I had the opportunity to attend the ISEAI 2025 event "ISEAI 2025 Fall Symposium" on November 7-8, 2025.  

It has long been my opinion that many of the complex conditions we face today are the result of our external environment.  ISEAI is a leading organization sharing this message; as well as fostering collaboration and sharing solutions to improve the quality of our lives.

I strongly encourage practitioners working with complex, chronic illnesses to join ISEAI; become part of the conversation and ultimately the solution.

Disclaimer: Nothing in this text is intended to serve as medical advice. All medical decisions should be made only with the guidance of your own personal licensed medical authority.

Disclaimer: This information was taken as notes during the training course and may not represent the exact statements of the speakers. Errors and/or omissions are likely present.

Note: As this information may be updated as any errors are found, I kindly request that you link to this single source of information rather than copying the content below. If any updates or corrections are made, this will help to ensure that anyone reading this is getting the most current and accurate information available.

Paul Anderson, NMD spoke on "Approaches to Detoxification and Depuration for Troubleshooting Complex Cases” and shared:

  • Toxicants are ubiquitous and immune dysregulating; more so to the chronically ill patients who have difficulty with detoxification
  • Some treatments may unearth other toxins or the body may be pushing out more toxins as reserves build
  • Detox has to happen throughout and match patient tolerance
  • May need to deal with histamine or immune-modulation
  • As they detoxify, other treatments will change; hormones may need to be decreased; antimicrobials may work better
  • Thinking of detoxification as a single toxicant is easier to learn but is not reality
  • Metal detox will liberate other mycotoxins, chemicals, etc.; detoxing one thing may open the doors for others to be released
  • Support all types of elimination; you never want to support just one thing like heavy metals
  • Today, people also have spike proteins to consider
  • External sources are food, drink, air
  • Toxins may be cell sequestered in bone, adipose tissue, hepatocytes
  • Reabsorbed in GI, plasma, cell sequestered
  • Circulation -> Phase 1, 2, and 3 -> Elimination
  • Elimination via kidneys, liver/gallbladder/stool, sweat, respiration
  • There can be a bottleneck where detox aggravates the patient; something in the body is overwhelmed
  • Have to think in reverse in sensitive people and work on elimination first, then phase 3, phase 2, phase 1, and toxin removal; each step could take weeks or months
  • Phase 1 often metals, minerals, superoxide support
  • Phase 2 has many pathways that are nutrient dependent
  • Phase 3 is preparing for elimination; fluids, stool regularity, binders
  • Phase 1 raises oxidative stress; hydroxylation; need SOD and glutathione
  • Phase 2 is conjugation; vitamins/minerals/amino acids
  • Elimination supports:
    • Kidneys: water, B6, Magnesium, Glutamine (shuttle out nitrogen waste)
    • Liver/Gallbladder/Stool: choleretics, binders
    • Sweat: heat, movement
    • Respiratory: respiration, movement
  • FIR sauna may be better but still better to use heat than not at all
  • If having less than 1 bowel movement per day, recirculating toxins -> sicker
  • People can have less frequent bowel movements when starting detox
  • Need hydration and binders
  • Binders:  Cholestyramine, Colestipol, Colesevelam
  • Some may only tolerate small amounts as they may only be able to tolerate so much
  • Bile must be flowing for the binder to work; sludgy bile will impeded progress
  • Food source binders: konjac flour, guar gum; psyllium, if tolerated
  • Highest bile acid binding with foods: asparagus, collard greens, mustard greens, kale, eggplant okra, beets; diet needs to be the base of binding; steaming best; boiling worst; while all good options, the order is from least to most binding
  • Charcoal works well on certain chemicals and not on others; not good for many metals
  • Humic acids effect the microbiome beneficially; humic/fulvic/zeolites bind well in the gut; do nothing systemically
  • Zeolites can help to heal the intestinal barrier
  • Zeolites can bind histamine
  • Binders are best given away from anything you want to absorb (food, supplements, medications); at least one hour prior or two hours after eating
  • Start with one dose of binder per day to not make the schedule too overwhelming
  • Can use bedtime as an opportunity to take binders
  • Between meals can be very difficult
  • Oral chelators are also binding substances; not well absorbed generally; less absorbed with gluten
  • Non-absorbed chelators bind in the GI tract
  • Can weaken biofilms in the gut; can pull metals from fungi and other microbes in the gut; sucking the energy source out of fungi
  • DMPS orally is 60-70% not absorbed; DMSA 75-80%, EDTA 90-95%, liposomal EDTA 50-80%
  • With immune-suppression and toxicity, best to not use non-human strains; use human strains; HMF trade name
  • Prebiotic and probiotic foods as tolerated; lists of high binding and pre/probiotic overlap notably
  • Cholagogues: curcumin, most fats, PC/PS; curcumin also helps with inflammation and protection from metals
  • GI health: demulcent herbs (ulmus, althaea, DGL, etc.), GI cell support (glutamine, carnosine), probiotics; can take these with binders at bedtime
  • Curcumin or EGCG to protect against heavy metal effects; curcumin may chelate metals from the CNS
  • Both can protect the person as they detoxify; green tea in the morning can be very helpful; turmeric root tea; the more you eat, the less you have to take
  • Phase 2
    • Acetylation uses B5; primary backup for histamine and cytokines; pantothenic acid or pantethine  
    • COMT and MAO use B6, magnesium, ascorbic acid; most steroid hormones, histamine go through MAO
    • Hippurates uses glycine
    • Mercapturates uses glutathione
    • Glucuronic Acid uses glucuronides; phytonutrients; polyphenols; triggered by glutathione
    • Sulfation uses molybdenum, sulfates; sulfates are post sulfite stable molecules; sulfite is what we want to get rid of
  • Phase 1: FAD (B2), NAD (B3), iron, zinc, manganese; counterbalance/slow down superoxide with glutathione/SOD
  • Adjuncts: TPE, plasma donation, blood donation, EBOO
  • Good elimination of metals with TPE; may help microplastics
  • TPE can "clear the deck"
  • Cell membrane: phospholipids, chelation, detox, taurine
  • Cytosolic enzymes: C, E, glutathione, melatonin, chelation, RED/NIR, heat
  • Mitochondria: B5 for CoA support
  • Ox-Phos slowed by metals
  • Mitochondria: B5, lipids, carnitine, PC, melatonin, C, B5, NAD, glutathione, chelation, CoQ10, ALA, heat, RED/NIR
  • Modalities: sauna, HBOT, exercise, hydration, binders, choleretics, colonics, phospholipids, TPE, EBOO, chelation
  • Must have binders, hydration, bowel movements, sweating, glutathione, movement, mitochondrial support
  • Support for detox: prebiotics, probiotics, binders, bowel movements, urination, hydrocortisone, H1/H2, antimicrobials
  • High value supplements: NAC, ALA, curcumin, EGCG, milk thistle, food and supplement binders; movement, heat, RED/NIR/FIR, colonics, enemas
  • Information from the Q&A
    • INUSpheresis with a specific filter is not yet available in the US
    • Plasma exchange removes a large amount of native plasma; replaced with albumin
    • EBOO does not remove plasma proteins; filtration and ozone components
    • Plastic exposures: medical plastics have been present forever; probably less than eating, drinking, breathing sources; harder to get glass IV bottles today; less heat to IV bag and tubing the better; tube warmer safer than heating up the bag; don't let the fluid sit in the bag longer than needed; heat, light, temperature speed up release of plastics; make IVs and then put in fridge
    • Might do TPE and then follow with a phospholipid protocol for cell membranes
    • Every liquid medical product has aluminum; most research on zeolite is done with powders; he does not use liquid zeolite
    • Uses humic and fulvic acids separately to optimize their effectiveness
    • Has not seen any systemic effect from humic or fulvic acids
    • Supporting bile / phase 2 before binders will add to what is being bound; glutathione and fats
    • Taking binders when you wake up to urinate is a good option
    • Cholestyramine taken with food to decrease intolerance; not with medications or supplements
    • Biofilm disrupters go after bigger, badder biofilms; body will remake any healthy biofilms
    • DMSA often not tolerated without food but don't want to take something with a lot of minerals to maximize the impact of the DMSA; raw vegetables; not with a big meal
    • Metals seem to be the biggest problem
    • Always want some binder going through the body
    • Mold patients considered to be immune suppressed early on
    • High MPA is a potent immune suppressant
    • Phospholipids may not be tolerated early in a protocol if the patient is not strong enough; get stronger first; sort of painting the house; get the old paint off first before you paint the house
    • Best PC for IV is Essentiale-N; often unavailable; in US, easier to get Plaquex
    • If there was a true deletion in glutathione genes, the person would not be alive; many backups; the treatment is to give glutathione
    • Any time, you stir things up (sauna, exercise, etc.), good to have binders moving through the system
    • Gliotoxin with glutathione study was very narrow; a balanced amount of glutathione, C, E, and elimination support no concerns
    • Glutathione after a chelator increases benefit many fold

