Full specifications for every recommended test — what it measures, which cascade node it confirms, where to order it, and when.
In regressive presentations, tests marked HIGH in the regression column should be prioritized immediately regardless of standard sequencing. These markers reflect active system instability rather than background dysfunction.
This document is the lookup companion to Document 07 — Where to Start. If you have not yet identified which channels are most relevant to your child's presentation, begin there. This reference is for when you know which direction you are headed and need full test specifications: what a test measures, which cascade node it confirms, where to order it, and how it is prioritized within the channel investigation sequence.
First-line tests are ordered routinely for all individuals investigating that channel — they give the broadest directional signal. Second-line tests are ordered when first-line results confirm the channel is active and you need to quantify severity or narrow the mechanism. Third-line tests are for specific circumstances, unexplained findings, or when precision mapping of a confirmed channel is required for intervention design.
All tests in this reference are used to identify which upstream biological channels are active in a given individual — not to diagnose autism. Abnormal findings guide the reordering of the intervention protocol. They do not confirm or deny the diagnosis. All testing decisions require clinical oversight. For results interpretation and protocol routing, see Document 07C — Interpreting Your Results.
| Test | What it measures | Cascade node confirmed | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| Zonulin (serum or stool) | Intestinal tight junction protein. Elevated = active barrier disruption and LPS translocation risk. Most direct measure of leaky gut. | Upstream trigger — LPS entry point. Elevated = gut is active ongoing cascade driver. | Cyrex Array 2; Doctor's Data stool panel | First-line | High |
| LPS-Binding Protein (LBP) | Acute phase protein that binds circulating LPS. Elevated = systemic LPS translocation actively occurring, driving TLR4/NF-κB activation. | Upstream trigger — confirms active LPS-driven NF-κB signaling. Makes gut Layer 1 priority. | LabCorp, Quest (order as LBP) | First-line | High |
| GI-MAP (comprehensive stool) | Pathogenic and commensal bacteria, H. pylori, parasites, fungi, secretory IgA (mucosal defense), calprotectin (gut inflammation), pancreatic elastase (enzyme output). | Upstream trigger + SST node — low elastase confirms SST inhibition of pancreatic secretion. Calprotectin quantifies gut inflammation severity. | Diagnostic Solutions (GI-MAP); Genova GI Effects | First-line | High |
| OAT — gut dysbiosis markers | Arabinose (yeast overgrowth), HPHPA (Clostridia), other dysbiosis metabolites in urine. Captured within the full OAT panel. | Upstream trigger — dysbiosis metabolites confirm gut is driving LPS load and propionate excess. Guides antimicrobial/antifungal sequencing before probiotic protocol. | Great Plains Laboratory OAT (included); Genova Organix | First-line | High |
| Anti-LPS IgG / IgM | Antibodies against LPS — marker of cumulative chronic LPS exposure. Elevated = gut has been leaking LPS for an extended period, not just acutely. | Upstream trigger — confirms chronic vs. acute LPS exposure; guides urgency and depth of gut repair protocol. | Cyrex Array 2; specialty functional labs | Second-line | Conditional |
| Secretory IgA (stool) | Mucosal immune defense layer. Low sIgA = gut immune surveillance compromised; predicts dysbiosis persistence and LPS vulnerability even after antimicrobial treatment. | Upstream trigger — low sIgA predicts failure of probiotic interventions without concurrent sIgA support. Colostrum and saccharomyces boulardii support sIgA restoration. | Included in GI-MAP and Genova GI Effects panels | Second-line | High |
| Test | What it measures | Cascade node confirmed | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| OAT — TCA cycle markers | Succinic, fumaric, malic, and citric acids in urine. Elevated = TCA cycle blockade indicating mitochondrial dysfunction. Also captures lactate and pyruvate metabolites. | SIRT1/PGC-1α node — confirms mitochondrial biogenesis failure downstream of SIRT1 suppression. Two or more elevated TCA markers = channel confirmed. | Great Plains Laboratory OAT (included in full panel); Genova Organix | First-line | High |
| Plasma lactate:pyruvate ratio | Direct measure of mitochondrial respiratory chain function. Ratio >20 at rest = Complex I/III dysfunction with anaerobic glycolysis active. Most specific marker of active respiratory chain failure. | SIRT1/PGC-1α node — elevated L:P ratio is the strongest single confirmatory marker of mitochondrial respiratory chain failure. Distinguishes true mito dysfunction from secondary metabolic strain. | LabCorp, Quest standard metabolic panels; specify lactate:pyruvate ratio. Order as fasting, resting sample. | First-line | High — motor regression |
