Selenium and Thyroid Disease: From Pathophysiology to Treatment

Ventura, Mara; Melo, Miguel; Carrilho, Francisco

doi:10.1155/2017/1297658

Cited by 256 publications

(203 citation statements)

References 50 publications

(54 reference statements)

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“…Optimal GPX activity within the thyroid is essential to prevent excessive oxidative stress within the thyroid, a process required to ameliorate the autoimmune responses implicated in thyroid dysfunction (McGregor, 2015). When GPX activity is insufficient within the thyroid gland, thyroid autoimmunity can result with the formation of thyroid-stimulating hormone receptor antibodies contributing to hyperthyroidism, or formation of thyroid peroxidase or thyroglobulin antibodies contributing to hypothyroidism (Ventura et al 2017). Future animal studies are required to tease apart these mechanisms to determine if selenium supplementation may reduce the frequency of thyroid disorders in pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth

Hofstee

Bartho

McKeating

et al. 2019

The Journal of Physiology

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Key points Inappropriate intake of key micronutrients in pregnancy is known to alter maternal endocrine status, impair placental development and induce fetal growth restriction. Selenium is an essential micronutrient required for the function of approximately 25 important proteins. However, the specific effects of selenium deficiency during pregnancy on maternal, placental and fetal outcomes are poorly understood. The present study demonstrates that maternal selenium deficiency increases maternal triiodothyronine and tetraiodothyronine concentrations, reduces fetal blood glucose concentrations, and induces fetal growth restriction. Placental expression of key selenium‐dependent thyroid hormone converting enzymes were reduced, whereas the expression of key placental nutrient transporters was dysregulated. Selenium deficiency had minimal impact on selenium‐dependent anti‐oxidants but increased placental copper concentrations and expression of superoxide dismutase 1. These results highlight the idea that selenium deficiency during pregnancy may contribute to thyroid dysfunction, causing reduced fetal growth, that may precede programmed disease outcomes in offspring. Abstract Selenium is a trace element fundamental to diverse homeostatic processes, including anti‐oxidant regulation and thyroid hormone metabolism. Selenium deficiency in pregnancy is common and increases the risk of pregnancy complications including fetal growth restriction. Although altered placental formation may contribute to these poor outcomes, the mechanism by which selenium deficiency contributes to complications in pregnancy is poorly understood. Female C57BL/6 mice were randomly allocated to control (>190 µg kg–1, n = 8) or low selenium (<50 µg kg–1, n = 8) diets 4 weeks prior to mating and throughout gestation. Pregnant mice were killed at embryonic day 18.5 followed by collection of maternal and fetal tissue. Maternal and fetal plasma thyroid hormone concentrations were analysed, as was placental expression of key selenoproteins involved in thyroid metabolism and anti‐oxidant defences. Selenium deficiency increased plasma tetraiodothyronine and triiodothyronine concentrations. This was associated with a reduction in placental expression of key selenodependent deiodinases, DIO2 and DIO3. Placental expression of selenium‐dependent anti‐oxidants was unaffected by selenium deficiency. Selenium deficiency reduced fetal glucose concentrations, leading to reduced fetal weight. Placental glycogen content was increased within the placenta, as was Slc2a3 mRNA expression. This is the first study to demonstrate that selenium deficiency may reduce fetal weight through increased maternal thyroid hormone concentrations, impaired placental thyroid hormone metabolism and dysregulated placental nutrient transporter expression. The study suggests that the magnitude of selenium deficiency commonly reported in pregnant women may be sufficient to impair thyroid metabolism but not placental anti‐oxidant concentrations.

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Section: Discussionmentioning

confidence: 99%

Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth

Hofstee

Bartho

McKeating

et al. 2019

The Journal of Physiology

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“…It is also possible that other nutrient deficiencies beyond iodine (e.g. selenium, iron [36,37]) interact with thyroid metabolism. Finally, thyroid size, reflected by DBS-Tg, may be larger in the Swedish population, as shown for school-aged children when compared with an age-matched reference international population [16].…”

