The trace element selenium and the thyroid gland.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic biology, animal models, and observational associations.
PubMed 10403185 · doi:10.1016/s0300-9084(99)80105-9
What was done
This narrative review synthesized biochemical, animal, and clinical observations regarding the role of selenium in thyroid physiology and disease. The authors examined the expression of selenoproteins in thyrocytes, mechanisms of antioxidant defense against hydrogen peroxide, consequences of dual iodine and selenium deficiency, and correlations between selenium status and thyroid pathologies.
What was found
The abstract reports no numerical data or effect sizes. It notes qualitatively that the human thyroid has the highest selenium content per gram of tissue of any organ. Selenoproteins expressed in thyrocytes include three glutathione peroxidases (cGPx, pGPx, PH-GPx), type I 5-deiodinase, thioredoxin reductase, and selenoprotein P. In animal models, severe selenium deficiency coupled with high iodide causes thyroid necrosis and fibrosis. In humans, combined deficiency is linked to myxedematous endemic cretinism, and low selenium levels correlate with thyroid carcinoma, though tissue selenium does not directly correlate with selenoprotein expression in diseased thyroid tissue.
Why it matters
The paper outlines how selenium is essential alongside iodine for thyroid hormone metabolism and antioxidant protection against reactive oxygen intermediates produced during hormone synthesis.
Limits
As a narrative review, it lacks a systematic literature search, standardized study selection, and quantitative data synthesis. The abstract provides no sample sizes, effect estimates, or statistical significance metrics.
Cited by
- supports Selenium supports the enzymatic conversion of T4 to T3 and lowers thyroid peroxidase (TPO) autoantibody levels in Hashimoto's thyroiditis.