This document summarizes a presentation on the evaluation and treatment of mold toxicity using mycotoxin assays. It discusses evaluating patients for mold toxicity based on their symptoms and biomarkers, as mold toxicity can mimic many other conditions. Treatment involves removing mold toxins from the body, eliminating mold exposure, and repairing the damage caused by toxins, as outlined in Dr. Shoemaker's biotoxin pathway model. Genetic testing for HLA-DR is also discussed as valuable to diagnosis.

1. EVALUATION & TREATMENTEVALUATION & TREATMENT
OF MOLD TOXICITY WITHOF MOLD TOXICITY WITH
THE USE OF MYCOTOXINTHE USE OF MYCOTOXIN
ASSAYSASSAYS
SymposiumSymposium
August 3-5th, 2018August 3-5th, 2018
Presented by Neil Nathan MDPresented by Neil Nathan MD

2. CONFLICT OF INTEREST?CONFLICT OF INTEREST?
DISCLAIMER:DISCLAIMER:
I have NO financial ties to any laboratory,I have NO financial ties to any laboratory,
medication, or supplement product to bemedication, or supplement product to be
discussed in this presentation (nor does mydiscussed in this presentation (nor does my
wife).wife).
Level of Evidence for Patient CareLevel of Evidence for Patient Care
Recommendations: Level B-publicationsRecommendations: Level B-publications

3. ADDITIONAL DISCLAIMERADDITIONAL DISCLAIMER
 The “Science” of the diagnosis andThe “Science” of the diagnosis and
treatment of mold toxicity is currentlytreatment of mold toxicity is currently
in its infancy. This presentation is anin its infancy. This presentation is an
attempt to synthesize the currentattempt to synthesize the current
information and approaches andinformation and approaches and
represents a work in progress withrepresents a work in progress with
change inevitable as our knowledgechange inevitable as our knowledge
advances.advances.

4. MY CURRENT PATIENTS:MY CURRENT PATIENTS:
AN OVERVIEWAN OVERVIEW
 This presentation is intentionally basedThis presentation is intentionally based
on my experience with unusually toxicon my experience with unusually toxic
and sensitive patients. Many patientsand sensitive patients. Many patients
who present to you can be treated muchwho present to you can be treated much
more aggressively; but if you can treatmore aggressively; but if you can treat
the sensitive patient, the rest will be a lotthe sensitive patient, the rest will be a lot
more straightforward.more straightforward.

6. ““MOLD” IS MUCH MORE THANMOLD” IS MUCH MORE THAN
MOLDMOLD
OTHER COMPONENTS INCLUDE;OTHER COMPONENTS INCLUDE;
 FungiFungi
 ActinomycetesActinomycetes
 MycobacteriaMycobacteria
 VOCs (Volatile Organic Compounds)VOCs (Volatile Organic Compounds)
 Beta glucans, hemolysinsBeta glucans, hemolysins
 Mannans, proteinasesMannans, proteinases

7. MOLD HEALTHMOLD HEALTH
EFFECTSEFFECTS
ALLERGIESALLERGIES
INFECTIONSINFECTIONS
TOXINSTOXINS

8. WHAT IS MOLDWHAT IS MOLD
TOXICITY?TOXICITY?
 InIn genetically susceptiblegenetically susceptible individuals, (25%individuals, (25%
of the population), mold toxicity is theof the population), mold toxicity is the
inability to process moldinability to process mold toxintoxin, which, which
leads to a series of biochemicalleads to a series of biochemical
alterations called the Biotoxin Pathwayalterations called the Biotoxin Pathway

9. ARE ALL MOLDS TOXIC?ARE ALL MOLDS TOXIC?
NO, butNO, but thesethese are:are:
Stachybotrys (“Black mold”)Stachybotrys (“Black mold”)
PenicilliumPenicillium
AspergillusAspergillus
Chaetomium AlternariaChaetomium Alternaria
FusariumFusarium
Wallemia

10. ARE ALL MOLDS TOXIC?ARE ALL MOLDS TOXIC?
We are exposed to hundreds ofWe are exposed to hundreds of
mold species out-of-doors, whichmold species out-of-doors, which
can affectcan affect allergyallergy. It is usually when. It is usually when
indoor molds grow withoutindoor molds grow without
competition from their naturalcompetition from their natural
enviroment that we get into troubleenviroment that we get into trouble
This is calledThis is called Sick Building SyndromeSick Building Syndrome

11. INFLAMMATIONINFLAMMATION
INFLAMMATION & IMMUNITY:INFLAMMATION & IMMUNITY:
 INNATE IMMUNITYINNATE IMMUNITY
Dr. Shoemaker’s Biotoxin PathwayDr. Shoemaker’s Biotoxin Pathway
 ACQUIRED IMMUNITYACQUIRED IMMUNITY
Mold Allergy Added to Mold ToxicityMold Allergy Added to Mold Toxicity

12. KEEP IN MINDKEEP IN MIND
THESE MOLD EFFECTSTHESE MOLD EFFECTS
 INTERACTIONS WITHINTERACTIONS WITH LYMELYME
DISEASEDISEASE ANDAND VIRAL INFECTIONSVIRAL INFECTIONS
 MULTIPLE CHEMICALMULTIPLE CHEMICAL
SENSITIVITIES (MCS)SENSITIVITIES (MCS)
 ELECTROMAGNETIC DYSTHYMIAELECTROMAGNETIC DYSTHYMIA
 FOOD ALLERGIES/AUTOIMMUNITYFOOD ALLERGIES/AUTOIMMUNITY
 MOLD MAKES EVERYTHING ELSEMOLD MAKES EVERYTHING ELSE
MUCHMUCH WORSE!WORSE!

13. SYMPTOMS OF MOLD TOXICITYSYMPTOMS OF MOLD TOXICITY
GLOBAL/UNDERAPPRECIATEDGLOBAL/UNDERAPPRECIATED
 Molds and Mycotoxins: Effects on theMolds and Mycotoxins: Effects on the
Neurological and Immune Systems inNeurological and Immune Systems in
HumansHumans
by Campbell, A, Thrasher, J, Gray, Mby Campbell, A, Thrasher, J, Gray, M
Vojdani, A inVojdani, A in Advances in AppliedAdvances in Applied
MicrobiologyMicrobiology, Vol 53, 2004, Vol 53, 2004

14. Mold Toxin Symptoms: 1Mold Toxin Symptoms: 1
 Fatigue, weaknessFatigue, weakness
 Muscle aches, cramps, unusual pain (ice-pick orMuscle aches, cramps, unusual pain (ice-pick or
“lightning bolt”)“lightning bolt”)
 HeadacheHeadache
 Sensitivity to bright light, tearing, blurred visionSensitivity to bright light, tearing, blurred vision
 Chronic sinus congestionChronic sinus congestion
 Cough, chest pain, shortness of breathCough, chest pain, shortness of breath
 Abdominal pain (IBS), often secretory diarrheaAbdominal pain (IBS), often secretory diarrhea

