📊 Risk Dashboard
Overall summary of genetic risk markers found across all 9 analyzed pathways.
34
Total SNPs Analyzed
23
Normal / Optimal
68% of analyzed SNPs
8
Heterozygous / Risk
24% of analyzed SNPs
1
Mixed (COMT)
3% — dual implications
2
Missing / Not Found
+ 21 not on 23andMe chip
SNP Distribution by Status
Normal (68%)
Risk (24%)
Mixed (3%)
Missing (5%)
⛽ Section 1: Oxidative Stress & Antioxidant Defense
6 SNPs tested across SOD2, GPX1, GSTP1, NQO1, NFE2L2, HMOX1
Oxidative stress is a primary proposed mechanism in EMF/EHS pathology. These genes encode key antioxidant enzymes that neutralize reactive oxygen species (ROS).
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs4880 | SOD2 | Ala16Val | AG | ⚠️ Heterozygous — one G (Val) risk allele. SOD2 is the primary mitochondrial antioxidant enzyme; this variant reduces SOD2 activity by ~40%, potentially increasing susceptibility to oxidative damage from EMF exposure. |
| rs1050450 | GPX1 | Pro198Leu | AG | ⚠️ Heterozygous — one G (Leu) risk allele. GPX1 (glutathione peroxidase 1) is a major cellular antioxidant; the Leu variant is associated with reduced enzyme activity. Combined with SOD2 AG, this suggests a double-hit on antioxidant defenses. |
| rs1695 | GSTP1 | Ile105Val | AA | ✅ Normal — the common/Ile-Ile genotype. GSTP1 is a phase II detoxification enzyme that conjugates glutathione to toxic electrophiles. AA = wild-type with full activity. |
| rs1800566 | NQO1 | Pro187Ser | GG | ✅ Normal — the common/non-risk genotype. NQO1 protects cells from oxidative stress by reducing quinones and stabilizing p53 and Nrf2. GG = optimal enzyme stability and activity. |
| rs3856440 | NFE2L2 (Nrf2) | — | AG | ⚠️ Heterozygous — one G risk allele. NFE2L2 encodes Nrf2, the master transcription factor regulating antioxidant response element (ARE) genes. This variant may influence baseline antioxidant gene expression levels. |
| rs2071746 | HMOX1 | — | TT | ✅ Normal — the common/non-risk genotype. HMOX1 encodes heme oxygenase-1, a stress-induced cytoprotective enzyme with antioxidant and anti-inflammatory properties. |
🧪 Section 2: Methylation & Catecholamine Metabolism
3 SNPs tested across MTHFR and COMT
Methylation pathways influence detoxification capacity and neurotransmitter regulation. COMT is particularly relevant as it breaks down stress hormones (adrenaline/noradrenaline) which may be elevated in EHS.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs1801133 | MTHFR | C677T | GG | ✅ Normal — the common/non-risk genotype. MTHFR C677T is the most studied methylation variant; GG means optimal enzyme function for folate metabolism and homocysteine regulation. |
| rs1801131 | MTHFR | A1298C | TT | ✅ Normal — the common/non-risk genotype. MTHFR A1298C is the second most studied variant; TT = normal enzyme activity. |
| rs4633 | COMT | Val108/158Met | CC | ℹ️ Met/Met — homozygous Met, lower COMT enzyme activity, higher prefrontal dopamine. In the context of EHS, lower COMT means slower breakdown of catecholamines (adrenaline, noradrenaline, dopamine), potentially amplifying stress hormone responses to EMF exposure. However, more SAMe is available for other methylation reactions. |
⚡ Section 3: Calcium Channels & Ion Excitability
2 SNPs tested in CACNA1C
