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MediBalans › Diagnostics › MethylDetox — 38-Gene Methylation Analysis
MediBalans Proprietary Test · Genetic SNP Analysis

38 genes.
Your methylation blueprint.

Methylation governs how you process B-vitamins, clear homocysteine, synthesise neurotransmitters and detoxify hormones. Standard tests check 2–5 genes. MethylDetox covers 38 — with complete SNP coverage across every pathway that matters clinically.

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Top-rated clinic in Sweden Verified patient reviews · Reco.se
38Genes Analysed
FullSNP Coverage
6Pathways Covered
Sweden'sMost Comprehensive
What Methylation Governs

Why methylation genetics changes everything

Methylation is one of the most fundamental biochemical processes in human physiology. It controls: the conversion of folic acid to its active usable form (5-MTHF), the regeneration of methionine and SAMe — the body's universal methyl donor, the clearance of homocysteine, neurotransmitter synthesis and breakdown, hormone detoxification, DNA methylation and gene expression, and the activation of B12.

Genetic variants in the enzymes governing these pathways — MTHFR, MTR, MTRR, COMT, CBS and others — determine how efficiently each step occurs. The variants are not rare: MTHFR C677T is carried by approximately 40–60% of the population. They are simply unknown in most patients because standard medicine does not routinely test them.

The consequence of not knowing: patients receive B-vitamin protocols that structurally cannot work — folic acid for someone who cannot convert it, methylcobalamin in a form their MTR variant cannot utilise, or antidepressant medication for COMT-driven neurotransmitter accumulation that would respond to nutritional support.

Proprietary · 38 genes vs standard panels

Consumer genetic services like 23andMe or standard MTHFR tests cover 2–5 genes and omit the regulatory regions. MethylDetox was developed by MediBalans to fill this diagnostic gap — providing clinically actionable data across all methylation-relevant pathways in a single, interpretable report.

Test Facts — MethylDetox

38-gene panel overview

Genes analysed38 methylation-relevant genes with complete SNP coverage
PathwaysMethylation · Methionine cycle · Folate pathway · B12 metabolism · COMT & transulfuration · Neurotransmitters
Sample typeBuccal swab or venous blood — home collection available
Turnaround7–10 business days
Developed byMediBalans AB — proprietary Swedish panel
InterpretationFull clinical consultation with Dr Mario Anthis — integrated with CMA and NutrEval findings
38 Genes · Complete SNP Coverage

What MethylDetox analyses

Methylation Capacity

MTHFR — Full Coverage

MTHFR C677T and A1298C with complete regulatory region coverage. The rate-limiting enzyme of the folate-methionine cycle. Variants reduce conversion of folic acid to active 5-MTHF by 35–70%. MethylDetox includes the full regulatory region — not just the two standard SNPs.

Methionine Cycle

MTR, MTRR & BHMT

MTR C3518T (methionine synthase), MTRR (methionine synthase reductase) and BHMT. These genes govern how homocysteine is remethylated back to methionine — and how B12 is activated and maintained in its functional form. MTR C3518T is uniquely covered by MethylDetox.

COMT & Transulfuration

COMT V158M & CBS Pathway

COMT V158M determines dopamine, noradrenaline and oestrogen clearance speed. CBS and CTH govern the transulfuration pathway — how homocysteine is converted to glutathione and taurine. These pathways are central to psychiatric, hormonal and detoxification phenotypes.

Neurotransmitter Synthesis

MAOA, MAOB & TPH

Monoamine oxidase A and B govern serotonin, dopamine and noradrenaline breakdown. TPH1 and TPH2 determine serotonin synthesis capacity. HNMT regulates histamine metabolism. Variants in these genes explain neurotransmitter phenotypes that resist pharmacological intervention.

B12 Metabolism

TCN1, TCN2 & MMACHC

Transcobalamin 1 and 2 govern B12 transport and cellular uptake. MMACHC is involved in intracellular B12 processing. Variants explain why patients with normal serum B12 continue to have neurological symptoms and methylation impairment.

Antioxidant & Detox

NOS, SOD2 & GPX1

Nitric oxide synthase variants (NOS1/2/3), SOD2 (mitochondrial antioxidant) and GPX1 (glutathione peroxidase). Govern oxidative stress resilience — clinically relevant in cardiovascular risk, mitochondrial dysfunction and chronic inflammatory conditions.

You've done 23andMe

Here's what it didn't show you.

Consumer genetic services check 2–5 genes and provide raw data without clinical interpretation. MethylDetox provides clinical analysis — 38 genes, complete SNP coverage, and results reviewed in the context of your actual health status.

23andMeStandard MTHFR TestMethylDetox
Genes covered2–3 methylation SNPsMTHFR C677T, A1298C only38 genes, all pathways
MTR C3518TNot includedNot included✓ Full coverage
COMT V158MSometimesNot included✓ Complete
Neurotransmitter genesNot includedNot included✓ MAOA, MAOB, TPH1, TPH2
Regulatory regionsNot includedPartial✓ Full regulatory coverage
Clinical interpretationNone (raw data)Minimal✓ Full consultation
CMA/NutrEval integrationNot possibleNot possible✓ Integrated protocol
Questions

MethylDetox explained

MethylDetox is MediBalans' proprietary 38-gene methylation analysis — the most comprehensive methylation panel available in Sweden. Standard methylation tests typically analyse 5–10 genes, covering only MTHFR C677T and A1298C. MethylDetox covers the entire methylation cycle including the folate pathway, methionine cycle, B12 metabolism, transulfuration pathway, COMT detoxification, and neurotransmitter synthesis. The result is a complete SNP profile that cannot be obtained from consumer genetic services like 23andMe.

