Selenium for Hashimoto's Thyroiditis by Jeffrey Dach MD
Susan has Hashimoto's thyroiditis, an autoimmune thyroid disorder causing fatigue, puffy face and muscle weakness. For the past year, she had been under the care of other doctors who started thyroid medication (Synthroid), and tested her thyroid antibody levels. The disturbing thing was that her antibodies kept climbing higher on each follow up lab test. The doctors had no explanation, so she asked me if there was something else that could be done.
Selenium Can Decrease Antibody Levels
As it turns out, there is a trace mineral called selenium that plays an important role in thyroid biochemistry. Selenium deficiency has been implicated in the etiology of Hashimoto's thyroiditis, and selenium supplementation has been found beneficial.
Three Selenium Studies Published in the Peer Reviewed Medical Literature
Showing Selenium is Beneficial in Hashimoto's Thyroiditis
The first study from Crete was published in the 2007 Thyroid Journal. This study reported a 21 % reduction in TPO antibodies after one year of selenomethionine supplements (200 mcg per day).
A second study from Germany from the 2002 Journal of Clinical Endocrinology & Metabolism showed a 40 % reduction in antibody levels after selenium supplementation with 9 of 36 (25%) patients completely normalizing their antibody levels.Left images: selenium diagrams courtesy of wikimedia commons.
A third study done in Turkey by Omer Turker et al. was published in the 2006 Journal of Endocrinology. They showed a 30% decrease in anti-thyroid antibodies after three months of L-selenomethionine supplementation at 200 mcg per day in women with Hashimotos thyroiditis. The starting average TPO antibodies of 803 and after three months the average was 572. The below bar chart shows the data from Omer Turker et al.
Left chart: Thyroid antibody (TPOAb) concentrations at the beginning of the study (light pink) and 3 months after treatment (arrow) with 200 mcg L-selenomethionine/day (group S2).
The light pink bar shows higher antibody levels before starting treatment.
Lower Dark pink bar (red arrow) shows decrease in antibody levels after three months of selenium supplementation. Left Bar Chart Image courtesy of Omer Turker et al. Journal of Endocrinology.
Why is Selenium So Important for Thyroid Function?
Recent advances in research into thyroid cell physiology shows that selenium is very important for thyroid function. There are at least 30 selenium dependent proteins, including the glutathione peroxidase enzyme, and the Iodothyronine deiodinases enzyme (this is the one that converts thyroxine (T4) to bioactive (T3). These preteins all need selenium as a co-factor in order to function properly. The selenoprotein, glutathione peroxidase, protects thyroid cells from damage by H2O2 produced by the thyroid cell. H2O2 is needed as a normal step in thyroid hormone production, However, too much H202 can damage the thyroid cell. In the event of selenium deficiency, the glutathione peroxidase enzyme cannot do its job protecting the thyroid cell, and the thyroid cells are damaged by excess H2O2. The current theory is that this damaged cell material is then recognized by the immune system as foreign, leading to Hashimoto's autoimmune disease.
Back to the Patient
Susan was started on her selenium supplements. In addition, her thyroid medication was switched from Synthroid to natural dessicated thyroid. Three months later Susan returned for follow up labs which showed decline in antibody levels. Although not all patients will see a dramatic decline in antibody levels, I have found that many patients will benefit from selenium supplementation.
A quick note about thyroid testing and treatment
A good thyroid testing protocol includes the following lab values, TSH, Free T3, Free T4, TPO Abs, Tgb Abs, reverse T3, selenium level, and iodine level. The thyroid panel is usually part of a larger evaluation with additional lab tests tailored to the clinical history and examination. A good thyroid treatment protocol uses natural dessicated thyroid medication such as Nature-throid from RLC labs. Dosage for natural dessicated thyroid medication varies, based on residual thyroid function, body weight, starting thyroid labs, and other variables.
Selenium Safety or Toxicity Depends on Dosage
Although Selenium is an inexpensive mineral supplement available without a prescription at the health food store, I would recommend working closely with your physician if you are considering selenium supplementation. Although selenium is generally considered safe at standard doses, very high dosage can cause selenium toxicity. In addition, your physician will determine if you need thyroid medication, the type and dosage of the medication, etc. By the way, for those looking for a food source for selenium, Brazil nuts are high in selenium.
Testing and Treatment in Hashimoto's Thyroiditis
Thyroid function in Hashimoto's Thyroiditis can have a variable course, with thyroid function varying over time. The need for thyroid medication will also vary depending upon thyroid function which can change over time. Lab studies at any one time may show low, normal or high thyroid function in patients with elevated antibody levels and Hashimoto's thyroid disease.
Recommended Books and Web SItes
1) David Brownstein's protocols are excellent.
His book is .
(left above image, book cover, Overcoming Thyroid Disorders courtesy of David Brownstein MD).
2) Janie Bowthorpe's Stop the Thyroid Madness Blog is excellent. Her book, is also recommended:
3) Mary Shomon's, Thyroid web site is excellent. Her book is .
4) Elaine Moore's Thyroid Web Site and her book is:.
