Mold Treatment Matcher

mold.practiced.health · The Mold Treatment Playbook · S/CS differentiated dosing · tolerance ladders · sequenced protocol

Confidence runs in one direction. Culture and stool PCR identify organisms. OAT measures metabolites — it infers overgrowth, it cannot speciate. Urine mycotoxins reflect environmental and dietary intake. Environmental panels describe the building, not the patient. And not every organism that grows needs treating.

Patient type Choose one — every dose below changes. Sensitive: reacts to ⅛–¼ doses, mast-cell pattern, limbic looping, dysautonomia, paradoxical responses.

Terrain first — limbic & vagus retraining the most sensitive patients may need to start and stay here before anything else

When a patient reacts to everything, the answer is almost never to push harder on the kill — settle the terrain. The limbic system is binary: safe or dangerous. Repeated sympathetic dominance teaches it that everything is a threat, and it becomes sensitised to read any input — a food, a smell, a supplement, a peptide — as danger. In the ⅛-to-¼-dose reactor, limbic and vagal work is not an adjunct; it is the prerequisite. ≥6 weeks before layering mast-cell agents in the very sensitive. These patients do not tolerate the protocol until the nervous system feels safe.

Limbic retraining programs

All are built on neuroplasticity — using the conscious mind to reteach the limbic system to leave the hypervigilant state, "like training a guard dog not to bark at everything." The basic structure is awareness/trigger → interruption → acknowledgment → visualisation/mood elevation. Different programs suit different patients; they can be combined. Sound- or light-based programs may not suit the light/sound-sensitive.

DNRS — Dynamic Neural Retraining System (Annie Hopper). retrainingthebrain.com. Structured, at-home video program, 20+ hours: targeted desensitisation and visualisation, incremental neural shaping, focused attention, cognitive reappraisal. Timed sessions, shortenable early on. The most-used program in this practice.

Gupta Program (Amygdala Retraining). guptaprogram.com. More meditative than DNRS. Retrain the brain / relax the nervous system / re-engage with joy — NLP, meditation, timeline therapy, breathwork, parts therapy, visualisation. Free 28-day mini-course to trial. Another mainstay in this practice.

Primal Trust (Dr. Cathleen King). primaltrust.org. Brain-retraining plus vagal and somatic work in one membership — frequently the next step when DNRS or Gupta alone stall. Named in the CIRS sequence alongside the two above.

Acceptance & Commitment Therapy (ACT). Not symptom reduction but psychological flexibility — cognitive de-fusion ("don't believe everything you think"), acceptance, present contact, observing self, values clarification, committed action. With a therapist or self-directed.

BrainTap (Dr. Patrick Porter). braintap.com. Brainwave entrainment via sound, music and pulsed light through a headset; pre-set packages for sleep, stress, focus. Passive — caution in the light/sound-sensitive.

Brainspotting (Dr. David Grand). brainspotting.com. Eye-position work to locate and release trauma held in the limbic system. Therapist-guided.

Vagus nerve — stimulating the ventral branch

Polyvagal frame: ventral vagal = calm, safe, socially engaged (where healing happens); dorsal vagal = freeze, shutdown, exhaustion; sympathetic = fight-or-flight. Acetylcholine is the vagal neurotransmitter. "When we do not feel safe, we cannot heal." Directly relevant here because a hypervigilant nervous system produces a hyper-reactive body — the MCAS-mold overlap.

Deep breathing — slower, deeper, belly, exhale longer than inhale, exhale through the mouth. A common pattern: in 2, hold 1, out 4, hold 1, repeated through the day. Buteyko technique for anxiety/panic overlap.
Gargling, humming, singing, chanting — direct motor stimulation of vagal fibres; cheap and daily.
Cold exposure — titrated; face/neck cold, cool rinse after sauna. Start gentle in the reactive patient.
Meditation & gratitude — combine with breathing; can be done walking, showering, doing dishes. Anchor to a sensory cue.
Laughter — genuine or self-induced; raises vagal tone (the coughing/fainting after hard laughter is vagally mediated).
Auricular acupuncture / aroma acu-therapy — ear points, especially Point Zero (the "autonomic brain" master point); essential oils on points for the needle-averse.
Aromatherapy — "euphorics" — olfactory nerve is a direct brain extension, no blood-brain barrier. Jasmine, rose, ylang-ylang, neroli, sandalwood, cacao, vanilla; natural-source oils only. Highly individual.
Gut & probiotics — the microbiota-vagus axis. In MCAS/histamine intolerance, mind the strains: raise histamine — L. casei, bulgaricus, helveticus, Strep thermophilus; lower/neutral — Bifidobacterium infantis, bifidum, breve, longum, and L. plantarum, rhamnosus, gasseri, salivarius.
TRE — Trauma Release Exercises (Berceli/Levine) — somatic tremoring through the psoas to complete an interrupted fight-flight response; a fatigue-to-tremor sequence releasing trauma held in the body core.
Rosenberg basic exercise and transcutaneous vagus nerve stimulation (the tVNS ear location is Point Zero) for the patient who wants a device.

