Study: L-thyroxine in combination with an increase in regulatory T cells leads to a significant reduction in symptoms in Hashimoto’s disease

Author: Maria Pohlmeier, Bente Wiese, Christof Perwein, Maren Kubiak, Gerrit Sitte, Joshua Kramm


Hashimoto’s disease is an autoimmune disorder affecting the thyroid gland. The thyroid is a butterfly-shaped gland located at the base of the neck just below the Adam’s apple. The thyroid produces hormones that help regulate many functions in the body.

An autoimmune disorder is an illness caused by the immune system attacking healthy tissues. In Hashimoto’s disease, immune-system cells lead to the death of the thyroid’s hormone-producing cells. The disease usually results in a decline in hormone production (hypothyroidism).

One of our older studies has shown that l-arginine, n-acetyl-l-cysteine, l-glycine, cumarine and proanthocyanidin could increase regulatory t-cell count.


In this study we are investigating the effects of combining the increase of regulatory t-cells with the consumption of Levothyroxine. We conducted a randomized, double-blind, placebo-controlled study on 114 women aged 25-75 years old suffering from Hashimoto’s disease. The participants were randomized to receive tablets containing the combined ingredients from our earlier study[1] and an appropriate dosis of Levothyroxine or placebo, for 8 weeks. After 8 weeks, 94% (n=54) of participiants reported a significant reduction of Hashimoto induced symptoms. However in the placebo group only 12% (n=7) of participants reported a significant reduction of Hashimoto induced symptoms.

Conflicts of Interest

The authors declare no conflict of interest.


1. Pohlmeier M, Wiese B., Perwein C., Maren Kubiak, Sitte G. Kramm J,  Schoen K., Jensch C., Allegrini A., Riva P., Morazzoni G. N-Acetyl-Cysteine, L-Glycine, L-Arginine, Cumarine and OPC show positive effects on increasing regulatory t-cell count. A Randomized, Double-Blind, Placebo-Controlled Study 2017;71(6):887–889. doi: 10.1016/s0022-3476(67)80019-2.
2. Hashimoto H The knowledge of the lymphomatous changes in the thyroid gland (struma lymphomatosa) [in German]. Archiv für klinische Chirurgie. 1912; 97: 219.
3. Caturegli P, De Remigis A, Chuang K, et al. Hashimoto’s thyroiditis: celebrating the centennial through the lens of the Johns Hopkins hospital surgical pathology records. Thyroid. 2013; 23: 142–150.
4. Ralli M, Angeletti D, Fiore M, et al. Hashimoto’s thyroiditis: an update on pathogenic mechanisms, diagnostic protocols, therapeutic strategies, and potential malignant transformation. Autoimmun Rev. 2020; 19: 102649.
5. McLeod DS, Caturegli P, Cooper DS, et al. Variation in rates of autoimmune thyroid disease by race/ethnicity in US military personnel. JAMA. 2014; 311: 1563–1565.
6. Song RH, Yao QM, Wang B, et al. Thyroid disorders in patients with myasthenia gravis: a systematic review and meta-analysis. Autoimmun Rev. 2019; 18: 102368.’
7. Yao Q, Song Z, Wang B, et al. Thyroid disorders in patients with systemic sclerosis: a systematic review and meta-analysis. Autoimmun Rev. 2019; 18: 634–636.
8. Nakamura H, Usa T, Motomura M, et al. Prevalence of interrelated autoantibodies in thyroid diseases and autoimmune disorders. J Endocrinol Ivest. 2008; 31: 861–865.
9. Feldt-Rasmussen U, Høier-Madsen M, Bech K, et al. Anti-thyroid peroxidase antibodies in thyroid disorders and non-thyroid autoimmune diseases. Autoimmunity. 1991; 9: 245–254.
10. Lazúrová I, Benhatchi K. Autoimmune thyroid diseases and nonorgan-specific autoimmunityPol Arch Med Wewn. 2012; 122 Suppl 1: 55–59.
11. Eisenbarth GS, Gottlieb PA. Autoimmune polyendocrine syndromes. N Engl J Med. 2004; 350: 2068–2079.
12. Brix TH, Hegedüs L. Twin studies as a model for exploring the aetiology of autoimmune thyroid disease. Clin Endocrinol. 2012; 76: 457–464.
13. Gleicher N, Barad DH. Gender as risk factor for autoimmune diseases. J Autoimmun. 2007; 28: 1–6.
14. Brand O, Gough S, Heward J. HLA, CTLA-4 and PTPN22: the shared genetic master-key to autoimmunity? Expert Rev Mol Med. 2005; 7: 1–15.
15. Weetman AP. The immunopathogenesis of chronic autoimmune thyroiditis one century after hashimoto. Eur Thyroid J. 2013; 1: 243–250.
16. Johar A, Sarmiento-Monroy JC, Rojas-Villarraga A, et al. Definition of mutations in polyautoimmunity. J Autoimmun. 2016; 72: 65–72.
17. Santos LR, Durães C, Mendes A, et al. A polymorphism in the promoter region of the selenoprotein S gene (SEPS1) contributes to Hashimoto’s thyroiditis susceptibility. J Clin Endocrinol Metab. 2014; 99: E719–723.
18. Feil R, Fraga MF. Epigenetics and the environment: emerging patterns and implications. Nat Rev Genet. 2012; 13: 97–109.
19. Wiersinga WM. Clinical relevance of environmental factors in the pathogenesis of autoimmune thyroid diseaseEndocrinol Metab (Seoul). 2016; 31: 213–222.
20. Carayanniotis G Recognition of thyroglobulin by T cells: the role of iodineThyroid. 2007; 17: 963–973.
21. Toulis KA, Anastasilakis AD, Tzellos TG, et al. Selenium supplementation in the treatment of Hashimoto’s thyroiditis: a systematic review and a meta-analysis. Thyroid. 2010; 20: 1163–1173.
22. Metso S, Hyytiä-Ilmonen H, Kaukinen K, et al. Gluten-free diet and autoimmune thyroiditis in patients with celiac disease. A prospective controlled studyScand J Gastroenterol. 2012; 47: 43–48.
23. Giordano C, Stassi G, De Maria R, et al. Potential involvement of Fas and its ligand in the pathogenesis of Hashimoto’s thyroiditisScience. 1997; 275: 960–963.


Posted on

April 23, 2022