Robert Whitfield, MD spoke on "Breast Implant-related Illness & Explant Surgery” and shared:

  • Listens for symptoms of limited detoxification 
  • Can lead to more fatigue, brain fog, muscle/joint pain, GI symptoms, skin issues libido
  • Behavior: sleep, air, fluid, food, supplements
  • We only recover when we sleep; prioritize over all else
  • Water leaks -> mold -> poor air quality
  • No tap water: ground water can be a source of arsenic and other toxins; use filtered water
  • Ultra-processed foods cannot be consumed if you have acute or chronic inflammation
  • Methylation, antioxidants, vitamin D, glutathione
  • Looks at: genetics, toxicity, gut health, food sensitivities, hormones, blood spot (inflammation)
  • Hormone balance such as cortisol needed to optimize surgical procedures
  • Detox: home, work, travel, skin
  • Prepare instead of reacting: preop, marking, anesthesia block, surgery, nerve block, avoid narcotics
  • Antioxidants in high amounts can lead to more bleeding
  • Have to stop other "stacks", herbals, etc. in the lead-up to surgery
  • Post op: HBOT, Flowpresso, NanoVi, Red light; no IV therapy, use GI tract; protein and amino acids; filtered or hydrogen water only; don't alkalize 
  • Uses Human Regenerator to support healing
  • 100-200G protein per day
  • Tissue analyzed is the scar tissue after an explant
  • In 700 samples, 29% had bacteria -> oxidation of oleic acid -> macrophage polarization
  • Uses MicrogenDX for testing
  • https://www.mdpi.com/2076-2607/12/9/1830 
  • Body tries to extrude the implant like a splinter
  • Explant process uniquely positioned to help those with bacterial contamination 
  • Devices (implants) can leech heavy metals into the system; do not use sauna with breast implants; may increase chemical leeching from the device
  • Patients can lower symptoms in some cases without explant; more preparatory phase
  • Information from the Q&A
    • Sees people with autoimmunity that then get implants or those with implants that have indicators of autoimmunity
    • Capsule around an implant is similar to what you would see in an organ rejection
    • Most likely, the bacteremia is from another infection after implant placement that then moves through the blood
    • Has seen only 5 out of a couple thousand explants that had fungal components; it is not a thing
    • PEMF could potentially detrimentally increase blood flow after an explant
    • Sees SNPs in methylation, vitamin D, antioxidant, glutathione, estrogen

Kristine Profeta-Gedroic, MD spoke on "Parasites, Immune Regulation & MCAS” and shared:

  • Symptoms: dissociative thoughts, aggression rage, headaches, worst at full moon, oral rashes, bruxism, digestive problems including movement, liver pain, fecal urgency, loose stools, anal itching, rashes/histamine, insomnia, frequent waking, night terrors, restless leg
  • Types: nematodes, cestodes, trematodes, protozoan
  • Nematodes: roundworm, whipworm, hookworm, pinworm, threadworm, Strongyloides
  • Helminths: Cestodes (tapeworms), Trematodes (liver flukes, Schistosoma)
  • Osteoporosis is the result of osteoclast activation
  • Spectrum of macrophages: host defense, would healing, regulation; Th1, Th2, Treg
  • Treg cells downregulate excessive inflammatory reactions
  • Steroids clinically work by generating a regulatory reaction
  • Classically activated macrophage: IFN-y; increase production of superoxide anions, oxygen and nitrogen radicals; pro-inflammatory cytokines IL-1, IL-6, IL-23; persistently elevated cause expansion of Th17 and autoimmunity
  • COVID shifted everyone to more Th17 and chronic inflammation
  • Parasites invade through tissue; wound-healing macrophages respond to tissue injury; IL-4 production by basophils and mast cells; IL-4 a response to chitin in fungi and parasites; stimulates macrophages converting arginine to ornithine; increasing production of the ECM; mainly occurs in lungs and GI
  • We do not produce chitin but can produce chitinase 
  • Regulatory macrophages: later stages of adaptive immune response; downregulate IL-12 which turns off Th1; exploited by parasite, bacterial, and viral pathogens
  • Microglia are the brain's macrophages
  • M1 macrophages mediate defense with bacteria, protozoa, and virus; classically-activated
  • M2 is anti-inflammatory; alternatively-activated
  • Regulatory - secrete IL-10
  • Recruitment to Tissue -> Differentiation and Activation in Situ -> Conversion to Suppressive Cells -> Restoration of Tissue Homeostasis 
  • IL-4 and IL-13 Cellular Effects: T cells are primed to induce the B cells to class switch to IgE
  • IL-4/IL-13 inhibit autophagy and nitric oxide
  • Th1 shuts off Th2; Th2 shuts of Th1
  • Chitin found in parasites, fungi, insects
  • Occupations with high chitin associated with high asthma
  • Helminths trigger innate immune system which primes the adaptive system
  • Helminths do not replicate in the host; they produce eggs which go to an intermediate host
  • Body has a "weep and sweep" response using IL-4 to stimulate muscle hypercontractility to dislodge parasites
  • Parasites are clinically associated with MCAS, eosinophilic esophagitis/colitis, granulomatous diseases such as Sarcoid, collagenous colitis
  • Dealing with false negatives in stool tests...period.
  • Parasites are part of the normal microbiome
  • Parasites directly impact our Th2 response; suppress our immune response through stimulation of Treg cells
  • Consider treatment of parasites for all patients with chronic infections, allergy, and MCAS
  • Information from the Q&A
    • Real wasabi is a powerful antiparasitic 
    • Uses Byron White and Beyond Balance; uses Beyond Balance in children
    • May use an RX and then use an herbal until things settle down
    • Suspects that you would see a reduction in TGFb1 with parasite treatment; cytokine panels show reduction of IL-4, IL-13
    • TNF-a as a surrogate for Th1; IL-4 for Th2
    • Worms in the gut are the final stage; they expel thousands of eggs; those eggs will not become new worms in the same body
    • Parasites can be part of normal ecology and may not always need to be treated; it is about balance, not sterilizing 
    • Chitin in parasites binds metals and other toxins to the skeleton; must detoxify during a parasite cleanse
    • Albendazole does cross BBB and can cause an acute depressive syndrome