Devices & practitioner-applied modalities

Apollo (Apollo Neuro) — wearable. apolloneuro.com. Wrist- or ankle-worn band that delivers gentle low-frequency vibration ("touch therapy") to shift the autonomic balance toward ventral-vagal / parasympathetic; app-selectable modes for calm, sleep, focus, recovery, and rising HRV. Passive, sub-sensory-adjacent, and well tolerated in the reactive patient — a good first device when a patient wants something to wear rather than a program to do. Pairs well with the breathing and gargling work above.

FSM — Frequency Specific Microcurrent. frequencyspecific.com. Two-channel microamperage current (millionths of an amp — below sensory threshold, so the very sensitive patient usually feels nothing) run at paired frequencies: one channel targets the tissue (e.g. the vagus nerve), the other the condition (e.g. inflammation, scarring, the limbic/emotional component). Published work shows the "reduce inflammation" frequency lowering IL-1, IL-6, TNF-α and substance P. In this practice it is a gentle adjunct for vagal tone, limbic calming, and inflammation/pain in the ⅛-to-¼-dose reactor who cannot tolerate much else — practitioner-applied or take-home unit. It is preferred over Rife (which is often no help — or worse; FSM does not do that). FSM is a certification course (start with the 5-day Core); the site carries a practitioner locator for referral. Caution in tickborne patients: the 40 Hz "acute inflammation" frequency can reactivate quiescent Lyme (~50–60%) — use the subacute frequency instead. Caution only where microcurrent is generally contraindicated — pregnancy and implanted pacemaker/electrical devices.

Handouts: the full patient-facing limbic-programs, vagus, and TRE handouts live in the practice library — hand these directly to the sensitive patient. Refer to mold.practiced.health for the complete versions.

MCAS — treat it as a system, never in isolation

MCAS is comprehensive, and never treated apart from the limbic/vagal work above or the root cause (usually mold). H1 + H2 blockers alone are insufficient — escalate to a full stack: H1 + H2 → mast-cell stabilizer (ketotifen or cromolyn) + DAO + a leukotriene inhibitor (montelukast), run concurrently with limbic/vagal retraining and mold treatment. Titrate the very sensitive from 1 (or ¼) drop of cromolyn up over months — cromolyn inhalation solution taken orally is the cheap route and is better tolerated than ketotifen in mito-fragile children (dropping histamine too fast can unmask mito/adrenal errors). Ketotifen symptom return on stopping = ongoing MCAS need, not withdrawal — wean slowly (0.25 mg steps). IV ketamine is the limbic-logjam breaker — low dose 25–50 mg IV for limbic/mast-cell reactivity (start 5–10 mg in the exquisitely sensitive); IV is far more effective than nasal/topical, and avoid intranasal (abuse risk). "Electrical shock" / buzzing sensations are near-pathognomonic for mold (also Bartonella/Lyme and EMF).

GLP-1 microdosing — used here as anti-inflammatory / mast-cell therapy, NOT weight loss. Tirzepatide microdose ~1 mg SubQ 2×/week (from 18 mg/mL compounded), or 0.25–1 mg (max ~2.5 mg), starting at ½ the FDA schedule and titrating frequency/dose by symptom — "basically never go up on the dose." Only once detox is working; pause if mycotoxin dumping outpaces clearance, add broad binders when starting (expected toxin dump), and stop if unwanted weight loss. Retatrutide/GLP-1 myalgia is a class effect → lower dose + ketone esters. (This practice uses tirzepatide/retatrutide, not semaglutide.)

