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CCIM Hashimoto thyroiditis
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