Randomized controlled trial of the effect of selenium supplementation on thyroid function in the elderly in the United Kingdom

Nutritional Sciences Division, Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom.
American Journal of Clinical Nutrition (Impact Factor: 6.77). 02/2008; 87(2):370-8.
Source: PubMed


Thyroid function depends on the essential trace mineral selenium, which is at the active center of the iodothyronine deiodinase enzymes that catalyze the conversion of the prohormone thyroxine (T(4)) to the active form of thyroid hormone, triiodothyronine (T(3)).
Because selenium intake in the United Kingdom has fallen during the past 25 y, we wanted to determine whether current selenium status might be limiting conversion of T(4) to T(3) in the elderly, in whom marginal hypothyroidism is relatively common.
We investigated the effect of selenium supplementation in a double-blind, placebo-controlled trial in 501 elderly UK volunteers. Similar numbers of men and women from each of 3 age groups, 60-64 y, 65-69 y, and 70-74 y, were randomly allocated to receive 100, 200, or 300 microg Se/d as high-selenium yeast or placebo yeast for 6 mo. As part of the study, plasma selenium, thyroid-stimulating hormone, and total and free T(3) and T(4) were measured. Data from 368 euthyroid volunteers who provided blood samples at baseline and 6 mo were analyzed.
Although selenium status at baseline correlated weakly with free T(4) (r = -0.19, P < 0.001) and with the ratio of free T(3) to free T(4) (r = 0.12, P = 0.02), we found no evidence of any effect of selenium supplementation on thyroid function, despite significant increases in plasma selenium. However, baseline plasma selenium in our study (x: 91 microg/L) was somewhat higher than in previous supplementation studies in which apparently beneficial effects were seen.
We found no indication for increasing selenium intake to benefit T(4) to T(3) conversion in the elderly UK population.

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    • "The most important of these are the iodothyronine deiodinases (DIO1, DIO2) that catalyze the formation of T3 from T4, and the glutathione peroxidases (GPx1, GPx3, GPx4) that catalyze the removal of peroxides and protect the thyrocytes from oxidative stress [25]. Two randomized clinical trials have shown no effect of selenium supplementation on serum TSH and thyroid hormone concentrations in healthy adults, even in those with moderately deficient selenium status [26,27]. Meanwhile, in the majority of 13 randomized clinical trials, selenium, in various formulations, effectively decreased serum TPO-Ab concentrations in AIT patients [28-40]. "
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    ABSTRACT: Patients with chronic autoimmune thyroiditis have impaired health-related quality of life. The thyroid gland has a high selenium concentration, and specific selenoprotein enzyme families are crucial to immune function, and catalyze thyroid hormone metabolism and redox processes in thyroid cells. Previous randomized controlled trials have found that selenium supplementation decreases thyroid-disease-specific antibody levels. We hypothesize that selenium might be beneficial in the treatment of chronic autoimmune thyroiditis.Methods/design: The CATALYST trial is an investigator-initiated randomized, blinded, multicentre clinical trial of selenium supplementation versus placebo in patients with chronic autoimmune thyroiditis. Inclusion criteria: age >=18 years; serum thyroid peroxidase antibody level >=100 IU/ml within the previous 12 months; treatment with levothyroxine and written informed consent. Exclusion criteria: previous diagnosis of toxic nodular goitre, Graves' hyperthyroidism, postpartum thyroiditis, Graves' orbitopathy; previous antithyroid drug treatment, radioiodine therapy or thyroid surgery; immune-modulatory or other medication affecting thyroid function; pregnancy, planned pregnancy or breastfeeding; allergy towards any intervention or placebo component; intake of selenium supplementation >55 mug/day; inability to read or understand Danish or lack of informed consent. The trial will include 2 x 236 participants. The experimental intervention and control groups will receive 200 mug selenium-enriched yeast or matching placebo tablets daily for 12 months. The experimental supplement will be SelenoPrecise(R). The primary outcome is thyroid-related quality of life assessed by the Thyroid Patient-Reported Outcome (ThyPRO) questionnaire. Secondary outcomes include serum thyroid peroxidase antibody concentration; serum triiodothyronine/thyroxine ratio; levothyroxine dosage; adverse reactions and serious adverse effects and events. In this pragmatic trial, participating patients follow their usual treatment at their usual hospitals. In order to collect high-quality data on the clinical course and quality of life, and to minimize missing data, an elaborate trial management system has been designed. 12 months intervention duration was selected in consideration of the primary outcome, thyroid-related quality of life.Trial registration: ClinicalTrials.gov ID: NCT02013479.
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    • "This notion is well manifested by the interaction of the family of Se-dependent Dios with TH homeostasis and metabolism studied in several animal model systems [39], [40], [41], [42]. It has been corroborated in human cross-sectional analyzes and prospective intervention studies that have addressed the effects of Se status and Se supplementation on circulating TH levels [43], [44], [45]. However, the results are not fully consistent and even in Se supplementation studies of critically ill patients with low circulating Se levels and grossly disturbed TH metabolism, a similar lack of clear effects was reported [17]. "
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    ABSTRACT: Impaired expression of selenium-containing proteins leads to perturbed thyroid hormone (TH) levels, indicating the central importance of selenium for TH homeostasis. Moreover, critically ill patients with declining serum selenium develop a syndrome of low circulating TH and a central downregulation of the hypothalamus-pituitary-thyroid axis. This prompted us to test the reciprocal effect, i.e., if TH status would also regulate selenoprotein expression and selenium levels. To investigate the TH dependency of selenium metabolism, we analyzed mice expressing a mutant TH receptor α1 (TRα1+m) that confers a receptor-mediated hypothyroidism. Serum selenium was reduced in these animals, which was a direct consequence of the mutant TRα1 and not related to their metabolic alterations. Accordingly, hyperthyroidism, genetically caused by the inactivation of TRβ or by oral TH treatment of adult mice, increased serum selenium levels in TRα1+m and controls, thus demonstrating a novel and specific role for TRα1 in selenium metabolism. Furthermore, TH affected the mRNA levels for several enzymes involved in selenoprotein biosynthesis as well as serum selenoprotein P concentrations and the expression of other antioxidative selenoproteins. Taken together, our results show that TH positively affects the serum selenium status and regulates the expression of several selenoproteins. This demonstrates that selenium and TH metabolism are interconnected through a feed-forward regulation, which can in part explain the rapid parallel downregulation of both systems in critical illness.
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    • "[51] "
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