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