Calcium channel dysfunction is one of the most studied mechanisms in EMF/EHS. EMF exposure has been proposed to affect voltage-gated calcium channels, leading to calcium overload and cellular dysfunction.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs1006737 | CACNA1C | — | AA | ✅ Normal — the common/non-risk genotype. CACNA1C encodes the alpha-1C subunit of L-type voltage-gated calcium channels, the primary channel type proposed to be affected by EMF exposure (pulsed electromagnetic field resonance hypothesis). AA = favorable. |
| rs1042713 | CACNA1C | intragenic | AG | ⚠️ Heterozygous — one G risk allele present. This SNP is in the CACNA1C gene region and may influence calcium channel expression or function. The heterozygous state suggests a moderate effect on calcium channel signaling. |
🔫 Section 4: Nitric Oxide & Vascular Response
4 SNPs tested across NOS3 and NOS1
Nitric oxide (NO) dysregulation is implicated in EMF sensitivity. NOS variants affect endothelial function, vasodilation, and neurovascular coupling.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs1800779 | NOS3 | Intron 4 | AG | ⚠️ Heterozygous — one G risk allele. NOS3 (eNOS) produces nitric oxide for vascular regulation. This intron variant may affect NOS3 mRNA splicing or expression levels. |
| rs2070744 | NOS3 | Promoter | CT | ⚠️ Heterozygous — one T risk allele. This promoter variant may influence NOS3 transcription levels, potentially affecting baseline nitric oxide production. |
| rs1041983 | NOS3 | — | CC | ✅ Normal — the common/non-risk genotype for this NOS3 variant. |
| rs11549467 | NOS1 (nNOS) | — | GG | ✅ Normal — the common/non-risk genotype. NOS1 encodes neuronal nitric oxide synthase, important for neuronal signaling. |
🧠 Section 5: Neurotransmitter & Stress Response
7 SNPs tested across BDNF, DRD4, OPRM1, SLC6A4, MAOA, GNGT2
EHS symptoms often involve neurological and psychiatric manifestations. These genes regulate neurotransmitter production, transport, and receptor sensitivity.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs6265 | BDNF | Val66Met | CC | ✅ Normal — the common/non-risk genotype. BDNF (brain-derived neurotrophic factor) supports neuron survival and plasticity. CC = normal BDNF secretion and activity. |
| rs1800955 | DRD4 | 48-bp VNTR | CC | ✅ Normal — the common/non-risk genotype. DRD4 is the dopamine D4 receptor; CC = normal receptor function. |
| rs1799971 | OPRM1 | A118G | AG | ⚠️ Heterozygous — one G risk allele. OPRM1 (mu-opioid receptor) variant affects endogenous opioid signaling and pain perception. The G allele is associated with altered receptor binding affinity, potentially influencing pain sensitivity and stress response. |
| rs25532 | SLC6A4 | 5-HTTLPR | GG | ✅ Normal — the common/non-risk genotype. SLC6A4 encodes the serotonin transporter; GG = normal serotonin reuptake. |
| rs25531 | SLC6A4 | 5-HTTLPR | -- | ❌ Missing call — genotype could not be determined. This key serotonin transporter variant is one of the most studied in stress and mood research. |
| rs909562 | MAOA | uVNTR | AA | ✅ Normal — the common/non-risk genotype. MAOA (monoamine oxidase A) breaks down serotonin, dopamine, and norepinephrine. |
| rs10489385 | GNGT2 | — | CC | ✅ Normal — the common/non-risk genotype. GNGT2 encodes a G-protein subunit involved in signaling cascades. |
🔥 Section 6: Inflammation & Immune Response
5 SNPs tested across IL1B, TNF, IL1RN
Chronic low-grade inflammation is a hallmark of EHS. These genes regulate pro-inflammatory cytokine production.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs16944 | IL1B | -511 C/T | GG | ✅ Normal — the common/non-risk genotype. IL1B encodes interleukin-1 beta, a key pro-inflammatory cytokine. GG = normal expression levels. |
