Selenium for hypothyroid. Selenium and Thyroid Health: Unraveling the Connection for Optimal Function
How does selenium impact thyroid health. What role does selenium play in thyroid hormone production. Can selenium supplementation benefit thyroid disorders. What are the recommended selenium intake levels for thyroid health. How does selenium deficiency affect thyroid function.
The Crucial Role of Selenium in Thyroid Function
Selenium, an essential trace element, plays a vital role in maintaining optimal thyroid health. This micronutrient is integral to the production and metabolism of thyroid hormones, making it a key player in the complex endocrine system. But how exactly does selenium contribute to thyroid function?
Selenium is a component of selenoproteins, which are enzymes crucial for thyroid hormone synthesis and metabolism. These selenoproteins include iodothyronine deiodinases, which are responsible for converting the inactive thyroid hormone (T4) into its active form (T3). Without adequate selenium, this conversion process can be impaired, potentially leading to thyroid dysfunction.
Selenium’s Antioxidant Properties in Thyroid Protection
Beyond its role in hormone production, selenium acts as a powerful antioxidant in the thyroid gland. It helps protect thyroid cells from oxidative stress and damage caused by free radicals. This protective function is particularly important given the thyroid’s high metabolic activity and susceptibility to oxidative damage.
- Selenium supports glutathione peroxidase activity, a key antioxidant enzyme
- It helps neutralize hydrogen peroxide produced during hormone synthesis
- Selenium may prevent thyroid cell apoptosis (programmed cell death)
Selenium Deficiency and Thyroid Disorders
Inadequate selenium intake can have significant consequences for thyroid health. Selenium deficiency has been linked to various thyroid disorders, including hypothyroidism and thyroid autoimmune diseases. How does a lack of selenium contribute to these conditions?
In cases of selenium deficiency, the thyroid gland may struggle to produce sufficient amounts of thyroid hormones. This can lead to hypothyroidism, a condition characterized by an underactive thyroid. Additionally, selenium deficiency may increase the risk of thyroid autoimmune diseases such as Hashimoto’s thyroiditis and Graves’ disease.
Selenium Deficiency and Iodine Metabolism
Selenium deficiency can also impact iodine metabolism, another crucial element for thyroid function. Without adequate selenium, the body may struggle to utilize iodine effectively, potentially exacerbating thyroid problems in iodine-deficient areas.
Selenium Supplementation for Thyroid Health
Given the importance of selenium for thyroid function, can selenium supplementation benefit those with thyroid disorders? Research suggests that selenium supplementation may indeed have positive effects on thyroid health, particularly in cases of autoimmune thyroid diseases.
Studies have shown that selenium supplementation can reduce thyroid antibody levels in patients with autoimmune thyroiditis. This may help slow the progression of the disease and improve overall thyroid function. Additionally, selenium supplementation has been found to enhance the effectiveness of conventional treatments for Graves’ ophthalmopathy, an eye condition associated with thyroid autoimmunity.
Recommended Selenium Intake for Thyroid Health
While selenium is essential for thyroid health, it’s important to maintain appropriate intake levels. The recommended dietary allowance (RDA) for selenium varies by age and gender:
- Adults: 55 micrograms per day
- Pregnant women: 60 micrograms per day
- Lactating women: 70 micrograms per day
It’s worth noting that these recommendations are for general health, and optimal levels for thyroid function may vary. Some studies suggest that higher selenium intake (up to 200 micrograms per day) may be beneficial for individuals with thyroid disorders, but this should be discussed with a healthcare provider.
Selenium Sources: Dietary and Supplemental Options
Ensuring adequate selenium intake can be achieved through both dietary sources and supplementation. What are the best food sources of selenium, and when might supplementation be necessary?
Selenium-rich foods include:
- Brazil nuts (highest natural source)
- Seafood (tuna, halibut, sardines)
- Organ meats (liver, kidney)
- Poultry and eggs
- Whole grains and cereals
While a balanced diet can provide sufficient selenium for most individuals, those with thyroid disorders or living in selenium-deficient regions may benefit from supplementation. Selenium supplements are available in various forms, including selenomethionine and sodium selenite. High-selenium yeast has also been shown to be an effective way to raise selenium status.
Considerations for Selenium Supplementation
Before starting selenium supplementation, it’s crucial to consult with a healthcare provider. Excessive selenium intake can lead to toxicity, known as selenosis, which can cause symptoms such as hair loss, nail brittleness, and neurological problems. The upper tolerable intake level for adults is set at 400 micrograms per day.
Selenium and Thyroid Autoimmunity: A Closer Look
The relationship between selenium and thyroid autoimmunity is of particular interest to researchers and clinicians. How does selenium influence the development and progression of autoimmune thyroid diseases?
Selenium’s role in thyroid autoimmunity is multifaceted. It helps regulate the immune response and may reduce inflammation in the thyroid gland. Selenium also supports the production of regulatory T cells, which are crucial for maintaining immune tolerance and preventing autoimmune reactions.
Selenium’s Impact on Thyroid Antibodies
Several studies have demonstrated that selenium supplementation can reduce thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb) in patients with autoimmune thyroiditis. This reduction in antibodies may help slow the progression of the disease and potentially improve thyroid function over time.
- Selenium may decrease TPOAb levels by 20-50% in some studies
- Reduction in antibodies is often observed within 3-6 months of supplementation
- Effects may be more pronounced in areas with mild selenium deficiency
Selenium and Graves’ Disease: Potential Benefits
Graves’ disease, an autoimmune condition causing hyperthyroidism, may also benefit from selenium supplementation. How does selenium impact the course of Graves’ disease and its associated complications?
Research suggests that selenium supplementation may help improve outcomes in patients with Graves’ disease. It may reduce thyroid hormone levels and improve quality of life in some individuals. Additionally, selenium has shown promise in managing Graves’ ophthalmopathy, a condition affecting the eyes that often accompanies Graves’ disease.
Selenium in Graves’ Ophthalmopathy Management
Studies have demonstrated that selenium supplementation can significantly improve eye symptoms and quality of life in patients with mild Graves’ ophthalmopathy. It may help reduce inflammation and oxidative stress in orbital tissues, potentially slowing the progression of eye symptoms.
- Selenium may improve eye symptoms in 61% of patients compared to 36% with placebo
- It can enhance the effectiveness of standard treatments for Graves’ ophthalmopathy
- Supplementation may be most beneficial in the early, active phase of the disease
Selenium Interactions with Iodine and Other Nutrients
While selenium plays a crucial role in thyroid health, it doesn’t work in isolation. How does selenium interact with other nutrients, particularly iodine, in supporting thyroid function?
The relationship between selenium and iodine is particularly important for thyroid health. Both nutrients are essential for proper thyroid hormone production and metabolism. Selenium helps protect the thyroid gland from oxidative stress caused by iodine, especially in cases of iodine excess.