| Plasma / RBC carnitine panel | Free and total carnitine plus acylcarnitine profile. Low free carnitine = impaired beta-oxidation. Acylcarnitine ratios identify specific metabolic blocks in fatty acid oxidation. | PGC-1α / mitochondrial node — carnitine depletion prevents fatty acid entry into the TCA cycle. Acylcarnitine profile guides targeted L-carnitine or acetyl-L-carnitine supplementation. | LabCorp, Quest; request full carnitine panel with acylcarnitine profile. Specify plasma or RBC. | Second-line | Conditional |
| CoQ10 (plasma) | Direct ubiquinol and ubiquinone levels. CoQ10 deficiency is common in mitochondrial dysfunction and in children on certain medications. Guides ubiquinol dose selection. | Mitochondrial / PGC-1α node — low plasma CoQ10 confirms need for ubiquinol (reduced form) supplementation rather than ubiquinone. Dose confirmed by level, not estimated. | LabCorp, Quest; specify CoQ10 plasma (not RBC). Genova NutrEval includes CoQ10. | Second-line | Conditional |
| Test | What it measures | Cascade node confirmed | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| Kynurenine / Tryptophan ratio (K:T) | Direct measure of IDO1 enzyme activity. Elevated K:T = IDO1 activated by inflammation, diverting tryptophan from serotonin synthesis into the kynurenine pathway. Functional NAD⁺ insufficiency confirmed. | IDO1 node — most direct single confirmatory test for the core cascade mechanism. Elevated K:T = SIRT1 fuel supply inadequate. NMN/NR intervention is urgent. | Mayo Clinic Labs; Boston Heart Diagnostics; some functional labs. OAT captures downstream kynurenine metabolites as a proxy. | First-line | High — core mechanism |
| OAT — quinolinic / kynurenic ratio | Quinolinic acid (neurotoxic NMDA agonist) versus kynurenic acid (neuroprotective NMDA antagonist). High ratio = neurotoxic kynurenine pathway dominance. Quinolinic acid elevation = active oxidative pressure on neurons. | IDO1 / tryptophan hijack node — elevated quinolinic acid confirms active neurotoxic IDO1 pathway. NAC becomes urgent to protect against quinolinate-driven oxidative DNA damage. | Included in Great Plains OAT full panel; Genova Organix includes kynurenine metabolites. | First-line | High — NMDA pressure |
| hsCRP (high-sensitivity C-reactive protein) | Systemic inflammatory load marker. Elevated >1.0 mg/L in absence of acute infection = chronic NF-κB activation driving the inflammatory cascade. Accessible first-line screen. | NF-κB node — elevated hsCRP confirms chronic inflammatory state. Most accessible entry point for detecting active neuroinflammatory drive. Pair with ESR for confirmation. | LabCorp, Quest standard. Inexpensive, widely covered by insurance. Included in many standard panels. | First-line | High |
| Cytokine panel (IL-6, TNF-α, IL-1β) | Pro-inflammatory cytokines from activated M1 microglia and NF-κB-driven immune cells. IL-6 and TNF-α confirm active M1 microglial state; IL-1β confirms NLRP3 inflammasome activation. | NF-κB / M1 microglia node — together confirms active neuroinflammatory signaling. Luteolin + omega-3 move to Layer 1 when both IL-6 and TNF-α are elevated. | LabCorp, Quest (IL-6, TNF-α available standard); specialty labs for IL-1β. Order as fasting sample to reduce noise. | Second-line | High |
| BDNF (serum) | Downstream output of the cAMP/PKA/CREB pathway — the convergence point where both SST elevation and SIRT1 deficiency suppress the learning circuit. Chronically low in ASD. Primary treatment response outcome marker. | CREB/BDNF node — low BDNF confirms both arms of the cascade suppressing the learning pathway simultaneously. Order at baseline; retest at 3 and 6 months. Rising BDNF = cascade responding to protocol. | LabCorp, Quest; specify serum BDNF. Sample handling matters — EDTA tube, centrifuged promptly. Confirm lab protocol before ordering. | Second-line | Urgent baseline |
Regression — the loss of speech, language, motor skills, or social connection that were previously present — requires a specific test combination rather than a single channel panel. Biologically, regression is the observable downstream consequence of CREB/BDNF pathway failure: the learning consolidation circuit has been suppressed severely enough that previously encoded skills can no longer be maintained. Because both the SST/HPA arm and the SIRT1/neuroinflammation arm independently suppress CREB, the regression test battery must probe both pathways simultaneously rather than defaulting to one channel's panel.