15. Mold Toxin Symptoms: 2Mold Toxin Symptoms: 2
 Joint pain, tendonitis, morning stiffnessJoint pain, tendonitis, morning stiffness
 Cognitive impairment: difficulties with recentCognitive impairment: difficulties with recent
memory, assimilation of new information, wordmemory, assimilation of new information, word
finding, handling numbers, confusion, sustainingfinding, handling numbers, confusion, sustaining
concentration, disorientation, “brain fog”concentration, disorientation, “brain fog”
 Skin sensitivity to light touchSkin sensitivity to light touch
 Mood swings, appetite swings, sweats (often atMood swings, appetite swings, sweats (often at
night), difficulty with temperature regulationnight), difficulty with temperature regulation

16. Mold Toxin Symptoms: 3Mold Toxin Symptoms: 3
 Numbness, tingling, (often non-anatomic),Numbness, tingling, (often non-anatomic),
vertigo, metallic taste in the mouthvertigo, metallic taste in the mouth
 Excessive thirst, frequent urination, sensitivity toExcessive thirst, frequent urination, sensitivity to
static shocks (doorknobs, light switches, carstatic shocks (doorknobs, light switches, car
handles, kisses)handles, kisses)
 Impotence, menorrhagiaImpotence, menorrhagia
 Nausea and vomitingNausea and vomiting

17. MOLD DIAGNOSIS: 1MOLD DIAGNOSIS: 1
MISS ME?MISS ME?
MOLD TOXICITY MAY LOOK LIKEMOLD TOXICITY MAY LOOK LIKE::
 FIBROMYALGIAFIBROMYALGIA
 CHRONIC FATIGUE SYNDROMECHRONIC FATIGUE SYNDROME
 ““ATYPICAL” MS, RA, ALZHEIMER’SATYPICAL” MS, RA, ALZHEIMER’S
 PARKINSON’SPARKINSON’S
 ASTHMA/ CHRONIC SINUSITISASTHMA/ CHRONIC SINUSITIS

18. MOLD DIAGNOSIS: 2MOLD DIAGNOSIS: 2
MISS ME?MISS ME?
 PSYCHIATRIC DIAGNOSESPSYCHIATRIC DIAGNOSES
 ANXIETY (unrelated to stressors)ANXIETY (unrelated to stressors)
 DEPRESSIONDEPRESSION
 DEPERSONALIZATIONDEPERSONALIZATION
 COGNITIVE IMPAIRMENTCOGNITIVE IMPAIRMENT
 MOOD SWINGSMOOD SWINGS

19. MOLD DIAGNOSIS: 3MOLD DIAGNOSIS: 3
MISS ME?MISS ME?
UNIQUE or KEYNOTE SYMPTOMSUNIQUE or KEYNOTE SYMPTOMS
---ELECTRICAL SHOCKS---ELECTRICAL SHOCKS
---”ICE PICK PAINS”---”ICE PICK PAINS”
---PARESTHESIAS (“non-dermatomal”)---PARESTHESIAS (“non-dermatomal”)
---INTERNAL VIBRATION/TREMOR---INTERNAL VIBRATION/TREMOR
---INCREASED SENSITIVITY TO---INCREASED SENSITIVITY TO
EVERYTHINGEVERYTHING

20. HOW DO WE REMOVE MOLDHOW DO WE REMOVE MOLD
TOXIN FROM THE BODY?TOXIN FROM THE BODY?
 Dr. Ritchie Shoemaker, in hisDr. Ritchie Shoemaker, in his
groundbreaking book, published in 2005,groundbreaking book, published in 2005,
Mold WarriorsMold Warriors, outlined the entire Biotoxin, outlined the entire Biotoxin
Pathway, which provided clear guidelinesPathway, which provided clear guidelines
of how to remove toxin from the body,of how to remove toxin from the body,
but also how to evaluate and repair thebut also how to evaluate and repair the
damage that the toxin had produced.damage that the toxin had produced.

22. TREATMENT OF MOLDTREATMENT OF MOLD
TOXICITYTOXICITY
 We first must understand what mold toxinWe first must understand what mold toxin
is doing to the body, so that we can repairis doing to the body, so that we can repair
the damage.the damage.
 We must remove the toxin from the body.We must remove the toxin from the body.
 We must remove all significant exposure toWe must remove all significant exposure to
mold in the patient’s environment.mold in the patient’s environment.
 ThisThis isis treatable, but it istreatable, but it is complicatedcomplicated..

26. BIOTOXIN EVALUATION:BIOTOXIN EVALUATION:
SHOEMAKER MODELSHOEMAKER MODEL
 Central to diagnosis is a careful,Central to diagnosis is a careful,
detailed history and physical exam.detailed history and physical exam.
Symptoms are so varied, and theySymptoms are so varied, and they
fluctuate and may overlap with severalfluctuate and may overlap with several
other important conditions, so aother important conditions, so a
good diagnosis is critical.good diagnosis is critical.

27. BIOTOXIN EVALUATION:BIOTOXIN EVALUATION:
SHOEMAKER MODELSHOEMAKER MODEL
 MeasureMeasure: MSH, VIP, TGF beta-1, c4a,: MSH, VIP, TGF beta-1, c4a,
VEGF, MMP9, ADH, serum osmolalityVEGF, MMP9, ADH, serum osmolality
cortisol and Visual Contrast, MARCoNScortisol and Visual Contrast, MARCoNS
 Also measureAlso measure: Cortisol, Estrogen,: Cortisol, Estrogen,
Testosterone, Thyroid levels, HLA-DRTestosterone, Thyroid levels, HLA-DR
Autoimmune/Clotting markersAutoimmune/Clotting markers
if indicatedif indicated

28. MOLD GENETICS:MOLD GENETICS:
VALUE & USE OF HLA-DRVALUE & USE OF HLA-DR
 Dr. Shoemaker and many others value &Dr. Shoemaker and many others value &
use HLA-DR. He developed the “Rosettause HLA-DR. He developed the “Rosetta
Stone” to interpret it; several are linked toStone” to interpret it; several are linked to
mold specifically (7/2 or 3/53, 13/6/52A,mold specifically (7/2 or 3/53, 13/6/52A,
B & C, 17/2/52A, 18/4/52A) and othersB & C, 17/2/52A, 18/4/52A) and others
which he unfortunately terms “dreaded”which he unfortunately terms “dreaded”
are multisusceptible 4/3/53, 14/5/52B, 11are multisusceptible 4/3/53, 14/5/52B, 11
or 12/3/53 of note, especially “4”.or 12/3/53 of note, especially “4”.