Balancing Selenium and Iodine Intake
Maintaining an appropriate balance between selenium and iodine is crucial for optimal thyroid function. In areas with iodine deficiency, selenium supplementation should be approached with caution, as it may exacerbate the effects of iodine deficiency. Conversely, in regions with adequate iodine intake, selenium supplementation may be more beneficial for thyroid health.
- Selenium and iodine work synergistically in thyroid hormone production
- Adequate selenium intake may protect against the harmful effects of iodine excess
- Combined deficiency of both selenium and iodine can lead to more severe thyroid dysfunction
Future Directions in Selenium and Thyroid Research
As our understanding of the relationship between selenium and thyroid health continues to evolve, what are the key areas for future research? Several important questions remain to be answered:
- Optimal selenium dosage for different thyroid conditions
- Long-term effects of selenium supplementation on thyroid function
- Genetic factors influencing selenium metabolism and thyroid health
- Potential role of selenium in thyroid cancer prevention and treatment
Ongoing research in these areas will help refine our approach to selenium supplementation and its use in thyroid disorders. As we gain more insights, personalized recommendations based on individual needs and genetic profiles may become possible, leading to more targeted and effective interventions for thyroid health.
Emerging Technologies in Selenium Research
Advancements in research technologies are opening new avenues for understanding selenium’s role in thyroid health. Genomic and proteomic studies are shedding light on the complex interactions between selenium, selenoproteins, and thyroid function at the molecular level. These insights may lead to the development of novel therapeutic approaches for thyroid disorders.
Additionally, improved methods for assessing selenium status, such as biomarkers of selenium function rather than just serum levels, may help clinicians better evaluate the need for supplementation in individual patients. This could lead to more precise and effective selenium interventions for thyroid health.
Selenium and Thyroid Disease: From Pathophysiology to Treatment
1. Duntas L. H., Benvenga S. Selenium: an element for life. Endocrine. 2015;48(3):756–775. doi: 10.1007/s12020-014-0477-6. [PubMed] [CrossRef] [Google Scholar]
2. Rayman M. P. Selenium and human health. Lancet. 2012;379(9822):1256–1268. doi: 10.1016/S0140-6736(11)61452-9. [PubMed] [CrossRef] [Google Scholar]
3. Thiry C., Ruttens A., Pussemier L., Schneider Y. J. An in vitro investigation of species-dependent intestinal transport of selenium and the impact of this process on selenium bioavailability. The British Journal of Nutrition. 2013;109(12):2126–2134. doi: 10.1017/S0007114512004412. [PubMed] [CrossRef] [Google Scholar]
4. Waegeneers N., Thiry C., De Temmerman L., Ruttens A. Predicted dietary intake of selenium by the general adult population in Belgium. Food Additives & Contaminants. Part A, Chemistry, Analysis, Control, Exposure & Risk Assessment. 2013;30(2):278–285. doi: 10.1080/19440049.2012.746474. [PubMed] [CrossRef] [Google Scholar]
5. Park K., Rimm E., Siscovick D., Spiegelman D., Morris J. S., Mozaffarian D. Demographic and lifestyle factors and selenium levels in men and women in the U.S. Nutrition Research and Practice. 2011;5(4):357–364. doi: 10.4162/nrp.2011.5.4.357. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
6. Rayman M. P. The use of high-selenium yeast to raise selenium status: how does it measure up? The British Journal of Nutrition. 2004;92(4):557–573. [PubMed] [Google Scholar]
7. Kipp A. P., Strohm D., Brigelius-Flohe R., et al. Revised reference values for selenium intake. Journal of Trace Elements in Medicine and Biology. 2015;32:195–199. doi: 10.1016/j.jtemb.2015.07.005. [PubMed] [CrossRef] [Google Scholar]
8. Institute of Medicine (US) Panel on Dietary Antioxidants and Related Compounds; N. A. P. (US) Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington (DC), USA: 2000. Vitamin C, vitamin E, selenium, and β-carotene and other carotenoids: overview, antioxidant definition, and relationship to chronic disease. [Google Scholar]
9. Agency for Toxic Substances and Disease Registry (ATSDR) Toxicologic Profile for Selenium. Atlanta, GA, USA: US Department of Health and Human Services, Public Health Service; 2003. [Google Scholar]
10. MacFarquhar J. K., Broussard D. L., Melstrom P., et al. Acute selenium toxicity associated with a dietary supplement. Archives of Internal Medicine. 2010;170(3):256–261. doi: 10.1001/archinternmed.2009.495. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
11. Goyens P., Golstein J., Nsombola B., Vis H., Dumont J. E. Selenium deficiency as a possible factor in the pathogenesis of myxoedematous endemic cretinism. Acta Endocrinologica. 1987;114(4):497–502. [PubMed] [Google Scholar]
12. Kohrle J. Thyrotropin (TSH) action on thyroid hormone deiodination and secretion: one aspect of thyrotropin regulation of thyroid cell biology. Hormone and Metabolic Research Supplement. 1990;23:18–28. [PubMed] [Google Scholar]
13. Dickson R. C., Tomlinson R. H. Selenium in blood and human tissues. Clinica Chimica Acta. 1967;16(2):311–321. [PubMed] [Google Scholar]
14. Schomburg L. Selenium, selenoproteins and the thyroid gland: interactions in health and disease. Nature Reviews Endocrinology. 2012;8(3):160–171. doi: 10.1038/nrendo.2011.174. [PubMed] [CrossRef] [Google Scholar]
15. Saranac L., Zivanovic S., Bjelakovic B., Stamenkovic H., Novak M., Kamenov B. Why is the thyroid so prone to autoimmune disease? Hormone Research in Pædiatrics. 2011;75(3):157–165. doi: 10.1159/000324442. [PubMed] [CrossRef] [Google Scholar]
16. Drutel A., Archambeaud F., Caron P. Selenium and the thyroid gland: more good news for clinicians. Clinical Endocrinology. 2013;78(2):155–164. doi: 10.1111/cen.12066. [PubMed] [CrossRef] [Google Scholar]
17. Dharmasena A. Selenium supplementation in thyroid associated ophthalmopathy: an update. International Journal of Ophthalmology. 2014;7(2):365–375. doi: 10.3980/j.issn.2222-3959.2014.02.31. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
18. Kohrle J., Jakob F., Contempre B., Dumont J. E. Selenium, the thyroid, and the endocrine system. Endocrine Reviews. 2005;26(7):944–984. doi: 10.1210/er.2001-0034. [PubMed] [CrossRef] [Google Scholar]
19. Negro R. Selenium and thyroid autoimmunity. Biologics. 2008;2(2):265–273. [PMC free article] [PubMed] [Google Scholar]
20. morSanmartin C., Plano D., Font M., Palop J. A. Selenium and clinical trials: new therapeutic evidence for multiple diseases. Current Medicinal Chemistry. 2011;18(30):4635–4650. [PubMed] [Google Scholar]