Ruth Kriz, APRN spoke on "How Biofilms May Contribute to Chronic Mold-related Illness" and shared:

  • 15-20% of her patients also had mold; had to address to resolve their chronic UTIs
  • Mold lives in biofilms along with bacteria and viruses
  • The compromised immune system from mycotoxins makes other infection eradication more difficult
  • Hypercoagulation patients are prone to chronic infections
  • Antimicrobials will not work as effectively with biofilms in the way
  • Biofilms can be made by people; not just microbes
  • Biofilms have been found in the bladder wall
  • Biofilms grow and eventually rupture and spill out microorganisms
  • Pathogen-produced biofilms can combine with biofilms created from the person's own fibrin
  • Organisms are dormant and not sensitive to antifungals or antibacterials; persister cells
  • Mold makes an extracellular matrix biofilm; produces mycotoxins; periods of dispersal with other location colonization
  • Aspergillus, Fusarium, Penicillium can also have biofilms
  • Enhance survival and create resistance genes
  • Can make molds 100-1000s of times more resistant to antimicrobial treatments
  • Have to get rid of the biofilms to access the embedded infections
  • Antifungals cannot get to fungi in biofilms
  • Biofilms protect mold: limiting antifungal diffusion through the matrix, transmission of resistant genes, azoles produce expression of drug-efflux pumps, fungi remodel cell walls in response to pH building tolerance to antifungals, presence of persister cells
  • Surviving fungi can rebuild after antifungals are removed
  • Persister cells do not carry their resistance making antifungals less effective
  • Biofilm made by mold and by person
  • Mast cells release pro-inflammatory cytokines; triggering intrinsic pathway
  • Extrinsic pathway results from injury; intrinsic happens in everyone
  • Fibrin is the end product of the coagulation pathway
  • COVID resulted in clotting events for patients
  • People with MCAS are pushing the coagulation pathway and producing more fibrin than other people
  • Some people make too much fibrin; others make a normal amount but cannot break it down
  • Two genetic problems that result in too much fibrin: Factor II and Factor V
  • Factor II makes too much prothrombin -> thrombin; spin off Prothrombin Fragment 1+2; excess is too much fibrin being made in real time
  • Factor V pushes activated Factor X and too much fibrin production; PF 1+2
  • Activated Protein C Resistance is the screening test for Factor V.  Low = low resistance and no brakes on Factor V pushing Factor X
  • Low Protein S Activity also results in too much fibrin.  Hundreds with acquired Protein S deficiency due to too many antibiotics and microbiome being low in Lactobacillus 
  • Protein C and S are both Vitamin K dependent
  • Low Protein S Activity can use vitamin K and probiotics; butyrate helpful as they prefer an acidic environment; most are not genetic
  • Body makes plasminogen which required Plasminogen Activator to make Plasmin; if blocked, you will not make enough plasmin to breakdown fibrin
  • Degradation of fibrin is D-Dimer; does not tell you if they are making a clot; tells how well they are activating plasminogen and breaking down the extra fibrin
  • Fibrinolytics will increase D-Dimer; and this is a good thing!
  • Fibrinolysis genetic problems blocking activation of plasmingoen; elevated Lp(a) and PAI-1 4G deletion
  • Lp(a) is genetic and does not respond to diet or exercise; binds tissue plasminogen activator -> no plasmin -> poor fibrin breakdown
  • Cholesterol is not the big problem and statin can increase Lp(a) by 20%; check Lp(a) if someone has LDL
  • Lp(a) can be brought down with niacin or lumbrokinase (for fibrin breakdown) or PSCK9 inhibitor such as berberine or Repatha
  • Need to reduce Lp(a) and use a fibrinolytic for historical build-up to reduce CVD risk
  • PAI-1 4G deletion: 100% compromise; 1 or 2 copies; does not functionally matter in terms of production of plasmin; higher miscarriages in 4G/4G compared to 4G/5G; high levels of plasminogen activator inhibitor results in low PAI-1 activity
  • A2AP binds plasmin making plasmin/antiplasmin complexes which are biologically inactive
  • Long COVID shows even a year after COVID, 100% still had elevated A2AP; preventing plasmin to breakdown fibrin / biofilms that are harboring COVID and other infections
  • Overproduction of fibrin - Factor II, Factor V, Low Protein S
  • Not enough plasmin: PAi-1 4G or Lp(a)
  • 20% of population has 1 of the 4 genetic variations
  • Ancestors clotted better when wounded in battle; not beneficial today
  • LabCorp panel 505443
  • Fibrin goes to clots, biofilms, and atherosclerotic plaque
  • Fibrin is trapping cholesterol
  • Mold and Lyme are triggers for more fibrin production; combined with genetics have a much bigger problem
  • Biofilms disrupted with:
    • Overproduction of fibrin
      • Lovenox
      • Apixaban
      • Low Protein S Activity: vitamin K, probiotics, butyrate
      • lumbrokinase
    • Poor fibrinolysis
      • PAI-1 4G - Lumbrokinase
      • Elevated Lp(a) - niacin + lumbrokinase or Repatha + lumbrokinase
  • Normalizing Lp(a) can make addressing infections much more effective
  • eDNA biofilms - Biofilm Phase 2 Advanced with bismuth; made by many bacteria including H. Pylori
  • Amyloid fibers - EGCG, NAC, Curcumin
  • Testing: MicroGenDX over 60,000 pathogens with 34,000 mold species; can do nasal testing; use Xlear to disrupt biofilms, lie on the side, do the other side, blow into a tissue; can do sputum specimen for lung colonization; has seen fungal colonization with both sinus and sputum samples
  • LabCorp 505443 is about $800 for cash pay; often covered by insurance when indicated
  • Information from the Q&A
    • Protein S Deficiency can look like Leiden Factor V; may present the same but are not
    • Boluoke is 600,000 units or 32mg for 2 capsules; pretty standard for other products
    • Researched Nutritionals is 880,000 units and 40mg
    • Dosing does not have to be terribly precise
    • Does not like multi-enzyme formulas as it may impact the bioavailability
    • Based on her consulting, practitioners are pleased with the new Researched Nutritionals product; only comes in 60 capsule bottle
    • Could look at D-Dimer to see how well any fibrinolytic might be working
    • COVID biofilms need Lumbrokinase
    • Have to use fibrinolytics to lower CVD risk