| rs1143627 | IL1B | +3953 T/C | AA | ✅ Normal — the common/non-risk genotype. Another IL1B variant regulating expression. |
| rs1800629 | TNF | -308 G/A | GG | ✅ Normal — the common/non-risk genotype. TNF-alpha is a major pro-inflammatory cytokine. GG = lower promoter activity. |
| rs2227956 | TNF | — | AA | ✅ Normal — the common/non-risk genotype for this TNF variant. |
| rs3789069 | IL1RN | VNTR | CT | ⚠️ Heterozygous — one T risk allele. IL1RN encodes the IL-1 receptor antagonist, which blocks IL-1 signaling. This variant may alter the ratio of IL-1 to IL-1Ra, potentially increasing net inflammatory signaling. |
🔗 Section 7: DNA Repair Capacity
4 SNPs tested across XRCC1, XRCC3, XPD/ERCC2
EMF exposure has been proposed to cause DNA damage through oxidative mechanisms. Efficient DNA repair is critical for maintaining genomic stability.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs25487 | XRCC1 | Arg194Trp | CC | ✅ Normal — the common/non-risk genotype. XRCC1 is a scaffold protein in DNA base excision repair. CC = optimal repair capacity. |
| rs861539 | XRCC3 | Thr241Met | GG | ✅ Normal — the common/non-risk genotype. XRCC3 is involved in DNA double-strand break repair via homologous recombination. |
| rs2383206 | XPD/ERCC2 | Lys751Gln | GG | ✅ Normal — the common/non-risk genotype. XPD is a DNA helicase in nucleotide excision repair. |
| rs2304274 | XPD | — | GG | ✅ Normal — the common/non-risk genotype for this XPD variant. |
🎮 Section 8: Detoxification & Metal Metabolism
2 SNPs tested in HFE
Impaired metal homeostasis and detoxification capacity may increase EMF susceptibility. Iron overload can amplify oxidative stress.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs1800562 | HFE | C282Y | GG | ✅ Normal — the common/non-risk genotype. HFE C282Y is the primary hemochromatosis mutation; GG = no increased iron absorption risk. |
| rs1800567 | HFE | H63D | CC | ✅ Normal — the common/non-risk genotype. HFE H63D is a secondary hemochromatosis variant; CC = normal. |
🏆 Section 9: Lipid Transport & Neuroinflammation
2 SNPs tested in APOE
APOE genotype influences neuroinflammation, lipid transport across the blood-brain barrier, and Alzheimer's risk.
| SNP | Gene | Variant | Genotype | Status |
|---|---|---|---|---|
| rs429358 | APOE | υ4 | TT | ✅ Normal — combined with rs7412 CC, this indicates APOE υ3/υ3 genotype (the most common, non-risk variant). No increased Alzheimer's or neuroinflammation risk from APOE. |
| rs7412 | APOE | υ2 | CC | ✅ Normal — confirms APOE υ3/υ3 genotype when combined with rs429358 TT. |
❌ Genes Not Found on 23andMe Chip
The following well-studied EMF-relevant markers were not included on the 23andMe genotyping array. Full assessment would require whole genome sequencing or a targeted gene panel.
❌ Oxidative Stress Genes Not Found
These well-studied oxidative stress markers were not included on the 23andMe genotyping chip used.
- rs1001179 CAT Catalase promoter variant (-262C/T) — critical peroxide-detoxifying enzyme in peroxisomes
- rs1050449 GPX1 Additional GPX1 variant
- rs1050448 GPX1 Additional GPX1 variant
- rs1565456 GSTM1 Tag SNP for GSTM1 null status — GSTM1 deletion is present in ~50% of population
- rs9282861 GSTT1 Tag SNP for GSTT1 null status — GSTT1 deletion affects ~20% of population
❌ Calcium Channel & Ion Excitability Genes Not Found
These well-studied ion channel markers were not included on the 23andMe genotyping chip used.