21. Schweizer U., Streckfuss F., Pelt P., et al. Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply. Biochemical Journal. 2005;386(Pt 2):221–226. doi: 10.1042/BJ20041973. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
22. Hill K. E., Wu S., Motley A. K., et al. Production of selenoprotein P (Sepp1) by hepatocytes is central to selenium homeostasis. The Journal of Biological Chemistry. 2012;287(48):40414–40424. doi: 10.1074/jbc.M112.421404. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
23. Schomburg L., Riese C., Michaelis M., et al. Synthesis and metabolism of thyroid hormones is preferentially maintained in selenium-deficient transgenic mice. Endocrinology. 2006;147(3):1306–1313. doi: 10.1210/en.2005-1089. [PubMed] [CrossRef] [Google Scholar]
24. Gartner R., Gasnier B. C., Dietrich J. W., Krebs B., Angstwurm M. W. Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. The Journal of Clinical Endocrinology and Metabolism. 2002;87(4):1687–1691. doi: 10.1210/jcem.87.4.8421. [PubMed] [CrossRef] [Google Scholar]
25. Duntas L. H., Mantzou E., Koutras D. A. Effects of a six month treatment with selenomethionine in patients with autoimmune thyroiditis. European Journal of Endocrinology. 2003;148(4):389–393. [PubMed] [Google Scholar]
26. Turker O., Kumanlioglu K., Karapolat I., Dogan I. Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses. The Journal of Endocrinology. 2006;190(1):151–156. doi: 10.1677/joe.1.06661. [PubMed] [CrossRef] [Google Scholar]
27. Gartner R., Gasnier B. C. Selenium in the treatment of autoimmune thyroiditis. BioFactors. 2003;19(3-4):165–170. [PubMed] [Google Scholar]
28. Nacamulli D., Mian C., Petricca D., et al. Influence of physiological dietary selenium supplementation on the natural course of autoimmune thyroiditis. Clinical Endocrinology. 2010;73(4):535–539. doi: 10.1111/j.1365-2265.2009.03758.x. [PubMed] [CrossRef] [Google Scholar]
29. Mao J., Pop V. J., Bath S. C., Vader H. L., Redman C. W., Rayman M. P. Effect of low-dose selenium on thyroid autoimmunity and thyroid function in UK pregnant women with mild-to-moderate iodine deficiency. European Journal of Nutrition. 2016;55(1):55–61. doi: 10.1007/s00394-014-0822-9. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
30. Negro R., Greco G., Mangieri T., Pezzarossa A., Dazzi D., Hassan H. The influence of selenium supplementation on postpartum thyroid status in pregnant women with thyroid peroxidase autoantibodies. The Journal of Clinical Endocrinology and Metabolism. 2007;92(4):1263–1268. doi: 10.1210/jc.2006-1821. [PubMed] [CrossRef] [Google Scholar]
31. Winther K. H., Watt T., Bjorner J. B., et al. The chronic autoimmune thyroiditis quality of life selenium trial (CATALYST): study protocol for a randomized controlled trial. Trials. 2014;15:p. 115. doi: 10.1186/1745-6215-15-115. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
32. Rasmussen L. B., Schomburg L., Kohrle J., et al. Selenium status, thyroid volume, and multiple nodule formation in an area with mild iodine deficiency. European Journal of Endocrinology. 2011;164(4):585–590. doi: 10.1530/EJE-10-1026. [PubMed] [CrossRef] [Google Scholar]
33. Derumeaux H., Valeix P., Castetbon K., et al. Association of selenium with thyroid volume and echostructure in 35- to 60-year-old French adults. European Journal of Endocrinology. 2003;148(3):309–315. [PubMed] [Google Scholar]
34. Wu Q., Rayman M. P., Lv H., et al. Low population selenium status is associated with increased prevalence of thyroid disease. The Journal of Clinical Endocrinology and Metabolism. 2015;100(11):4037–4047. doi: 10.1210/jc.2015-2222. [PubMed] [CrossRef] [Google Scholar]
35. Vrca V. B., Skreb F., Cepelak I., Romic Z., Mayer L. Supplementation with antioxidants in the treatment of Graves’ disease; the effect on glutathione peroxidase activity and concentration of selenium. Clinica Chimica Acta. 2004;341(1-2):55–63. doi: 10.1016/j.cccn.2003.10.028. [PubMed] [CrossRef] [Google Scholar]
36. Wang L., Wang B., Chen S. R., et al. Effect of selenium supplementation on recurrent hyperthyroidism caused by Graves’ disease: a prospective pilot study. Hormone and Metabolic Research. 2016;48(9):559–564. doi: 10.1055/s-0042-110491. [PubMed] [CrossRef] [Google Scholar]
37. Bahn R. S. Graves’ ophthalmopathy. The New England Journal of Medicine. 2010;362(8):726–738. doi: 10.1056/NEJMra0905750. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
38. Marcocci C., Kahaly G. J., Krassas G. E., et al. Selenium and the course of mild Graves’ orbitopathy. The New England Journal of Medicine. 2011;364(20):1920–1931. doi: 10.1056/NEJMoa1012985. [PubMed] [CrossRef] [Google Scholar]
39. Bartalena L., Baldeschi L., Boboridis K., et al. The 2016 European Thyroid Association/European Group on Graves’ Orbitopathy Guidelines for the Management of Graves’ Orbitopathy. European Thyroid Journal. 2016;5(1):9–26. doi: 10.1159/000443828. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
40. Carlson B. A., Yoo M. H., Shrimali R. K., et al. Role of selenium-containing proteins in T-cell and macrophage function. The Proceedings of the Nutrition Society. 2010;69(3):300–310. doi: 10.1017/S002966511000176X. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
41. Patrick L. Selenium biochemistry and cancer: a review of the literature. Alternative Medicine Review. 2004;9(3):239–258. [PubMed] [Google Scholar]
42. Shen F., Cai W. S., Li J. L., Feng Z., Cao J., Xu B. The association between serum levels of selenium, copper, and magnesium with thyroid cancer: a meta-analysis. Biological Trace Element Research. 2015;167(2):225–235. doi: 10.1007/s12011-015-0304-9. [PubMed] [CrossRef] [Google Scholar]
43. Jonklaas J., Danielsen M., Wang H. A pilot study of serum selenium, vitamin D, and thyrotropin concentrations in patients with thyroid cancer. Thyroid. 2013;23(9):1079–1086. doi: 10.1089/thy.2012.0548. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
44. Rayman M. P., Stranges S. Epidemiology of selenium and type 2 diabetes: can we make sense of it? Free Radical Biology & Medicine. 2013;65:1557–1564. doi: 10.1016/j.freeradbiomed.2013.04.003. [PubMed] [CrossRef] [Google Scholar]
45. Stranges S., Navas-Acien A., Rayman M. P., Guallar E. Selenium status and cardiometabolic health: state of the evidence. Nutrition, Metabolism, and Cardiovascular Diseases. 2010;20(10):754–760. doi: 10.1016/j.numecd.2010.10.001. [PubMed] [CrossRef] [Google Scholar]
46. Rocourt C. R., Cheng W. H. Selenium supranutrition: are the potential benefits of chemoprevention outweighed by the promotion of diabetes and insulin resistance? Nutrients. 2013;5(4):1349–1365. doi: 10.3390/nu5041349. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
