Related Experiment Video
Updated: Jul 18, 2026

04:39
Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
Selenium and goiter prevalence in borderline iodine sufficiency
Volker F H Brauer1, Ulrich Schweizer, Josef Köhrle
1Third Department of Medicine, University of Leipzig, Ph-Rosenthal-Street, 27, 04103 Leipzig, Germany.
European Journal of Endocrinology
|November 30, 2006
Summary
Selenium (Se) does not significantly impact thyroid volume in areas with borderline iodine sufficiency. Higher urinary Se in goiter patients was likely coincidental, with iodine status being the primary determinant.
Area of Science:
- Endocrinology
- Nutritional Science
- Thyroid Research
Background:
- Selenium (Se) is crucial for selenocysteine protein synthesis, including thyroid selenoenzymes like deiodinases that regulate thyroid hormones.
- Investigating Se's role in goiter is complex due to population variations in Se intake and bioavailability, and confounding iodine deficiency in prior studies.
Purpose of the Study:
- To assess the influence of selenium on thyroid volume in an iodine-sufficient population.
- To determine if selenium status is an independent risk factor for goiter development.
Main Methods:
- Evaluated urinary iodine (UI) and creatinine, and prevalence of goiter/nodules via ultrasonography in randomly selected individuals.
- Compared urinary Se excretion (USe) in goiter patients versus controls, adjusting for age, gender, thyroid history, smoking, and UI.
Main Results:
- The study population exhibited borderline selenium and iodine sufficiency (mean USe: 24 µg/L; mean UI: 96 µg/L).
- Individuals with goiter (n=89) had significantly higher USe levels than those with normal thyroid volume (n=83; P < 0.05).
- Urinary Se excretion was not affected by smoking or pregnancy.
Conclusions:
- Urinary Se was not found to be an independent risk factor for goiter development.
- The observed higher USe in goiter patients is likely coincidental.
- Iodine status appears to be the more critical determinant of thyroid volume in this population, rather than selenium.
Related Concept Videos
Goiter
Goiter refers to an abnormal enlargement of the thyroid gland that may appear as a diffuse goiter (uniform enlargement) or nodular (single or multiple nodules). Functionally, it is classified as nontoxic (normal/low hormone levels) or toxic (excess hormone production).PathophysiologyDiffuse thyroid enlargement typically results from prolonged stimulation by thyroid-stimulating hormone (TSH) or TSH-like agents, commonly seen in hypothyroidism or iodine deficiency. In contrast, in hyperthyroid...
Graves' Disease I: Introduction
Graves' disease is an autoimmune disorder that causes hyperthyroidism, or overactivity of the thyroid gland. It results from autoantibodies called thyroid-stimulating immunoglobulins (TSIs), which bind to thyroid-stimulating hormone (TSH) receptors, leading to overstimulation of hormone production and a hypermetabolic state.EtiologyAlthough considered idiopathic, Graves’ disease has well-established contributing factors. There is a strong genetic component, with increased prevalence in...
Hyperthyroidism I: Introduction
Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hyperthyroidism II: Pathophysiology
Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
Synthesis and Regulation of Thyroid Hormones
Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Upon reaching the thyroid gland, TSH stimulates the follicular cells' active uptake of iodide ions from the blood. The ions diffuse to the apical surface of the cells and are oxidized to iodine. The iodine is then...
Graves Disease II: Pathophysiology
Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...