29. MOLD GENETICS:MOLD GENETICS:
MY EXPERIENCEMY EXPERIENCE
 I have measured hundreds of HLA-DRsI have measured hundreds of HLA-DRs
and have NOT noted correlation betweenand have NOT noted correlation between
the results and clinical improvement. Thethe results and clinical improvement. The
“dreaded” (a word“dreaded” (a word II dread) genetics oftendread) genetics often
do well with treatment and those notdo well with treatment and those not
having those genes may do poorly. Ihaving those genes may do poorly. I
suspect much more will be revealed assuspect much more will be revealed as
genetic information accumulatesgenetic information accumulates

30. Biotoxin Illness: DiagnosisBiotoxin Illness: Diagnosis
FACT: Visual Contrast SensitivityFACT: Visual Contrast Sensitivity
Functional Acuity Contrast Test (FACT)Functional Acuity Contrast Test (FACT)::
 NoninvasiveNoninvasive
 Neurologic function of the optic nerveNeurologic function of the optic nerve
 Eliminates near, far, color, motion andEliminates near, far, color, motion and
peripheral vision variablesperipheral vision variables
 In prior studies by Ken Hudnell, Ph.D.,In prior studies by Ken Hudnell, Ph.D.,
neurotoxicologist at the Environmentalneurotoxicologist at the Environmental
Protection Agency (EPA) used for screening andProtection Agency (EPA) used for screening and
monitoringmonitoring

31. Measuring Visual Contrast Sensitivity

33. TESTING YOUR HOME FORTESTING YOUR HOME FOR
MOLDMOLD
 Mold pour plates: open the top, let it sit forMold pour plates: open the top, let it sit for
2 hours and replace top. Evaluate plates2 hours and replace top. Evaluate plates
if significant growth notedif significant growth noted
 ERMI testingERMI testing
 Independent environmental evaluationIndependent environmental evaluation
 Remediation may be really expensive andRemediation may be really expensive and
may not work!may not work!

34. HERTSMI-2HERTSMI-2
 POINT SYSTEMPOINT SYSTEM::
 10 Points are awarded for:10 Points are awarded for:
Apergillus penicilloides >500 spore E/mgApergillus penicilloides >500 spore E/mg
Aspergillus versicolor >500 spore E/mgAspergillus versicolor >500 spore E/mg
Chaetomium globosum >125 spore E/mgChaetomium globosum >125 spore E/mg
Stachybotrys chartarum >125 spore E/mgStachybotrys chartarum >125 spore E/mg
Wallemia sebi >2500 spore E/mgWallemia sebi >2500 spore E/mg

35. HERTSMI-2HERTSMI-2
 6 Points are awarded for:6 Points are awarded for:
A. penicilloides or A. versicolor >100A. penicilloides or A. versicolor >100
Chaetomium or Stachybotrys >25Chaetomium or Stachybotrys >25
Wallemia >500Wallemia >500
 4 points awarded for:4 points awarded for:
A. penicilloides or A. versicolor >10A. penicilloides or A. versicolor >10
Chaetomium or Stachybotrys >5Chaetomium or Stachybotrys >5
Wallemia >100Wallemia >100

36. HERTSMI-2HERTSMI-2
 SCORING INTERPRETATIONSCORING INTERPRETATION::
Any score overAny score over 1515 is too dangerous foris too dangerous for
ill patients to occupy the buildingill patients to occupy the building
Any score underAny score under 1111 is viewed as safeis viewed as safe
Any score fromAny score from 11-1511-15 is borderline andis borderline and
the building should be evaluatedthe building should be evaluated
carefully for safetycarefully for safety

38. MOLD TOXIC PATIENTSMOLD TOXIC PATIENTS
& URINE MYCOTOXINS& URINE MYCOTOXINS
 ““Mycotoxin detection in human samplesMycotoxin detection in human samples
from patients exposed to environmentalfrom patients exposed to environmental
molds”, Hooper, D, Guilford, F, Straus, Dmolds”, Hooper, D, Guilford, F, Straus, D
Int J Mol SciInt J Mol Sci, 2009, 10, 1465-1475, 2009, 10, 1465-1475

39. SINUS MYCOTOXINSSINUS MYCOTOXINS
 ““Measurement of mycotoxins inMeasurement of mycotoxins in
patients with chronic rhinosinusitis”patients with chronic rhinosinusitis”
Lieberman, S, Jacobs J, Lebowitz, R,Lieberman, S, Jacobs J, Lebowitz, R,
Fitzgerald, M, Feigenbaum, B,Fitzgerald, M, Feigenbaum, B,
Otolaryg Head Neck SurgOtolaryg Head Neck Surg, 2011,, 2011,
145, 327-329.145, 327-329.

40. FUNGAL SINUSITISFUNGAL SINUSITIS
 ““The diagnosis and incidence of allergicThe diagnosis and incidence of allergic
fungal sinusitis”, Ponikau, J, Sherris D,fungal sinusitis”, Ponikau, J, Sherris D,
Kern, EB, Homburger, H, Frigas E,Kern, EB, Homburger, H, Frigas E,
Gaffey T, Roberts, G,Gaffey T, Roberts, G, Mayo Clin ProcMayo Clin Proc
1999 Sep; 74 (9): 877-84. 96% of surgical1999 Sep; 74 (9): 877-84. 96% of surgical
nasal cultures were positive with thenasal cultures were positive with the
presence of eosinophils prominent.presence of eosinophils prominent.

41. MYCOTOXIN EVALUATION:MYCOTOXIN EVALUATION:
BREWER MODELBREWER MODEL
 Measure mycotoxins: Urine or nasalMeasure mycotoxins: Urine or nasal
washings sent to laboratorywashings sent to laboratory
 Challenge testing preferred for mostChallenge testing preferred for most
accurate results:accurate results:
 Use 500mg glutathione twice daily for 7Use 500mg glutathione twice daily for 7
days, collecting urine on 7days, collecting urine on 7thth
dayday
 And/or use sweating: sauna, bath, hot tubAnd/or use sweating: sauna, bath, hot tub

42. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
CAUTIONSCAUTIONS
 Anything that mobilizes mold toxins mayAnything that mobilizes mold toxins may
inadvertently pull more toxin into theinadvertently pull more toxin into the
body than it is capable of dealing with.body than it is capable of dealing with.
 This may lead to an exacerbation (whichThis may lead to an exacerbation (which
may be severe) of mold toxic symptomsmay be severe) of mold toxic symptoms
 If this happens with glutathione or saunaIf this happens with glutathione or sauna
STOP IT and collect urine immediatelySTOP IT and collect urine immediately