47. Bleys J., Navas-Acien A., Guallar E. Serum selenium levels and all-cause, cancer, and cardiovascular mortality among US adults. Archives of Internal Medicine. 2008;168(4):404–410. doi: 10.1001/archinternmed.2007.74. [PubMed] [CrossRef] [Google Scholar]
48. Sunde R. A., Paterson E., Evenson J. K., Barnes K. M., Lovegrove J. A., Gordon M. H. Longitudinal selenium status in healthy British adults: assessment using biochemical and molecular biomarkers. The British Journal of Nutrition. 2008;99(Suppl 3):S37–47. doi: 10.1017/S0007114508006831. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
49. Gonzalez S., Huerta J. M., Fernandez S., Patterson E. M., Lasheras C. Food intake and serum selenium concentration in elderly people. Annals of Nutrition & Metabolism. 2006;50(2):126–131. doi: 10.1159/000090633. [PubMed] [CrossRef] [Google Scholar]
50. Emmanuelle B., Virginie M., Fabienne S., et al. Selenium exposure in subjects living in areas with high selenium concentrated drinking water: results of a French integrated exposure assessment survey. Environment International. 2012;40:155–161. doi: 10.1016/j.envint.2011.07.007. [PubMed] [CrossRef] [Google Scholar]
51. Pograjc L., Stibilj V., Falnoga I. Impact of intensive physical activity on selenium status. Biological Trace Element Research. 2012;145(3):291–299. doi: 10.1007/s12011-011-9204-9. [PubMed] [CrossRef] [Google Scholar]
52. Valent F., Horvat M., Mazej D., Stibilj V., Barbone F. Maternal diet and selenium concentration in human milk from an Italian population. Journal of Epidemiology. 2011;21(4):285–292. [PMC free article] [PubMed] [Google Scholar]
53. Hughes C. M., Woodside J. V., McGartland C., Roberts M. J., Nicholls D. P., McKeown P. P. Nutritional intake and oxidative stress in chronic heart failure. Nutrition, Metabolism, and Cardiovascular Diseases. 2012;22(4):376–382. doi: 10.1016/j.numecd.2010.08.006. [PubMed] [CrossRef] [Google Scholar]
Zinc and Selenium and Their Effect on Thyroid Health — Genesis Performance Chiropractic of Elverson, PA
If you’ve been following us, you know our passion for restoring the health of those suffering. In our experience, many of our patients, particularly women, do not have optimal function of the thyroid. You may remember that the thyroid is a butterfly-shaped gland in the lower front of the neck. Its responsibilities include:
There are a number of nutrients that contribute to thyroid health. In this article, we’ll discuss two of them: selenium and zinc.
Selenium
Selenium is an essential trace element that’s found in the soil. Selenium is found naturally in water and in some foods, including Brazil nuts, fish, ham, pork, beef, turkey, chicken, eggs, brown rice, mushrooms, oatmeal, spinach, lentils, cashews, bananas, some dairy products, and some enriched food products.
Selenium has wonderful antioxidant properties, which protect against oxidative damage and infections. Lack of selenium has been associated with a number of conditions, including heart disease, neuromuscular disorders, cancer, male infertility, and inflammation. Selenium has been positively associated with mammalian development, immune function, and even delaying the progression of AIDS in HIV-positive patients (1). Selenium is thought to have these protective effects because of its positive influence on immune response. Those who especially need to watch for a selenium deficiency are those who have digestive issues, such as Celiac disease or Crohn’s disease due to a lowered ability to absorb nutrients.
Selenium and the thyroid
Selenium is also key to thyroid health. It is a necessary micronutrient for thyroid hormone synthesis and function. The concentration of selenium in the thyroid is higher than in any other organ in the body and is needed for optimal thyroid function. Selenium works together with iodine to activate three different selenium-dependent iodothyronine deiodinases, which can then activate or deactivate thyroid hormones. This process (and selenium) is essential for normal growth, development, and metabolism (2).
Selenium deficiency is associated with hypothyroidism, Hashimoto’s, an enlarged thyroid (goiter), thyroid cancer, and Graves’ disease.
One study with 1900 participants found an inverse relationship between serum selenium concentrations and thyroid volume. They also observed a protective effect of selenium against goiter and thyroid tissue damage. In this particular study, these results were significant only for the women participants (3).
Another study looked at the effects of selenium on Graves’ orbitopathy, which is thyroid eye disease from hyperthyroidism (when the thyroid gland produces too much thyroid hormone). The researchers compared treatment with selenium to treatment with pentoxifylline, which is an anti-inflammatory. The selenium treatment group reported an improved quality of life, reduced ocular involvement, and slowed progression of Graves’ orbitopathy in comparison to the pentoxifylline treatment group (4).
Table information from https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/
* It is important to note that with a thyroid condition, these dose recommendations will increase.
Zinc
Zinc is another trace element that is essential for growth, development, and a healthy immune system. Zinc also has a major impact on the nervous and reproductive systems (5).
Zinc is found in meat (including beef, lamb, and pork), shellfish, legumes, hemp seeds, pumpkin seeds, squash seeds, sesame seeds, pine nuts, peanuts, cashews, almonds, eggs, whole grains, potatoes, green beans, kale, dark chocolate, and dairy products.
Zinc and the thyroid
Zinc is another element that is needed for the synthesis of thyroid hormones. Zinc is needed for the production of hormones T3, T4, and thyroid stimulating hormone (TSH).
A deficiency in zinc can lead to hypothyroidism. On the other hand, hypothyroidism can lead to a zinc deficiency, as thyroid hormones are required for the absorption of zinc. When supplementing with thyroid hormones, taking a zinc supplement is also important (6).
In a case study with two college women who were zinc deficient, researchers asked the women to supplement with zinc for four months. At the end of four months, both women showed improvement on all thyroid levels (especially T3) as well as resting metabolic rate (7).
Another research study showed that taking zinc alone or in combination with selenium can improve thyroid function in women who have hypothyroidism (8)
Table information from https://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/
* It is important to note that with a thyroid condition, these dose recommendations will increase.
