Functional Support for Hashimoto's Thyroiditis

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Hashimoto’s thyroiditis is an acquired and autoimmune type of hypothyroidism that destroys the thyroid tissues.  It is the most frequent cause of hypothyroidism in the U.S. and occurs more often in women versus men at a ratio of 20:1 (1).  Certain environmental toxins such as perchlorate, fluoride, lithium, mercury, bisphenol A, and Teflon can trigger the disease by concentrating in the thyroid follicles and generating free radicals that activate immune response (2).

            In Hashimoto’s, antibodies attack certain thyroid proteins, including thyroid peroxidase (TPO) enzyme, thyroglobulin (TG), and thyroid-stimulating hormone (TSH) receptors, which prevents the manufacture of the thyroid hormones, T3 and T4, and eventually destroys thyroid follicular cells (3).  Hashimoto’s may be present in the absence of overt hypothyroidism but will likely progress to this condition with time.  Thyroid replacement, dietary elimination, and DHEA have all been implicated in the treatment of this disease.

Thyroid Replacement

            Thyroid replacement has shown positive clinical responses in the majority of Hashimoto cases (2).  Administration of desiccated and synthetic hormones normalizes the decreased levels of thyroid hormones, suppresses thyroid activity, and eventually decreases the autoimmune process (2).  Thyroid replacement should be used in high enough doses to decrease TSH to 0.1 or 1.5 (a healthy euthyroid level) and careful monitoring should continue in order to prevent the hyperthyroid side effects experienced in some individuals (2).  Additionally, frequent TSH and antibody tests should be administered to verify proper suppression of thyroid activity and to monitor autoimmune activity, and thyroid replacement may be contraindicated if a hyperthyroid scenario is present.

Dietary Adjustments

            The strong correlation between autoimmune disorders, intestinal permeability, and food allergies suggests that dietary adjustments may present significantly beneficial results.  In fact, the prevalence of autoimmune thyroid disease in patients with Celiac disease (CD) is measurably higher than those without CD, which may be due to certain genetic factors that are over-expressed in affected individuals (4, 5).  While some studies show positive clinical results after incorporating a gluten-free diet (Mainardi, Montanelli, & Dotti as cited by Pizzorno & Murray, 2013), other studies show little evidence as to its efficacy in reducing the development of associated autoimmune disorders, including Hashimoto’s (4, 5).  However, early diagnosis and elimination of allergenic foods may reduce the complications often seen in autoimmune disorders, such as malabsorption and osteoporosis (4).  Incorporating an elimination diet and detoxification regime may help decrease antigen load, strengthen and repair the intestinal lining, remove chemical toxins, and mitigate autoantibody activity (2). 

Dehydroepiandrosterone (DHEA)

            Lastly, some studies have indicated the administration of DHEA in the range of 5 to 10 mg/day for women and 10 to 20 mg/day for men as beneficial and safe in various autoimmune conditions (6).  However, higher doses have resulted in hirsutism and acne in some cases (6).  Moreover, the effects of long-term DHEA administration are not well-known and should be monitored as such (2).

            In conclusion, hormone replacement therapy currently presents with the best clinical results, though complications may arise in some individuals.  Though evidence for dietary adjustments are controversial, incorporating a diet free of typical allergens may help mitigate the autoimmune process by relieving the antigen load, removing toxins, and encouraging tissue repair.

References

1. Burkhart, N. (2013). Hashimoto’s thyroiditis. RDH, 13, 66-68. Retrieved from https://search.proquest.com/docview/1326413972?accountid=158302

2. Pizzorno, J. E., & Murray, M. T. (2013). Textbook of natural medicine (4th ed.). Philadelphia, PA, United States: Elsevier/Churchill Livingstone.

3. Copstead, L.-E. C., & Banasik, J. L. (2013). Pathophysiology (5th ed.). Amsterdam: Elsevier Health Sciences.

4. Ch’ng, C. L., Jones, M. K., & Kingham, J. G. C. (2007). Celiac disease and autoimmune thyroid disease. Clinical Medicine & Research, 5(3), 184-192. doi:10.3121/cmr.2007.738

5. Sun, X., Lu, L., Yang, R., Li, Y., Shan, L., & Wang, Y. (2016). Increased incidence of thyroid disease in patients with Celiac disease: A systematic review and meta-analysis. PLOS One, 6-13. doi: 10.1371/journal.pone.0168708

6. van Vollenhoven, R. F. (2002). Dehydroepiandrosterone for the treatment of systemic lupus erythematosus. Expert Opinion on Pharmacotherapy, 3(1), 23-31. doi:10.1517/14656566.3.1.23