Krishna Doniparthi, MD spoke on "Lipid Replacement Therapy in Complex Chronic Illness" and shared:

  • Environment impacts our genetics through epigenetics
  • Epigenetic drifts are a change in how our genes are expressed
  • COVID-19 is a stressful event on the body
  • 4 epigenetic mechanisms: DNA methylation, histone modification chromatin remodeling, non-coding RA
  • DNA methylation: changes how a gene is expressed; essential for brain development, detoxification, regulating inflammation, neurotransmitter production
  • Histone modification: COVID can cause abnormal histone modification leading to immune dysregulation, inflammation, metabolic issues, neurological issues; DNA is in tact
  • Non-coding RNA: can be impacted by COVID which leads to altered gene expression and symptoms
  • Epigenetic drift is a gradual, random change in the switches that control our genes; COVID accelerates the drift; accelerated aging
  • Infection triggers inflammation/oxidation/immune activation -> disrupts epigenetic maintenance -> random DNA methylation changes
  • Long COVID: altered DNA methylation for immune and metabolic genes; age accelerators; increased drift 6 months after infection
  • Impacts neurotransmitters, mitochondria, neuroinflammation, blood-brain barrier integrity, neurogenesis, and myelin repair
  • Lipid Replacement Therapy can support against the impacts of epigenetic drift
  • Cell membrane repair and enhanced function
  • LRT: membrane repair and stability, mitochondria, reduce oxidative stress, methylation/epigenetic support, improved cell signaling and neurotransmission
  • Plasmalogens are a cousin; reduce oxidative stress, antioxidants
  • PC is a choline contributor but serves many other roles
  • Can replace lipids with liquid, capsules, powders, or IV
  • Nutrients: MB12/folate, NAC, CoQ10, magnesium, omega 3
  • ProdromeScan, DNA methylation, homocysteine, OAT testing may be helpful
  • May start with glutathione or NAC and then add PC or plasmalogens; later methylation support with B12 and folate
  • Radiance Diagnosis cytokine panel
  • Nutritional support: methyl donors such as folate/B12/B5/betaine; antioxidants such as NAC, ALA, C, sulforaphane; adaptogens such as ashwagandha; mitochondrial such as CoQ10, NAD, phospholipids
  • Restore sleep, physical activity, stress reduction, low toxin environment
  • Low fatty acids, phospholipids, and plasmalogens can be an indication of liver dysfunction
  • There are epigenetic drifts and there are substrates and supplements that can help
  • Information from the Q&A
    • C15 is an odd chain fatty acid; we don't have much use for odd chain fatty acids
    • Omega 3 and 6 are all even chain fatty acids
    • Enzymes in the cell covert C15 to C16 or C18
    • All fatty acids are stored as phospholipids
    • Phospholipids have an ester bond in the first connection (sn-1) which is an ether bond in plasmalogens; the head groups are the same
    • Oral PC: most cells ~40% PC; ~35% PE; ~15% PI/PS; you don't want to just use PC as it supports only one side of the cell lipid bilayer; PE inner; PC outer; he created a product by Precision Nutrients which has all 4 lipids; soy, sunflower are common sources; chicken, egg yolks, sea food in low quantities; raw egg yolk is the most natural
    • For IV, only uses Sanofi from Europe; Essentiale-N
    • Lipid droplets are a single layer of lipid that surround a toxin; escorts it out; glutathione as a natural binder
    • Phospholipids are ~75% of cellular architecture; plasmalogens are the rest

Kat Toups, MD spoke on "Reversing Cognitive Decline – Updates on Emerging Research" and shared:

  • Working on a clinical trial
  • Dementia is preventable and treatable
  • Find and correct the underlying causes
  • Dementia is not a death sentence
  • They did a trial in 2022 that showed 84% improvement; 12% declined; 4% no change
  • Some that declined were living in mold
  • RX options are still resulting in decline; not addressing what caused the amyloid in the first place
  • Patients increased gray matter volume; hippocampal volume decreased but far less than study participants
  • New study in 2025
  • More than 7 million in US with dementia; younger and younger
  • COVID impacts blood vessels and brain; seeing brain dementia even at young ages
  • Had a control arm in this study; could be argued to be unethical
  • Harder to help people with a MoCA of 18 or less; were not part of the study
  • 72 patients in 2 different groups; 2/3 active treatment; 1/3 standard of care
  • Home sleep testing for 3 nights
  • Testing with MyPerioPath
  • You can't fix some of the factors; you have to fix all of them
  • Large battery of tests used in the study
  • Infections tested: Lyme, Babesia, Bartonella, Ehrlichia/Anaplasma, TBRF, EBV, HSV 1/2, HHV6, Toxoplasmosis, Mycoplasma, CMV, Chlamydia, Syphilis, HIV, Hepatitis, COVID
  • COVID has really changed the landscape of the brain
  • Brain biomarkers: p-Tau 217 (inside neurons), A-beta 42/40 (lower ratio is worse; outside neurons), GFAP (less specific; neurodegeneration and head trauma; can be in TBI, MS, PD, FTD), NfL (neuronal injury indicator; neurodegeneration; useful in ALS), BDNF (essential for neuroplasticity; not available commercially)
  • Amyloid is antimicrobial and is protective
  • ApoE 4 have more robust amyloid secretion
  • NeuroCode uses a very sensitive platform for testing
  • Wearables: Oura, CGM, Cronometer, BrainHQ, HeartMath, Keto Mojo
  • More cognitive benefits the higher the ketone levels; they were shooting for 1-4
  • Diet: Ketogenic, grain free, dairy free, Paleo type, time restricted eating (eat 8-12 hours a day), avoid eating 2-3 hours before bedtime
  • Optimized sleep, exercise, brain training, mindfulness, dental health
  • Nutritionist, health coach, exercise coach, study partner
  • With aging, cannot utilize glucose properly and need more ketones as a workaround
  • Used basic nutrients and mitochondrial supports, nootropics; hormone optimization
  • Phobobiomodulation, neurofeedback, HBOT, EWOT, cold laser
  • Patients with 4/4 can do fine; you just have to work harder
  • Results (not yet published) showed the treatment group did better than the standard of care group; the degree of improvement varied somewhat based on the measurement being used
  • Information from the Q&A
    • If people don't get out of mold, the hopefulness index goes down. - Mary Ackerley, MD
    • When the brain is degenerating, you need even more mitochondrial support
    • COVID and COVID vaccines appear to attack the blood vessels and lead to white matter disease
    • Arterosil, nitric oxide, pycnogenol for vascular support
    • All of your patients are potential Alzheimer's patients.  - Mary Ackerley, MD
    • Need to know more about the right candidate for plasmapheresis; some have notably worsened after
    • Auragen light therapy was helpful for her patients; has seen rapid improvements in visual processing
    • She saw notable improvements in her own brain scans with the Auragen; Renew with gamma stimulation for the brain
    • You cannot heal when in a high stress state
    • New HeartMath device that shows HRV in real-time
    • Oxytocin can be very calming
    • Lithium is a wonderful nutrient that can lower P-tau and amyloid and improve BDNF
    • BDNF - exercise, meditation, ketosis, PBM, lithium, nattokinase, butyrate, whole fruit coffee extract, Cerebrolysin, carnosine, peptides
    • One of the best predictors of longevity is muscle strength