For optimal thyroid health, we recommend testing for your levels of these important trace elements. We will work with you to address deficiencies and supplement adequately, but without moving into toxic levels of selenium or zinc. Making sure your selenium and zinc levels are at optimal levels will improve your thyroid health along with your overall health and wellness.
Works cited:
https://www. ncbi.nlm.nih.gov/pmc/articles/PMC4101630/#B40
https://pubmed.ncbi.nlm.nih.gov/19594417/
https://pubmed.ncbi.nlm.nih.gov/12611611/
https://pubmed.ncbi.nlm.nih.gov/21591944/
https://pubmed.ncbi.nlm.nih.gov/11115789/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746228/#:~:text=Zinc%20and%20other%20trace%20elements,result%20in%20acquired%20zinc%20deficiency.
https://pubmed.ncbi.nlm.nih.gov/17541266/
https://pubmed.ncbi.nlm.nih.gov/25758370/
Ryan VermeeschGenesis Performance Chiropractic
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Use of selenium in medical practice | Shestakova T.P.
The article is devoted to the possibilities of using selenium in medical practice. Selenium is a trace element that is part of the enzymes that play an important role in the functioning of the thyroid gland, reproductive, immune systems and in carcinogenesis. Lack and excess of selenium are unfavorable for human health. The main organ that uses selenium is the thyroid gland. Selenium effectively reduces the level of antibodies to thyroperoxidase (TPO) in patients with autoimmune thyroiditis, improves the quality of life of patients with endocrine ophthalmopathy. Selenium is used in the clinical practice of endocrinologists for autoimmune thyroiditis and endocrine ophthalmopathy.
Introduction
Selenium is a trace element that was first described in 1817 by the Swedish chemist John Berzelius. It belongs to the 16th subgroup of the table of chemical elements of D.I. Mendeleev, where it stands between arsenic and bromine, and in its chemical properties it is similar to sulfur. Due to its ability to donate electrons, selenium is widely used in industry. In 1957, researchers Schwartz and Foltz found that selenium supplementation prevented the development of muscular dystrophy and liver cirrhosis in rats [1]. In subsequent years, it was revealed that selenium is an important element of the glutathione peroxidase enzyme [2], after which the study of the effect of selenium deficiency on human health and the possibility of using it in medical practice began. Its role in the functioning of the immune, endocrine and reproductive systems, metabolism, cellular homeostasis, and carcinogenesis was revealed.
Sources of selenium
The main source of selenium for a person is food, therefore, the content of selenium in the body is determined by the dietary preferences of a person. In turn, the content of selenium in food products depends on the place where the plants grow. The average content of selenium in the soil is 0.4 mg/kg [3]. But this number is not constant. It depends on the composition of the soil, including the proportion of organic matter in it, and the amount of precipitation falling in a given area [4]. In mountainous areas (Finland, Sweden, Scotland), soils are deficient in selenium, while clay soils and soils in regions with low rainfall usually contain an increased amount of this trace element. In most European countries, Egypt, Brazil, India, China, Saudi Arabia, Nepal, Burundi, New Guinea, separate regions with selenium deficiency have been identified. An excess of selenium is also found in certain regions of India, China, USA, Canada, Brazil, Venezuela, Japan. For comparison: in Europe, the average intake of selenium is 40 mcg / day, and in the USA – 93 µg/day for women and 134 µg/day for men [5].
Selenium is found not only in soil, but also in water. The average concentration of selenium in tap water is 10 µg/l, which is defined by the World Health Organization (WHO) as the minimum acceptable level of selenium in drinking water. In underwater waters, the concentration of selenium is somewhat higher, but it reaches the highest level in sea water, where it ranges from 4000 to 12000 μg of selenium per 1 l [6].
The content of selenium in plants varies considerably. It depends not only on the place of growth, but also on the ability of plants to capture selenium from the soil and accumulate it. In general, the selenium content is higher in vegetables than in fruits. The selenium content in cereals varies from 0.01 to 0.55 µg/g, in dairy products – from 0. 001 to 0.17 µg/g [7]. According to a Belgian study, the main source of selenium for humans is meat products (31%), followed by fish (19%).%), bread and cereals (11%) [8].
In nature, selenium exists in the form of organic (selenomethionine and selenocysteine) and inorganic compounds (selenite and selenate). Considering that organic forms are better absorbed in the gastrointestinal tract, some experts consider them as the main ones for the prevention and treatment of diseases caused by selenium deficiency. Selenomethionine is found in plants, mainly in cereals, while selenocysteine is found mainly in animal products. In food supplements, inorganic forms of selenium are more commonly used. Selenium is absorbed mainly in the small intestine (50-80%) and excreted through the kidneys (60%). Another 35% is excreted through the large intestine, 5% through sweat and saliva [9]. For reasons not yet understood, selenium levels are lower in smokers and decrease with age. In addition, selenium content is lower in individuals who consume large amounts of coffee and alcohol. Eating large amounts of rice and eggs is also associated with a reduced concentration of selenium in the body [10]. WHO recommends an intake of 50–55 micrograms of selenium per day [11].
Influence of deficiency and excess of selenium on human health
Both the lack of selenium and its excess are dangerous for humans. Deficiency manifestations appear when selenium intake is less than 40 μg/day, and excess – when more than 400 μg/day is consumed [12]. Severe selenium deficiency leads to the development of Keshan disease, manifested by heart failure due to cardiomyopathy, atrophy, degeneration and necrosis of articular cartilage, and fever. But even a less pronounced lack of this microelement adversely affects the state of human health. Selenium acts as a catalytic site for several enzymes, such as glutathione peroxidase, thioreduxin reductase, and iodothyronine deiodinase, which protect the cell from oxidative stress, the action of free radicals, strengthen the immune system, are involved in the metabolism of thyroid hormones, etc. [7].
In some studies, selenium deficiency was associated with an increased risk of cardiovascular disease, which decreased when the deficiency was replenished. Selenium has an anticarcinogenic effect on the prostate, liver, pancreas, and large intestine. In addition, selenium is involved in embryo implantation, placental development, fertility enhancement by increasing sperm motility, testosterone and sperm synthesis [6].
With the consumption of more than 400 micrograms of selenium per day, the so-called selenite develops. This rare situation has been described in population studies with chronic selenium intoxication in regions with high natural content [13]. Symptoms of selenitis are nausea, vomiting, abdominal pain, diarrhea, hair loss, brittle nails, peripheral neuropathy, and a characteristic garlic odor in sweat and exhaled air. Cases of the development of selenite are described in case of an overdose of food additives with an increased content of it [14].