Regression test battery — order together at first evaluation
| Test | What it confirms in regression | Lab source | Priority | |
|---|---|---|---|---|
| BDNF (serum — urgent baseline) | Directly confirms CREB pathway output is suppressed. The most specific single marker that the learning consolidation circuit has failed. Low BDNF at regression onset sets the recovery benchmark — rising BDNF at 3 and 6 months confirms the protocol is restoring pathway function. | LabCorp, Quest; specify serum BDNF. EDTA tube, centrifuge promptly. | First-line | High |
| OAT — kynurenine metabolites + TCA markers | Quinolinic acid elevation confirms IDO1-driven SIRT1 fuel depletion (neuroinflammation arm suppressing CREB). Elevated TCA markers confirm mitochondrial dysfunction — especially relevant when motor regression accompanies speech regression. | Great Plains Laboratory OAT full panel. First-morning urine. | First-line | High |
| K:T ratio (kynurenine:tryptophan) | Confirms IDO1 is actively diverting tryptophan — the mechanism depleting NAD⁺ and starving SIRT1. In regression, this is often the most actionable finding because NMN/NR can be introduced urgently once confirmed. | Mayo Clinic Labs; Boston Heart Diagnostics. | First-line | High |
| Salivary cortisol (4-point) + IGF-1 | Confirms whether the SST/HPA arm is also suppressing CREB independently. Abnormal cortisol pattern + low IGF-1 means both arms are active simultaneously — CREB is being suppressed from two directions at once, the most treatment-resistant configuration. | ZRT Laboratory (saliva); IGF-1 via LabCorp/Quest standard. | First-line | High |
| Zonulin + LBP (if regression followed a gut event or illness) | When regression followed a febrile illness, vaccination, or GI event, active LPS translocation may have been the immune trigger. Zonulin + LBP confirm whether the gut is still an active upstream driver sustaining the cascade after the initial triggering event. | Cyrex Array 2 (Zonulin); LabCorp or Quest (LBP — order as LPS-Binding Protein). | Second-line | High |
| Plasma lactate:pyruvate ratio + carnitine panel | Add when motor regression accompanies speech or social regression. Elevated L:P ratio confirms respiratory chain dysfunction is contributing independently. Motor regression has a stronger association with active mitochondrial dysfunction than speech regression alone. | LabCorp, Quest; specify fasting resting sample for L:P ratio. | Second-line | High — motor regression |
For the cascade interpretation of regression findings and protocol implications, see Document 07C — Regression interpretation. For scripts to use when discussing regression with a practitioner, see Document 07D — Regression script.
| Test | What it measures | Cascade node confirmed | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| Salivary cortisol (4-point diurnal) | Cortisol at waking, midday, afternoon, and evening. Maps the full diurnal rhythm pattern. Flat or inverted curve = HPA axis dysregulated, SST tonically elevated, cAMP/CREB suppressed around the clock. | SST node — HPA dysregulation is the primary driver of chronic SST elevation. Abnormal pattern confirms AC/cAMP/CREB chronically suppressed. Sleep/circadian optimization becomes non-negotiable Layer 1. | ZRT Laboratory (saliva); DUTCH Test (Precision Analytics); Genova Adrenocortex Stress Profile. Not available through standard LabCorp/Quest. | First-line | High |
| IGF-1 (serum) | SST inhibits growth hormone (GH), which drives IGF-1 production. Low IGF-1 for age = functional downstream marker of chronically elevated SST tone. Documented low in a subset of ASD individuals. | SST node — low IGF-1 confirms SST chronically suppressing the GH axis via a second independent pathway. When both cortisol pattern and IGF-1 are abnormal, SST channel is doubly confirmed. | LabCorp, Quest standard serum test. Inexpensive and widely available. Age-reference ranges are essential — use pediatric norms. | First-line | High |
| Fasting insulin / HOMA-IR | Insulin resistance index. Metabolic strain and hyperinsulinemia are direct SST release triggers — the pancreas responds to elevated insulin demand by increasing somatostatin output. HOMA-IR = fasting insulin × glucose / 405. | SST / upstream metabolic node — elevated HOMA-IR confirms a metabolic component driving SST elevation independent of HPA stress. Dietary intervention and insulin sensitization become protocol priorities. | LabCorp, Quest standard. HOMA-IR requires fasting glucose and fasting insulin drawn at the same time. Specify fasting draw. | First-line | Conditional |
