This document discusses neuroinflammation and its relationship to chronic pain and depression. It begins by outlining the common neurobiology of these conditions, including involvement of the hypothalamic-pituitary-adrenal axis, inflammatory cytokines, neurotransmitters, and glial cells like microglia and astrocytes. It then discusses the role of the gut-brain axis and gut microbiome in neuroinflammation. The document proposes that chronic pain and depression are actually symptoms of underlying neuroinflammation in the brain. It concludes by outlining a 3-phase treatment approach focused on eliminating triggers of neuroinflammation, treating the underlying issue, and reducing mast cell and microglial activation.

1. Gary Kaplan D.O. DABFM, DABPM, FAAMA
The Kaplan Center of Integrative Medicine
Associate Professor-Georgetown University School of Medicine
The Management of Mold Toxicity in Patients with
Chronic Neuro-immunologically Mediated
Neuroinflammatory Disease

2. Osteopathic Medicine

3. BRAIN ON FIRE!
Phase 1
Identify the issue
Phase 2
Treat the issue
Phase 3
Put out the fire!

5. GARY KAPLAN
What if the beginning,
isn’t the beginning?

6.  Common genetic vulnerabilities
 Common neurobiology
• Neuroanatomy
• Neuroendocrinology
• Neuroimmunology
• Neurotransmitters
Chronic Pain and Depression

7. Diagram of the brain. Adapted from “Depression and Pain,” by M.J. Robinson, S.E. Edwards, S. Iyengar, F. Bymaster, M. Clark, W. Katon, 2009, Frontiers in
Bioscience, 14, p. 5033.
Anatomy of the Brain

8.  Inflammatory cytokines alter the metabolism of
serotonin and dopamine
 Dysregulation of serotonin and norepinephrine
 Dysregulation of glutamate
16,18
Neurotransmitters

9. Hypothalamic
CRF
Anterior
Pituitary
ACTH
Adrenals
Hippocampus Amygdala
• Disruption of the normal
circadian cycle
• Reduced basal cortisol level
Glucocorticoids
Damage to hippocampal neurons and reduces neurogenesis
Deregulation of the hypothalamic-pituitary-adrenal axis
1,8,9,30,47
Deregulation of the Hypothalamic-pituitary-
adrenal Axis

10.  Elevated inflammatory cytokines
 IL-1
 IL-6
 (TNF)-alpha
 Loss of grey matter
17, 35, 37, 41
Inflammatory Biomarkers

11.  Depression and Chronic Pain are
1. Neuroinflammatory
2. Neurodysregulatory
3. Neurodegenerative
Chronic Pain and Depression

12. What is Inflammation?

13. AstrocytesMicroglia
Glial Cells Mast Cells
What are the mediators of Inflammation in the
brain and CNS?

14. Oligodendrocytes
Astrocytes
Microglia
Other
6.5% 0.6%
Pie chart of the distribution of neuroglia cerebral cortex
17.3%
75.6%
Chronic Pain and Depression
27,28

15. Photo Credit www.shutterstock.com, by Yanushevskaya Victoria
Microglia

16.  Microglia are resident cells of the brain involved in regulatory
processes critical for development, maintenance of the neuronal
environment, injury and repair”
 “Electricians” of the CNS
 Innate immune cells of the CNS
18,19,25,41
Microglia

17. 17,50

18. 17,50,51

19. What are DAMPs and PAMPs?

20. Pathogen-Associated Molecular Patterns
(PAMPs)
 Molecules present in diverse organisms, but absent in
humans
 Provide exogenous signals that alert the immune system to
the presence of pathogens, thereby promoting immunity
52,53

21. Etiology of PAMPs
 Brucellus abortus
 Coxiella burnetii
 Porphyromonas gingivalis
 Salmonella enterica
 Chlamydia trachomatis
 Listeria monocytogenes
 Group A Streptococcus
 Mycobacterium
 Tuberculosis
 Herpes simplex virus
 Dengue virus
 Coronavirus
 Spirochete Borrelia Burgdorferi
52,53