The role of selenium in the functioning of the thyroid gland
Selenium plays a special role in the functioning of the thyroid gland. This organ contains the largest amount of selenium per 1 g of tissue in the form of selenoproteins. The participation of selenium in the synthesis of thyroid hormones was first suspected after studies conducted in Zaire, where not only severe iodine deficiency was revealed, but also severe selenium deficiency. At the same time, the population had severe myxedematous cretinism and a pronounced intellectual deficit. After that, many studies have been conducted on the role of selenium in the functioning of the thyroid gland. As a result, it was shown that selenium affects the synthesis of thyroid hormones indirectly via selenoproteins [15] (Table 1). Thyroid status is mainly affected by selenium-containing deiodinases, which convert the inactive form of thyroid hormones (T 4 ) into active (T 3 ) by removing one iodine atom from the outer ring. In addition, they are able to convert T 4 into an inactive form of the hormone – reverse T 3 , splitting off one iodine atom from the inner nucleus.
But this is not limited to the role of selenium in the functioning of the thyroid gland. So, selenoprotein – glutathione peroxidase protects the thyroid gland from oxidative stress. The fact is that in the process of synthesis of thyroid hormones in thyrocytes, hydrogen peroxide (H 2 O 2 ), which is a powerful oxidant. Glutathione peroxidase has the ability to inactivate hydrogen peroxide and free radicals and thereby limit their damaging effects on thyroid tissue. It has been proven that when exposed to glutathione peroxidase, the concentration of prostaglandins and leukotrienes decreases, which indicates a decrease in inflammation [16].
With a deficiency of selenium, a lack of deiodinases of various types is formed, the formation of T9 decreases0024 3 , leading to stimulation of the hypothalamic-pituitary axis through a negative feedback system and an increase in the synthesis of thyroid-stimulating hormone (TSH). TSH stimulates the production of thyroid hormones and increases the activity of deiodinases, restoring the level of thyroid hormones. But at the same time, it stimulates the formation of hydrogen peroxide, for the inactivation of which, again, selenoprotein, glutathione peroxidase, is required, the activity of which is reduced under conditions of selenium deficiency. Hydrogen peroxide accumulates in the thyroid gland, which leads to damage to thyrocytes and the development of fibrosis [17, 18]. An increased formation of hydrogen peroxide in the thyrocyte is observed in all cases of excessive stimulation of the thyroid gland by TSH, for example, in patients with autoimmune thyroiditis and subclinical hypothyroidism. As a result, damage to thyrocytes, progression of hypothyroidism and development of fibrosis are observed. In such a situation, selenoproteins, having antioxidant activity, can prevent or at least slow down the destruction of thyrocytes and reduce their functional activity [15].
Thioreduxin reductase, like glutathione peroxidase, has antioxidant activity, but the role of this enzyme in the functioning of the thyroid gland is less studied.
Selenoprotein P is the main source of selenium in plasma, it performs the transport function and distribution function of the microelement in the body [19]. It is synthesized in the liver and is responsible for retaining selenium in the body and distributing it between organs. The main organs into which selenium enters from the blood are the liver, thyroid gland, and brain. However, the thyroid gland and the brain have the ability to retain and accumulate selenium even in conditions of selenoprotein P deficiency [20].
Place of selenium in the treatment and prevention of thyroid diseases
Autoimmune thyroiditis
Studies have shown that selenium deficiency plays an important role in damage to thyrocytes and a decrease in their functional activity in autoimmune thyroiditis. In a population study conducted by Q. Wu et al., it was shown that subclinical hypothyroidism (RR 0.68; 95% CI 0.58–0.93), overt hypothyroidism (RR 0 .75;95% CI 0.63–0.90), autoimmune thyroiditis (RR 0. 47; 95% CI 0.35–0.65). In total, the prevalence of these diseases was almost two times less in the region with sufficient selenium supply compared to the selenium-deficient region (18% compared to 30.5%, p<0.001) [21].
But are selenium preparations able to prevent or at least slow down the development of autoimmune thyroiditis and, subsequently, hypothyroidism? There is currently no single answer to this question.
In studies of patients with autoimmune thyroiditis, the effect of selenium on the level of antithyroid antibodies (to thyroperoxidase (TPO) and thyroglobulin (TG)), thyroid function, echogenicity of thyroid tissue, and quality of life of patients was determined (Table 2). None of the studies evaluated the incidence of hypothyroidism, which is probably due to the short duration of the studies (no more than 12 months). Organic forms of selenium were mainly used, apparently due to their greater bioavailability.
Most authors [22–26] have found a statistically significant decrease in the level of anti-TPO antibodies after the use of selenium at doses of 83–200 µg/day. In a study by O. Turker et al. it was shown that the dose of 100 mcg/day is insufficient to reduce the level of antithyroid antibodies, while the dose of 200 mcg was determined to be optimal. On the other hand, D. Nacamulli showed a sustained decrease in TPO antibodies with 83 µg of selenium per day, and the effect persisted for 1 year. Only one study demonstrated a decrease in the level of anti-TG antibodies, while in most studies the level of these antibodies did not change significantly [26].
O. Turker D. et al. found an “escape” effect, since the decrease in the level of antibodies to TPO continued for 6 months. therapy with selenium, but by the 9th month. the level of antibodies increased again, although it did not reach the initial level [27]. However, in other studies, the effect of treatment was stable and lasted up to 12 months. the use of the drug.
But the effect on the level of antibodies was not confirmed in all studies against the background of taking the same doses of selenium (83–200 µg/day) [28, 29].
There was no effect of selenium on the level of TSH and thyroid hormones. Only in the study of D. Esposito was an increase in St. T 3 and decrease in St. T 4 in the group of patients taking selenium, while in the control group there was a decrease in the level of St. Т 3 after 3 and 6 months. compared to the original. This result may reflect an increase in the activity of deiodinases and an increase in the conversion of T 4 to T 3 . The effect on the level of T 3 appeared after 3 months. drug intake [28].
In the study of L. Yu in the group of patients with hypothyroidism, a weak negative correlation of selenium concentration in the blood with TSH was revealed. In addition, it was demonstrated that the concentration of interleukin-2 decreases against the background of selenium, which indicates a decrease in inflammation [26].
Some studies have assessed the severity of changes in thyroid tissue typical of autoimmune thyroiditis during ultrasound. In two of the three studies, an improvement in echostructure was found, which indirectly indicates a decrease in autoimmune inflammation. Such positive changes were revealed in studies that simultaneously demonstrated a decrease in the level of antibodies to thyroid tissue [22, 23]. D. Esposito noted the absence of changes in the ultrasound picture, while there was no effect on the level of antibodies [28].
Gartner and Nacamulli evaluated the quality of life of patients with autoimmune thyroiditis (AIT) while taking selenium. Both studies showed an improvement in the quality of life, and there was also a decrease in the level of antibodies to TPO [22, 23].