43. MYCOTOXIN LAB TESTSMYCOTOXIN LAB TESTS
 TWO MAIN TYPES OF TESTINGTWO MAIN TYPES OF TESTING
ARE CURRENTLY AVAILABLE:ARE CURRENTLY AVAILABLE:
 ELISA TESTING THROUGHELISA TESTING THROUGH
RealTime or Bio-Trek LabsRealTime or Bio-Trek Labs
 LIQUIDLIQUID
CHROMATOGRAPHY/MASSCHROMATOGRAPHY/MASS
SPECTROMETRY THROUGHSPECTROMETRY THROUGH

44. DIFFERENCES BETWEENDIFFERENCES BETWEEN
MASS SPEC & ELISA TESTINGMASS SPEC & ELISA TESTING
 Currently available labs measure aflatoxin,Currently available labs measure aflatoxin,
ochratoxin and tricothecenesochratoxin and tricothecenes
 The ELISA testing from RealTime alsoThe ELISA testing from RealTime also
includes gliotoxin (MCAR covered)includes gliotoxin (MCAR covered)
 The mass spec testing from Great PlainsThe mass spec testing from Great Plains
includes zearalenone and enniatin B-1includes zearalenone and enniatin B-1
They don’t measure the same thingsThey don’t measure the same things

45. WHAT THEY TEST FOR 1WHAT THEY TEST FOR 1
 RealTime measures:RealTime measures:
 ochratoxin Aochratoxin A
 tricothecene group (macrocyclics)tricothecene group (macrocyclics)
 aflatoxin group (B1, B2, G1, G2)aflatoxin group (B1, B2, G1, G2)
 gliotoxingliotoxin

46. WHAT THEY TEST FOR 2WHAT THEY TEST FOR 2
at GPL:at GPL:
 Zearalenone (made by fusarium)Zearalenone (made by fusarium)
 Aflatoxin M1Aflatoxin M1
 Ochratoxin AOchratoxin A
 Sterigmatocystin (related to aflatoxin)Sterigmatocystin (related to aflatoxin)
 Riordin E (macrocyclic tricothecene)Riordin E (macrocyclic tricothecene)
 Verrucarin A (macrocyclic tricothecene)Verrucarin A (macrocyclic tricothecene)
 Enniatin B1 (made by fusarium)Enniatin B1 (made by fusarium)

48. DIFFERENCES BETWEENDIFFERENCES BETWEEN
MASS SPEC & ELISA TESTINGMASS SPEC & ELISA TESTING
 Mass spectrometry is theoretically moreMass spectrometry is theoretically more
accurate and reproducible but moreaccurate and reproducible but more
specific as to what is measuredspecific as to what is measured
 ELISA testing may measure the toxinsELISA testing may measure the toxins
andand their metabolitestheir metabolites

50. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
 Any positive testing may be significant.Any positive testing may be significant.
 The initial testing numbers may notThe initial testing numbers may not
reflect the total toxin load. Many ofreflect the total toxin load. Many of
our patients have compromised abilitiesour patients have compromised abilities
to detoxify and can barely, even withto detoxify and can barely, even with
a challenge, get the toxins out of theira challenge, get the toxins out of their
bodies.bodies.

51. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
 I have come to view the initial testingI have come to view the initial testing
as the “tip of the iceberg”as the “tip of the iceberg”
 With treatment, as patients improveWith treatment, as patients improve
and the toxic load is lowered, it is quiteand the toxic load is lowered, it is quite
common for the next testing to reflectcommon for the next testing to reflect
much higher mycotoxin levels whichmuch higher mycotoxin levels which
probably more accurately reflect baselineprobably more accurately reflect baseline

52. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
 It is important to understand that urineIt is important to understand that urine
testing reflects not only the presence oftesting reflects not only the presence of
mycotoxins, but also the body’s abilitymycotoxins, but also the body’s ability
to mobilize and release those toxins.to mobilize and release those toxins.
 The testing numbers need to be alignedThe testing numbers need to be aligned
with the clinical picture for it to makewith the clinical picture for it to make
sense.sense.

53. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
On Repeat Testing, higher results may mean:On Repeat Testing, higher results may mean:
 1. Re-exposure to mold1. Re-exposure to mold
 2. Improved detoxification2. Improved detoxification
 3. Excessive binding of toxin3. Excessive binding of toxin
 4. Excessive killing of mold-releasing toxin4. Excessive killing of mold-releasing toxin
 5. Stimulating mold to make mycotoxins?5. Stimulating mold to make mycotoxins?
Must put the results in context!Must put the results in context!

54. TREATMENT STIMULATESTREATMENT STIMULATES
MOLDS TO MAKE TOXINSMOLDS TO MAKE TOXINS
 ““Amphotericin B enhances the synthesisAmphotericin B enhances the synthesis
and release of the immunosuppressiveand release of the immunosuppressive
agent gliotoxin from the pulmonaryagent gliotoxin from the pulmonary
pathogen Aspergillus fumigatus”, Reeves,pathogen Aspergillus fumigatus”, Reeves,
EP, Murphy, T, Daly, P, Kavanagh, K,EP, Murphy, T, Daly, P, Kavanagh, K,
J Med MicrobiolJ Med Microbiol; 2004, 53: 719-25; 2004, 53: 719-25

55. EXCESS BINDING vs POOREXCESS BINDING vs POOR
DETOXIFICATIONDETOXIFICATION
 60 yo woman with long standing Lyme60 yo woman with long standing Lyme
disease who had improved (“70-80%”): ondisease who had improved (“70-80%”): on
initial mold tests showed high tricothecene.initial mold tests showed high tricothecene.
She increased her binders rapidly and gotShe increased her binders rapidly and got
much worse, with exacerbation of jointmuch worse, with exacerbation of joint
pain, cognition and fatigue. Note initial testpain, cognition and fatigue. Note initial test
and follow up showing marked increase inand follow up showing marked increase in
all toxin levels.all toxin levels.

56. URINE MYCOTOXIN TESTING 1URINE MYCOTOXIN TESTING 1
EXCESS BINDER/POOR DETOXEXCESS BINDER/POOR DETOX

57. URINE MYCOTOXIN TESTING 2URINE MYCOTOXIN TESTING 2
EXCESS BINDER/POOR DETOXEXCESS BINDER/POOR DETOX

58. EXCESS BINDING vs POOREXCESS BINDING vs POOR
DETOXIFICATIONDETOXIFICATION
 How Do We Distinguish an Increase inHow Do We Distinguish an Increase in
Toxicity from Improved Detox?Toxicity from Improved Detox?
 She was getting worse, steadily (not seenShe was getting worse, steadily (not seen
with improved detox) and when wewith improved detox) and when we
stopped her binders for several weeks, herstopped her binders for several weeks, her
exacerbation resolved. When we got theexacerbation resolved. When we got the
dose of binders right, she improveddose of binders right, she improved
steadily.steadily.

59. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
 While testing gives us theWhile testing gives us the
most detailed information available,most detailed information available,
we still see patients who are almostwe still see patients who are almost
certainly mold toxic with negative tests.certainly mold toxic with negative tests.
 Sometimes we can clarify this with aSometimes we can clarify this with a
nasal wash test.nasal wash test.
 We may need to treat empirically.We may need to treat empirically.

