Hashimotos is an Autoimmune Disease that attacks the thyroid. As the thyroid is attacked by antibodies, it begins to struggle to function. This in turn affects the amount of thyroid hormone being produced, eventually leading to not or barely producing. Thyroid hormones regulate metabolism, the T3 hormone affects just about every organ of the body, modulating cell functions. Thyroid hormones also stimulate the synthesis of protein, increase the use of glucose for ATP production, increase Lipolysis (Chemical breakdown of fats), enhance cholesterol excretion, reducing blood cholesterol levels. Thyroid hormones T4 and T3 regulate Oxygen use and Basal metabolic Rate (BMR), cellular Metabolism, growth and development and the activity of the nervous system.
Using the 3-legged Stool Analogy, Hashimotos possible triggers are more likely to involve genetics. It is related to Type IV: Delayed Hypersensitivities. A Type IV: Delayed reaction is a hypersensitivity reaction and represents classic delayed food hypersensitivity and can also be seen in organ specific autoimmune conditions. Immune responses in these cases generally occur within 48-72 hours of exposure to things like foods, viral, fungal or bacterial pathogens or heavy metals. Because they involve recognition of MHC Complexes, they are mediated by T cells (generally Th1 or Th17) and macrophages. The specific symptoms that a person may develop are very strongly influenced by their genetics. Therefore, you may see various family members with different issues, or multiple issues, like Non Celiac Gluten Sensitivity, Celiac, Hashimotos, Chron’s Disease and Multiple Sclerosis.
Food sensitivities may be a trigger in some for this Autoimmune disease. Heavy Metals, bacterial of fungal or vial pathogens may also be a trigger.
Epigenetics
Epigenetic exposures that may be contributing to Hashimotos are diet, medications, hormone imbalances, environmental chemicals, microbiota, viruses, inflammation, stress and trauma. Hashimotos is associated with a Type IV: delayed food hypersensitivity. This involves the recognition of MHC complexes, that are mediated by T cells (Usually Th1 or Th17) and microphages.
“There are two types of MHC complexes, MHC Type I and MHC Type II. T cells use them to determine what to attack and how to differentiate between “self-cells” and “non-self-cells”. Because of this, some scientists propose that MHCs play a key role in autoimmunity.” (Immunity Student Guide, NTA 2019)
- Gluten and Casein are two of the molecular mimicries of thyroid. This happens after Leaky Gut has begun BY gluten, leaking out the gluten and the Casein proteins and triggering T cells to form and clone themselves.
Molecular Mimicry
An unexpected cross-reaction of the antibodies with autologous components may occur. This process is in fact at the basis of the progression of autoimmune diseases and is called molecular mimicry. In the gut, inflammatory pathologies that are related to dysbiosis associated with various factors, such as genetic factors and food, cause alterations of the immune system characterized in IBD and CD (9, 10, 14). Those enteric eco-events induce systemic inflammatory responses, leading to the systemic manifestations of IBD and/or CD, affecting remote organs including the thyroid (10, 14).” (Gut-thyroid axis and celiac disease; Aaron Lerner, Patricia Jeremias, and Torsten Matthias, May 2017)
Recommendations to help a person with Hashimotos Thyroiditis:
It would be a good idea to eliminate gluten and dairy. Also, any inflammatory foods and any food sensitivity foods as shown on a Cocas Pulse Test. The gut needs to be repaired, and stomach acid replaced. Good bacteria will have to be replaced as well as bad bacteria removed.
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