One of the most common causes of hypothyroidism – a slow thyroid -- is Hashimoto’s thyroiditis. This thyroid-damaging autoimmune disease typically affects women more than men, generally between the ages of 40 and 60.
While there are drug treatments for Hashimoto’s, nutrients can also help restore healthy levels of thyroid hormones. One of the most critical nutrients is selenium.
Selenium is found naturally in foods, including tuna, liver, oysters, pork, clams, and Brazil nuts. But that doesn’t guarantee a consistent amount of the mineral, at least not in a meaningful way that can counteract a slow thyroid.
Instead, researchers have been studying the effects of selenium supplementation for individuals with Hashimoto’s, and have seen some positive results.
In four months, about half of the patients enrolled in the study saw a return to normal thyroid activity – and that was simply using selenium supplementation with no other treatment. Even six months after the study, when no selenium supplements were taken, over 80 percent of the positive responders still had restored, healthy thyroid activity.
There are many forms of supplemental selenium available – some are based on yeast, and have yielded excellent results for a variety of health conditions, including tumor reduction. Others are chelated (bound) to the amino acid glycine for better absorption in the intestines. These forms may be the best for relatively fast and ultimately sustainable, results.
Pirola I, Rotondi M, Cristiano A, et al. Selenium supplementation in patients with subclinical hypothyroidism affected by autoimmune thyroiditis: Results of the SETI study. Endocrinol Diabetes Nutr. 2020;67(1):28‐35.
Objective: The purpose of this prospective study was to assess the effects of selenium supplementation on TSH and interferon-γ inducible chemokines (CXCL9, CXCL10 and CXCL11) levels in patients with subclinical hypothyroidism due to Hashimoto's thyroiditis.
Patients and methods: Patients with subclinical hypothyroidism due to Hashimoto thyroiditis were prospectively enrolled in the SETI study. They received 83mcg of selenomethionine/day orally in a soft gel capsule for 4 months with water after a meal. No further treatment was given. All patients were measured thyroid hormone, TPOAb, CXCL9, CXCL10, CXCL11, iodine, and selenium levels at baseline and at study end.
Results: 50 patients (43/7 female/male, median age 43.9±11.8 years) were enrolled, of which five withdrew from the study. At the end of the study, euthyroidism was restored in 22/45 (48.9%) participants (responders), while 23 patients remained hypothyroid (non-responders). There were no significant changes in TPOAb, CXCL9, CXCL10, CXCL11, and iodine levels from baseline to the end of the study in both responders and non-responders. TSH levels were re-tested six months after selenomethionine withdrawal: 83.3% of responding patients remained euthyroid, while only 14.2% of non-responders became euthyroid.
Conclusions: The SETI study shows that short-course supplementation with selenomethionine is associated to a normalization of serum TSH levels which is maintained 6 months after selenium withdrawal in 50% of patients with subclinical hypothyroidism due to chronic autoimmune thyroiditis. This TSH-lowering effect of selenium supplementation is unlikely to be related to changes in humoral markers of autoimmunity and/or circulating CXCL9.
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