60. WHAT DOES A NEGATIVEWHAT DOES A NEGATIVE
TEST MEAN?TEST MEAN?
 THERE ARE 4 POSSIBILITIES:THERE ARE 4 POSSIBILITIES:
 1. The Patient Is Not Mold Toxic1. The Patient Is Not Mold Toxic
 2. The Patient’s ability to detoxify is so2. The Patient’s ability to detoxify is so
compromised they can’t excrete toxincompromised they can’t excrete toxin
 3. The test is not measuring the toxin3. The test is not measuring the toxin
which is causing symptoms (Wallemia)which is causing symptoms (Wallemia)
 4. The test is not accurate4. The test is not accurate

61. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
INTERPRETATIONINTERPRETATION
 It is important to understand theIt is important to understand the
numbers that accompany test results.numbers that accompany test results.
In ELISA tests only positive numbersIn ELISA tests only positive numbers
are significant. This test is reported asare significant. This test is reported as
““semi-quantitative” meaning that theresemi-quantitative” meaning that there
can be variations in numerical results,can be variations in numerical results,
not to be taken completely literally.not to be taken completely literally.

62. MY CURRENT TESTINGMY CURRENT TESTING
RECOMMENDATIONSRECOMMENDATIONS
 To get the most accurate picture of whichTo get the most accurate picture of which
mycotoxins are present in the patientmycotoxins are present in the patient
(so we can optimize treatment):(so we can optimize treatment):
---Great Plains Mycotoxin Panel---Great Plains Mycotoxin Panel
andand
---RealTime panel with gliotoxin---RealTime panel with gliotoxin
or Bothor Both

63. URINE MYCOTOXIN TESTING:URINE MYCOTOXIN TESTING:
EXPENSIVE & VALUABLEEXPENSIVE & VALUABLE
 Given the need for accurate diagnosis,Given the need for accurate diagnosis,
and the value of knowing the specificand the value of knowing the specific
mycotoxins present, this test has becomemycotoxins present, this test has become
invaluable in my practice.invaluable in my practice.
 Treatment is usually a year or more; it isTreatment is usually a year or more; it is
complicated and expensive----so testingcomplicated and expensive----so testing
is usually well worth the cost.is usually well worth the cost.

65. BIOTOXIN TREATMENT:BIOTOXIN TREATMENT:
SHOEMAKER MODEL BASICSSHOEMAKER MODEL BASICS
 EVALUATE HOME/WORK/CAR FOREVALUATE HOME/WORK/CAR FOR
MOLD & FIND SAFE ENVIRONMENTMOLD & FIND SAFE ENVIRONMENT
 USE BINDERS TO REMOVE MOLD TOXINSUSE BINDERS TO REMOVE MOLD TOXINS
 IF PATIENT ISN’T RESPONDING TOIF PATIENT ISN’T RESPONDING TO
BINDERS: TREAT BIOCHEMICAL MARKERSBINDERS: TREAT BIOCHEMICAL MARKERS
PER PROTOCOL, TREAT MARCONS THENPER PROTOCOL, TREAT MARCONS THEN
FOLLOW WITH VIPFOLLOW WITH VIP

66. TWO IMPORTANT MOLDTWO IMPORTANT MOLD
PAPERSPAPERS
 Structural brain abnormalities in patients with inflammatoryStructural brain abnormalities in patients with inflammatory
illness acquired following exposure to water-damaged buildings:illness acquired following exposure to water-damaged buildings:
A volumetric MRI study using NeuroQuant by Shoemaker, R,A volumetric MRI study using NeuroQuant by Shoemaker, R,
et al,et al, Neurotoxicology and Teratology,Neurotoxicology and Teratology, 45 (2014) 18-2645 (2014) 18-26
 Vasoactive intestinal polypeptide (VIP) correctsVasoactive intestinal polypeptide (VIP) corrects
chronic inflammatory response syndrome (CIRS) acquiredchronic inflammatory response syndrome (CIRS) acquired
following exposure to water-damaged buildings, byfollowing exposure to water-damaged buildings, by
Shoemaker, R, et al,Shoemaker, R, et al, HealthHealth, Vol 5, No.3, (2013) 396-401, Vol 5, No.3, (2013) 396-401
 Available throughAvailable through www.survivingmold.comwww.survivingmold.com

67. CholestyramineCholestyramine
 Work up to 1 scoop 4 times a day (1 scoop=1 ¾ tsp)Work up to 1 scoop 4 times a day (1 scoop=1 ¾ tsp)
 The more toxic and ill the patient, the smaller theThe more toxic and ill the patient, the smaller the
dose: start with ¼ scoop once a daydose: start with ¼ scoop once a day
 If there are problems with toxin-release or treatmentIf there are problems with toxin-release or treatment
reactions, start with pioglitazone 15-45mg a day, for 5reactions, start with pioglitazone 15-45mg a day, for 5
days, then start cholestyramine again.days, then start cholestyramine again.
 Side effects (heartburn and constipation) need to beSide effects (heartburn and constipation) need to be
addressedaddressed
 Colesevelam ii cap tid may be better toleratedColesevelam ii cap tid may be better tolerated

68. Cholestyramine & Colesevelam:Cholestyramine & Colesevelam:
How To Take ThemHow To Take Them
 Take cholestyramine powder mixed withTake cholestyramine powder mixed with
water or juice (e.g. pomegranate) one halfwater or juice (e.g. pomegranate) one half
hour before a meal (usually lunch). Best tohour before a meal (usually lunch). Best to
have some fat in the meal (to get thehave some fat in the meal (to get the
gallbladder to empty) and to wait 90gallbladder to empty) and to wait 90
minutes after eating before taking any otherminutes after eating before taking any other
supplements or medications (probiotics aresupplements or medications (probiotics are
OK )OK )

69. Cholestyramine: Side EffectsCholestyramine: Side Effects
Dealing with ConstipationDealing with Constipation
 With small doses of cholestyramine, mostWith small doses of cholestyramine, most
patients have few side effects; butpatients have few side effects; but
constipation is the commonest problemconstipation is the commonest problem
and needs to be addressed:and needs to be addressed:
 Use magnesium to stimulate peristalsisUse magnesium to stimulate peristalsis
and titrate dose to bowel function. Ifand titrate dose to bowel function. If
necessary add Vitamin C powder using anecessary add Vitamin C powder using a
challenge test to determine dosage.challenge test to determine dosage.