| DHEA-S (serum) | Adrenal androgen produced alongside cortisol. Low DHEA-S with abnormal cortisol pattern = HPA exhaustion — the adrenal axis is in a conservation phase after chronic activation. Chronic SST elevation is strongly confirmed. | SST / HPA node — low DHEA-S + flat cortisol curve is the HPA exhaustion signature. Adrenal recovery must precede SIRT1 restoration. Phosphatidylserine 100–200mg evening is the first intervention. | LabCorp, Quest standard serum test. Inexpensive and widely covered. Interpret always in the context of the cortisol diurnal curve — DHEA-S alone is insufficient. | First-line | Conditional |
| Hair cortisol (3-month integrated) | Cortisol incorporates into the hair shaft at approximately 1 cm/month. A 3 cm proximal segment captures the preceding 3 months of integrated HPA output. Distinguishes chronic load from acute or transient HPA activation. | SST / HPA node — hair cortisol quantifies sustained chronic HPA burden sustaining long-term SST elevation. Complements salivary cortisol: rhythm pattern (saliva) + total load (hair). Elevated hair cortisol = chronic load confirmed, not a transient stress response. | ZRT Laboratory (hair); Stratech/Ciatec; Eurofins; some LabCorp specialty labs. Collect 3 cm proximal segment close to scalp. | Second-line | Conditional |
| Glutamate / GABA ratio | Excitatory / inhibitory (E/I) neurotransmitter balance. Elevated glutamate or depressed GABA = E/I imbalance. Correlates with sensory hypersensitivity, anxiety, and repetitive behaviors in ASD. | SST node + connectivity node — E/I imbalance is the synaptic signature of SST interneuron loss and glypican deficiency. Elevated ratio confirms the cascade has reached architectural impact level, not just signaling suppression. | OAT includes glutamate metabolites (most accessible); plasma amino acid panels (LabCorp, Quest); CSF requires lumbar puncture at specialized centers only. | Second-line | Conditional |
| Actigraphy / sleep study (PSG) | Objective sleep architecture measurement. Identifies slow-wave sleep (SWS) deficit — the glymphatic-active sleep phase when neuroinflammatory debris is cleared. SWS <15% of total sleep time = clearance failure. | SST / glymphatic node — SWS deficit confirms glymphatic clearance is impaired; inflammatory debris (quinolinic acid, cytokines) accumulates nightly. Melatonin timing and sleep optimization become non-negotiable before other interventions. | Polysomnography via sleep specialist for clinical PSG. Consumer actigraphy (Oura Ring, Garmin, Apple Watch) for directional monitoring. Clinical PSG required for formal diagnosis of sleep disorder. | First-line | Conditional |
| Test | What it measures | Cascade node confirmed | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| GPL-TOX (toxic organic chemicals) | Urine screen for 172+ environmental chemicals including glyphosate, organophosphates (pesticides), phthalates (plastics), benzene, styrene, and MTBE. Captures both agricultural and urban chemical exposure. | Upstream trigger — environmental channel. Positive findings confirm ongoing toxin-driven oxidative load contributing to IDO1 activation, gut microbiome disruption, and SIRT1 inhibition simultaneously. | Great Plains Laboratory (GPL-TOX urine panel). Direct-to-consumer ordering available in most states. | First-line | Conditional |
| Glyphosate (urine, specific) | Quantitative glyphosate measurement. Glyphosate disrupts gut microbiome by inhibiting the shikimate pathway in bacteria, depletes tryptophan precursors, and is epidemiologically associated with increased ASD risk. | Upstream trigger — glyphosate depletes Lactobacillus and Bifidobacterium, compounding IDO1 pathway dysregulation and gut barrier vulnerability. Positive = gut repair more urgent, dietary glyphosate reduction essential. | Great Plains Laboratory (included in GPL-TOX); The Detox Project; HRI Labs. Can be ordered standalone or as part of GPL-TOX. | First-line | Conditional |
| RBC heavy metals (Hg, Pb, As, Cd) | Red blood cell metal levels reflecting chronic tissue exposure rather than recent acute exposure (serum measures only recent). Mercury disrupts mitochondria; lead elevates inflammatory cytokines; arsenic directly impairs SIRT1 catalytic activity. | Upstream trigger + FOXO node — metal burden drives oxidative stress, GSH depletion, and SIRT1 inhibition from a second independent direction. Must specify RBC — serum metals miss chronic tissue burden. | Doctor's Data RBC Elements panel; LabCorp metals panel with RBC specification. Must specify RBC not serum when ordering. | First-line | Conditional |