Patient factors — these change what is safe

Current medications & supplements

Immune state — drives thymic peptide choice (read from the cytokine panel)

Cytokine / immune panel — how to read the immune state and pick the thymic peptide order this before committing to TA-1

The panel is how you turn "which thymic peptide?" from a guess into a decision. It reads the TH1/TH2/TH17/Treg polarisation and the mold signal, which maps directly onto the immune-state selector above — anergic/exhausted (low IL-2, low IFN-γ, paradoxical TNF-α) points to TA-1; a hot inflammatory profile (high IL-1β, IL-6, TNF-α) says lead with Thymalin/Thymagen first.

Reading the pattern — mold vs COVID vs tick-borne. Elevated sCD40L + high-normal RANTES (even when the other cytokines are low, or the patient is improving) points to mold — these are the two mold-relevant cytokines. A high Long Hauler Index with IL-6 / IL-10 / VEGF up = a COVID component; low IL-13 argues against active tick-borne; a cytokine pattern that doesn't reflect Lyme despite positive serology → look at mold instead. Note the cheaper broad serum panel does not measure sCD40L or produce the Long Hauler Index, so it can't replace the Long-COVID plasma panel for that specific question — "they answer different questions." Use the panel to prioritise limited testing dollars and to decide mold-first vs COVID-first sequencing.

Panel	Order via	Best for
CytoDx (Diagnostic Solutions)	Fullscript / Rupa / Evexia — much cheaper (~$242)	The default broad serum panel you can order on a portal. This is the practical, affordable choice for immune-state mapping.
Radiance / IncellDx, 14-cytokine plasma multiplex	Radiance / IncellDx direct	Long-COVID phenotyping — the validated Long Hauler Index (0–1, 0.70 cutoff) is the deliverable. Worth the premium only when long-COVID is genuinely the question.
Mayo/ARUP "Cytokine 13"	Institutional send-out by code	When a protocol names those exact 13. Not on Fullscript/Rupa.
À la carte (IL-6, IFN-γ…)	Fullscript (Quest/Access)	Targeted follow-up only — assembling ~13 this way runs $1,200–2,000.

The non-portability rule — read before you compare two results. Serum ELISA (CytoDx) and plasma multiplex (IncellDx) use different matrices and reference values — never cross-compare absolute numbers between panels. The same patient can read "high" on one and "normal" on the other. What travels is the pattern: the TH1/TH2/TH17/Treg polarisation and the mold signal — sCD40L and RANTES, elevated in mold. Read the shape, trend on one platform. The Long Hauler Index cannot be reproduced from another platform — its equation is proprietary.

When to re-test: cytokines have short half-lives, so the panel is a snapshot — re-test on the same ~3–4-month cadence as urine mycotoxins, or after a meaningful protocol change. Expect sCD40L/RANTES to drift down as load falls; if they stay up despite good treatment, hunt for ongoing exposure, sinus/gut colonisation, or a second driver (Lyme, viral reactivation). Why it matters clinically: a stuck patient after the mold is handled may be idling in the Cell Danger Response — the cytokine panel reveals what the immune system is still reacting to, and whether the answer is TH1/TH2/TH17 rebalancing, antivirals, biofilm/coagulation work, or membrane repair (phosphatidylcholine) rather than more binder.

Immunoglobulins (IgG · IgA · IgM · IgE) — the blood tests, and how they steer treatment

Order these on the initial comprehensive panel (they’re part of the CIRS work-up), then add the targeted antibodies when a specific question comes up. They answer two different things: is the immune system competent (the quantitative totals) and is a specific organism actually driving disease (the specific antibodies).

Quantitative totals — IgG, IgA, IgM

Baseline immune competence. Low totals point to immunodeficiency — CVID, selective IgA deficiency — the recurrent-infection, won’t-clear phenotype. In that patient, be cautious with immune-suppressing moves, expect slower clearance, and consider immunoglobulin support or an immunology referral. High IgG can reflect chronic antigen load.

Total IgE (+ allergen-specific IgE)

High total IgE flags the allergic / atopic (and parasite) axis. With a positive Aspergillus-specific IgE it points to allergic fungal disease — ABPA or allergic fungal rhinosinusitis — which is a different treatment path (corticosteroid + antifungal), not pure colonisation. Distinguishing this changes the whole plan.

Aspergillus IgG (precipitins)

The best serologic proxy for colonisation / chronic exposure — a sustained IgG response means persistent antigen, i.e. the organism is established rather than a passing exposure. It’s the backbone of the chronic-pulmonary-aspergillosis diagnosis and the highest-yield antibody when you’re deciding whether a systemic azole is justified.

