Immune Dysregulation Triggers Hashimoto’s Thyroiditis
The mechanism implicated in Hashimoto’s thyroiditis is the activation of auto-aggressive lymphocytes, or white blood cells directed against self which trigger the production of antibodies against enzymes involved in thyroid hormone production and storage called thyroid peroxidase (TPO) and thyroglobulin (TG) (4). Development of anti-thyroid antibodies, correlated with progressive thyroid damage and lymphocytic inflammation (5), represents an eight-fold and 25-fold increased risk of the subsequent development of clinical hypothyroidism in women and men, respectively (6).
As a result of autoantibody formation, inflammatory cytokine production, and migration of immune cells toward the thyroid gland, auto-destruction of thyroid epithelial cells occurs, and hypothyroidism is the end product (2). As a compensatory reaction, levels of the upstream pituitary hormone thyroid stimulating hormone (TSH) rise in an attempt to prompt the remaining thyroid cells to increase thyroid hormone production (2). Once levels of TSH meet an arbitrary diagnostic threshold, established based on a reference group uncorrected for chronic or occult disease (7), Hashimoto’s patients are unilaterally offered levothyroxine, a synthetic analog of thyroxine (T4) that is the conventional treatment of choice.
However, even when thyroid parameters return to so-called normal levels, a significant proportion of patients on thyroid hormone replacement continue to report fatigue and diminished quality of life (8). This is unsurprising, since thyroid replacement therapy does nothing to arrest the underlying autoimmune pathogenesis responsible for Hashimoto’s, but rather applies a hormonal Band-Aid to keep symptoms at bay. This failure to practice root-cause resolution medicine, and address the immune dysregulation that invokes Hashimoto’s in the first place, also accounts for the three-fold increased likelihood of developing another autoimmune disease after the first autoimmune diagnosis (9).