| 8-OHdG (urine) | 8-hydroxy-2-deoxyguanosine — a DNA oxidative damage marker produced when reactive oxygen species modify guanine. Elevated in ASD and correlates with behavioral severity. Confirms active oxidative DNA damage. | FOXO / antioxidant node — elevated 8-OHdG confirms ROS burden has reached genomic level. NAC + sulforaphane are prioritized to restore antioxidant enzyme capacity. Retest at 3 months to confirm response. | Great Plains OAT includes 8-OHdG (most accessible); standalone via LabCorp. Also included in some comprehensive oxidative stress panels. | Second-line | Lower priority |
| Glutathione GSH:GSSG ratio | Ratio of reduced (active) to oxidized glutathione. Low ratio = antioxidant system overwhelmed and FOXO axis depleted. Quantifies antioxidant depletion depth more precisely than 8-OHdG alone. | FOXO / antioxidant node — low GSH:GSSG is the primary indicator for urgency of NAC intervention. Severely low ratio (<80% GSH) may indicate need for direct liposomal glutathione in addition to NAC. | Doctor's Data; Genova Diagnostics; some specialty labs. Not available through standard LabCorp/Quest — requires functional lab ordering. | Second-line | Lower priority |
| Test | What it measures | Cascade nodes covered | Lab source | Priority | Regression |
|---|---|---|---|---|---|
| OAT — full panel | Single first-morning urine collection covering: mitochondrial TCA cycle markers, kynurenine/IDO1 pathway metabolites, gut dysbiosis metabolites (arabinose, HPHPA), oxidative stress markers (8-OHdG), neurotransmitter metabolites, and B-vitamin functional status. | Covers IDO1, mitochondrial, gut/LPS, FOXO/antioxidant, and CREB nodes in a single collection. Highest-yield single test in the entire testing suite for initial channel mapping. | Great Plains Laboratory OAT (most comprehensive version). Genova Organix as alternative. First-morning urine; no vitamin B supplementation 48 hours prior. | First-line | High — start here |
| Intracellular micronutrient panel | Intracellular (not serum) levels of B vitamins, zinc, magnesium, selenium, CoQ10, vitamin D, and antioxidants. Co-factor deficiencies limit the efficacy of every cascade node intervention — supplements underperform without adequate cofactors. | All nodes — must be identified before building the intervention protocol. B6 and magnesium have the strongest ASD-specific RCT data. Zinc is essential for metallothionein and gut barrier function. Selenium is required for glutathione peroxidase. | Spectracell Micronutrient Panel; Genova NutrEval; LabCorp ION Panel. Serum nutrient levels are insufficient — intracellular or functional testing required for meaningful results. | First-line | Conditional |
| Vitamin D (25-OH-D) | VDR (vitamin D receptor) modulates NF-κB transcription. Deficiency is near-universal in ASD, correlates with severity, and permits unchecked NF-κB activation. Target range 50–70 ng/mL. | NF-κB / microglial node — deficiency amplifies the inflammatory arm of the cascade from a separate direction. Inexpensive to test, easy to correct. Order for every individual regardless of other findings. | LabCorp, Quest standard. Inexpensive, widely covered by insurance. Order as 25-OH-D (calcidiol), not 1,25-OH-D (calcitriol). | First-line | High |
| CBC + CMP | Complete blood count (CBC) and comprehensive metabolic panel (CMP). Screens for anemia, liver and kidney function, glucose and insulin indicators, and inflammatory markers. Universal safety baseline before initiating any supplement protocol. | Multi-node baseline — identifies systemic constraints on detoxification, nutrient delivery, and metabolism that limit protocol efficacy. Abnormal LFTs or creatinine require clinical review before hepatically-cleared supplements. | LabCorp, Quest standard. Covered by virtually all insurance. Available through primary care without specialist referral. | First-line | High |
| ApoE genotyping | ApoE4 allele impairs glymphatic clearance of neuroinflammatory debris, Aβ, and tau during sleep. ApoE4 carriers have 3–4× higher risk of neuroinflammatory debris accumulation for any given level of sleep disruption. | Glymphatic / sleep node — ApoE4 status identifies individuals where sleep disruption has compounding neuroinflammatory consequences. Melatonin timing and circadian repair become non-negotiable Layer 1 in ApoE4 carriers. Once-in-lifetime result. | LabCorp, Quest standard genetic test. Single blood draw. 23andMe raw data can be parsed for ApoE status via Promethease or similar. | Second-line | Lower priority |
The following sequence is the recommended ordering framework for families working through the full testing bridge. Each stage builds on the previous — second-line tests are only meaningful after first-line results establish which channels are active. The sequence prevents over-testing before direction is established and under-testing once a channel is confirmed.