Candida antibodies — IgG, IgA, IgM (the fluconazole decision)

These decide whether to treat gut / systemic Candida. IgA = mucosal / gut involvement — the SIFO driver. IgM = recent or active. IgG = established or ongoing (or past). Read them with arabinose on the OAT and stool Candida: positive antibodies + high arabinose + stool Candida → treat (fluconazole, ± luminal nystatin/ampho). An isolated low titre with no symptoms and nothing corroborating → don’t chase it.

Quick routing: immune competence & the sick-often patient → totals · allergic/ABPA picture → total + Aspergillus IgE · is the mould colonising? → Aspergillus IgG · treat gut Candida or not? → Candida IgG/IgA/IgM (IgA leads).

MyMycoLab — the serum-antibody mycotoxin test, and where it earns its place

What it measures. IgG + IgE antibodies to 14 mycotoxins (28 markers) from a single blood draw. It reads the immune footprint of exposure, not what the body excretes — so it does not depend on hydration, kidney function, binders, or a glutathione challenge. It does not include IgA or IgM.

Where it earns its place — the sick-but-urine-negative patient

Our most exposed patients are often our worst detoxifiers — weak glutathione, sluggish phase II, impaired kidney, bound up on binders, dehydrated. A urine panel only shows what they can mobilise and excrete, so that exact patient can be genuinely loaded and still test low. MyMycoLab sidesteps that, because an antibody response doesn't care whether they can excrete. Its highest-yield moment is the patient whose story, exposure history and symptoms say mould but whose urine won't confirm it — it rescues that case and gives you something concrete to stand on before committing someone to a months-long azole course.

The IgG / IgE split — phenotyping that changes how you dose

IgE-dominant (especially with an allergic picture) is the hypersensitivity / atopic patient — the MCAS overlap, the ⅛-to-¼-dose reactor. Read it as this person will react — settle the terrain and stabilise mast cells before you push the kill, and look harder at the allergic-fungal / ABPA pathway (a different treatment path). It's objective backup for treating someone as Sensitive. IgG-dominant with little IgE reads more like established chronic exposure / burden without the hyperallergic arm — the patient you can move through a systemic antifungal more confidently. And because IgE skews current / active and IgG skews memory / past, a strong IgE signal is also a nudge to re-examine the building — if they're still actively reacting, remediation may not really be done.

Diagnose with serum, trend with urine

Use MyMycoLab to identify and diagnose exposure. Do not repeat it to follow progress — antibody titres lag and persist for months, so they won't track treatment. To trend response, repeat a urine panel (RealTime). Serum answers "was there real exposure?"; urine answers "is it clearing?"

Where it does NOT help

It does not speciate the organism or tell you which azole — it's at the toxin level, so you still need nasal culture, OAT and stool to pick the agent. It doesn't identify the source building, doesn't quantify severity, and isn't FDA/CDC-validated as a standalone diagnosis — it's confirmatory and phenotyping, read alongside the clinical picture, never in isolation. Practical fit: cash-pay, ~$380, blood draw, no physician order required.

One-line version: your best "was there real exposure?" test in the patient who can't excrete, plus a read on how allergic / reactive they are — not a progress tracker and not a drug-picker.

The non-responding "mold" patient — when to broaden to tick-borne & viral

Mold first — but when a mold patient stalls, or presents with features mold doesn't cause, broaden the differential. The governing rule for taking these on: treat within your competence or refer — "never go past your comfort level." Formal training (ILADS, ISEAI, LLMD shadowing) is strongly advised before treating tick-borne disease.

When to suspect a coinfection behind a non-responding patient

Lymphadenopathy — "rarely occurs with mold toxicity, so look for an infectious cause, with Lyme and Bartonella high on the list." Extreme sensitivity + tendon/ligament pathology (contractures, tendinopathies) → Bartonella. "Air hunger" ± night sweats / temperature dysregulation → Babesia (also seen in mold). Electrical shocks / brain shivers, restless legs → mold first, but Bartonella/Babesia on the differential. Incomplete Lyme responders ("80% better then declined") → look harder at Bartonella and test for mold. Most mold patients deny exposure — "that in no way takes it off the table."

