Dushyant Viswanathan, MD, ABIM, ABOIM, AACE

CCIM Hashimoto Autoimmune Thyroiditis


  • 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


  • 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


  • 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


  • 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