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Graves Disease

Speaker

Sarah Zielsdorf, MD, MS

Description: 

Graves Disease, eponym of Robert James Graves, MD,  (1835), is an autoimmune condition fraught with misunderstanding, misdiagnosis and mistreatment by the medical community. Graves’ Disease is characterized by hyperthyroidism secondary to circulating autoantibodies in which Thyroid-Stimulating Immunoglobulins (TSIs) bind to and activate thyrotropin receptors (TSH receptors), causing thyroid enlargement with subsequent thyroid hormone over-synthesis.  

Graves’ Disease may present as hyperthyroidism alone (toxic diffuse goiter), or a patient may swing hyper or hypothyroid due to concomitant Hashimoto’s Disease (characterized by the production of Thyroid Peroxidase and/or Thyroglobulin antibodies). A patient may have Hashimoto’s alone (causing hyper/hypothyroid swings) or a single thyrotoxic nodule producing thyroid hormone.

In some patients, Graves’ disease is only one of a related group of existing autoimmune conditions, which leads to dysfunction of multiple organs (i.e. polyglandular autoimmune syndromes). Graves’ and Hashimotos (representing a spectrum of autoimmune thyroid disease) are associated with Celiac disease, vitiligodiabetes mellitus type 1autoimmune adrenal insufficiency (Addison’s Disease), systemic sclerosismyasthenia gravisSjögren syndromerheumatoid arthritis, and systemic lupus erythematosus

Females are more predisposed to Graves’ Disease with precipitating or causal factors including genetics, physical/emotional trauma, acute or a chronic infections, and environmental toxins/food antigens. Epstein-Barr Virus (EBV) is an example of a viral trigger via molecular mimicry. Three traditional treatments for Graves’ Disease include anti-thyroid medications, radioiodine therapy, and thyroidectomy. Our functional medicine approach has changed the paradigm of Graves’ Disease treatment to include a root cause approach of treatment. Low Dose Naltrexone (LDN) is a critical therapy in conjunction with removal of autoimmune triggers/environmental stressors, intense diet, nutritional, and lifestyle modifications, herbal therapies, and treatment of underlying causes (e.g. infections).

Session Learning Objective: 

Participants will understand that Graves’ Disease (also known as toxic diffuse goiter) is an autoimmune-mediated thyroid disease, which causes hyperthyroidism. Exophthalmos and non-pitting edema (pretibial myxedema) are diagnostic signs of Graves’ Disease. The three traditional treatments for Graves’ Disease include anti-thyroid medications, radioiodine therapy (RAI), and thyroidectomy. Though definitive management is the removal of the thyroid by destruction or surgery, the underlying autoimmune disease process remains. Thus, the individual is predisposed to further morbidity and risk of developing additional autoimmune diseases. Using a functional medicine approach, our clinic views Graves’ Disease with a root-cause approach, looking for the underlying reasons the patient expressed autoimmunity. A brief case study will illustrate this paradigm. Low Dose Naltrexone (LDN) is an important immune system modulator in the treatment of autoimmune disease.

Session Outline: 

  • Graves’ Disease: definitions
  • Spectrum of related autoimmune conditions, concomitant Hashimotos disease possible
  • Predisposing factors for development of Graves’ Disease
  • Three traditional treatments for Graves’ Disease include anti-thyroid medications, radioiodine therapy, and thyroidectomy
  • Removal of the thyroid does not cure the underlying autoimmune process
  • Functional medicine is a roadmap seeking the underlying root causes for the development of autoimmunity
  • Brief Graves’ Disease case study: adjunctive use of LDN in conjunction with removal of autoimmune triggers/environmental stressors, intense diet, nutritional, and lifestyle modifications, herbal therapies, and treatment of underlying causes (e.g. infections)