Lab tiering the group trusts

IGeneX is first-line — order immunoblots AND FISH, never FISH alone (both false-negative patterns are common). Bundles: write-in panel 41B (~$1,200) or 4IB Plus (immunoblots + FISH, $1,599); under Medicare, TBD4/4IB are covered (add the two FISH tests, ~$40 copay each); Medicare Advantage covers essentially nothing; LymeTAP reimburses IGeneX for cost-limited patients. Bands: 18 & 23 kDa are Lyme-specific; 41 kDa is nonspecific (cross-reacts with EBV); a positive IgM alone supports Lyme; a positive FISH = active infection. Always check total immunoglobulins in the chronically ill (poor antibody production → false-negative blots). Galaxy (Bartonella) and T-Labs (fluorescent smear — best for knowing a microbe is active) are adjuncts; ArminLabs / REDlabs are the affordable European routes.

Labs the group distrusts: DNA Connexions (over-diagnoses), Vibrant & LabCorp for Lyme, ImmunoSciences, the Fry smear, urine PCR (low-yield), and CD57 (deprecated). Testing is insensitive overall — Lyme/coinfections are a clinical diagnosis; treatment response is the arbiter. Keep testing on record before starting antibiotics.

Treatment — in brief (refer if outside your scope)

Herbs first, then layer antibiotics (herbs make the antibiotics more effective). Bartonella — a commonly used regimen is clarithromycin + rifampin, plus a Bartonella tincture (Beyond Balance Bar-1/2/3 or Byron White A-Bart) titrated by Herx. Babesia: atovaquone 750 mg BID (or tafenoquine) and/or herbals (Woodland Essence CSA, Beyond Balance BAB-1) — don't delay coverage, Babesia can cause fatal cardiac/pulmonary disease. Neuro-Lyme is treated across all three forms (spirochete/cyst/biofilm), ≥3–4 months. Methylene blue is safe with SSRIs below ~300 mg/day (check G6PD).

Viral reactivation (EBV / HSV / COVID spike)

Mold is usually the root — don't chase the virus. "Once the mold has cleared, the immune system reboots and the EBV is no longer an issue." For refractory HSV/EBV, immune modulation beats escalating antivirals: TA-1 (thymosin α-1) to raise NK/antiviral capacity, ± SOT + thymic peptides — but SOT only works once mold is substantially treated and terrain optimized (given prematurely it fails or flares). COVID spike antibody is an unreliable monitor — don't chase the number; symptomatic-but-stuck with low/flat spike → look for mold.

Systemic antifungal — coverage

Add findings from any tab. Everything selected combines into one plan.

1 reliable2 partial 3 not active– no data

Environmental → expected mycotoxins

Sinus ladder assume colonisation — escalate by tolerance, not by organism

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Gut ladder assume colonisation — nystatin first, azole added as tolerance builds

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Binders — matched to toxin

Binders in place BEFORE antifungals. Get the matched binders dosed and tolerated first — opening a systemic antifungal on an unbound patient risks a severe, weeks-long die-off (~40% in the cognitive-decline population) that derails the whole plan. And when a patient isn't responding, check the order: (1) is the home/environment fully remediated — by far the #1 cause of poor response; then (2) have limbic, vagal and mast-cell been addressed. "The body cannot heal if it does not feel safe."

Special-population safety. Pregnancy: binders OK except Welchol/cholestyramine; nystatin, nasal sprays and biofilm agents OK; avoid Sporanox and the systemic azoles. Preconception (male): same — binders OK except Welchol/CSM, nystatin OK, hold azoles. Chemo / oncology: start low-dose binders early, hold antifungals — oral non-absorbed binders don't interfere with injected chemo. eGFR <50: fluconazole −50%; itraconazole oral solution is problematic (cyclodextrin) but capsules / SUBA are fine.

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Herx management

Prescriptions nasal regimen in ladder order · copy-ready · confirm compounded strengths

Compounded strengths vary by pharmacy. Confirm the formulation before writing — most compounders do not publish exact percentages, and they genuinely differ. Culture susceptibilities override any default. Click through to set up a provider account or call.