- rs1801759 FXYD2 Na+/K+ ATPase regulatory subunit — critical for cellular ion homeostasis
- rs1355382 ATP2A2 Plasma membrane calcium pump (PMCA) — regulates intracellular calcium
- rs17822555 KCNK3 Potassium channel (two-pore domain) — affects neuronal excitability
- rs11912629 GRIN2B NMDA receptor subunit — calcium-permeable glutamate receptor
- rs1351652 GRIA3 AMPA receptor subunit — ionotropic glutamate receptor
- rs7569578 SCN8A Voltage-gated sodium channel NaV1.6 — neuronal excitability
- rs732915 SCN9A Voltage-gated sodium channel NaV1.7 — pain signaling and nerve excitability
- rs2071012 ATP1A2 Na+/K+ ATPase alpha-2 subunit — ion homeostasis
- rs1782935 GRIK4 Glutamate receptor (AMPA) — associated with bipolar disorder
- rs9342723 FOSL1 Immediate early gene — calcium/calmodulin signaling
- rs1056324 CHRNA3/A5 Nicotinic acetylcholine receptor — cellular signaling
❌ Nitric Oxide Genes Not Found
These well-studied NOS markers were not included on the 23andMe genotyping chip used.
- rs1799983 NOS3 Glu298Asp — the most studied NOS3 variant affecting enzyme activity
- rs2071014 NOS3 Additional NOS3 variant
❌ DNA Repair Genes Not Found
These well-studied DNA repair markers were not included on the 23andMe genotyping chip used.
- rs25489 XRCC1 Arg399Gln — another well-studied XRCC1 variant
- rs1047846 XPD Lys31Asn — nucleotide excision repair helicase variant
❌ Detoxification Genes Not Found
These well-studied detoxification markers were not included on the 23andMe genotyping chip used.
- rs1565456 GSTM1 Tag SNP for GSTM1 null — ~50% of population carries GSTM1 deletion
- rs9282861 GSTT1 Tag SNP for GSTT1 null — ~20% of population carries GSTT1 deletion
❌ Additional EMF-Relevant Genes Not Found
These additional markers were not included on the 23andMe genotyping chip used.
- rs2234670 TRPV1 Transient receptor potential vanilloid — sensory receptor involved in pain and thermal perception
- rs2070640 HSP90AA1 HSP90 alpha catalytic subunit — heat shock protein involved in cellular stress response
📊 Summary Analysis
Overall EMF/EHS Genetic Risk Assessment
| Category | Risk Level | Risk Variants | Normal Variants | Key Findings |
|---|---|---|---|---|
| Oxidative Stress | ⚠️ Moderate | 3 (SOD2 AG, GPX1 AG, NFE2L2 AG) | 3 (GSTP1, NQO1, HMOX1) | Multiple heterozygous antioxidant variants suggest reduced oxidative stress defense capacity |
| Methylation | ℹ️ Mixed | 0 risk | 2 normal (MTHFR) | MTHFR optimal; COMT Met/Met has dual implications for stress response |
| Calcium Channels | ⚠️ Moderate | 1 (CACNA1C AG) | 1 (CACNA1C AA) | One heterozygous variant in the key EMF-target gene CACNA1C |
| Nitric Oxide | ⚠️ Moderate | 2 (NOS3 AG, NOS3 CT) | 2 (NOS3 CC, NOS1 GG) | Two heterozygous NOS3 variants may affect NO signaling |
| Neurotransmitter | ⚠️ Low-Moderate | 1 (OPRM1 AG) | 5 normal | One risk variant in opioid signaling; BDNF, DRD4, MAOA all normal |
| Inflammation | ⚠️ Low-Moderate | 1 (IL1RN CT) | 4 normal | Most inflammatory markers normal; one IL1RN variant may alter IL-1 balance |
| DNA Repair | ✅ Low | 0 | 4 | All tested DNA repair variants are normal — favorable for genomic stability |
| Detoxification | ✅ Low | 0 | 2 | HFE variants normal — no hemochromatosis risk |
| Lipid Transport | ✅ Low | 0 | 2 | APOE υ3/υ3 — optimal for neuroinflammation and lipid transport |
Overall Risk Score
| Metric | Count |
|---|---|
| Total SNPs Analyzed | 34 |
| ✅ Normal/Optimal | 23 (68%) |
| ⚠️ Heterozygous/Risk | 8 (24%) |
| ℹ️ Mixed (COMT) | 1 (3%) |
| ❌ Missing/Not Found | 2 on chip (rs25531 missing call) + 21 not on chip |
Key Takeaways
1
Oxidative stress defense is the primary concern — Three heterozygous variants (SOD2 AG, GPX1 AG, NFE2L2 AG) suggest a reduced capacity to neutralize reactive oxygen species. SOD2 and GPX1 work in tandem in the mitochondrial antioxidant defense system, and having risk variants in both represents a compounding vulnerability. If EMF exposure does increase oxidative stress, your genetic profile suggests you may be less equipped to handle it efficiently.
