Why Dysbiosis, SIBO, Hydrogen Sulfide Intolerance, MCAS, and Long COVID May All Be Downstream of a Single Event — The hidden regulators: local thyroid signaling and iron trafficking

Two more systems round out the picture, and both reinforce the same theme — what's in the blood is not what's in the tissue. Local thyroid signaling. We usually judge thyroid status from blood markers — TSH, free T4, free T3. But thyroid hormone is activated and inactivated locally, in tissues, by enzymes called deiodinases. Inflammation upregulates deiodinase 3 (D3), which inactivates thyroid hormone right at the tissue level. The result: a colonocyte can be functionally hypothyroid — its mitochondrial, beta-oxidation, and transporter genes under-stimulated — while the patient's blood thyroid panel reads perfectly normal. Not every gut case is a thyroid case. But systemic blood markers genuinely cannot see local epithelial thyroid suppression, and that blind spot matters. Iron trafficking. Iron is never simply "high" or "low" — it has to be routed correctly. Chronic inflammation reshapes the whole logistics network: it raises hepcidin (the hormone that locks iron away inside cells by blocking the exporter ferroportin), alters ferritin storage, and drops transferrin saturation. The classic inflammatory signature is high ferritin with low serum iron and low transferrin saturation — iron sequestered, not absent. And here's the paradox that ties back to our core mechanism: while the body looks iron-restricted in the blood, the colonocyte may be drowning in loose, reactive iron int