Some researchers have studied the effectiveness of combining selenium with other drugs that affect thyroid function. So, in patients with AIT and euthyroidism, who took a combination of selenium and myoinositol, which also affects thyroid function, there was a significant decrease in the level of both TSH and antithyroid antibodies, while in the comparison group, in which patients took only selenium at a dose of 83 mcg / days, no such changes were detected [29].
Thus, encouraging data have now been obtained on a decrease in the level of antithyroid antibodies in AIT with the help of selenium. However, additional studies are required to formulate recommendations on the regimen of the drug and the duration of treatment.
The effect of selenium on thyroid function was studied in pregnant women with elevated titers of anti-TPO antibodies. It is known that with an increased level of antibodies to TPO before pregnancy in women, the risk of postpartum thyroiditis and the development of hypothyroidism during pregnancy is significantly increased. The results of the use of 200 μg of selenomethionine during pregnancy were a decrease in the titer of antibodies to TPO, an improvement in the structure of the thyroid gland according to ultrasound, a decrease in the incidence of postpartum thyroiditis and permanent hypothyroidism in the postpartum period [30].
Thus, at present, the role of selenium in reducing the level of antithyroid antibodies, especially antibodies to TPO, can be considered proven, but the clinical significance of this phenomenon has not been proven. In addition, only one study determined the concentration of selenium in the blood before and during the administration of selenium preparations, which does not allow determining the initial deficiency of the microelement and replenishing it during the administration of the preparation. Currently, a study is underway on the effectiveness of selenium in patients with AIT with reduced thyroid function. The end point of the study is not only the level of antibodies to thyroid tissue, but also the dose of replacement therapy with levothyroxine sodium, and the quality of life of patients. It is planned to complete the study in 2018 [31].
Selenium and diffuse toxic goiter (DTG)
DTG belongs to the group of autoimmune thyroid diseases. In connection with the positive effect of selenium on the level of antithyroid antibodies, a study of its effect on the course of this disease is being carried out. V. Vrca studied the course of thyrotoxicosis with the addition of selenium to traditional therapy for DTG. A fixed combination of 60 micrograms of selenium was used with other antioxidants: vitamin E, vitamin C and beta-carotene. The study showed that in the group receiving a combined selenium-containing antioxidant drug simultaneously with methimazole, euthyroidism was achieved faster than in the group taking only methimazole [32]. But in a randomized study by M. Leo et al. no benefit was found for the combination of 166 μg selenium and methimazole over methimazole monotherapy [33]. In a similar study by J. Calissendorff, using 200 μg of selenomethionine in the treatment regimen for patients with thyrotoxicosis, a more pronounced decrease in the level of thyroid hormones and an increase in the level of TSH were demonstrated [34]. When comparing these studies, only one difference was revealed that could affect the result – in the study by J. Calissendorff, patients were with laboratory-confirmed selenium deficiency. It is possible that selenium has a positive effect on the treatment of thyrotoxicosis only when it is deficient, and when there is a sufficient level, it is pointless to add it to the treatment. But this hypothesis requires confirmation. In addition, perhaps it is the combination of selenium with other antioxidants (vitamins E and C) that has a positive effect.
In another study, selenium was added to methimazole in the treatment of patients with recurrent DTG. An accelerated achievement of euthyroidism and a pronounced decrease in the level of antibodies to TSH receptors were also shown. At the final visit, a large proportion of patients in the group treated with selenium did not have antibodies to TSH receptors, which improves the prognosis in the near future [35].
Another area of research is the use of selenium in the treatment of endocrine ophthalmopathy (Graves’ disease). It is one of the clinical manifestations of DTG. This disease significantly affects the quality of life of patients, and the treatment regimens used are not always sufficiently effective and safe. S. Marcocci conducted a randomized double-blind study to study the effect of selenium and pentoxifylline on the course of endocrine ophthalmopathy. 152 patients with endocrine ophthalmopathy were divided into groups receiving selenium, pentoxifylline or placebo. The study used the inorganic compound sodium selenite at a dose of 100 mcg 2 times a day. Treatment continued for 6 months. followed by follow-up for 6 months. It was concluded that the use of selenium improved the quality of life of patients, slowed down the progression of endocrine ophthalmopathy after 6 months. treatment. The effect persisted for 6 months. observations. Pentoxifylline has not been proven effective [36]. Although the data are clearly insufficient, the international organization EUGOGO, based on this study, included selenium in its recommendations for the treatment of mild endocrine ophthalmopathy [37]. This is important because for severe forms, a treatment regimen with the use of glucocorticoids has been developed, and for mild forms, which sometimes significantly worsen the patient’s quality of life, no treatment was previously offered, but only observation.
Currently, the GRASS study is ongoing, planned for completion in 2018, which should answer the questions whether the addition of selenium to the therapy of Graves’ disease will accelerate the achievement of euthyroidism, reduce the risk of disease recurrence, and improve the quality of life of patients [38].
Of interest is a pilot study on the treatment of patients with subclinical thyrotoxicosis with a combination of selenium and L-carnitine. Subclinical thyrotoxicosis is much more common than manifest, and, according to various sources, ranges from 0.6 to 16%, depending on the diagnostic criteria, the age of the patients, and the provision of the region with iodine. The causes of subclinical thyrotoxicosis may be different: the onset of Graves’ disease, nodular or multinodular toxic goiter, thyrotoxic phase of thyroiditis, etc. But regardless of the causes, persistent subclinical thyrotoxicosis affects the quality of life of patients, and in elderly patients significantly increases the risk of cardiovascular diseases – mainly atrial fibrillation and thromboembolic complications. To date, no effective and safe treatment regimens have been developed for these patients. At a TSH level of 0.1-0.4 mU/L, observational tactics are recommended, while at a lower TSH level, treatment with small doses of thyreostatics and/or beta-blockers is used. This study was planned as a pilot study, and the number of patients was small (n=18), which allows only preliminary conclusions to be drawn. As a result of the use of 83 micrograms of selenium and 500 mg of L-carnitine for 1 month. managed to significantly increase the level of TSH to almost normal values, reduce the level of antibodies to TPO and TG, reduce the clinical manifestations of thyrotoxicosis, such as trembling, palpitations, weakness. The treatment lasted for 1 month, and after 1 month. observation after discontinuation of therapy, a return of hormonal parameters and clinical manifestations to the initial level was recorded, which demonstrated an insufficient duration of treatment. Side effects were not recorded. Of course, a larger study is required, but this pilot study gives hope for the development of an effective and safe regimen for the treatment of patients with subclinical thyrotoxicosis [39].
Selenium, diffuse and nodular goiter and thyroid cancer
Some researchers have studied the effect of selenium on the formation of goiter – both diffuse and nodular. Most of the studies are few, but it is suggested that there is an inverse relationship between blood and urine selenium levels and thyroid volume and hypoechogenicity. So, L. Rasmussen et al. found that a low concentration of selenium in the blood in combination with iodine deficiency is associated with an increased risk of developing both diffuse goiter and nodules in the thyroid gland [40].
