SPECT
Blood flow and activity. What is working, working too hard, or running low.
PRESENTATION MODE — PRESS P TO EXIT
Kevin Meuret · IntellxxDNA · Sept 2026
My source code, and what it says about my brain.
SPECT showed blood flow. QEEG showed rhythm. This is the third view — the genomic panel I was issued, read through IntellxxDNA, and translated the same way as the scans: technical finding first, then how it shows up. None of what follows is a prescription for you. It is mine.
WHY GENOMICS
SPECT showed blood flow. QEEG showed rhythm. This shows the hardware I was issued.
The knocks came later. The two machines looked at what my brain is doing now. This panel is older than both of those stories — it is the starting kit. I wanted it in the same walk-through, in the same voice, sitting between the question and the two doctors.
150
SNPs across 31 panels
~20
Findings with real consequence
Sept 4
Report date · 2026
QEEG
Electrical rhythm. What the cortex is doing, band by band, against an age-matched map.
Genomics
The letters I inherited. Not a diagnosis — a set of small changes that can stack with how I live.
READING THE PANELS
First — how to read one of these rows.
Every card below is the same three-beat translation the rest of this site uses: the gene and the letters I carry, the mechanism in the report’s language, then how that can show up. A few words get used a lot. Here they are once, in plain English.
This is not a diagnosis.
IntellxxDNA describes itself as a clinical decision-support tool for licensed providers — one input next to a full history, an exam, and labs — not something meant to diagnose or treat illness on its own. Nothing on this page is a diagnosis. These are small DNA changes that by themselves are not disease-causing. They can matter as they interact with each other and with diet, lifestyle, and environment. The report belongs to me. Take whatever is useful.
A single-letter change in the DNA sequence.
The less common version of the sequence. It can convey benefit or risk — it is not automatically bad.
The two letters actually carried, one allele inherited from each parent.
0, 1, or 2 minor alleles. Two copies generally means a stronger effect.
How common this exact genotype is in the population.
The report’s own Low / Medium / High rating for likelihood and strength of contribution.
1.0 means no difference from baseline. 2.79 means roughly 2.79× the reference risk. Printed for some SNPs only.
Both copies are the same.
Using genotype to predict how someone will respond to a specific drug.
THEME 1 · AMYLOID CLEARANCE
Four independent genes, all pointing the same direction.
Amyloid clearance is hit from four separate directions on my panel, which is why the response stacks more than one lever instead of picking a favorite. A SNP here is a letter change. The genotype is the pair I actually carry.
Mechanism
Decreased levels of the protein that processes amyloid-beta, so more can accumulate.
How it shows up
The clearance side of the story starts thin. That is why this page does not treat amyloid as a single-gene problem.
Mechanism
Reduced ability to break down amyloid-beta peptide in the brain.
How it shows up
The enzyme that should chew the peptide is slower. Coffee and intermittent fasting show up later on this page because of this row — and they collide with the caffeine story.
Mechanism
Mitochondrial outer-membrane pores more prone to clogging with amyloid; long-run mitochondrial damage.
How it shows up
The power plants of the cell get a dirtier doorway. This is the third independent angle, not a repeat of ABCA7.
Mechanism
The K-variant promotes fibril formation and plaque buildup.
How it shows up
The fourth direction: not just clearance, but a tilt toward forming the plaque itself. This gene also returns in the anesthesia ledger.
APOC1 only matters if APOE e4 is also in the picture.
APOC1 came back RI, high impact, odds ratio 2.79. The report is explicit: there is no risk identified for people who have this variant but do not have an APOE e4 variant. APOC1 acts as the “on switch” for APOE e4 and is found in about 70% of APOE e4 individuals. I am not going to let that 2.79 stand unqualified.
LGALS3 — the loudest single line in the report.
Two separate SNPs, both high impact, both homozygous. The clinician summary escalates to a printed all-caps callout: two copies of this SNP makes me a predicted non-responder to TB006 anti-galectin-3 antibody treatment based on initial research, and other modalities should be considered. That belongs here and again on the drug ledger.
