufficient to maximize glutathione peroxidase activities. The suppression rate decreases with time." Vitasearch Comment: The doses of selenomethionine studied refer to micrograms of elemental selenium supplied as L-selenomethionine



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