The largest study in this area was conducted by Q. Wu et al. More than 6,000 people took part in the study. The aim of the study was to compare the prevalence of thyroid diseases in regions of China with different levels of selenium availability. It has been found that high selenium levels are associated with a lower incidence of goiter (RR 0.75, 95% CI 0.59–0.97) [21].
Thus, preliminary data have now been obtained on a greater prevalence of diffuse and nodular goiter in regions with low selenium intake. But studies are needed to confirm that selenium supplementation can prevent the development of AIT and multinodular goiter.
Several studies have examined the association of cancer and low levels of selenium in the blood and urine. It has been found that the incidence of cancer increases with selenium deficiency. A meta-analysis was conducted of 8 studies involving more than 1200 patients, which studied the relationship of the level of certain micronutrients (selenium, copper and magnesium) with thyroid cancer (TC). Patients with thyroid cancer have been shown to have reduced levels of selenium and magnesium and increased levels of copper compared to healthy controls [41]. J. Jonklaas, in his study of 65 patients who underwent thyroidectomy for thyroid cancer and nodular goiter, confirmed that selenium deficiency is associated with a high degree of cancer. The exact mechanisms of the effect of selenium deficiency on cancer development are still unknown, but it is assumed that the lack of selenoenzymes leads to an increase in free radicals that contribute to carcinogenesis and disease progression [42].
Selenium, general morbidity and mortality
Some studies have shown that there is a U-shaped relationship between the concentration of selenium in the blood and general morbidity, i.e., both a deficiency and an excess of selenium affect the incidence [43]. In other words, the supplementation of selenium is beneficial in the presence of selenium deficiency, but the use of additional selenium preparations in the absence of deficiency can lead to various side effects, such as hyperglycemia and accelerated progression of atherosclerosis [44, 45].
Mortality from all causes also increases with a deficiency or excess of selenium. A study involving more than 13,000 patients and lasting 12 years showed a weak positive association between selenium levels above 150 ng/mL and overall mortality, as well as mortality from cancer [46].
Practical application of selenium
Despite the fact that data on the effectiveness of selenium is rather contradictory, it is already used in real clinical practice. In Italy, endocrinologists were surveyed about their experience with selenium. 778 doctors took part in the survey. 85.2% of respondents indicated that they use selenium in the treatment of patients, and about 30% prescribe it often, the main nosology for prescribing selenium was AIT. Two-thirds of the respondents prescribed selenium for subclinical hypothyroidism in patients with AIT. One fifth of the respondents used this microelement in the treatment regimen for mild endocrine ophthalmopathy. Most physicians used doses of 100 to 200 μg of selenium per day [47].
An example of a selenium-containing agent is the dietary supplement Oksilik containing 50 µg of selenium. Oxylik also contains vitamins C and E, lycopene and β-carotene. It is the combination of selenium with other vitamins with antioxidant activity that has demonstrated its effectiveness in the treatment of autoimmune thyroid diseases [32]. This is probably due to the synergy of their action.
Oxilik has a high synergistic combination of antioxidants in doses corresponding to the physiological need for them. The components are surrounded by a complex of phospholipids, which is a high-tech pharmaceutical method for the manufacture of such products and significantly increases absorption in the gastrointestinal tract.
Statement
At present, areas of endocrinology have been identified in which the use of selenium can be beneficial. These are autoimmune thyroid diseases (autoimmune thyroiditis, Graves’ disease), thyroid nodules and thyroid cancer. In addition, an adverse effect of selenium deficiency on overall mortality has been shown. However, taking into account the side effects of selenium in its overdose, it is necessary to develop effective and safe treatment regimens that require additional research in this area.
Why Selenium is a Recommended Supplement to Take
Why Selenium is a Recommended Supplement Especially for Thyroid Diseases
Selenium is a micronutrient found in food and soil that is vital for immune response and thyroid function, including the conversion of T4 to T3 thyroid hormone, making it essential for good health. metabolic function. It is often recommended that those of us who suffer from hypothyroidism and Hashimoto’s consider selenium supplementation.
Symptoms of low selenium levels may include: fatigue, low immunity, poor concentration (brain fog), reproductive problems, heart problems. However, selenium does not occur naturally in the body, so we must take it through our diet and sometimes even supplements.
Selenium is converted into one of three types of selenoproteins, which are:
- Gluthione Peroxidases – antioxidants.
- Thioredoxin reductase – active in cell structure and growth.
- Iodothyronine deiodinases are responsible for the conversion of T4 to T3. (The reason many thyroid patients still feel ill on their thyroid medications.)
During a selenium deficiency, you may have symptoms of brain fog and cognitive decline, as well as lack of energy and blood results that look “normal” even if you still feel unwell. You may also have low Free T3 levels.
Many people with hypothyroidism have trouble converting their T4 medication to the active T3 thyroid hormone, so a lack of iodothyronine deiodinase protein (which requires selenium) may be the cause. A sign is that if you are taking T4-only drugs such as levothyroxine or synthroid and are not feeling better, especially if your thyroid blood test results look “normal” or you have low free T3 levels, then you may have low or deficiency of iodothyronine deiodinases and hence selenium.
Research has also shown that selenium can lower thyroid antibodies, helping to manage Hashimoto’s more effectively. A study published in 2002 discussed the effects of selenium on thyroid antibodies. The researchers reported that they gave 200 micrograms of selenium daily to Hashimoto’s patients with high TpoAB levels. Three months later, their levels were redrawn and a 66.4% decrease in TpoAB was found. [1]
This certainly was the case for me as my Hashimoto is now in remission and I still take a selenium supplement religiously, every day.
The NHS recommends a conservative 0.06mg per day for women and 0.075mg per day for men, while Dr Ex recommends no more than 0.055mg per day, which is more or less in line with NHS guidelines.
However, the recommended dose by many thyroid sources is 200 micrograms per day, such as STTM and thyroid pharmacist Isabella Wentz, who also promote 200 micrograms per day. The study mentioned above also used this amount.
Because we don’t yet know the potential risks of long-term selenium supplementation, the safest option may be to satisfy your needs by eating selenium-rich foods such as brazil nuts, cod, tuna, mushrooms, and meats. Brazil nuts are generally considered the most popular option, and only two to three per day provide approximately 200 micrograms of selenium, but they must be of very good quality to contain the selenium you need. It can be hard to tell if they contain enough, which is why so many people choose to just take supplements.
If you are looking to supplement, organic forms of selenium such as selenium yeast or selenomethionine are said to be safer and easier to absorb, and as with most supplements, selenium can have toxic effects when used in excess, so be aware.