Articles with related Interest:
Selenium and Thyroid , More Good News !!
Selenium
Selenium, Essential Mineral, Part One
The Case for Selenium, Part Two
Selenium, Your Vitamins Are Killing You, Part Three
Selenium for Hashimotos, Part Four
Hashimoto’s Thyroiditis Articles
Hashimotos Thyroiditis and Selenium Part One
Hashimotos, Selenium and Iodine, Part Two
Thyroid Articles
Ann Nicole Smith and Hypothyroidism
Why Natural Thyroid is Better than Synthetic Part One
Why Natural Thyroid is Better Part Two
The TSH Reference Range Wars – Part One
Jeffrey Dach MD
7450 Griffin Rd Suite 180/190
Davie, FL 33314
Phone: 954-792-4663
Blog
References
1) http://www.ncbi.nlm.nih.gov/pubmed/17696828
Thyroid. 2007 Jul;17(7):609-12. Effects of 12 months treatment with L-selenomethionine on serum anti-TPO Levels in Patients with Hashimoto's thyroiditis. Mazokopakis EE, Papadakis JA, Papadomanolaki MG, Batistakis AG, Giannakopoulos TG, Protopapadakis EE, Ganotakis ES. Department of Internal Medicine, University Hospital of Heraklion, Crete, Greece.
OBJECTIVE: We studied the effects of selenium (Se) treatment on serum anti-thyroid peroxidase (TPO) levels in Greek patients with Hashimoto's thyroiditis (HT). DESIGN: We prospectively studied 80 women with HT, median age 37 (range 24-52) years, for 1 year.
All patients received 200 microg Se in the form of l-selenomethionine orally for 6 months. At the end of the 6-month period, 40 patients continued taking 200 microg Se (Group A) and 40 patients stopped .
Serum thyrotropin (TSH), free triiodothyronine (FT(3)), free thyroxine (FT(4)), anti-TPO, and anti-thyroglobulin (Tg) levels were measured at baseline and at the end of each 3-month period.
MAIN OUTCOME: There was a significant reduction of serum anti-TPO levels during the first 6 months (by 5.6% and 9.9% at 3 and 6 months, respectively). An overall reduction of 21% (p < 0.0001) compared with the basal values was noted in Group A. In Group B, serum anti-TPO levels were increased by 4.8% (p < 0.0001) during the second 6-month period.
CONCLUSIONS: Our study showed that in HT patients 6 months of Se treatment caused a significant decrease in serum anti-TPO levels, which was more profound in the second trimester. The extension of Se supplementation for 6 more months resulted in an additional 8% decrease, while the cessation caused a 4.8% increase, in the anti-TPO concentrations.
2) http://jcem.endojournals.org/cgi/content/full/87/4/1687
The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 4 1687-1691, 2002 Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. Gärtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW. Department of Endocrinology, Medizinische Klinik Innenstadt, University of Munich, D-80336 Munich, Germany.
In areas with severe selenium deficiency there is a higher incidence of thyroiditis due to a decreased activity of selenium-dependent glutathione peroxidase activity within thyroid cells. Selenium-dependent enzymes also have several modifying effects on the immune system. Therefore, even mild selenium deficiency may contribute to the development and maintenance of autoimmune thyroid diseases.
We performed a blinded, placebo-controlled, prospective study in female patients (n = 70; mean age, 47.5 +/- 0.7 yr) with autoimmune thyroiditis and thyroid peroxidase antibodies (TPOAb) and/or Tg antibodies (TgAb) above 350 IU/ml. The primary end point of the study was the change in TPOAb concentrations. Secondary end points were changes in TgAb, TSH, and free thyroid hormone levels as well as ultrasound pattern of the thyroid and quality of life estimation.
Patients were randomized into 2 age- and antibody (TPOAb)-matched groups; 36 patients received 200 microg (2.53 micromol) sodium selenite/d, orally, for 3 months, and 34 patients received placebo. All patients were substituted with L-T(4) to maintain TSH within the normal range. TPOAb, TgAb, TSH, and free thyroid hormones were determined by commercial assays. The echogenicity of the thyroid was monitored with high resolution ultrasound.
The mean TPOAb concentration decreased significantly to 63.6% (P = 0.013) in the selenium group vs. 88% (P = 0.95) in the placebo group. A subgroup analysis of those patients with TPOAb greater than 1200 IU/ml revealed a mean 40% reduction in the selenium-treated patients compared with a 10% increase in TPOAb in the placebo group. TgAb concentrations were lower in the placebo group at the beginning of the study and significantly further decreased (P = 0.018), but were unchanged in the selenium group.
Nine patients in the selenium-treated group had completely normalized antibody concentrations, in contrast to two patients in the placebo group (by chi(2) test, P = 0.01). Ultrasound of the thyroid showed normalized echogenicity in these patients. The mean TSH, free T(4), and free T(3) levels were unchanged in both groups. We conclude that selenium substitution may improve the inflammatory activity in patients with autoimmune thyroiditis, especially in those with high activity. Whether this effect is specific for autoimmune thyroiditis or may also be effective in other endocrine autoimmune diseases has yet to be investigated.
