Dushyant Viswanathan, MD, ABIM, ABOIM, AACE

    CCIM Hashimoto Autoimmune Thyroiditis

    Intro:

    • Hashimoto Thyroiditis is an autoimmune inflammatory disease of the thyroid, in which antibodies (TPO, anti-thyroglobulin) are made to attack the thyroid because of immunologic dysfunction originating in the gut microbiome.
    • The thyroid cells can be destroyed by cytotoxic T cells activated to attack them, and by the antibodies, however the presence of the antibodies doesn’t automatically mean the thyroid cells are being destroyed. 
    • Little to no symptoms, Normal TSH, free T3, free T4 levels suggests that there’s no active thyroid cell destruction

    Immunology:

    • Hashimoto’s is a Th1 inflammatory process (cytokines IL-1β, IL-12, IFN-γ, TNF-α) are involved in activating the inflammation
      • Gut dysbiosis  activates IFN-gamma and TNF-alpha  Th1 inflammation
      • Antibiotic exposure  promotes antibiotic resistant gram-negative bacterial dominance of the intestine  leads to high dose LPS in the gut  activates Th1 inflammation
      • EBV infection can induce Th1 inflammation and is implicated in Hashimoto’s
    • Th17 inflammation can also contribute to Hashimoto’s
      • Gut dysbiosis & Candidiasis  TGF-beta increases  promotes Th17 inflammation

    Treatment

    • High Dose IV Vitamin C is useful to treat EBV
    • CCIM Enteroimmunology (Gut microbiome balancing) can treat gut dysbiosis and lessen autoimmune inflammation
    • Vit A is a useful immunomodulator
    • Resveratrol beneficially modulates Th17 inflammation

    Miscellaneous:

    • Thyroglobulin Ab is assoc with thyroid cancer, so lowering that titer suggests lower thyroid cancer risk; acute inflammation can transiently raise levels
    • TPO antibody titer doesn’t necessarily correspond to degree of disease / thyroid inflammation, and acute inflammation can transiently raise levels.
    • Excess iodine intake (iodine is in salt) can increase TPO antibody production