Hashimoto's Thyroiditis

Hashimoto's thyroiditis is not a primary autoimmune attack but rather the final stage of a simple colloid goiter, driven by chronic overstimulation and metabolic blockage. 2 Peat argued that the condition, originally defined by lymphocytic infiltration of the gland, is now diagnosed by "pure guesswork" based on blood antibodies without biopsy, and that the presence of antithyroid antibodies does not prove the immune system is causally destroying the gland. 3 Instead, the antibodies are part of a cleanup process, mobilized to remove debris from tissue injured by prolonged stress. 3 The root injury stems from factors that block thyroid hormone production and release, forcing the pituitary to secrete excess thyroid stimulating hormone (TSH), which itself acts as an inflammatory agent. 3

The pathogenic sequence begins when hormone release from the gland is inhibited. Estrogen activates the formation of the viscous protein thyroglobulin (colloid) but blocks its proteolytic digestion into active hormones, causing the gland to enlarge even as systemic hypothyroidism develops. 2 Progesterone, conversely, activates the proteolytic enzymes that release the hormones. 3 Other blocking agents include excess iodine, which can suppress hormone formation and induce classical hypothyroid signs, and polyunsaturated fats (PUFA). 3 The resulting deficiency in thyroid hormone triggers a compensatory surge in TSH, and the mechanical and chemical stress of this chronic overstimulation creates an inflammation-like state within the gland. 3 Peat noted that TSH itself causes many symptoms blamed on hypothyroidism by acting on bone marrow, the liver, and other tissues to increase inflammatory cytokines. 5

The antibodies measured in diagnosis—such as antithyroglobulin and antithyroperoxidase—are not specific to the thyroid and appear whenever connective tissue is disrupted. 2 Peat cited evidence that these antibodies are found more frequently in rheumatoid arthritis and Sjogren's syndrome than in Hashimoto's disease, and that they interact with joint cartilage, making the condition fundamentally a connective tissue inflammatory disease accompanying hypothyroidism. 2 The immune system treats the stressed, debris-filled tissue as if it were infected, and the antibodies serve to help phagocytes clear the accumulated junk. 3 This explains why the condition is five to ten times more frequent in women: estrogen not only blocks thyroid secretion but also causes rapid thymic atrophy, degrading the normal regulation of immune functions. 2

Treatment, in Peat's framework, does not require immunosuppression but rather the removal of the underlying thyroid inhibition. He observed that simply supplementing thyroid hormone—even synthetic thyroxine (T4)—for six months to a year usually suppresses TSH, resolves the inflammatory drive, and causes the antibodies to decrease or disappear. +4 However, he cautioned that women with high estrogen often cannot convert T4 to the active T3 hormone in the liver, making T3 supplementation necessary in some cases. 2 Because the antibodies reflect a repair process rather than a self-destructive one, Peat considered thyroid, along with progesterone, pregnenolone, and DHEA, as the effective cure for so-called autoimmune thyroiditis, restoring the metabolic balance that halts the initial tissue injury. 8