Selenium supplementation. There seem to be two different approaches. One approach regards selenium supplementation as a direct pharmaceutical treatment. For example, it is considered a form of medication administered to thyroid disorder patients. Alone or together with thyroid disorder medication, the selenium supplementation is intended to 1) alleviate symptoms, 2) slow the progression of the disorder, and 3) perhaps provide a cure [Schomburg 2019].
A second approach to selenium supplementation does not regard the administration of selenium as a pharmaceutical intervention. Rather, the second approach considers selenium supplementation to be a nutritional intervention designed to address and correct a deficiency condition. This approach recognizes that both sub-optimal selenium status and selenium deficiency limit the body’s expression of vital selenoproteins. These selenoproteins are needed to minimize health risks and to alleviate disease symptoms. Supplemental selenium can be necessary to enable the full endogenous expression of selenoproteins [Schomburg 2019].
In the context of selenium status as it relates to thyroid disease, Schomburg notes that the situation is complicated. Long-term low selenium intake is associated with increased thyroid disease risk, both hypothyroidism and hyperthyroidism, especially in males.
Priority Supply of Selenium to the Thyroid Gland
Schomburg points out that the brain and endocrine glands, including the thyroid gland, are supplied with selenium in a prioritized manner. Consequently, he says, it is not likely that selenium status and selenoprotein expression in thyroid gland cells will be much affected by relatively small differences in dietary selenium intake.
Even so, clinical studies do show that some patients with Hashimoto’s thyroiditis, Graves’ disease, or Graves’ orbitopathy respond positively to selenium supplementation. How can this positive response be explained?
Effect of Selenium Supplementation on the Immune System
Schomburg suggests that the most likely explanation for the clinical improvement in individuals with thyroid disorders has to do with the effect of the selenium supplementation on the immune system. The immune system does not get the same high-level supply of selenium in periods of low dietary selenium intakes as the thyroid gland does. Consequently, in a condition of selenium deficiency, the immune system cannot express fully the selenoproteins that it needs to make a gradual and adequate immune response to a challenge [Schomburg 2019].
In conditions of inadequate selenium intake, the relationship between thyroid gland cells and lymphocytes (= white blood cells that participate in immune system response) is disturbed and suboptimal. This is especially the case whenever there is a challenge to the immune system, e.g., challenges from viral infections such as HIV and SARS infections, iodine deficiency, pregnancy, severe illness, shock, trauma, etc. [Schomburg 2019].
There is evidence for a causal link between selenium deficiency and the development and progression of hypothyroidism (mainly Hashimoto’s thyroiditis) and autoimmune-related thyroid gland damage. There is also evidence, in males only, for a connection between selenium deficiency and hyperthyroidism, mainly Graves’ disease [Schomburg 2021].
Identifying Selenium Deficiency
Schomburg notes that diagnosing moderate selenium deficiency is difficult. Selenium deficiency as a medical condition is essentially symptom-free. Low selenium status is associated with long-term health risks that extend beyond autoimmune thyroid disease [Schomburg 2019].
Based on analyses of data from the European Prospective Investigation into
Cancer and Nutrition (EPIC), Schomburg and colleagues have identified the following significantly increased health risks associated with low selenium intake and status:
- risk of cancer (colorectal and hepatocellular)
- risk of death in the intensive care unit
- risk of pregnancy complications
- risk of cardiovascular morbidity and mortality
- risk of all-cause and cardiovascular mortality in seniors
- higher postoperative mortality
- risk of age-related diseases
Sufficient selenium intake is needed for the expression of selenoproteins that have the following relevant biological properties necessary for good thyroid gland health:
- antioxidant protection of thyroid gland cells
- anti-inflammatory protection of the thyroid gland
- effect on immune system response (T cell and natural killer cell activation)
Misunderstanding of the Selenium and Type 2 Diabetes Data
Just as the relationship between selenium status and thyroid disorders is complex, so too is the relationship between selenium status and type 2 diabetes.
Schomburg makes the following points[Schomburg 2019]:
- Selenium deficiency seems to be a risk factor for metabolic disorders. Well-controlled studies show that low selenium intake may be associated with high BMI, high body fat percentage, and greater waist circumference. The relevant data show a dose-dependent relationship.
