Hashimoto's thyroiditis
An autoimmune condition before it is a thyroid one, which is why antibodies, conversion and nutrient cofactors are assessed alongside your replacement therapy.
Hashimoto's is an autoimmune process in which the immune system targets thyroid tissue. The hypothyroidism is the downstream consequence. Replacement therapy addresses the consequence, which is why symptoms often persist on an adequate dose. The immune driver is a separate clinical question, and it is the one addressed here.
Genetic susceptibility, then triggers: loss of intestinal barrier integrity, gluten reactivity in a meaningful subset, selenium and iodine imbalance, low vitamin D, chronic stress physiology, and unresolved infection including Epstein–Barr. Antibody titers often move when these are addressed, even where TSH is already controlled.
Replacement therapy stays with the prescriber managing it. Alongside it: barrier and microbiome work, gluten elimination where reactivity is demonstrated, selenium and vitamin D repletion to target, and stress and sleep physiology. Conversion of T4 to T3 is assessed rather than assumed, since impaired conversion explains many residual symptoms.
TPO and thyroglobulin antibodies. TSH, free T4, free T3 and reverse T3 rather than TSH alone. Vitamin D, selenium, ferritin and B12. Barrier permeability and inflammatory markers. Where nodules or structural change are suspected, imaging and endocrinology referral come first.
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Start with the fifteen-minute consultation. No cost, and a straight answer on whether this model fits your case.