Alexis Cutchins, MD spoke on "Venous Insufficiency" and shared:

  • Works with POTS, MCAS, and EDS
  • Patients with environmental illness often have POTS, MCAS
  • No FDA approved treatments for POTS; off-label
  • Compression of veins may lead to collateral vessel formation
  • May be treated with a stent
  • Conditions associated with POTS: HSD/EDS, venous disease, infectious contributions
  • POTS: Autoimmune, GI/dysmotility, MCAS, venous disease/vascular compression, small fiber neuropathy, cognitive dysfunction, infection, CCI/TC, endocrine, mixed connective tissue/HSD
  • POTS is a condition that has to be addressed from many different aspects
  • POTS is a physiological condition; not just in your head
  • When you stand, 300-800 ml of blood go to abdomen and lower extremities; results in 10-15 beat increase in HR and 5-10 diastolic increase in normal patients
  • Symptoms: dizziness, lightheaded, weakness, blurred vision, brain fog, fatigue, migraine, palpitations, tremulousness, anxiety, shortness of breath/cheat pain, nausea, abdominal cramps, bloating, constipation/diarrhea, GERD, dysphagia, pelvic pain, menorrhagia, allergies, intolerances, hives
  • Symptoms often started after COVID, EBV, Lyme
  • Looks for hypermobility, venous pooling/edema, elasticity or translucence of the skin, stretch marks, adipose tissue distribution (lipedema), flushing/rash/dermatographia
  • In hEDS, difficult venous access, skin is thin, stretchy, translucent; 90% of EDS population; results in defects in collagen
  • Venous disease/pooling can be a driver of POTS; less blood returned to heart and less blood to brain
  • Pro-thrombotic state
  • Long COVID can create a cascade of problems including mitochondria, microbiome, thromboinflammation, HPA axis issues, neuroinflammation
  • Venous insufficiency: aching, heavy, cramping, uncomfortable legs, swollen feet and ankles, burning, throbbing, tingling in legs, muscle cramps in in legs, dry itching think skin over affected vein, restless legs, leg ulcers, discoloration of skin, pain that worsens when standing and improves with legs up, pelvic pain, pain with intercourse, low back pain
  • Iliac vein compression; May-Thurner Syndrome
  • If the body makes collaterals, why do we need to fix the main flow?  They do not work as well, do not have valves, limited blood capacity, irritate structures the blood is pooling in; opening allows for more blood to the heart and closes the collaterals  
  • Iliac vein compression can lead to scar tissue formation; vein walls are rubbing against each other
  • Veins in the venous system are overlooked in medicine
  • Veins hold more volume; arteries have more pressure
  • Most of her POTS patients have some form of hypermobility and some MCAS; 80% have venous disease
  • Pelvic Venous Insufficiency can occur in POTS
  • Treatment of iliac vein compression: iliac vein stent, sclerotherapy/coiling
  • Venous stenting is quite safe; some risk of stent migration; less common with longer-stents; may need a short course of anticoagulation for a thrombus; stent placement can lead to significant back pain that results in a couple of weeks
  • Other tools: fascial counter-strain; Sulodexide (oral heparin) may repair the glycocalyx; not approved in US
  • Treatment of Venous Disease with no pelvic/leg pain; no approved indications for stenting for orthostatic intolerance
  • General population venous insufficiency 7-60%; same for iliac vein compression
  • POTS is more common in women
  • Venous disease plays a large role i POTS
  • Symptoms worsen with infections leading to endothelial inflammation
  • There is a link between POTS/HSD/Pelvic Venous Disorder
  • Information from the Q&A
    • Radiologist often see these conditions as incidental findings
    • Checks all POTS patients with an ultrasound for venous insufficiency
    • Many have an ultrasound for pelvic pain before they explore the potential for vein compression
    • A normal study does not necessarily mean it is normal
    • Lower extremity doppler
    • Fibroids could be a contributor to venous compression/insufficiency
    • Has seen interstitial cystitis resolve with pelvic disease treatment
    • Population of patients that are pre-disposed to complications from infections
    • Patients may be born with abnormal connective tissue that is triggered by a later insult
    • Has found success with GLP1 in lipedema patients; inflammation, glucose regulation
    • Diosmin and horse chestnut extract for venous disease; not a robust response but some do respond well
    • Has had patients that get worse when anticoagulants are stopped and improve when restarted
    • Has seen POTS after COVID or HPV injections; sees similar presentations in some patients after reaction to injections; further trigger the inflammatory cascade
    • Feels you are born with a predisposition and later have a "hit" that results in a debilitating condition
    • Compression, lymphatic therapies can be very helpful adjuncts
    • Many patients are intolerant to treatment options
    • Salt, water, compression, exercise; early options tried in every patient
    • Every patient with POTS has some spectrum of MCAS activity
    • Treating MCAS helps tremendously in POTS patients
    • Can have vein-related issues from head to toe

Lawrence Afrin, MD spoke on "Diagnosis of MCAS" and shared:

