Hypothyroidism
Feeling unwell on an adequate levothyroxine dose is a real problem, because TSH shows whether your dose is right and not whether you convert T4 to active T3.
TSH is a pituitary signal, not a measure of tissue thyroid activity. A patient can have a perfect TSH, an adequate dose and persistent symptoms — because T4 must be converted to T3 to do anything, and that conversion depends on selenium, zinc, iron, cortisol status and inflammatory load. None of that is visible on TSH alone.
Hashimoto's thyroiditis, the most common cause in the United States, which makes this an autoimmune problem first. Impaired T4 to T3 conversion. Selenium, zinc, iron and ferritin insufficiency. Elevated cortisol and inflammatory load, both of which suppress conversion and raise reverse T3. Post-surgical and post-radioiodine states. And certain medications.
Replacement therapy stays with the prescriber managing it, and dose changes are theirs to make. Alongside it: cofactor repletion — selenium, zinc, iron and ferritin to target. Cortisol and inflammatory load addressed, since both throttle conversion. Antibody drivers addressed where Hashimoto's is present. Where T3 therapy is clinically appropriate, that is a prescriber conversation with monitoring.
TSH, free T4, free T3 and reverse T3, rather than TSH alone. TPO and thyroglobulin antibodies, since the cause matters. Ferritin and full iron studies, selenium, zinc, vitamin D and B12. hs-CRP. Cortisol rhythm where the picture suggests it.
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