- The often repeated assumption that selenium supplementation might cause type 2 diabetes may be upside down. Schomburg presents the following explanation for the appearance of a relationship between selenium status and increased risk of type 2 diabetes:
- Diabetes may well cause increased selenoprotein P (SELENOP) biosynthesis in the liver and thus increase circulating SELENOP and selenium levels. Note: SELENOP is the primary transporter of selenium in the blood circulation to the tissues and organs.
- In non-diabetic individuals, the normal supply of insulin decreases the extent of the liver biosynthesis and secretion of SELENOP. Thus, the absence of diabetes is associated with lower selenium status.
- In individuals with insulin resistance, however, there is less inhibition of SELENOP biosynthesis, resulting in higher circulating SELENOP levels and thus higher circulating selenium levels. The direction of causation is from higher insulin resistance towards higher selenium status, not from higher selenium status to higher insulin resistance. The insulin resistance induces higher SELENOP and higher selenium levels, not the other way around.
- In the later stages of type 2 diabetes development, insulin levels decrease because of the decline in beta-cell function. However, the high blood glucose concentrations continue to promote SELENOP biosynthesis and secretion. In this way, the supposed relationship between type 2 diabetes and higher selenium status remain susceptible to misinterpretation.
Conclusion: Selenium’s Role in Thyroid Disorder and Type 2 Diabetes
Selenium deficiency limits the extent of selenoprotein expression and increases the risk of autoimmune disorders. Adequate selenium intake is necessary to counteract ill health risks and to alleviate disease symptoms.
Inadequate intakes of selenium adversely affect thyroid gland health through the resulting diminished immune response. We need more clinical research to investigate the effect of selenium supplementation on the immune system, on oxidative stress, and on low-grade inflammation in patients with thyroid diseases [Larsen 2024].
Selenium supplementation in selenium-poor regions enables full selenoprotein expression. To optimize the expression of SELENOP, serum selenium must be in the range of 120-130 mcg/L. Attaining that selenium status requires a selenium intake of at least 100 mcg per day [Larsen 2024].
The best explanation for a relationship between higher selenium status and greater risk of type 2 diabetes indicates that supplemental selenium does not cause type 2 diabetes. Rather, insulin resistance and type 2 diabetes cause greater SELENOP biosynthesis and secretion, resulting in higher circulating levels of selenium.
Schomburg [2021] finds it unfortunate that clinicians too often neglect the health risks of selenium deficiency. At the same time, they too often exaggerate the possibility of adverse side effects of selenium supplementation. This tendency is especially unfortunate in cases of viral infections (including COVID-19), pregnancy, and severe illness. In these situations, selenium deficiencies will increase the risk of developing autoimmune disorder, will cause long-lasting health impairments, and will slow recovery [Schomburg 2021].
Sources
Alehagen U, Alexander J, Aaseth JO, Larsson A, Opstad TB. Supplementation with selenium and coenzyme Q10 in an elderly Swedish population low in selenium – positive effects on thyroid hormones, cardiovascular mortality, and quality of life. BMC Med. 2024 May 7;22(1):191.
Larsen C, Winther KH, Cramon PK, Rasmussen ÅK, Feldt-Rasmusssen U, Knudsen NJ, Bjorner JB, Schomburg L, Demircan K, Chillon TS, Gram J, Hansen SG, Brandt F, Nygaard B, Watt T, Hegedus L, Bonnema SJ. Selenium supplementation and placebo are equally effective in improving quality of life in patients with hypothyroidism. Eur Thyroid J. 2024 Jan 1;13(1):e230175.
Schomburg L. The other view: the trace element selenium as a micronutrient in thyroid disease, diabetes, and beyond. Hormones (Athens). 2020 Mar;19(1):15-24.
Schomburg L. Selenium deficiency due to diet, pregnancy, severe illness, or COVID-19: a preventable trigger for autoimmune disease. Int J Mol Sci. 2021 Aug 8;22(16):8532.
The information presented in this review article is not intended as medical advice. It should not be used as such.
30 August 2024