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MediBalans›Autoimmunity & Chronic Inflammation
Investigation · Stockholm

Your immune system is attacking you.
But why did it start?

Autoimmune diseases are treated in conventional medicine with immunosuppression — damping the attack. MediBalans asks a different question: what is driving the immune system to attack in the first place? The answer is almost always found in the gut, the diet, and the epigenome.

"You have an autoimmune disease. There is no cure — we manage symptoms."
Immunosuppression does not address trigger factors. Patients who identify and eliminate their biological drivers frequently achieve remission — measurable with antibodies and inflammatory markers.

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The biology of autoimmunity

Three mechanisms that start the immune attack

01

Leaky gut and molecular mimicry

Compromised tight junctions (measurable with zonulin and claudin/occludin IgA/IgG in GI Effects) allow unprocessed protein fragments to cross the intestinal barrier. The immune system produces antibodies against these fragments. If they structurally resemble the body's own proteins — molecular mimicry — the antibodies attack own tissues. Gluten-gliadin and thyroid antigen share epitopes, explaining the Hashimoto connection.

02

ALCAT reactivities as chronic triggers

Food reactivities drive constant immune activation that sustains autoimmune inflammation. ALCAT identifies the specific foods triggering NF-κB-driven inflammation — the central signalling pathway in most autoimmune conditions. Elimination reduces the total inflammatory burden.

03

Methylation capacity governs immune regulation

MethylDetox 38-gene panel identifies variants in MTHFR, COMT and immune-regulatory genes that determine the body's ability to regulate its inflammatory response. Impaired methylation of pro-inflammatory genes perpetuates autoimmune activity genetically.

The GCR framework

The gut is the starting point

More than 70% of the immune system resides in the gut's lymphoid tissue (GALT). The gut microbiome and barrier integrity fundamentally determine the immune system's tolerance threshold. A compromised gut barrier is the most consistently identified factor in autoimmune diseases.

GCR sequence for autoimmunity

GI Effects (gut barrier) + ALCAT (immunological triggers) → MethylDetox (immune regulation) → CMA (cofactors for healing). In this order — not in parallel. Without knowing which triggers are driving the activity, we cannot know whether barrier repair is having effect.

Genova Diagnostics

GI Effects® + Zonulin

Intestinal barrier integrity: zonulin, occludin/claudin IgA/IgG, pancreatic elastase, calprotectin. Reveals whether the gut is the source of immune activation.

Cell Science Systems

ALCAT 250+ — Immune Reactivity

Identifies food reactivities maintaining chronic NF-κB activation. Often the single most important step towards remission.

MediBalans

MethylDetox — 38 genes

MTHFR, COMT and immune-regulatory SNPs. Maps the genetic capacity for inflammation suppression and epigenetic regulation.

Cell Science Systems

CMA — 55 intracellular markers

Vitamin D (critical for immune regulation), zinc, selenium and omega-3 index. Identifies nutritional cofactors for immune tolerance.

FAQ

Questions about autoimmune investigation

Remission — absence of measurable autoimmune activity — is possible and is achieved in some patients who identify and eliminate their biological trigger factors. It is not guaranteed and depends on disease duration, organ damage and genetic profile. The goal is to reduce the immunological burden sufficiently for inflammatory markers and autoantibodies to normalise.
Molecular mimicry means that an external antigen (e.g. a protein motif in gluten, a bacterial protein or a food) structurally resembles a body-own protein. The immune system produces antibodies against the antigen — and these antibodies cross-react against own tissue. It is the primary molecular mechanism behind Hashimoto's, type 1 diabetes and a range of other autoimmune conditions.
Hashimoto's thyroiditis has a documented association with intestinal permeability and coeliac disease. Gliadin antigens share epitopes with thyroid antigens — a documented molecular mimicry link. Gut dysbiosis and SIBO increase systemic inflammation that can trigger and sustain antibody production against thyroid peroxidase (TPO) and thyroglobulin (Tg).
Related tests

Diagnostic protocols used in this investigation

Diagnostics
GI Effects® + Zonulin
Intestinal barrier integrity — zonulin, tight junction markers, calprotectin. The gut as the starting point for immune activation.
Diagnostics
ALCAT 250+ — Food Immune Reactivity
Identifies food reactivities maintaining chronic NF-κB activation — the central pathway in autoimmune conditions.
Diagnostics
MethylDetox — 38 Genes
MTHFR, COMT and immune-regulatory SNPs. Maps the genetic capacity for inflammation suppression.
Diagnostics
CMA — Cellular Micronutrient Assay
Vitamin D, zinc and selenium — critical cofactors for immune tolerance. Intracellular measurement, not serum.
Next step

Investigate your autoimmune profile

Book a consultation to map your biological trigger factors and remission strategy.

Book Consultation → 08-530 210 20
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