MTR C3518T is a polymorphism in the methionine synthase gene — the enzyme responsible for regenerating methionine from homocysteine using B12 as cofactor. The variant can reduce enzyme activity, impairing B12 utilisation even when serum B12 is normal. Clinical consequences include elevated homocysteine despite supplementation, neuro-psychiatric symptoms, and impaired methylation capacity. MethylDetox analyses MTR C3518T with complete coverage of the entire regulatory region including the 3' UTR, which many standard tests omit.

Yes. MTHFR polymorphisms are among the most common genetic variants in the population — up to 40–60% carry at least one. The heterozygous C677T variant reduces MTHFR enzyme activity by approximately 35%; the homozygous form reduces it by 70%. Most people are unaware because symptoms — fatigue, mood fluctuations, recurrent infections, poor recovery — are non-specific and attributed to other causes. Standard medical screening does not test MTHFR. MethylDetox identifies all MTHFR variants with full SNP coverage.

CMA measures intracellular nutrient stores. NutrEval measures metabolic pathway function. MethylDetox identifies genetic variants that determine how efficiently you convert and utilise nutrients — regardless of how much you take. A patient homozygous for MTHFR C677T cannot convert folic acid to active 5-MTHF even with high folic acid intake. Without knowing the genetic variant, the supplementation approach is structurally incorrect. MethylDetox provides the genetic layer that CMA and NutrEval cannot.

MethylDetox covers: methylation capacity (MTHFR C677T, A1298C, MTHFR regulatory region), methionine cycle (MTR, MTRR, MAT, BHMT, AHCY), folate pathway (FOLH1, DHFR, TYMS, SHMT), B12 metabolism (TCN1, TCN2, MMACHC), COMT and transulfuration (COMT V158M, CBS, CTH, CDO1), neurotransmitter synthesis (MAOA, MAOB, HNMT, DDC, TPH1, TPH2), and detoxification (NOS1, NOS2, NOS3, SOD2, GPX1, CAT). This multi-pathway approach is what distinguishes MethylDetox from single-gene or limited-panel tests.

MethylDetox informs the interpretation of every other diagnostic result. B-vitamin levels on CMA must be understood in the context of methylation genetics — a patient with low-activity MTHFR may show normal folate on CMA but be functionally folate-deficient at the enzymatic level. Homocysteine on NutrEval only makes sense when you know whether the elevation is driven by B6 deficiency (CBS pathway), B12/folate deficiency (methionine cycle), or a genetic variant in MTR or MTRR. MethylDetox makes every other test interpretable at its deepest level.

Next Step

Understand your methylation at genetic level.

MethylDetox results are reviewed by Dr Mario Anthis and interpreted alongside your CMA and metabolomic findings for a complete biochemical portrait.

Book Consultation Also: CMA Nutrient Analysis →
Related Diagnostics

Often combined with MethylDetox

Intracellular · Cell Science Systems

CMA — Cellular Micronutrient Analysis

55 intracellular nutrients. B-vitamin status on CMA is only interpretable in the context of methylation genetics — MethylDetox explains why.
Metabolomics · Genova

NutrEval® Metabolomics

Homocysteine and organic acid markers on NutrEval gain full clinical meaning when interpreted alongside MethylDetox SNP data.
Immune Reactivity · Cell Science Systems

ALCAT Food Intolerance

Food reactivity drives systemic inflammation that compounds methylation pathway burden. ALCAT + MethylDetox addresses both the trigger and the biochemical bottleneck.
Scientific References

Published evidence behind methylation genetics

The biology of MTHFR polymorphisms and the methylation cycle is among the most robustly established in nutritional biochemistry, with thousands of published studies and documented clinical significance across neurology, oncology and cardiovascular medicine.

[1]
Tsang BL et al. Meta-analysis confirming MTHFR 677C→T polymorphism is associated with folate and homocysteine concentrations. Homozygous TT genotype reduces enzyme activity by approximately 60–70%, establishing the biological mechanism for impaired methylation. Am J Clin Nutr. 2015;101(6):1286–1294 ↗
[2]
Crider KS et al. Comprehensive review of molecular mechanisms linking folate to DNA methylation. Established that folate status directly impacts epigenetic regulation, neurotransmitter synthesis and homocysteine metabolism. Adv Nutr. 2012;3(1):21–38. — Also: Am J Clin Nutr. 2011;93(6):1365–1372.
[3]
Regland B et al. ME/CFS and fibromyalgia patients responded to vitamin B12 and folic acid supplementation, with improvements correlating to methylation support. Supports clinical relevance of methylation assessment in fatigue conditions. PLoS One. 2015;10(4):e0124648 ↗
[4]
Hickey SE et al. (ACMG Practice Guideline). American College of Medical Genetics guideline stating standalone MTHFR testing has limited utility for thrombophilia evaluation — a position that does not address multi-gene functional methylation assessment or precision supplementation. Genet Med. 2013;15(2):153–156 ↗
[5]
Bottiglieri T. Comprehensive review of folate, B12 and methionine cycle in neuropsychiatric disease — establishing the biochemical basis for methylation defects in depression, cognitive decline and neurological conditions. Drugs. 2013;73(15):1590–1596.
[6]
Lerner V et al. High-dose folic acid + B12 supplementation in schizophrenia patients with MTHFR polymorphisms produced significant improvement in negative symptoms vs non-carriers — demonstrating genotype-guided dosing clinical utility. JAMA Psychiatry. 2012;69(12):1255–1262.
Evidence context: MediBalans does not use MTHFR data in isolation. MethylDetox analyses 38 genes, and results are always interpreted alongside functional biomarkers — homocysteine, B12, folate, SAMe. The multi-gene panel approach identifies the specific pathway bottleneck driving dysfunction, enabling precision intervention rather than empirical supplementation.
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