70. Biotoxin Treatment:Biotoxin Treatment:
Shoemaker ModelShoemaker Model
Identify Treatable DeficienciesIdentify Treatable Deficiencies::
 ADH/osmolality: Vasopressin spray qohs.ADH/osmolality: Vasopressin spray qohs.
Recheck parameters after 5 treatmentsRecheck parameters after 5 treatments
 Adrenal deficiencies: DHEA, Cortisol,Adrenal deficiencies: DHEA, Cortisol,
Mineralocorticoids; define and treatMineralocorticoids; define and treat
 MARCoNS: Treat by culture sensitivities.MARCoNS: Treat by culture sensitivities.
Rifampin 600mg/d helpful, with BEG nasallyRifampin 600mg/d helpful, with BEG nasally

71. Biotoxin Illness: TreatmentBiotoxin Illness: Treatment
Shoemaker ModelShoemaker Model
 Thiazolidinediones (TZD’s)Thiazolidinediones (TZD’s)
 Pioglitazone 15-45mg/dPioglitazone 15-45mg/d
 Improve genetic responses and PPAR blocks.Improve genetic responses and PPAR blocks.
Specifically lowers TNF, Leptin, MMP9, PAI-1Specifically lowers TNF, Leptin, MMP9, PAI-1
and raises VEGF.and raises VEGF.
 Avoid TZDs if Leptins are Low (until they rise)Avoid TZDs if Leptins are Low (until they rise)
or if patient is slender.or if patient is slender.
 Especially helpful if fasting insulin is elevatedEspecially helpful if fasting insulin is elevated

72. Other Adjunctive TreatmentsOther Adjunctive Treatments
Shoemaker ModelShoemaker Model
 Melatonin may help if MSH is lowMelatonin may help if MSH is low
 If c3a is elevated, high dose statin medication areIf c3a is elevated, high dose statin medication are
helpful (Simvastatin 80mg/d). Pretreat with CoQ 10helpful (Simvastatin 80mg/d). Pretreat with CoQ 10
150mg/d and use concurrently)150mg/d and use concurrently)

73. Adjunctive Treatments: 2Adjunctive Treatments: 2
Shoemaker ModelShoemaker Model
 If VIP is low, (with increased pulmonary arteryIf VIP is low, (with increased pulmonary artery
pressure, poor response to exercise) considerpressure, poor response to exercise) consider
VIP by nasal spray,VIP by nasal spray, IF mold and MARCoNSIF mold and MARCoNS
adequately treatedadequately treated. Tadalafil, 20mg 3x/wk. is a. Tadalafil, 20mg 3x/wk. is a
weak alternative.weak alternative.
 If VEGF is low, and/or cardiolipins are high,If VEGF is low, and/or cardiolipins are high,
consider low dose heparin, 5000u sub Q bid forconsider low dose heparin, 5000u sub Q bid for
2 weeks and follow parameters.2 weeks and follow parameters.
 Pentoxifylline, 400 mg tid may also help withPentoxifylline, 400 mg tid may also help with
low VEGF and decreased blood flow.low VEGF and decreased blood flow.

74. Adjunctive treatments: 3Adjunctive treatments: 3
Shoemaker ModelShoemaker Model
 If TGF beta-1 is persistently elevated and notIf TGF beta-1 is persistently elevated and not
responding to treatment, consider the ARBresponding to treatment, consider the ARB
((AAngiotensin IIngiotensin II RReceptoreceptor BBlocker):locker):
Losartan: 25-50mg/day for adultsLosartan: 25-50mg/day for adults
0.4mg/kg for children0.4mg/kg for children
 If MMP9 remains elevated, consider:If MMP9 remains elevated, consider:
Down-regulation with Actos andDown-regulation with Actos and
the no amylose diet orthe no amylose diet or
High doses of omega-3 fatty acids: 2.4 EPA/1.8 DHAHigh doses of omega-3 fatty acids: 2.4 EPA/1.8 DHA

76. EVALUATING & TREATINGEVALUATING & TREATING
MYCOTOXINMYCOTOXIN
TESTING: MY RECOMMENDATIONSTESTING: MY RECOMMENDATIONS
UrineUrine Mycotoxin TestingMycotoxin Testing
Visual Contrast Testing (survivingmold.com)Visual Contrast Testing (survivingmold.com)
Shoemaker testing: (Shoemaker testing: (OptionalOptional)) VIPVIP (from ARUP), c4a,(from ARUP), c4a,
TGF beta 1, MSH, MMP-9, VEGF, ADHTGF beta 1, MSH, MMP-9, VEGF, ADH
Home evaluation: Mold plates, ERMI (including newHome evaluation: Mold plates, ERMI (including new
HERTSMI2 format) indoor/outdoor air testingHERTSMI2 format) indoor/outdoor air testing
Endocrine evaluation: adrenal/thyroid/sex hormonesEndocrine evaluation: adrenal/thyroid/sex hormones

77. VALUE OF MYCOTOXIN URINEVALUE OF MYCOTOXIN URINE
TESTINGTESTING
 Is Mycotoxin Present? (confirms dx)Is Mycotoxin Present? (confirms dx)
 Which mycotoxins? (helps informWhich mycotoxins? (helps inform
specifics of treatment program)specifics of treatment program)
 Do the levels of toxin agree with theDo the levels of toxin agree with the
degree of toxic symptomatology?degree of toxic symptomatology?
If not, “tip of the iceberg” toxicityIf not, “tip of the iceberg” toxicity
 Repeat tests help refine treatmentRepeat tests help refine treatment

78. DIET & MOLD TOXICITYDIET & MOLD TOXICITY
 BASIC DIETBASIC DIET::
HIGH PROTEIN/LOW CARB DIETHIGH PROTEIN/LOW CARB DIET
20-60gm carbs daily20-60gm carbs daily
KETO CURRENTLY PREFERREDKETO CURRENTLY PREFERRED
Does Yeast (Cheese, Vinegar, Mushroom)Does Yeast (Cheese, Vinegar, Mushroom)
consumption matter?consumption matter?
SHOEMAKER DIET: LOW AMYLOSESHOEMAKER DIET: LOW AMYLOSE

79. DIET & MOLD TOXINSDIET & MOLD TOXINS
IS THERE AIS THERE A SIGNIFICANTSIGNIFICANT AMOUNTAMOUNT
OF MOLD/TOXIN IN FOOD?OF MOLD/TOXIN IN FOOD?
WE DON’T KNOW…..WE DON’T KNOW…..
There isThere is somesome in dried fruit, aged cheese,in dried fruit, aged cheese,
mushrooms, coffee, beer, wine, processedmushrooms, coffee, beer, wine, processed
meat, tomato products and many fermentedmeat, tomato products and many fermented
food products.food products.