2
COMT Met/Met (CC) amplifies stress sensitivity — While not a "risk" variant per se, the homozygous Met genotype means significantly lower COMT enzyme activity (~20-25% of normal). This results in slower breakdown of catecholamines (adrenaline, noradrenaline, dopamine), which could amplify the physiological stress response to any environmental trigger, including EMF exposure. The upside: more SAMe is available for other methylation reactions.
3
CACNA1C heterozygous variant — One of the two CACNA1C variants tested (rs1042713) is heterozygous. CACNA1C encodes the L-type voltage-gated calcium channel, which is the primary molecular target proposed in the pulsed electromagnetic field resonance (PEFR) hypothesis of EMF effects. While the primary tested variant (rs1006737) is normal, the secondary variant (rs1042713 AG) may still influence channel function or expression.
4
Nitric oxide signaling may be altered — Two heterozygous NOS3 variants (rs1800779 AG + rs2070744 CT) suggest potential alterations in endothelial nitric oxide production. Nitric oxide plays roles in neurovascular coupling, immune function, and cellular signaling — all systems potentially affected by EMF exposure.
5
DNA repair capacity appears robust — All four tested DNA repair variants (XRCC1, XRCC3, XPD × 2) are the common/non-risk genotypes. This is a significant positive finding, as efficient DNA repair is critical if EMF exposure causes oxidative DNA damage.
6
Inflammatory profile is largely favorable — IL1B and TNF variants are all normal, which is reassuring. The single heterozygous IL1RN (rs3789069 CT) variant may slightly alter the IL-1/IL-1Ra balance, but this is a mild concern.
7
OPRM1 variant may influence pain perception — The heterozygous OPRM1 A118G variant (rs1799971 AG) affects mu-opioid receptor binding affinity, potentially influencing pain sensitivity and endogenous opioid signaling. This could be relevant for EHS-related pain symptoms.
8
Significant genetic gaps — 21 important EMF-relevant SNPs were not on the 23andMe chip, including key calcium channel genes (ATP2A2, SCN9A, KCNK3), the primary NOS3 variant (rs1799983 Glu298Asp), and GST null status markers. Full assessment would require additional testing or a whole genome sequencing panel.
9
No single "EMF gene" — There is no single SNP that determines EMF sensitivity. The current scientific understanding suggests that EMF/EHS susceptibility arises from a combination of genetic factors (particularly in oxidative stress, calcium signaling, and stress response pathways), environmental exposures, and psychological/physiological factors.
10
Genetics is only part of the picture — This analysis identifies genetic predispositions, NOT diagnoses. Environmental factors (diet, lifestyle, EMF exposure levels, sleep quality), epigenetic modifications, and psychosocial factors are equally or more important in determining actual EHS symptoms and severity.
Medical Disclaimer
This analysis is for educational and informational purposes only. It is not a medical diagnosis, nor should it be used to guide medical treatment. Genetic predisposition ≠ destiny. Many people carry risk alleles without ever developing the associated conditions. The relationship between genetic variants and EMF/electromagnetic hypersensitivity is an active area of research with no established clinical consensus. If you have concerns about EMF sensitivity or any aspect of your health, please consult qualified healthcare professionals for proper assessment and personalized guidance.