| Stage | Tests | What you learn | Action threshold |
|---|---|---|---|
| 1 | Map active channels OAT (full panel) · Intracellular micronutrient panel · Vitamin D (25-OH-D) · CBC + CMP · hsCRP | Active channels across gut, mitochondria, IDO1/kynurenine, and oxidative stress identified in a single round. Co-factor depletions limiting all subsequent interventions identified. Baseline inflammatory status and safety markers captured. | OAT abnormalities route to channel-specific Stage 2 tests. Vitamin D <40 ng/mL: supplement immediately regardless of other findings. CMP abnormalities: clinical review before advancing protocol. hsCRP elevated: anti-inflammatory layer prioritized. |
| 2 | Confirm channel dominance K:T ratio · Salivary cortisol (4-point) · Hair cortisol (3-month) · IGF-1 · DHEA-S · Fasting insulin / HOMA-IR · Zonulin + LBP (if OAT gut markers elevated) | Primary cascade driver identified and quantified. SST/HPA load assessed from two angles — rhythm (saliva) and chronic burden (hair). Gut as active vs. resolved ongoing trigger clarified. Protocol layer reordering determined. | K:T elevated: NMN/NR to Layer 1 urgently. Abnormal cortisol curve: sleep/circadian as Layer 1. Elevated hair cortisol: chronic HPA load confirmed. Low IGF-1 + abnormal cortisol: SST doubly confirmed. Low DHEA-S + flat cortisol: HPA exhaustion pattern — adrenal recovery before SIRT1 restoration. Elevated Zonulin + LBP: gut repair before all other layers. |
| 3 | Quantify severity Cytokine panel (IL-6, TNF-α) · GSH:GSSG ratio · BDNF (serum baseline) · GI-MAP stool (if gut channel confirmed active) | Neuroinflammation severity and M1 microglial activation depth mapped. Antioxidant depletion depth quantified. Learning circuit impairment baseline established via BDNF. Gut microbiome composition and pathogen load detailed for targeted antimicrobial protocol. | Cytokines both elevated: luteolin + omega-3 move to Layer 1; curcumin added as adjunct. Low GSH:GSSG: NAC becomes urgent; liposomal glutathione considered if severely low. Low BDNF: establishes baseline — retest at 3 and 6 months. GI-MAP calprotectin very high: gastroenterology review before probiotic protocol. |
| 4 | Environmental burden GPL-TOX + glyphosate (urine) · RBC heavy metals · 8-OHdG (if not captured in OAT) · Carnitine panel (if mito channel confirmed) | Environmental toxin contribution to the cascade quantified. Metal burden and its impact on SIRT1 and GSH depletion identified. Mitochondrial fatty acid oxidation capacity assessed when TCA markers were elevated in Stage 1. | GPL-TOX positives: detox support (NAC, sulforaphane, glycine) + dietary exposure reduction. Metals elevated: NAC/glutathione urgently; physician-supervised chelation consultation if Hg or Pb significantly elevated. Low carnitine: L-carnitine 500–1000mg with meals. 8-OHdG elevated: NAC + sulforaphane urgently. |
Many of the tests in this reference are not available through standard pediatric primary care. Understanding where each type of test lives — and how to access it — is essential to navigating the testing bridge without unnecessary friction.
Most Stage 1 baseline tests and many Stage 2 confirmatory tests are available through LabCorp and Quest via a physician order or direct-to-consumer. This includes CBC, CMP, hsCRP, ESR, vitamin D, IGF-1, DHEA-S, fasting insulin, cytokines (IL-6, TNF-α), RBC metals, serum BDNF, and CoQ10.
The OAT, GI-MAP, GPL-TOX, salivary cortisol, hair cortisol, GSH:GSSG ratio, and intracellular micronutrient panel require specialty labs not connected to LabCorp/Quest.
If your current pediatrician is unfamiliar with functional panels, these practitioner types typically order them routinely:
Insurance coverage varies significantly by plan and by test type.