Forte Rx California · ready-to-use nasal sprays — itraconazole 1%, EDTA, amphotericin B, BEG-I, Synapsin. A primary source for this protocol. PD Labs Cedar Park, TX · closest to central Texas · nasal spray preparations · vegan capsules, AGS-safe. A primary source for this protocol. Park Compounding Irvine, CA · (855) 876-3060 · dedicated biotoxin/CIRS line; will compound Argentyn 23 + xylitol into the EDTA spray Richie's Specialty Pharmacy Conroe, TX · (877) 231-8386 · nasal anti-infective line, but supplied as capsules the patient reconstitutes in 120 mL distilled water with salt — an irrigation, not a spray. Irrigation may not reach or dwell in the sinuses as well, and twice-daily reconstitution is cumbersome for patients. Prefer a spray preparation where you can. Drug Crafters Frisco, TX · (214) 618-3511 · sterile & non-sterile, provider portal · not yet used in this practice ScriptWorks Walnut Creek, CA · (925) 934-4400 · BEG and fungal sinusitis preparations · not yet used in this practice Pavilion Compounding Atlanta, GA · (404) 350-5780 · not yet used in this practice

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Recovery — immune, barrier & mitochondrial step 4 · peptides earn their place here, not earlier

Synapsin (intranasal) — the three variants, and how to choose

What “Synapsin” actually is. The patent-pending base is ginsenoside Rg3 + nicotinamide riboside (NR) — Rg3 for neuroprotection and microglial modulation (it calms the neuroinflammatory arm), NR to hold NAD⁺ and mitochondrial energy up in the same tissue. Every product on the market is that base with something bolted on, so you are really only ever choosing the add-on — not a different drug.

Base — Rg3 + NR

The cleanest option, fewest moving parts. Reach for it when the target is neuroinflammation plus cognitive fatigue and you want to see what Rg3 / NAD⁺ do on their own before layering anything. A sensible first trial in a reactive patient.

+ Methylcobalamin B12 (“RG3-Synapsin”, “Methylcobalamin (Synapsin)”)

The most commonly dispensed form (Strive, Welltopia, Rock Ridge, Wells). The B12 adds myelin-sheath integrity, nerve repair and methylation / neurotransmitter support. This is the default upgrade in the mold / CIRS population, where a functional B12 need, methylation strain, and a peripheral-nerve or autonomic component are all common. When unsure, this is the sensible middle.

+ Alpha-GPC (± B12)

Alpha-GPC is a cholinergic precursor — it feeds acetylcholine. Add it when the dominant complaint is memory, attention and executive function specifically — the acetylcholine-flavoured picture — rather than diffuse inflammatory brain fog. Acetylcholine is also the vagal neurotransmitter, so this variant carries a mild autonomic rationale in the dorsal-vagal / limbic patient.

Methylene blue — a pairing, not an ingredient (the common confusion)

Low-dose methylene blue is frequently co-prescribed alongside Synapsin, and a few pharmacies co-compound the two — but it is not part of the Synapsin blend. MB is an alternative electron carrier in the mitochondrial chain and a low-dose antioxidant, with its own cognitive / mitochondrial literature. Reserve it and screen first: it is serotonergic (MAO-inhibiting) — real serotonin-syndrome risk with SSRIs / SNRIs / MAOIs — avoid in G6PD deficiency, and it turns urine and tears blue-green. A deliberate add, never a default.

How to choose, in one line: clean neuroinflammation + energy → base · myelin / nerve / methylation in play (most mould patients) → + B12 (the usual pick) · memory / acetylcholine cognition → + alpha-GPC · deeper mitochondrial push → consider a methylene-blue pairing, after a medication and G6PD screen.

The cognitive-decline workup it belongs to

Mold is a leading driver of unexplained cognitive decline — dementia patients carry many-fold the mycotoxin burden of controls, with a near-universal sinus link. Full workup for unexplained neuro-decline / aphasia: RealTime urine mycotoxins + IGeneX (Lyme / Bartonella / Babesia) + DMSA-provoked urine metals to Doctor's Data + Cyrex neural autoantibodies, and get the patient out of the sick environment (the rate-limiting step). Get binders fully in place before antifungals in this population — the die-off risk is highest here.

Where it sits in the sequence — early, not late. Unlike VIP (which waits until VCS and MARCoNS clear and exposure is gone), Synapsin can go in while the patient is still symptomatic — one of the few cognitive tools available during the messy middle. Dose early in the day, refrigerate, warm to room temperature before spraying. More context in the app’s Recovery section →

Heavy metals & environmental medicine treat mold first — chelate only what is real

Treat mold / mycotoxins before chelating metals. Clearing the mycotoxins improves detoxification and passively drops metals; minimally elevated provoked metals usually do not need treatment. And amalgams must come out before chelation is coherent — you cannot effectively chelate mercury with amalgams still in the mouth (biologic dentist first; expect a flare afterward).