  • No FDA approved treatments for MCAS; FDA may not even know the disease exists
  • MCAS is a chronic and inappropriate release of many mediators by mast cells
  • More than 1200 mediators produced by mast cells
  • Drive inflammatory effects; the universal constant is inflammation
  • Some MCAS patients do not have allergy; others life-threatening anaphylaxis 
  • Many mediators are involved in growth and development of tissues; can lead to cysts, fibrosis, aneurysms, weak connective tissues (EDS), neurodevelopmental (autism)
  • 17% of the general population
  • Mastocytosis is a very rare disease 
  •  MCAS is probably a primary disease in most MCAS patients; rooted in genes in mast cells
  • The mutations are not inherited but are acquired; leads to a step-wise worsening
  • Autoantibodies may attack mast cells; anti-IgE; the attach triggers the mast cells; more rare
  • Can be a secondary disease; chronic inflammation, malignancy, toxic exposures
  • The vast majority of MCAS are not clonal; KIT mutations; commonly found in mastocytosis and not in MCAS
  • May be 10-20 years before highly specialized genetic testing is commercially available
  • Do not have the ability today to adequately test for the clonality of the disease
  • No true consensus yet in diagnosing MCAS
  • Far wider range of symptoms than acknowledged in the "consensus-1" criteria; increase in tryptase; demonstrated response to treatment 
  • Tryptase is quite stable in MCAS even when having a flare
  • "Consensus-2" requires some laboratory evidence of mast cell activation
  • High familial propensity even without genetically-inherited mutations
  • Symptoms often chronic/recurrent, episodic/intermittent, and waxing/waning
  • Can see escalations around puberty, college, marriage, pregnancy, stressful employment events, relocations, surgeries, traumas, immune events
  • Long COVID is probably an escalation of pre-existing MCAS that is sparked by severe inflammation that the virus or vaccine lead to
  • Reactions to medications are generally related to fillers, binders, dyes, preservatives; not the drug itself
  • Patients learn not to share their symptoms; have to extract them out of them
  • Most tissues in the body have few or no mast cells; dominant at environmental interfaces; skin, respiratory, GI genitourinary, vessels, neurons
  • Normal number of mast cells but activation of the mast cells
  • Looks for at least two points of evidence
  • MCAS can be a life-changing diagnosis for the person and the family
  • Mediator testing is challenging
  • Certain drugs may interfere with some of the tests; such as PPIs interfering with chromogranin A testing
  • Many tests are negative even with obvious symptoms
  • Find 2 or more abnormal mediators commonly within 3 rounds of testing
  • Specimen temperature is critical
  • If you cannot get positive testing with proper process, tissue biopsy may be used; can re-stain old biopsies
  • Checks: CBCD, CMP, magnesium, PT/PTT, tryptase, chromogranin A, prostaglandin D2, histamine, heparin, PGD2, 11-beta-PGF2-alpha, N-methylhistamine, leukotriene E4, anti-IgE or receptor antibodies
  • 5-6% of population have hereditary alpha-tryptasemia (HAT); overproduce tryptase
  • HAT patients have very similar symptoms to MCAS patients
  • May have to have patients off medications and supplements to maximize lab sensitivity
  • Plasma, whole blood, 24 hour urine histamine; no clear advantage in terms of plasma vs. serum vs. whole blood
  • Plasma heparin is the one most commonly positive
  • Antibodies can be mimicking antibodies of no significance
  • Information from the Q&A
    • Various somatic or acquired mutations underly MCAS; mutations are generally permanent
    • Growing studies suggesting increased risk in dementia, Alzheimer's, Parkinson's in those with chronic use of H1 and H2 blockers
    • The papers have not shown that the drugs are causal; there is an association; mast cell disease is a chronic, multi-system, inflammatory disease
    • Chronic inflammation assaulting the CNS for decades may increase brain diseases
    • Great majority of people with mildly elevated tryptase may have HAT
    • The mediators being measured are not, for the most part, the mediators driving the symptoms
    • If testing is done properly, the vast majority will find 2 or more abnormal indicators
    • Ask local labs if they have a refrigerated centrifuge; it not, keep looking
    • Chromogranin, PGD2, and heparin are the most commonly elevated in research
    • Chromogranin is the least specific to the mast cell

Ritchie Shoemaker, MD spoke on "CIRS Update – GENIE: The Last Six Years" and shared:

  • GENIE - Genetic Expression: Inflammation Explained
  • 64 published biomarkers looking at CIRS; many in GENIE
  • Specific causation allows us to say with certainty that the cause is fungi/mycotoxins, Actinobacteria, endotoxins, beta glucans, etc.; can be more than one
  • GENIE looks at 200 genes that are important for CIRS
  • Inflammation, metabolism, and transcriptomic problems in CIRS
  • Looking at activated and suppressed genes
  • Transcription factors turn on gene expression
  • Bacteria turn on toxin production; toxin/antitoxin; shown in over 6000 species
  • Molecular hypometabolism: suppression of ribosomal activity; 37 mitochondrial genes; source of chronic fatigue in 85% of patients
  • Ribosomal inhibitory proteins (RIPs) can be called ribotoxins
  • Impact ATP Synthases and cyclooxygenases 
  • Metabolic acidosis - 80% with MA will have Treg deficiency, gray matter nuclear atrophy, pulmonary hypertension, insulin resistance, and/or widened anion gap
  • IRS2 elevation = proliferative physiology; lactic acidosis
  • Sarcin/ricin loops; removal of adenosine; one gene change
  • Normal mitochondria (not mitochondrial disease); but they don't work
  • When you fix the illness, the mitochondria go back to working normally
  • IRS2 activated glucose transport proteins 1 and 4 and allows glucose to flood into the cell; converted to pyruvate
  • What does the cell do with pyruvate if it cannot cross the mitochondrial membrane?  The mitochondria are on spike
  • Warburg Effect = proliferative physiology; not just in cancer; metabolic acidosis linked to elevated IRS2
  • Keto diet works well if IRS2 is suppressed otherwise, will make things a lot worse
  • Anion gap > 13 (not equal to); (sodium + potassium) - (trichloride + CO2)
  • Linked to Actinobacteria; left behind by failed remediation
  • Saw low CO2 findings in patients
  • Without GENIE, many things you will never know
  • Coagulation genes, localized ischemia micro clots, bleeds; binds to tau; use HIF1A for hypoxia, pulmonary hypertension; Akt activation controls autophagy in CNS and protein-misfolding; autophagy suppressed by Akt -> Lewy Bodies -> Parkinson's
  • Apoptosis is programmed cell death; if fungal causation, see 2 caspase genes and 1 other MAP kinase; defective apoptosis; source of endogenous inflammation
  • BCL2 active with HIV and COVID; says you had COVID before
  • Long COVID: is there evidence of TGFBR1, 2, 3 receptors?  
  • CLU/clusterin important in apoptosis; involved in triple positives
  • Specific causation: Actinos/endos/fungi/beta glucans
  • Correlates specific exposure to inflammation
  • Causation: 42% Actinos, 28% endos, fungi 7%, beta glucans ~10%
  • Actinos: looking for one or more TGFBR1, 2, 3 and one or more of 6 MAPK
  • > 10,000 P Acnes (PA) or Corynebacterium tuberculostearicum (CT)
  • Soil-based Actnios are related to ribosomal inhibitory proteins
  • RELA, TLR2, AKT, are new CIRS biomarkers; now 64 markers
  • Endotoxins: CD14 or TLR2 >= 1.3 or +TLR4
  • 100 endotoxin level is the cutoff on Envirobiomics testing 
  • AKT, RELA, TLR2 are new biomarkers
  • Fungi: 2 or more caspase genes and 3 ore more MAPK genes
  • Beta glucans: hypometaolism and no other causation with T cell Synapse 
  • Fungi like acidic environments, Actinos like alkaline
  • 3 or more COAG genes in triple positives
  • Lyme: mean of Z-scores of CD40LG, IL1B, TGF BETA-1, and TNF > 1.3
  • Defensins look at free viruses and bacteria in blood (not tissue)
  • IKAROS and VIPR1 involved in environmental susceptibility; negative/positive is rare; positive/negative MCS, food/drug sensitivity
  • Low dose VIP protocol for MCS published in textbook of CIRS
  • TLR2 > 1.5 represents microglial activation
  • Defective T cell presentation CD3D
  • PTSD, FKBP5 not specific for any specific source; has seen a few cases of suicide
  • Histamine CCL5, HDC; every nucleated cell in the body; not just mast cells
  • TUBA4A, TUBB1 are the third leg of triple positives
  • Treg cell deficiency; Th17/TReg imbalance; looks like CIRS but is not; metabolic acidosis
  • Triple positives in about 10% of cases; find 10-16 CIRS biomarkers
  • Role of endotoxins in the brain: contributes to neurodegeneration 
  • Plumbing is the leading cause of endotoxin exposure
  • LPS injected in research leads to microglial activation for 12 months
  • Nasal wtTIDM peptide reduces glial inflammation and alpha-synuclein spreading
  • GENIE can be applied to approach neurodegeneration
  • Information from the Q&A
    • wtTIDM is not related to VIP
    • Endotoxins from urinary, GI bacterial infections; could be an inflammatory illness
    • LPS binding protein should mean you could have all the LPS you want and not lead to illness
    • Jury is still out on a role for endogenous LPS; cannot say absolutely no but has not seen data that says yes
    • Sees correction of endotoxin, TLR2, TLR4, CD14 with removal of external exposure