BDNF GG — fertilizer for the neurons
BDNF came back GG, two copies, high impact. The report calls BDNF essentially fertilizer for the neurons. Lower BDNF means more difficulty stimulating brain growth. The panel ties BDNF variants to Alzheimer’s, autism, cognitive decline, and depression, and notes that BDNF levels drop in depression and normalize with remission.
Named levers, straight from the report: moderate-to-intense aerobic exercise, butyrate, curcumin, and prebiotic high-fiber foods to feed butyrate-producing gut bacteria. This is the most actionable optimistic finding on the page. It balances an otherwise heavy section.
Mechanism
Impaired endogenous phosphatidylcholine synthesis; men and post-menopausal women flagged higher risk.
How it shows up
Choline production from inside the body is weaker. Diet has to carry more of that load.
Mechanism
Brain ischemia panel; factor 5 interaction note printed.
How it shows up
This is the row that later drives lumbrokinase on my supplement table. Prevalence printed at 10.4%.
THEME 2 · THE CATECHOLAMINE HUB
The same gene showed up in four different panels.
COMT V158M is the single most cross-cutting finding in the brain dataset. AA, two copies, high impact. It sits under anxiety, rumination, attention, and stimulant response at the same time.
Mechanism
Slow clearance of catecholamines — dopamine, norepinephrine, epinephrine — from the synapse.
How it shows up
Stress chemistry lingers longer than it should. Caffeine hits harder and stays. The printed list also includes an SSRI non-responder flag, heightened opiate and post-surgical pain sensitivity, an estrogen interaction, explicit caution against quercetin with two copies, decreased stimulant response in males, and lower response to both methylphenidate and bupropion.
SLC1A1 carries an explicit gene-gene interaction note with COMT V158M — which I carry as AA.
THEME 3 · ANXIETY & RUMINATION
The anxiety hardware, and the serotonin story on top of it.
COMT is the hub. These rows are the rest of the anxiety and rumination stack — adrenergic, adenosine, and serotonin receptors the report treats as hardware, not personality.
Mechanism
Over double the anxiety risk on the printed panel.
How it shows up
This one gene drives four action-plan entries at once: magnesium threonate, vitamin B6 (P5P), a low-carb diet, and meditation.
Mechanism
Allele T homozygous, linked to 3× multiple-chemical-sensitivity risk via rs2298383; caffeine- and amphetamine-triggered anxiety. Allele C homozygous adds a seizure-risk note, again caffeine-worsened.
How it shows up
This is one of the three independent caffeine flags. The other two sit on COMT.
Mechanism
Roughly 3× depression risk. Appears in both the Depression and Anxiety panels.
How it shows up
Serotonin receptor one. It is not the whole mood story — HTR2A, HTR3C, and HTR1B stack on top.
Mechanism
HTR2A allele T TT and allele A AA both high in the obsession / rumination / compulsions panel. HTR3C AA carries a male-specific OCD risk note.
How it shows up
The rumination hardware is not one SNP. It is a pile.
The caffeine paradox
Caffeine is called out three times independently as a problem: twice under ADORA2A (caffeine-worsened anxiety) and once under COMT (caffeine intolerance). Meanwhile coffee is simultaneously recommended under MME for amyloid-beta suppression. That tension is in the source. I am leaving it unresolved. Show the data, including where it disagrees with itself.
HTR1B prints advice to avoid SSRIs and 5-HTP — less likely to respond, and they may worsen symptoms. DRD2 C71572T came back GG, two copies, high impact: that is the SNP behind the velvet-bean recommendation later.
THEME 4 · REWARD, OPIOIDS, ADDICTION
Two percent of people have this one.
OPRMI is the highest-stakes practical finding on the page. It is rare, it is homozygous, and the printed multiples are not small.
OPRMI GG — opioid non-responder, elevated severe-outcome risk.