Testing — provoked vs unprovoked

Doctor's Data is the reliable toxic-metals lab. Blood mercury is unreliable — mercury is stored in brain/tissue (sulfhydryl-bound), so a non-quantitative "<5" is useless; if the patient eats fish, repeat at a lab quantifying to 1.0. Use provoked testing: DMSA in 3 divided doses × 3 days → a timed 6-hour urine to Doctor's Data, and do a pre-provocation first-morning baseline first so you can read the ratio. Arsenic is measured in urine. Oral DMSA is contraindicated in celiac / gluten-sensitivity / IBD (poorly absorbed).

Action thresholds

Act only if post-provocation Lead >20 or Mercury >11, or the level is >10× the pre-provocation baseline. Thallium on a panel is often dietary (kale / spinach smoothies) — confirm a markedly elevated urine level plus symptoms before treating. Note 10 mg/kg TID DMSA is a treatment dose, not a true provocation dose (~1,000–2,000 mg).

Gadolinium (post-contrast MRI)

Gadolinium deposition disease is distinct: only EDTA and DTPA raise urinary gadolinium, and only Zn / Ca-DTPA directly chelates it from the brain — with steroid / antihistamine premedication (critical for tolerating the DTPA). Refer to a gadolinium-literate clinic. "Detox" botanicals (cilantro, chlorella, modified citrus pectin, ALA, NAC) reduce Gd-driven inflammation but do not chelate gadolinium.

PFAS & pesticides

PFAS: serum panel (EmpowerDx / Eurofins, ~$279); the only proven depletion is plasma / blood donation (plasma more effective, every ~3 months); cholestyramine helps only PFOS. Organochlorine pesticides + benzene are adipose-stored and may need apheresis to clear. Fipronil — binders + probiotics (fecal route), sauna, glutathione / vitamin C / selenium / milk thistle.

Environmental-medicine first principles. Health effects come from the total toxic load — the cumulative burden across all toxicants and the body's capacity to eliminate them — not any single chemical. So: avoidance first (stop ongoing exposure — no depletion strategy beats continued intake); match the test to the toxicant's storage and kinetics (blood = recent, unprovoked urine = ongoing / renal-cleared, provoked urine = stored metal burden read against a baseline, sweat / adipose for lipophilic POPs); and support elimination — bile→stool (binders + regular bowel movements), sweat / sauna, hydration — with glutathione and nutrient cofactors introduced only as fast as a sensitive patient tolerates, so mobilization never outpaces elimination.

Structural rate-limiters — why the ultra-sensitive patient won't progress check when everything else is optimized and they're still stuck

When a very sensitive patient plateaus despite good mold, limbic, vagal and mast-cell work, look for a structural block that caps all progress:

Craniocervical instability (CCI) / CSF leak — often the reason a hypersensitive patient can't move forward. Work up with flexion / extension / rotation CT + upright MRI (an hEDS-familiar neurosurgeon).
TMD / bite & the ALF appliance — cranial / TMD dysfunction impairs vagal function (→ impaired detox) and glymphatic drainage.
Dental cavitations — an occult inflammatory block (CBCT to find).
Pelvic venous congestion — an under-recognized driver of POTS / orthostatic pooling; evaluate the pelvis (duplex Doppler) before any permanent leg-vein procedure.

Pediatric mold — quick module gentler, slower, mast-cell-first

EOE (eosinophilic esophagitis)

Usually mast-cell-driven and rooted in mold (or Lyme). Sequence: clean the environment + heavy mast-cell support (a mast-cell stabilizer — cromolyn if mitochondrial fragility — taurine, aloe, flavonoids) → compounded anhydrous nystatin 1 → 3 mL/day once stable; remove top allergens, then slowly reintroduce. Use OAT + RealTime over stool tests; screen zinc / iron / IgA (IgA deficiency = slower healing).

Pediatric candida

High OAT arabinose: bentonite clay + S. boulardii (to bind gliotoxin released on kill) → nystatin 500,000 U BID → fluconazole 100 mg daily; expect mycotoxins to surface on repeat RealTime as detox improves.