 Jill Crista, ND spoke on "Herbal Anti-Fungal Interventions" and shared:

  • Some feel better when they are removed from exposure; some do not
  • Fungi become unwelcome residents rather than tourists
  • Normal controls and CFS with WDB all had fungi in the sinuses; the fungi in sick patients had mycotoxins not found in healthy controls
  • The result is colonization/biofilms
  • Intranasal antifungals led to patients getting better much faster
  • Colonization is when the fungi take up residence; sinuses, lungs, GI tract
  • Colonization = dysbiotic biome
  • Once a patient is recovered, MPA or mycotoxin exposure can trigger old patterns; immunosuppression
  • Affects all mucosa/mucocutaneous tissue 
  • Slower growing molds tend to be the more toxic; Stachybotrys, Chaetomium, Wallemia, Trichoderma 
  • Mycotoxins, MPA, mVOCs, alcohols, aldehydes all involved
  • Just Well Law winning mold cases and doing amazing work
  • Herbal antifungals: don't need to wait until someone has dementia, GI problems, neuropsych problems, etc.
  • Peel the orange: Avoidance, Fundamentals (diet/sleep), Protect (tissues), Repair (immune modulation), Fight
  • In an ideal world would be out of mold before starting antifungals
  • Few clinical trials on herbs as they can't be patented
  • Drug companies come to rainforest, learn from them, and then burn the rainforests
  • Natures has compounds to potentiate the active component or mitigate the side effects
  • Antifungals to reset the body's biome; reduce body burden; reset to commensal working to the benefit of the host
  • Antifungals sooner minimize histamine, sulfur, oxalate, salicylate issues
  • Fungal overgrowth is the fire; mycotoxins are the smoke
  • Mop up the smoke and reset the microbiome; add the antifungals to put out the fire and minimize the smoke
  • Herbals: often more gentle on person (not fungus), broad-spectrum, prevents mycotoxin production as a defense, anti-inflammatory, antioxidant, mast cell stabilizers, not hard on the mycobiomes, prevents fungal resistance and biofilms
  • Disadvantages: frequent dosing required; higher doses often required; taste expense; may use up to 6 times per day
  • Not everything that can eradicate yeast can eradicate mold
  • Mushrooms/mycelium are wise; mold are worker bees; Candida are dummies
  • Candida formulas may not impact multi-cellular organisms
  • Most gentle to more aggressive
  • Holy Basil - when still stuck in mold; affinity for lungs, inhibits fungal adhesion and invasion; reduces MMP9 (marker for mast cell), action against drug resistance; likes in a glycerite
  • Thyme - a favorite; can help PANS kids; inhibits Aflatoxin production; pre-dose with thyme before more aggressive interventions to minimize mycotoxin production
  • Oregano - antifungal broadly; anti-mycotoxin effects
  • Neem - broad antifungal; long-standing asthma/SIBO/Babesia; good to minimize drug resistance; whole plant needed for broader effects
  • Pau D' Arco - deeply embedded mucous/sinusitis/asthma; MIC similar to Amphotericin B; immune modulation; can help in those with potential cancers
  • Clove - broad antifungal; eradicates all the big guys; disrupts biofilms; anti-mycotoxin 
  • Finds biofilms in prostate after mold
  • Sneak in with the plants to shutdown mold's ability to defend itself before using bigger guns if needed
  • Holy basil, thyme, oregano, neem, Pau D'Arco, Clove have positive effects on the microbiome; may protect the microbiome
  • Respirator masks used by IEPs do not block from mycotoxins
  • Resistance vs. Persistence - person feeling great; symptoms creeping back; could be not strong enough treatment or could be fungal resistance; feel good on a therapy but then the benefits seem to run out
  • Symptom return when stopping treatment could be a biofilm thing
  • Colonization and biofilm are a continuum, kind of the same thing
  • MARCoNS, Pseudomonas, or Klebsiella in sinuses; assume biofilms
  • ENTs do not treat biofilms
  • Zearalenone can reduce testosterone 
  • Stachybotrys in the sinuses can produce trichothecenes; the nose matters
  • Sinus treatments
    • Antifungals - essential oils, lauricidin/monolaurin, manuka honey, propolis
    • Antibiotics - colloidal silver, allicin
    • Biofilm - xylitol, NAC, ozone
    • Only use STERILE water with nasal treatments
    • Lactobacillus sakeii and casei 
  • Essential oils reduce fungal growth, reduce mycotoxin production; safe to use long term
  • Can use essential oil nasal sticks
  • Essential oils do have aldehydes
  • People do not get all the way better until they get out of mold
  • Visualization to get out of coherence with mold
  • Information from the Q&A
    • MicrobiologyDx and MicroGenDx (many different body fluids can be tested)
    • B6 is important as a nutrient on agar plates; needed for some molds; a reason people become B6 deficient; the molds eat B6
    • Need both sinus and GI/systemic antifungals
    • Holy basil improves microbial diversity
    • Uses bioflavonoids to provoke urine mycotoxin testing
    • Treats the nose until there are no urinary mycotoxins
    • Fish oil can be helpful for those with salicylates 
    • Symptoms need to be 80% better or more before considering stopping antifungals
    • Resistance would be getting to 80%, continuing treatment, but losing ground
    • Looks for zero on MyMycoLab and urine mycotoxin
    • 10 or above on her questionnaire is a strong correlation with mold-related illness; 5-9 mold should be considered as a differential/further exploration
    • Chitin is Actinos favorite food
    • Does not use glutathione with gliotoxin; the sulfur will lead to more gliotoxin; similar with Patulin and salicylates
    • Glutathione, NAC, ALA, butyrate; sulfur-foods; avoided in gliotoxin
    • Aloe, hops, nettle, holy basil for mast cells
    • Amphotericin better for those with salicylate sensitivity 
    • Azoles may further tax the glucuronidation pathway
    • Bioflavonoids before binders for mycotoxin clearance through kidneys
    • Uses many different binders; aloe (binder that gives back; with food for nutrient absorption); steamed kale, mustard greens, collard greens, finely ground okra or lemongrass (trichothecene)
    • Chaetoglobosin needs Colesevalam for a month; then moves on to other binders
    • Uses a bioflavonoid mix rich in antioxidants; 3 capsules at bed; 3 in the morning; and then collects urine for 6 hours; for urine mycotoxin provocation

Michael Schrantz, CIEC spoke on "IEP Lecture: Fungal Ecology in the Indoor Environment" and shared:

