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MediBalans›Chronic Fatigue & Burnout
Investigation · Stockholm
Energy · HPA Axis · Mitochondria

All your tests are normal.
But you are exhausted.

Chronic fatigue is frequently diagnosed as depression, stress or burnout — without actually investigating the biochemical state. MediBalans measures what is actually happening at the cellular level: immunological load, mitochondrial energy production, the HPA axis cortisol profile, and intracellular nutritional status.

"You're burned out. Rest and take it easy."
If you have rested for months without improvement, that is a signal that the fatigue has a biological, not psychological, primary constraint. These mechanisms are measurable and addressable — but they are not measured with standard blood work.

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The biology of fatigue

What actually drives your exhaustion

01

Chronic immune activation

ALCAT-identified food reactivities drive constant cytokine production. Cytokines — particularly IL-6, TNF-α and IL-1β — are directly inhibitory to mitochondrial function and ATP production. This is the most common and least diagnosed cause of treatment-resistant fatigue.

02

Mitochondrial dysfunction

NutrEval organic acids reveal whether the Krebs cycle, beta-oxidation and electron transport chain are functioning correctly. Blockades in these pathways — often secondary to CoQ10 deficiency, carnitine deficiency or B-vitamin deficiency — give direct and measurable energy limitation.

03

HPA axis cortisol dysregulation

Adrenocortex Stress Profile (ASP) maps the cortisol curve across 4 time points. Flat pattern, low amplitude or absent cortisol awakening response (CAR) are biological signs of HPA axis exhaustion — not psychological weakness.

04

Intracellular deficiency of energy substrates

CMA measures CoQ10, carnitine, magnesium, B12 and B6 directly inside cells. These are the primary cofactors for mitochondrial energy production. Deficiency is rarely visible in serum — but is consistently found in white blood cells of chronic fatigue patients.

The GCR protocol

The sequence that determines results

Chronic fatigue is MediBalans' most common multi-domain presentation. Almost always there is an immunological primary constraint — ALCAT reactivities driving chronic cytokine production that suppresses both the HPA axis and mitochondrial function.

Treating fatigue with cortisol, adaptogens or B12 injections without addressing the immunological driver gives temporary effect. Symptoms recur as the underlying inflammation continues.

Clinical pattern

Patients with chronic fatigue who are treated solely with rest, B12 and thyroid medication without ALCAT data respond inconsistently. Those who initiate with ALCAT elimination and CMA-based supplementation have consistently better and faster responses — regardless of severity.

Cell Science Systems · Primary instrument

ALCAT 250+ — Immune Reactivity

Identifies food reactivities driving chronic cytokine load. The single most important step in the investigation of treatment-resistant fatigue.

Cell Science Systems · 55 markers

CMA — Cellular Micronutrient Assay

CoQ10, carnitine, magnesium, B12, B6, folate — directly inside the cell. The energy substrates without which mitochondria cannot produce sufficient ATP.

Genova Diagnostics

Adrenocortex Stress Profile (ASP)

Four saliva samples map the cortisol curve and DHEA. Cortisol awakening response (CAR) add-on reveals the HPA axis' actual state — not just that you are stressed.

Genova Diagnostics

NutrEval® Metabolomics

Organic acids reveal exactly where in energy production the blockade lies. Methylmalonate (B12 function), xanthurenic acid (B6), succinate/fumarate (mitochondrial blockade) — all measurable.

FAQ

Questions about chronic fatigue

GP investigation addresses structural causes of fatigue: anaemia, hypothyroidism, diabetes, depression. MediBalans measures the biological processes driving fatigue when these are excluded: immunological load (ALCAT), mitochondrial function (NutrEval), HPA axis cortisol profile (ASP) and intracellular nutritional status (CMA). It is complementary — we assume serious disease has already been excluded.
Functionally the boundary is blurred. Biologically they often share the same pattern: immune activation, HPA axis dysregulation and mitochondrial impact. ME/CFS is characterised by post-exertional malaise (PEM) — symptoms worsening after exertion — and is more biologically fixed. The MediBalans protocol is the same regardless of diagnostic label; we measure the underlying biological mechanisms.
Yes. TSH measures the pituitary signal, not tissue response to thyroid hormone. Conversion of T4 to active T3 can be impaired during chronic inflammation, high cortisol or selenium deficiency — without TSH deviating. Reverse T3 (rT3) blocks thyroid receptors and is not included in standard thyroid panels.
Related tests

Diagnostic protocols used in this investigation

Diagnostics
ALCAT 250+ — Food Immune Reactivity
Identifies food reactivities driving chronic cytokine production that suppresses energy production.
Diagnostics
CMA — Cellular Micronutrient Assay
CoQ10, carnitine, magnesium and B12 directly inside cells — primary cofactors for mitochondrial function.
Diagnostics
NutrEval® Metabolomics
125+ metabolomic markers. Reveals exactly where in energy production the blockade lies.
Diagnostics
Adrenocortex Stress Profile (ASP)
Cortisol curve and DHEA at 4 time points. Cortisol awakening response reveals the true HPA axis state.
Next step

Investigate
your fatigue

Book a consultation to determine which diagnostic layers provide the most information for your situation.

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