80. BASICS OF MOLD TREATMENTBASICS OF MOLD TREATMENT
BREWER MODELBREWER MODEL
 1. EVALUATE THE PATIENT’S1. EVALUATE THE PATIENT’S
ENVIRONMENT (Home, Work, Car)ENVIRONMENT (Home, Work, Car)
 2. PROVIDE THE APPROPRIATE2. PROVIDE THE APPROPRIATE
BINDER FOR THE TOXINSBINDER FOR THE TOXINS
FOUNDFOUND
 3. IF COLONIZED, TREAT THE3. IF COLONIZED, TREAT THE
SINUS/GUT WITH ANTIFUNGALSSINUS/GUT WITH ANTIFUNGALS

81. DR. BREWER’S PAPERSDR. BREWER’S PAPERS
1.1. Brewer, JH, Thrasher JD, Straus DC,Brewer, JH, Thrasher JD, Straus DC,
MadisonMadison
RA, Hooper D. Detection of mycotoxins inRA, Hooper D. Detection of mycotoxins in
patients with chronic fatigue syndrome,patients with chronic fatigue syndrome, ToxinsToxins
2013; 5:605-6172013; 5:605-617
2. Brewer JH, Thrasher JD, Hooper D.2. Brewer JH, Thrasher JD, Hooper D.
Chronic illness associated with mold andChronic illness associated with mold and
mycotoxins: Is naso-sinus fungal biofilm themycotoxins: Is naso-sinus fungal biofilm the

82. DR. BREWER’S PAPERSDR. BREWER’S PAPERS
3. Brewer JH, Hopper D, Muralidhar S3. Brewer JH, Hopper D, Muralidhar S
Intranasal antifungal therapy inIntranasal antifungal therapy in
patients with chronic illnesspatients with chronic illness
associated with mold and mycotoxins:associated with mold and mycotoxins:
an observational analysisan observational analysis GJMRGJMR
2015 volume 15 issue 2: 29-332015 volume 15 issue 2: 29-33

83. DR. BREWER’S PAPERSDR. BREWER’S PAPERS
4. Brewer, JH, Hooper, D & Muralidhar, S4. Brewer, JH, Hooper, D & Muralidhar, S
Intranasal Nystatin Therapy in PatientsIntranasal Nystatin Therapy in Patients
with Chronic Illness Associated withwith Chronic Illness Associated with
Mold and MycotoxinsMold and Mycotoxins
Global Journal of Medical Research: KGlobal Journal of Medical Research: K
Interdisciplinary Vol. 15, Iss 5, 2015Interdisciplinary Vol. 15, Iss 5, 2015

84. MYCOTOXIN TREATMENT:MYCOTOXIN TREATMENT:
BREWER MODELBREWER MODEL
FIRST STEP:FIRST STEP: BINDERSBINDERS
OCHRATOXINOCHRATOXIN: Cholestyramine or: Cholestyramine or
Colesevelam, weakly bound by charcoalColesevelam, weakly bound by charcoal
Use compounded cholestyramineUse compounded cholestyramine
Start low 1/16-1/8 tsp in sensitive patientsStart low 1/16-1/8 tsp in sensitive patients
Colesevelam: 625mg/capsule 1-2 capsules dailyColesevelam: 625mg/capsule 1-2 capsules daily
One-half hour before fatty meal?One-half hour before fatty meal?

85. MYCOTOXIN TREATMENT:MYCOTOXIN TREATMENT:
BREWER MODELBREWER MODEL
TRICOTHECENETRICOTHECENE
AFLATOXINAFLATOXIN
Best binders: Activated charcoal (500mg caps)Best binders: Activated charcoal (500mg caps)
Bentonite clay (500mg caps/liquid)Bentonite clay (500mg caps/liquid)
Chlorella (200mg tabs)Chlorella (200mg tabs) glass grownglass grown
May be taken together, between meals: best toMay be taken together, between meals: best to
separate by two hours each way (e.g. 3 pm)separate by two hours each way (e.g. 3 pm)
START SLOW!!! (One or ¼ every 3-4 days)START SLOW!!! (One or ¼ every 3-4 days)

86. GLIOTOXINGLIOTOXIN
 WHAT MAKES GLIOTOXIN?WHAT MAKES GLIOTOXIN?
In sinus isolates:In sinus isolates:
----Aspergillus fumigatus 6-32%----Aspergillus fumigatus 6-32%
----Aspergillus niger 2-17%----Aspergillus niger 2-17%
----Aspergillus flavus 1-6%----Aspergillus flavus 1-6%
 HOW ABOUT CANDIDA?HOW ABOUT CANDIDA?
Yes or No? Or Maybe?Yes or No? Or Maybe?

87. GLIOTOXINGLIOTOXIN
 BEST BINDERS:BEST BINDERS:
Bentonite Clay (caps or liquid)Bentonite Clay (caps or liquid)
Saccharomyces boulardii (with food)Saccharomyces boulardii (with food)
 BEST TREATMENTSBEST TREATMENTS
NAC (N-Acetyl Cysteine) 500mg 1-2/dNAC (N-Acetyl Cysteine) 500mg 1-2/d
ANTIFUNGALSANTIFUNGALS
BIOFILM TREATMENT AGENTSBIOFILM TREATMENT AGENTS

88. MYCOTOXIN TREATMENT:MYCOTOXIN TREATMENT:
BREWER MODELBREWER MODEL
SECOND STEP:SECOND STEP: KILLING MOLDKILLING MOLD
NASAL COLONIZATION:NASAL COLONIZATION:
TREAT BIOFILMTREAT BIOFILM: BEG spray (G necessary?): BEG spray (G necessary?)
EDTA: compounding pharmacyEDTA: compounding pharmacy
TREAT MOLD DIRECTLYTREAT MOLD DIRECTLY: Amphotericin B: Amphotericin B
(nasal sprays) 2% ketoconazole(nasal sprays) 2% ketoconazole
NystatinNystatin
Hydrosol silver nasal spray: one spray each nostril 1/dHydrosol silver nasal spray: one spray each nostril 1/d

89. MYCOTOXIN TREATMENT:MYCOTOXIN TREATMENT:
BREWER MODELBREWER MODEL
COLONIZATION OF GI TRACT:COLONIZATION OF GI TRACT:
TREAT BIOFILM:TREAT BIOFILM:
TREAT MOLD DIRECTLY:TREAT MOLD DIRECTLY:
Itraconazole 100mg (1/week to start, mayItraconazole 100mg (1/week to start, may
increase to 2 bid if tolerated)increase to 2 bid if tolerated)
Ketoconazole (black box), Amphotericin BKetoconazole (black box), Amphotericin B
Hydrosol silver ½ tsp twice dailyHydrosol silver ½ tsp twice daily

90. AAEM PEARLSAAEM PEARLS
 At the spring AAEM meeting this year,At the spring AAEM meeting this year,
Ruth Grant, MD, pointed out that theRuth Grant, MD, pointed out that the
hyphae forms of mold are onlyhyphae forms of mold are only
responsive to amphotericin Bresponsive to amphotericin B
 Michael Gray, MD, shared that 0.06%Michael Gray, MD, shared that 0.06%
amphotericin B oral and nasal is wellamphotericin B oral and nasal is well
tolerated and is effective here.tolerated and is effective here.