Section: Discussionmentioning

confidence: 99%

Iodine deficiency in pregnant women in Sweden: a national cross-sectional study

et al. 2019

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Purpose Voluntary salt iodization at 50 mg/kg salt ensures adequate iodine nutrition in Swedish school-aged children, but iodine status in pregnant women is uncertain. Methods We conducted a cross-sectional national study of 743 pregnant women, at median gestational age of 23 weeks (IQR 9, 38), recruited from maternal health care centers. We measured: urinary iodine concentration (UIC) and urinary creatinine concentration in spot urine samples; thyroglobulin (Tg), thyroid-stimulating hormone (TSH), and total thyroxine (tT4) on dried blood spots (DBS); and thyreoperoxidase antibodies in serum samples. Data on dietary supplement use were obtained, and women were classified as supplement users (consuming multivitamins containing ≥ 150 µg iodine/day) and non-supplement users (no supplements or < 150 µg iodine/day from supplements). Results Overall median UIC [bootstrapped 95% confidence interval (CI)] was 101 µg/L (95, 108; n = 737): 149 µg/L (132, 164) in supplement users (n = 253) and 85 µg/L (79, 92) in non-supplement users (n = 440) (p < 0.001). Overall geometric mean DBS-Tg (95% CI) was 22.1 μg/L (20.8, 23.5; n = 675) and the prevalence of elevated DBS-Tg was 19%. DBS-Tg was lower in supplement users (n = 229) than in non-supplement users (n = 405) (19.1 vs 24.4 μg/L, p < 0.001). DBS-TSH, DBS-tT4, and S-TPOab positivity did not differ between the two groups. Conclusions Pregnant women in Sweden have inadequate iodine nutrition. Women not taking iodine supplements containing ≥ 150 µg iodine/day are affected by mild iodine deficiency and are at higher risk for increased thyroid activity, while maintaining euthyroidism. Iodine intake should be improved in women both before and after conception by promotion of iodized salt instead of non-iodized salt. We urge regular monitoring of iodine status in the general Swedish population, as well as in risk groups.

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“…This clinical approach appears sound. Whereas the recommended daily intake for adults is 70 μg/day for men and 60 μg/day for women [34], a daily amount exceeding 400 µg should be avoided due to its potential toxic effects (a condition defined as “selenosis”), characterized by diarrhea, fatigue, hair loss, and nail discoloration [35-37]. Further, in a recent randomized controlled trial, the safety of this upper limit has been questioned.…”

Section: Discussionmentioning

confidence: 99%

A 2018 European Thyroid Association Survey on the Use of Selenium Supplementation in Graves’ Hyperthyroidism and Graves’ Orbitopathy

Negro¹,

Attanasio²,

Papini³

et al. 2018

Eur Thyroid J

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Objective: Selenium (Se) supplementation has been suggested in the treatment of Graves’ disease (GD). We sought to investigate Se prescription patterns for GD across European countries. Methods: Members of the European Thyroid Association were invited to participate in an online survey investigating the use of Se in GD either without or with orbitopathy (GO). Of 872 invited members, 244 (28%) completed the survey. After exclusion of basic scientists and non-European members, 197 responses were retrieved out of clinical trials (nearly half of clinician members), of whom 61 do not use Se. Thus, 136 respondents remained for further analyses. Results: Among the 136 analyzed respondents, most (64.7%) were not aware of the Se status in their populations, did not assess Se levels (78.7%), nor considered iodine status (74.3%). In GD without GO, 38.2% recommend Se supplementation (“sometimes” [27.2%], “frequently” [5.9%] or “always” [5.1%]). When GO occurs, 94.1% recommend Se supplementation (“sometimes” [39%], “frequently” [30.1%] or “always” [25%]). Of these, 60.1% recommend Se as an alternative to watchful waiting in patients with mild ocular involvement and 44.9% as an adjuvant to the established treatment modalities in patients with moderate to severe ocular involvement. Conclusions: In Graves’ hyperthyroidism without GO, 38.2% of ETA (European Thyroid Association) members recommend Se supplementation. Conversely, Se is recommended by the majority of respondents in GO, both in patients with mild and moderate to severe ocular involvement. This clinical practice is partially in disagreement with current European treatment guidelines that recommend Se as a 6-month treatment in mild GO only.

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Selenium and Thyroid Disease: From Pathophysiology to Treatment

Cited by 256 publications

References 50 publications

Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth

Maternal selenium deficiency during pregnancy in mice increases thyroid hormone concentrations, alters placental function and reduces fetal growth

Iodine deficiency in pregnant women in Sweden: a national cross-sectional study

A 2018 European Thyroid Association Survey on the Use of Selenium Supplementation in Graves’ Hyperthyroidism and Graves’ Orbitopathy

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