Two copies, high impact, 2.9% prevalence. Appears in both the Addiction and the Opioid & Pain Response panels. Predicted opioid non-responder for pain relief, with printed severe-outcome multiples of 12.9×, >5×, and ~4×, plus increased opioid-addiction risk, a psychosis association, and a specific instruction to avoid methamphetamine-containing stimulants. The gene regulates pain and the pleasure response to opioids. Carriers are prone to lower pain reduction with opioids.
Mechanism
1.74× opioid dependence risk.
How it shows up
A second opioid-side flag sitting next to OPRMI, not instead of it.
Mechanism
Over 9× cannabis dependence risk.
How it shows up
This sits in the endocannabinoid cluster with CNR1, CNR2, CYP2C9, and FAAH.
Endocannabinoid cluster
CNR2 GG two copies, high. CYP2C9 CT — slow THC metabolizer; dose reduction advised. FAAH AG — significantly increased THC/CBD-induced anxiety and psychosis risk; start at a lower CBD dose. CNR1 also carries a weight-gain-on-atypical-antidepressants note.
Other printed stimulant-response flags: CYP2B6 AG reduced bupropion smoking-cessation success; NTF3 AA methylphenidate-alternative caution; SLC6A2 GA decreased stimulant response; DBH T15791C less likely to respond to atomoxetine; DRD3 and DRD4 C8887A poorer stimulant response.
THEME 5 · WHAT LABS MISS
Normal bloodwork, wrong brain.
Nutrient status can look normal on labs and still be wrong in the brain. TCN2 is the clean example. The same logic runs through BHMT, CUBN, CBS, MUC1, FGFR2, and CYP2R1.
Mechanism
3.33× peripheral neuropathy risk, rising to 6.9× if folate exceeds 800 mg/day. Brain B12 can be low even when blood B12 reads normal.
How it shows up
A normal lab is not the same as a fed brain. This is why high-B12 foods land on the protocol table.
Mechanism
Explicit non-responder flag: two-copy carriers generally do not get significant homocysteine reduction with folate.
How it shows up
Folate is not the automatic homocysteine answer for this genotype. That is a ledger row, not a slogan.
Mechanism
16% prevalence. Drives magnesium threonate plus high-magnesium foods.
How it shows up
FGFR2 is the companion “rare SNP” at 14.6% prevalence. Both sit in the mineral story, not the amyloid story.
CYP2R1 is filed under benefit and then contradicted.
CYP2R1 AG sits in the Vitamin D Benefit panel, but the report prints that one variant is actually a risk for vitamin D deficiency. A variant filed under “benefit” that the report itself argues with is exactly the texture this page should surface.
CUBN prints 1.61× risk of severe B12 deficiency and 1.39× below-adequate B12, with dietary intake flagged as possibly insufficient. CBS CC prints 1.22× below-adequate B12.
THEME 6 · CLEARANCE & INFLAMMATION
The genes that take out the garbage.
Glutathione and inflammation rows. This is where “avoid glyphosate” and “avoid smoke” come from — not from a wellness slogan.
Mechanism
4.8× and 1.84× cognitive-impairment and glyphosate figures, plus lead-exposure cognitive effects.
How it shows up
This drives “avoid glyphosates” and “avoid smoke” on the protocol table.
Mechanism
Complete gene deletion. Alzheimer’s association. Additive interaction with the other glutathione genes.
How it shows up
The trash crew is short-handed, and the shortage stacks.
GCLC prints increased size of stroke damage and psychosis notes. GPX1: lower long-term visual memory, brain glioma note. ABCC1: mercury toxicity in the brain; mold-related cognitive issues. CARD8: brain inflammation; interferon non-response pharmacogenomic warning. GCKR TT 18.1% and LEPR CC sit on the CRP panel. CRP, CCL2, and IL10 carry stroke / Alzheimer’s notes.
THE LEDGER
Most of the drug flags came back negative.