Eczema with mold / Clostridia

Food-allergy elimination diet first, plus spore probiotics + oregano + S. boulardii; strict gluten / dairy removal.

ASD insomnia

Split by onset vs maintenance — onset: glycine 3 g, valerian, kava, GABA; maintenance: 5-HTP; low-dose doxepin / amitriptyline 10 mg. Always hunt the driver (mold, Lyme / Bartonella, copper:zinc ratio, methylation). An empiric leucovorin 5–10 mg trial is a fast (2–3 day) read for cerebral folate deficiency (worsening agitation = negative) — ideally run a FRAT first. Address EMF (grounding, opt out of smart meters).

Pediatric tick-borne

Gentle herbals first, rotating brands on plateau. A nicotine patch, if used, is dosed by weight + theanine; brand potency varies.

Maintenance & off-ramp — the improved-but-still-positive patient most patients land here, not at zero

Roughly 95% of patients get much better but don't hit "not present" in every category. The off-ramp: ongoing binders (chlorella / fiber for PCBs and microplastics), sauna, biofilm agents, and long-term fibrinolytics in the hypercoagulable — while continuing to hunt for ongoing exposure. Add broad binders whenever starting a GLP-1 (expected toxin dump). The goal is durable stability at the lowest maintenance burden, not endless escalation.

Dosing & monitoring at a glance

Sequence

0	Confirm & remove exposure. You cannot heal in it. Building test + urine mycotoxins to prove it; remediate or leave.
1	Prepare the terrain (if sensitive). Limbic + vagal first — ≥6 weeks in the very sensitive — then add mast cell. H1 + H2, quercetin/DAO/Perimine/PEA → cromolyn/ketotifen.
2	Bind & drain. Open the drains first — bowels, water, bile, sweat. Match the binder to the toxin; start at a fraction of a dose.
3	Clear colonization. Sinus + gut antifungals by tolerance; biofilm agents. Race to the antifungals when gliotoxin is high.
4	Recover. Immune reboot (LDN, VIP, peptides), hormones, mitochondria last. Ketamine/LDI for the truly untreatable.
5	Re-test & re-sequence at ~3–4 months. Numbers often rise before they fall as detox improves.

The functional-medicine exception: "treat the gut first" fails here. In mold + Candida you must clear the mold and Candida before the gut will respond.

Resources — vetted referral contacts remediation & inspection first · the medicine cannot outrun a mouldy building

Why this lives in the tool. Who you send a patient to for remediation decides whether the treatment works. Step 0 is not optional, you cannot heal in it, and a half-done tear-out with no containment does more harm than leaving it alone. Ripping out mouldy material aerosolises millions of spores and mycotoxin-laden dust, and without a sealed, negative-pressure enclosure that load spreads through the whole house and into the HVAC. The patient you are treating gets a fresh hit instead of a clean building. These are contacts I trust to do it right.

Mould remediation & inspection

Blackhill Restoration Central Texas — Round Rock, Austin, Cedar Park, Leander, Liberty Hill, the Hill Country and surrounding communities · (800) 931-1962 · ask for Ryan Walker. IICRC mould-certified crews, full containment with negative air and HEPA filtration, source removal and post-remediation verification testing. Excellent work, and trusted in this practice.

What proper containment looks like, so you know good work when you see it. Show this to a patient before they let anyone open a mouldy wall. Done right, the work zone is sealed into its own box: 6-mil poly walls run floor to ceiling and every seam is taped to the wall, the door frame and the floor. Crews come and go through a zippered entry so the seal is never peeled back. The enclosure is held under negative pressure by a HEPA air scrubber that pulls air out and exhausts it through a filter, so the plastic visibly draws inward and air only ever flows into the sealed room, never out of it. That negative pull, not the plastic alone, is what stops spores and mycotoxin dust from drifting into the rest of the home when the material gets disturbed. A commercial LGR dehumidifier runs to dry the structure, because mould does not return to a dry building. The floor is protected with taped ram board and the area is posted with a remediation-in-progress sign. The opposite, meaning no plastic, a box fan in a window, spray-and-pray, does the reverse of helping. It blows spores through the whole house. Insist on containment, negative air, and post-remediation verification testing every time.

Environmental inspectors / IEPs, building-biology surveyors and air-quality testing can be added here as the practice vets them. Compounding pharmacies and lab sources are listed in the Prescriptions and testing sections above.