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MediBalans›Thyroid & Hormonal Balance
Investigation · Stockholm

TSH is normal.
But you still feel terrible.

TSH measures the pituitary's signal to the thyroid — not what is actually happening in the tissues. Conversion of T4 to active T3, reverse T3 blocking receptors, antibodies against thyroid peroxidase, and adrenal interaction with thyroid function are not measured in standard TSH testing. MediBalans measures the complete picture.

"Your TSH is normal — your thyroid is fine."
Normal TSH excludes primary hypothyroidism. It does not exclude impaired T4-to-T3 conversion, reverse T3 blockade, early-stage Hashimoto's autoimmunity, or adrenal-thyroid interaction affecting tissue response.

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What standard tests miss

Four dimensions of thyroid function

01

T4→T3 conversion and reverse T3

T4 (levothyroxine) is a prohormone — it must be converted to active T3 by deiodinase enzymes in the liver, gut and peripheral tissues. Chronic inflammation, high cortisol and selenium deficiency impair this conversion and can increase reverse T3 (rT3) — an inactive T3 isomer that blocks T3 receptors. Standard thyroid panels do not include rT3.

02

Hashimoto's — autoimmunity before symptoms

Anti-TPO and anti-thyroglobulin antibodies can be elevated for decades before TSH deviates. Hashimoto's is an autoimmune disease where gut dysbiosis, molecular mimicry and food immune reactivity are documented trigger factors. Early antibody diagnosis enables interventions that may delay or prevent clinical hypothyroidism.

03

Adrenal-thyroid interaction

Chronically elevated cortisol (HPA axis stress) suppresses pituitary TSH secretion and reduces peripheral T3 uptake. Patients with HPA axis dysregulation may have suboptimal thyroid hormone tissue response despite normal TSH values — a state requiring that the adrenal axis be addressed before thyroid treatment can be optimised.

04

Selenium deficiency and thyroid peroxidase

Thyroid peroxidase — the enzyme producing T4 — is a selenoprotein-dependent enzyme. Selenium deficiency reduces thyroid hormone production and increases oxidative stress in thyroid tissue, worsening Hashimoto's. Intracellular selenium is measured in CMA — almost never in standard blood work.

The Hashimoto's protocol

Hashimoto's is an immunological disease

Hashimoto's thyroiditis is not primarily a thyroid disease — it is an autoimmune disease where the thyroid happens to be the target organ. Treatment with levothyroxine alone does not address the immunological process destroying thyroid tissue.

Documented trigger factors: gluten (molecular mimicry with thyroid antigens), gut dysbiosis, SIBO, food immune reactivities (ALCAT), and methylation capacity governing immune regulation. Eliminating these factors reduces anti-TPO antibodies in a subset of patients.

GCR sequence for Hashimoto's

ALCAT + GI Effects (leaky gut, dysbiosis) → MethylDetox (immune regulation) → Comprehensive Thyroid Assessment (full thyroid picture incl. rT3) → ASP (adrenal-thyroid interaction) → CMA (selenium, zinc, iodine).

Genova Diagnostics

Comprehensive Thyroid Assessment

TSH, free T4, free T3, reverse T3, anti-TPO, anti-thyroglobulin. The only complete thyroid picture — including rT3 that reveals T3 receptor blockade.

Genova Diagnostics

Adrenocortex Stress Profile (ASP)

Cortisol-DHEA curve determines whether adrenal-thyroid interaction impairs tissue response. Mandatory in treatment-resistant hypothyroid symptoms.

Cell Science Systems

ALCAT 250+ — Immune Reactivity

Food reactivities driving anti-TPO antibody production. Gluten is the most common single trigger but is part of a broader reactivity pattern.

Cell Science Systems

CMA — 55 intracellular markers

Selenium (thyroid peroxidase cofactor), iodine, zinc and vitamin D — the nutritional prerequisites for thyroid function.

FAQ

Questions about thyroid investigation

Normal TSH excludes primary hypothyroidism but does not guarantee optimal thyroid function at tissue level. Impaired T4→T3 conversion (due to inflammation or cortisol), reverse T3 blockade, subclinical Hashimoto's with normal TSH, or adrenal-thyroid interaction all produce hypothyroid-like symptoms with normal TSH.
In early stages — before significant thyroid tissue is destroyed — interventions addressing immunological trigger factors can slow disease progression and stabilise antibodies. If TSH is already elevated and symptoms are significant, levothyroxine is usually indicated. MediBalans always works in coordination with your endocrinologist.
Reverse T3 (rT3) is an inactive isomer of T3 produced during conversion of T4 under stress, inflammation and caloric restriction. rT3 binds to T3 receptors without activating them — it actively blocks active T3's effect. High rT3 with normal free T3 is called functional hypothyroidism. Standard thyroid panels do not measure rT3.
Related tests

Diagnostic protocols used in this investigation

Diagnostics
Comprehensive Thyroid Assessment
TSH, free T4, free T3, reverse T3, anti-TPO, anti-thyroglobulin. The only complete thyroid picture — including rT3 revealing T3 receptor blockade.
Diagnostics
Adrenocortex Stress Profile (ASP)
Cortisol-DHEA curve determines whether adrenal-thyroid interaction impairs tissue response. Mandatory in treatment-resistant hypothyroid symptoms.
Diagnostics
ALCAT 250+ — Food Immune Reactivity
Food reactivities driving anti-TPO antibody production. Gluten is the most common single trigger in Hashimoto's.
Diagnostics
CMA — Cellular Micronutrient Assay
Selenium (thyroid peroxidase cofactor), iodine, zinc and vitamin D. The nutritional prerequisites for thyroid function.
Next step

Complete thyroid investigation
at MediBalans

Book a consultation for complete thyroid and hormonal investigation — including rT3, antibodies and adrenal-thyroid interaction.

Book Consultation → 📞 08-530 210 20
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