Pharmacogenomics is where this report is most actionable, and most of the flags came back negative. That is the honest headline. Flags differ by border and label, not by color.
| Drug or compound | Predicted response | Flag | Driving SNP |
|---|---|---|---|
| TB006 anti-galectin-3 antibody | Predicted non-responder | Non-responder | LGALS3 ×2, homozygous |
| SSRIs | Non-responder flag | Non-responder | COMT V158M (2) |
| SSRIs and 5-HTP | Avoid — less likely to respond, may worsen symptoms | Caution | HTR1B |
| Methylphenidate | Reduced response | Reduced | COMT V158M (2), NTF3 (2), SLC6A2, DRD3, DRD4 |
| Bupropion | Reduced response; reduced smoking-cessation success | Reduced | COMT V158M (2), CYP2B6 AG |
| Atomoxetine | Less likely to respond | Reduced | DBH T15791C |
| Opioids | Non-responder for analgesia; elevated addiction and severe-outcome risk | Non-responder | OPRMI GG (2), TH AA (2) |
| Folate (for homocysteine) | No significant homocysteine reduction | Non-responder | BHMT R239Q (2) |
| Donepezil, rivastigmine, huperzine | Possible non-response; long-term use may worsen memory | Caution | BCHE |
| Propofol | ~20% less needed; falls asleep ~40% faster | Reduced | HTR2A AA (2), 18.6% prevalence |
| Succinylcholine-family anesthesia | Difficulty waking | Caution | BCHE CT |
| Methamphetamine-containing stimulants | Avoid | Caution | OPRMI GG (2) |
| Quercetin | Caution with two copies of COMT | Caution | COMT V158M (2) |
| THC (CYP2C9-metabolized) | Slow metabolizer — reduce dose | Caution | CYP2C9 CT |
| CBD | Increased anxiety and psychosis risk — start low | Caution | FAAH AG |
| Interferon | Non-response warning | Non-responder | CARD8 |
| t-PA | Pharmacogenomic warning printed | Caution | A2M |
Notify the anesthesiologist.
HTR2A AA, two copies, high impact, 18.6% prevalence: approximately 20% less propofol needed, asleep roughly 40% faster. The action plan turns that into a standing instruction. BCHE adds difficulty waking from succinylcholine-family anesthesia, an additive interaction with APOE e4 that the report links to sudden worsening of cognition with deep anesthesia (more significant over age 65), and a note that two-copy carriers may not respond to acetylcholinesterase inhibitors prescribed for memory problems — donepezil, rivastigmine, and the supplement huperzine — which may with long-term use even make memory worse.
WHAT I CHANGED
Six supplements, three foods, three things to avoid.
None of the above is a prescription for you — it is mine. Dosages are what the report printed for these SNPs. Verify with your own clinician before copying any of it.
Supplements
| Intervention | Dosage | Timing | For | Driving SNP(s) |
|---|---|---|---|---|
| Lumbrokinase | 800,000–4.8M IU/day (1–6 capsules/day) | With meal | Cognition | PROC (2) |
| Magnesium threonate | 200–350 mg/day elemental magnesium | With meal | Anxiety | ADRB2 (2) |
| Omega-3s (EPA/DHA) | 1–4 g/day based on EPA content | With meal | Cognition, inflammation, detox | ABCA7 (2), GCLC (1), ABCA2 (1) |
| Sulforaphane | 30–60 mg based on glucoraphanin, 1–2×/day with food | With meal | Cognition, detox | GSTP1 (2), BCHE (1), OPRMI (2), GCLC (1), MME (2) |
| Velvet bean (Mucuna pruriens) | 50–150 mg L-Dopa/day, standardized extract | With meal | Anxiety | DRD2 C71572T (2) |
| Vitamin B6 (P5P) | 10–40 mg/day | With meal | Anxiety | ADRB2 (2) |
Report language on the velvet-bean study, attributed: “The results of this study indicate that hydroalcoholic extract of MPE have antidepressant action, which may be mediated by an interaction with the dopaminergic system.”
Diet
- Coffee — associated with amyloid-beta suppression. Cognition · MME (2). This is the other half of the caffeine paradox.
