Clinical Thyroidology® for the Public

Summaries for the Public from recent articles in Clinical Thyroidology
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HYPOTHYROIDISM
Does selenium supplementation prevent hypothyroidism in Hashimoto’s Thyroiditis?

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BACKGROUND
Hashimoto’s thyroiditis is a chronic autoimmune inflammatory process which means that the body makes antibodies that attack and destroy the thyroid. This inflammatory process will lead to hypothyroidism over time. Indeed, Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the United States. Women are 10-fold more at risk of having Hashimoto’s thyroiditis than men.

Selenium is a mineral found naturally in various foods that is important for making thyroid hormones and for normal thyroid function. It is needed in small amounts by the body. Selenium also carries antioxidant benefits which helps to fight inflammation. Hashimoto’s thyroiditis has been associated with low selenium. Some studies have suggested that selenium supplementation may help stop the progression of Hashimoto’s thyroiditis and slow the onset of hypothyroidism. This study is a systematic review and analysis of prior studies that have been done to evaluate the effect of selenium supplementation on markers of thyroid function in patients with Hashimoto’s thyroiditis.

THE FULL ARTICLE TITLE
Huwiler VV et al. Selenium supplementation in patients with Hashimoto thyroiditis: a systematic review and metaanalysis of randomized clinical trials. Thyroid. Epub 2024 Feb 16. doi: 10.1089/thy.2023.0556. PMID: 38243784.

SUMMARY OF THE STUDY
The authors conducted a systematic review and analysis of trials that have evaluated the effect of selenium supplementation on markers of thyroid function, such as thyrotropin (TSH), free thyroxine (FT4), total triiodothyronine (TT3), and free triiodothyronine (FT3) and antithyroid antibody levels, either thyroid peroxidase autoantibodies (anti-TPOAb) or thyroglobulin autoantibodies (TgAbs).

A total of 687 articles were reviewed and 35 were identified and analyzed. From those, 18 studies checked blood selenium levels at baseline. Participants were severely selenium-deficient in 9 of these studies (50%), mildly deficient in 7 studies (39%), and only seleniumsufficient in 2 studies (11%). Of all the 35 studies, 30 studies (86%) diagnosed Hashimoto’s thyroiditis using the presence of anti-TPOAb. The studies ranged from 2 to 12 months.

This study showed that selenium supplementation was associated with slightly lower serum TSH than in controls in participants not using thyroid hormone. The one study that showed the strongest effect of selenium supplementation used 200 μg/day of selenium for 6 months. The study showed that after supplementation with selenium, serum TSH was 2.4 mIU/L vs 3.24 mIU/L prior to selenium supplementation. There was no significant change in FT3 levels after selenium supplementation as compared to controls. Similarly, there were no significant changes in FT4, anti-TgAb, or thyroid volume on ultrasonography, and adverse events with the use of selenium supplementation. The study also noted lower anti-TPOAb in patients with and without thyroid hormone therapy.

WHAT ARE THE IMPLICATIONS OF THIS STUDY?
The authors conclude that selenium supplementation in patients with Hashimoto’s thyroiditis was associated with slightly reduced serum TSH levels and anti-TPOAb levels. This study raises important questions about the autoimmune process that causes Hashimoto’s thyroiditis and whether selenium supplementation can delay progression or even prevent hypothyroidism in the future. Since data is still limited, further studies are needed to clearly examine the effect of selenium supplementation on slowing the onset of hypothyroidism.

— Joanna Miragaya, MD

ABBREVIATIONS & DEFINITIONS

Autoimmune thyroid disease: a group of disorders that are caused by antibodies that get confused and attack the thyroid. These antibodies can either turn on the thyroid (Graves’ disease, hyperthyroidism) or turn it off (Hashimoto’s thyroiditis, hypothyroidism).

Selenium: a mineral found naturally in various foods that is important for making thyroid hormones and for normal thyroid function. It is needed in small amounts by the body.

Hypothyroidism: a condition where the thyroid gland is underactive and doesn’t produce enough thyroid hormone. Treatment requires taking thyroid hormone pills.

Hashimoto’s thyroiditis: the most common cause of hypothyroidism in the United States. It is caused by antibodies that attack the thyroid and destroy the gland.

Thyroid hormone therapy: patients with hypothyroidism are most often treated with Levothyroxine in order to return their thyroid hormone levels to normal. Replacement therapy means the goal is a TSH in the normal range and is the usual therapy.

Thyroxine (T4): the major hormone produced by the thyroid gland. T4 gets converted to the active hormone T3 in various tissues in the body.

Triiodothyronine (T3): the active thyroid hormone, usually produced from thyroxine.

TSH: thyroid stimulating hormone — produced by the pituitary gland that regulates thyroid function; also the best screening test to determine if the thyroid is functioning normally.

TPO antibodies: these are antibodies that attack the thyroid instead of bacteria and viruses, they are a marker for autoimmune thyroid disease, which is the main underlying cause for hypothyroidism and hyperthyroidism in the United States.

Thyroglobulin antibodies: these are antibodies that attack the thyroid instead of bacteria and viruses, they are a marker for autoimmune thyroid disease, which is the main underlying cause for hypothyroidism and hyperthyroidism in the United States.