91. AAEM PEARLS 2AAEM PEARLS 2
 Virtually every speaker at that meetingVirtually every speaker at that meeting
emphasized that successful treatment ofemphasized that successful treatment of
mold toxicity often takesmold toxicity often takes 3-5 years3-5 years,,
especially if accompanied by otherespecially if accompanied by other
systemic conditions such as Lyme diseasesystemic conditions such as Lyme disease
and heavy metal toxicity.and heavy metal toxicity.

92. PROBIOTICS FOR MOLD RxPROBIOTICS FOR MOLD Rx
 Lactobacillus rhamnosusLactobacillus rhamnosus andand caseicasei protectprotect
against aflatoxin and increase catalaseagainst aflatoxin and increase catalase
and glutathione peroxidaseand glutathione peroxidase
 Lactobacillus plantarumLactobacillus plantarum help removehelp remove
aflatoxinaflatoxin
 Berevibacillus laterosporusBerevibacillus laterosporus protect againstprotect against
aflatoxin exposureaflatoxin exposure

93. PROBIOTICS FOR RxPROBIOTICS FOR Rx
 ““Reduction of Aflatoxin B1 Toxicity byReduction of Aflatoxin B1 Toxicity by
Lactobacilus plantarum C88” byLactobacilus plantarum C88” by
Li Huang, et al, in PLoS 12(1): e0170109Li Huang, et al, in PLoS 12(1): e0170109
““Effects of probiotic bacteria on theEffects of probiotic bacteria on the
bioaccessibility of aflatoxin B(1) and OTA”bioaccessibility of aflatoxin B(1) and OTA”
by Kabak, B,by Kabak, B, J. Environ Sci Health BJ. Environ Sci Health B
2009, Jun; 44(5): 472-802009, Jun; 44(5): 472-80

94. ANTIFUNGAL DRUGANTIFUNGAL DRUG
RESISTANCE?RESISTANCE?
 FromFrom: “Update on Antifungal Drug: “Update on Antifungal Drug
Resistance”, Perlin, D, Shor, E, Zhao,YResistance”, Perlin, D, Shor, E, Zhao,Y
Curr Clin Microbiol RepCurr Clin Microbiol Rep, 2015 Jun 1, 2015 Jun 1
2 (2): 84-95 “Resistance to antifungal2 (2): 84-95 “Resistance to antifungal
agents remains relatively uncommon asagents remains relatively uncommon as
the majority of fungi retain susceptibilitythe majority of fungi retain susceptibility
to commonly used fungal agents.” (HHS)to commonly used fungal agents.” (HHS)

95. MOLD TOXICITY:MOLD TOXICITY:
BREWER MODELBREWER MODEL
OTHER COMPONENTS OF TREATMENTOTHER COMPONENTS OF TREATMENT
(My version):(My version):
Ozone by nasal insufflation and ears: start slow 11 gammaOzone by nasal insufflation and ears: start slow 11 gamma
given 2-3 cc in each nostril; increase to 10cc if toleratedgiven 2-3 cc in each nostril; increase to 10cc if tolerated
Diet: limits carbs, especially sugarsDiet: limits carbs, especially sugars
Consider Candida as a component ofConsider Candida as a component of
treatment and incorporate this into treatment programtreatment and incorporate this into treatment program
Use oral nystatin and/or fluconazoleUse oral nystatin and/or fluconazole

96. MOLD & BIOFILMMOLD & BIOFILM
 ““Aspergillus fumigatusAspergillus fumigatus biofilm onbiofilm on
primary human sinonasal epithelialprimary human sinonasal epithelial
culture”, Singhal, D, Baker, L,culture”, Singhal, D, Baker, L,
Wormold, P, Tan L,Wormold, P, Tan L, Am J Rhinol AllergyAm J Rhinol Allergy
2011, 25, 219-2252011, 25, 219-225

97. ROLE OF GLUTATHIONEROLE OF GLUTATHIONE
IN TREATMENT?IN TREATMENT?
 ““Deficient Glutathione in the Patho-Deficient Glutathione in the Patho-
Physiology of Mycotoxin-Related Illness”Physiology of Mycotoxin-Related Illness”
Guilford, F, Hope, J inGuilford, F, Hope, J in ToxinsToxins 20142014
6, pp. 608-623. “Toxins can decrease the6, pp. 608-623. “Toxins can decrease the
formation of glutathione”formation of glutathione”

May use intranasal, oral or IVMay use intranasal, oral or IV BUTBUT
 May worsen sensitive patientsMay worsen sensitive patients

98. PRETREATMENT:PRETREATMENT:
For Very Sensitive &/or Toxic PtsFor Very Sensitive &/or Toxic Pts
 Some patients are so sensitive or toxicSome patients are so sensitive or toxic
that they cannot start binders withoutthat they cannot start binders without
intense reactions. Consider starting theseintense reactions. Consider starting these
first:first:
 Supplements to assist liver and GI detoxSupplements to assist liver and GI detox
 Help with lymphatic drainageHelp with lymphatic drainage
 Modalities for kidney and skin detoxModalities for kidney and skin detox
 Intravenous phosphatidyl cholineIntravenous phosphatidyl choline

99. NEW APPROACHESNEW APPROACHES
 OZONEOZONE
 By nasal insufflation: start low, atBy nasal insufflation: start low, at
11 gamma, with 2-3 cc each nostril11 gamma, with 2-3 cc each nostril
and slowly work up to 10cc each nostriland slowly work up to 10cc each nostril
once or twice a week. ? Injection?once or twice a week. ? Injection?
 Consider adding ear ozoneConsider adding ear ozone
 Consider rectal ozone: 2 min dailyConsider rectal ozone: 2 min daily

104. NEW APPROACHESNEW APPROACHES
 LDI: Low Dose ImmunotherapyLDI: Low Dose Immunotherapy
developed by Dr. Ty Vincent usingdeveloped by Dr. Ty Vincent using
patient’s own nasal washingspatient’s own nasal washings
(Note William Rea’s autogenous vaccine)(Note William Rea’s autogenous vaccine)
 Transfer FactorsTransfer Factors which includewhich include Penicillium,Penicillium,
Fusarium, Aspergillus sp., Cladosporium andFusarium, Aspergillus sp., Cladosporium and
Candida sp.Candida sp.

105. Still learning……..Still learning……..
 Our knowledge of mold toxicity andOur knowledge of mold toxicity and
its treatment is still in its infancy….its treatment is still in its infancy….
If you learn of new treatments andIf you learn of new treatments and
approaches, please share with meapproaches, please share with me
so we can disseminate this as soon asso we can disseminate this as soon as
possible…..possible…..
Thank you.Thank you.