  • Has done thousands of mold inspections
  • Must understand normal fungal ecology to interpret test results
  • Condition 1, 2, 3 from S520
  • Condition 1 defines normal fungal ecology: settled spores, fungal fragments, or traces of growth; may not be elevated
  • Condition 2- settled spores with primarily contaminated spores from a Condition 3 area or actual growth; SPC is typically the solution
  • Condition 3- microbial growth; indoor environment contaminated with actual growth; can be visible or hidden; or low density growth you cannot see with the eye; physical removal/remediation is needed
  • Normal background is normal fungal ecology; mold-free is not a thing; outdoors influences indoor levels
  • Normal fungal ecology outdoors is different in geographies, climates, seasons
  • Outdoor influence can be different from your home to your neighbor's home
  • Airborne levels of mold spores indoors will often be higher than normal background outdoors because of accumulation; does not necessarily indicate a mold growth problem
  • When accumulation is the cause of a high test result, cleaning/maintenance is the solution
  • 3 Myths
    • A good indoor environment is mold free; mold free does not exist
    • Any elevated test result automatically means there is a mold problem; must consider normal background; accumulation through normal build-up; or a mold problem
    • Testing is the best way to diagnose a mold problem in a building; more of a clinical diagnosis; history, inspection; testing as an adjunct; testing best when done professionally and secondary to interview/inspection which drives the sampling strategy 
  • Stachybotrys regularly exists at low levels outside
  • Homes that are not cleaned well will accumulate mold spores over time
  • A pea size mold growth on shower grout may be a very small exposure; and ironically, leaving the door open will bring in more mold from the outside
  • HVAC - heating, ventilation, air conditioning
  • Duct work is like carpeting; it is a reservoir that will build up over time; may have higher concentrations of molds
  • Normal use leads to normal background buildup
  • If your goal is mold-free, you would have to change your duct work every 7 seconds
  • Common to have Condition 2 in duct work; or even condition 3 in a coil
  • Duct work cleaning will impact the sequence of the process; must do before an SPC
  • Any porous component with condition 3 (or even 2 sometimes) will need to be replaced
  • Non-porous commonly need cleaning only; many components in HVAC are non-porous and cleanable
  • Mold growth common in components of HVAC such as an evaporator coil
  • Sometimes recommendations are extreme and impossible to achieve 
  • May have mold on the vent registers just in certain seasons; could be humidity touching the register; may be a topical issue
  • Musty smells may be observed when A/C starts up; some accumulation of microbial growth or damp dust within the evaporator coil or drain pan; takes stale area and delivers to the home; may be more related to how the system is functioning, drain pan drainage
  • Do you notice symptoms when turning on or off the system?

Michael Schrantz, CIEC spoke on "IEP Lecture: Abnormal Fungal Ecology (Leading to Mold Exposure) in HVAC Systems" and shared:

  • Not all about doom and gloom with mold sources in the HVAC system
  • HVAC systems are prone to mold/microbial problems
  • HVAC is the lungs of the home; the system efficiently distributes contamination throughout the living spaces
  • Traditional mold inspections overlook the HVAC; black sheep
  • Patients often overlook HVAC when doing DIY SPC
  • Radiator heating, radiant floor (heated water pipes or electric cords), baseboard heating (electric or heated water pipes), evaporative "swamp" coolers, A/C window units (common in rentals), package unit on roof, mini-split, gas furnace with A/C evaporator coil, or electric heat pump with A/C evaporator coil
  • Swamp coolers; if you push moisture-laden air, you could create condition for mold in the living space; great reservoir for mold and bacteria
  • Window units are ductless; common sources of growth; not maintained well
  • Package unit has everything in it; condensing unit on outside of house; one big box
  • Mini-split commonly ductless (but can have ducts); evaporator cooler, drain pain; known to get moldy
  • Evaporator coil and blower wheel in different locations in gas furnace with A/C evaporator coil vs electric heat pump with A/C evaporator coil
  • AC removes moisture which can result in condensation
  • Condensation can occur in/on/near the evaporator coil, plenum, ductwork
  • When A/C cools air, surfaces become a condensing surface which can create a microbial problem
  • The cooler you keep the home in a warmer, humid climates, the more the moisture wants to come into the home
  • Colder temperatures create more condensation potential
  • Refrigerant running through the coil absorbs heat from the living space
  • Blower wheel circulates cooled air; surfaces on coil get very cold; warmer air from living space holds more moisture; vapor turns to liquid form and to drain pain and out condensate line
  • Want to avoid standing water in the drain pain
  • Blower wheel can get mold on it; proximity to evaporator coil can create condensation
  • Packaged units have a separate blower wheel; gas furnace in the unit
  • Duct work can be rigid vs. flex ducting
  • Duct work lined with insulation is porous; metal only is better; pros and cons
  • Debris can buildup in duct work
  • Raised platforms; furnace may sit above the floor due to code requirements; can have a condensate leak that leads to a wet, damp environment supporting microbial growth
  • Take your time to inspect the HVAC system
  • The homeowner should provide physical access to the system including opening any panels
  • Inspect all sides of the evaporator coil; collect a swab sample
  • Visually inspect the drain pan; check for evidence of growth
  • May pour small amount of water into the drain pain to see how the water is draining; it should not stay
  • Check the Vent-T of the condensate line; can have microbial growth; if hooked to a gas furnace, the box would be under positive pressure and mold would not go into system; but electric would be negative air and could suck into the system
  • Look for rust on the blower wheel; related to moisture
  • Supply air plenum can be common area for microbial growth; insulated plenums are breeding grounds; wrap on the outside
  • HVAC Cleaning: ACR NADCA Standard for HVAC 2021; does support chemicals which they do not recommend
  • Clean the duct work before remediation and cleaning of the home
  • Seal registers and vents to prevent cross-contamination after the system is cleaned 
  • HEPA vacuum, damp wiping where possible
  • Compressed Air Whip System; agitates the duct surface and sucks the particulates out
  • Rotary brush is like a toothbrush for the duct work; probably the better option
  • What to what out for: duct cleaning machine may be exhausted back into your living air; want a truck mounted system
  • Duct cleaning should clean the blower wheel, evaporator coil, and registers
  • Ask for the components that will be cleaned to be put in writing
  • Clean HVAC and duct work before SPC
  • Limit release of debris into the home during the cleaning process
  • Ask if any chemicals will be used.  The answer should be no.
  • Information from the Q&A
    • Can get vent cover film on Amazon; any duct work should be sealed off to minimize cross contamination
    • Try to have the HVAC system in the conditioned space
    • Builders want to get the HVAC out of the space and into the attic; can have more condensation; often on the outside of the ducts and not the inside of the ducts
    • Crawlspace should be dry and be encapsulated
    • Metal round ducting with insulation on the outside preferred
    • When not a mold problem, cleaning often suggested every 3-5 years
    • NADCA recommends an annual inspection of the HVAC system
    • Cross-contamination into the living space after duct cleaning is a potential concern

Disclaimer: While I attempted to accurately represent the statements of the various speakers, it is possible (or even likely certain) that the above contains errors or inaccuracies. If you have any corrections to the content listed above, please Contact Me.