- Intermittent fasting — earlier dinner, later breakfast. Printed effects on amyloid precursor proteins, Aβ plaque, and cognitive decline. MME (2).
- Low-carbohydrate diet — avoid sugar; sugar triggers adrenaline. Anxiety · ADRB2 (2).
- High-magnesium foods — leafy greens, legumes, nuts, seeds, avocado, dark chocolate, whole grains, yogurt, fish. MUC1 (2).
- High-B12 foods — meats, poultry, fish. TCN2 (2).
Avoid / lifestyle
- High-sugar diet. Consider gluten-free if autoimmune, GI, autism, or PANDAS/PANS issues, to help lower zonulin. COMT V158M (2).
- Glyphosates — organic grains and flours; avoid smoke and charred foods and the “Dirty Dozen.” GSTP1 (2).
- Smoke — reduced detoxification activity, particularly for benzopyrene. GSTP1 (2).
- Quercetin — caution with two copies of COMT.
- Meditation — stressful thoughts stimulate adrenaline as if the event is happening. ADRB2 (2).
- Standing instruction: notify the anesthesiologist. HTR2A (2).
THE PLAIN-ENGLISH VERSION
What I actually took away from this.
These seven patterns are the page’s thesis. They are stronger than any individual SNP.
The repeating shape
- Two copies is the recurring theme. ABCA7, MME, PEMT, BDNF, TMEM106B, LGALS3 ×2, COMT V158M, ADRB2, ADORA2A ×2, DRD2, HTR2A ×3 across panels, HTR3C, OPRMI, TH, CNR1, CNR2, PENK, TCN2, MUC1, GSTP1, GSTM1, GCKR, and LEPR are all homozygous. This is not a scatter of single-copy carriers.
- Amyloid clearance is hit from four independent directions — ABCA7 (processing), MME (degradation), TOMM40 (mitochondrial pore clogging), BCHE-K (fibril formation) — which is why the response stacks fasting, coffee, omega-3s, sulforaphane, ashwagandha, curcumin, and choline rather than picking one.
Mind and meds
- The catecholamine and serotonin systems are the mental-health story. COMT V158M AA sits under anxiety, rumination, attention, and stimulant response at once, while HTR1A, HTR2A ×2, HTR3C, and HTR1B stack on the serotonin side. The practical read-through is a printed skepticism about SSRIs and 5-HTP for this genotype.
- Pharmacogenomics is where this report is most actionable, and most flags are negative. See the ledger.
- Caffeine is called out three times, and coffee is recommended once. The tension is real and stays unresolved.
What the report will not pretend
- Nutrient status can look normal on labs and still be wrong in the brain. TCN2 is the clean example; the same logic runs through BHMT, CUBN, CBS, MUC1/FGFR2, and CYP2R1.
- The report contains internal conflicts and does not hide them. Atomoxetine is recommended by SLC6A2 G47034T but contraindicated by DBH response. Stimulant-response direction conflicts between COMT/SLC6A2 and ADGRL3/DBH. 5-HTP is recommended by TPH2 and warned against by HTR1B. A genetics page that presents itself as certain is dishonest. This is the most important thing on the page.
One clean benefit — Clusterin (Apolipoprotein J)
Helps clear amyloid from inside the cell, affects inflammation and immune responses, and carriers have an associated decreased risk for Alzheimer’s, especially when combined with MS4A4E. I am putting the bright line on the page so the walk-through is not unrelievedly negative.
SOURCES
The underlying material.
The other two views of the same brain are the most valuable outbound links on this page.
IntellxxDNA
Clinical decision support · not a diagnosis
Mantality Health
Jessica Veasy · Union, MO
SPECT · Amen
The blood-flow view of the same brain
QEEG · Peak Brain
The rhythm view of the same brain
Report components: Hot Spot Summary, Cognition & Memory, Mental Wellness, Medical Overview, Clinician Summary & Action Plan.
Want to see the rest of the workup?
The two doctors’ pages sit next. Same brain, two more instruments.
Next: the brainwave maps from Peak Brain.
Next: QEEG · Peak Brain