3) http://www.ncbi.nlm.nih.gov/pubmed/12487769
Thyroid. 2002 Oct;12(10):867-78.The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health.
Zimmermann MB, Köhrle J.Laboratory for Human Nutrition, Swiss Federal Institute of Technology, Zürich, Switzerland.
Several minerals and trace elements are essential for normal thyroid hormone metabolism, e.g., iodine, iron, selenium, and zinc. Coexisting deficiencies of these elements can impair thyroid function. Iron deficiency impairs thyroid hormone synthesis by reducing activity of heme-dependent thyroid peroxidase. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. Combined selenium and iodine deficiency leads to myxedematous cretinism. The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and expresses many of the known selenocysteine-containing proteins. Among these selenoproteins are the glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes. Adequate selenium nutrition supports efficient thyroid hormone synthesis and metabolism and protects the thyroid gland from damage by excessive iodide exposure. In regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation in order to prevent hypothyroidism. Selenium deficiency and disturbed thyroid hormone economy may develop under conditions of special dietary regimens such as long-term total parenteral nutrition, phenylketonuria diet, cystic fibrosis, or may be the result of imbalanced nutrition in children, elderly people, or sick patients.
4) http://nuclmed.web.auth.gr/magazine/eng/jan07/8.pdf
Hashimoto’s thyroiditis and the role of selenium. Current concepts
by Hellenic in the Journal of Nuclear Medicine January - April 2007 Review Article
5) http://joe.endocrinology-journals.org/cgi/content/full/190/1/151
Journal of Endocrinology (2006) 190, 151-156
Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses
Omer Turker et al Thyroidology Unit, Department of Nuclear Medicine, GATA Haydarpasa, Istanbul, Turkey
The aim of this study is to investigate the long-term (9 months) effects of variable doses (200/100 µg/day) of L-selenomethionine on autoimmune thyroiditis (AIT) and the parameters affecting the success rate of this therapy.
The present study was designed in three steps:
(1) 88 female patients with AIT (mean age = 40.1 ± 13.3 years) were randomized into two groups according to their initial serum TSH, thyroid peroxidase antibody (TPOAb) concentrations, and age. All the patients were receiving L-thyroxine to keep serum TSH 2 mIU/l. Group S2 (n = 48, mean TPOAb = 803.9 ± 483.8 IU/ml) received 200 µg L-selenomethionine per day, orally for 3 months, and group C (n = 40, mean TPOAb = 770.3 ± 406.2 IU/ml) received placebo.
(2) 40 volunteers of group S2 were randomized into two age- and TPOAb-matched groups. Group S22 (n = 20) went on taking L-selenomethionine 200 µg/day, while others (group S21) lowered the dose to 100 µg/day.
(3) 12 patients of group S22 (group S222) went on taking L-selenomethionine 200 µg/day, while 12 patients of group S21 (S212) increased the dose to 200 µg/day.
Serum titers of TPOAb decreased significantly in group S2 (26.2%, P < 0.001), group S22 (23.7%, P < 0.01) and group S212 (30.3%, P < 0.01).
There were no significant changes in group C and group S222 (P > 0.05).
TPOAb titers increased significantly in group S21 (38.1%, P < 0.01).
A significant decrease in thyroglobulin antibody titers was only noted in group S2 (5.2%, P < 0.01).
L-selenomethionine substitution suppresses serum concentrations of TPOAb in patients with AIT, but suppression requires doses higher than 100 µg/day which is sufficient to maximize glutathione peroxidase activities. The suppression rate decreases with time.
Selenium is essential for optimal endocrine and immune function and for moderating the inflammatory response. These actions are mediated in most cases through the expression of at least 30 selenoproteins. There are at least six different glutathione peroxidases (GPX); Iodothyronine deiodinases type D1 and D2 convert thyroxine (T4) to bioactive 3,5,3'-tri-iodothyronine (T3);
http://edrv.endojournals.org/cgi/content/abstract/26/7/944
Endocrine Reviews 26 (7): 944-984, 2005
Selenium, the Thyroid, and the Endocrine System by J. Köhrle, F. Jakob, B. Contempré and J. E. Dumont Institut für Experimentelle Endokrinologie (J.K.), Charité Universitätsmedizin Berlin, Humboldt Universität, D-10098 Berlin, Germany;
Recent identification of new selenocysteine-containing proteins has revealed relationships between the two trace elements selenium (Se) and iodine and the hormone network. Several selenoproteins participate in the protection of thyrocytes from damage by H2O2 produced for thyroid hormone biosynthesis. Iodothyronine deiodinases are selenoproteins contributing to systemic or local thyroid hormone homeostasis. The Se content in endocrine tissues (thyroid, adrenals, pituitary, testes, ovary) is higher than in many other organs. Nutritional Se depletion results in retention, whereas Se repletion is followed by a rapid accumulation of Se in endocrine tissues, reproductive organs, and the brain.
Jeffrey Dach MD
7450 Griffin Road Suite 190
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954-792-4663
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