22. Examples of PAMPs
 Lipopolysaccharides
 Endotoxins
 Flagellin
 dsRNA
52,53

23. Damage-Associated Molecular Patterns
(DAMPs)
52,53
 Endogenous danger signals, cell derived molecules
 Initiate and perpetuate immunity in response to trauma, ischemia,
cancer and other settings of tissue damage in the absence of overt
pathogenic infections
 Alert the innate immune system to unscheduled cell death

24. Etiology of DAMPs
52,53
 Concussions
 Emotional Stress
 Hypoxia
 Environmental toxins
 Heavy metals
 Mold toxicity
 Autoimmune Diseases

25. Examples of DAMPs
 Localized within the nucleus and cytoplasm (HMGB1), cytoplasm
alone (S100 proteins), exosomes, the extracellular matrix and
plasma components
 Non-protein DAMPs: ATP, Uric Acid, Heparin, Sulfate
 RNA and DNA
52,53

26. 17,50,51

27. 18,21,23,39,43

28. 50,51

29. Microglia
Microglia cells possess “memory” and
repetitive stimulation can lead
to a chronic inflammatory state in the
CNS
17,29,45,50,51

30. Astrocytes
Photo Credit www.shutterstock.com, by Rost9

31. Astrocytes
 Support the blood brain barrier and modulate blood flow in the brain
 Structural support
 Modulate synaptic transmission
 Modulate microglial activity
 Role in spinal and central sensitization
 Role in nervous system repair “glial scar”
 Metabolic support contain glycogen and are capable of gluconeogenesis.
Provided nutrients to the neurons.
54,55,56

32. Astrocyte-Microglia Communication
Reprinted by permission from Macmillan Publishers Ltd: Nature Reviews Immunology (K;, Saijo, Kaoru; Glass, Christopher. 2011. Microglial cell origin
and phenotypes in health and disease., Nature reviews. Immunology, 11(11), 775 - 787. (ISSN: 1474-1733), copyright (2011)

33. Mast Cells
Photo Credit www.shutterstock.com, by Sciencepics

34. Mast Cells
 Type of white blood cells: Granulocyte
 Part of the immune and neuroimmune systems
 Common in areas of close contact to external
environment: skin, GI, airways
 Distributed in all organs and vascular tissue
 Can move across BBB and BSCF barrier in
inflamed and non-inflammatory conditions
57,58,59

35. Mast Cells
Mast cells release immune-modulators, chemo-
attractants, vasoactive compounds, neuropeptides and
growth factors in response to allergens, pathogens,
emotional stress and tissue damage constituting a first
line of host defense.
57,60,61

36. Common to all MCAD is the inappropriate activation of mast cells
62

37. Mast Cell Activation Syndrome
63,64,65
 A condition featuring chronic, inappropriate, non-neoplastic MC
activation
 MCAS results in multi-system signs and symptoms including but
not limited to gastrointestinal, cardiovascular, psychological,
neurologic, and genitourinary systems

38. Clinically Relevant Mediators Released from Mast
Cells & Putative Effects
From The New England Journal of Medicine. C. Theoharides, Peter Valent, Cem Akin, Mast Cells, Mastocytosis, and Related Disorders, Volume No.373 ,
Page No. 163-172 Copyright © (2017) Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society

39. Mast Cells in Nociception
Aich, A.; Afrin, L.B.; Gupta, K. Mast Cell-Mediated Mechanisms of Nociception. Int. J. Mol. Sci. 2015, 16, 29069-29092. , PMC4691098

40. What if we are thinking about this all wrong?

41. In the spinal cord, this chronic inflammatory state results in
neuropathic pain and myofascial pain, this is called
Central Sensitization

42. Central Sensitization Syndrome
CSS = Chronic Pain + Neuropsychiatric Condition
 Neuroinflammatory
 Neurodysregulatory
 Neurodegenerative

43. Depression and Chronic Pain
Depression and chronic pain share common
neurophysiology and neurobiology. They are the
result of mutually reinforcing neuro-pathologic
processes.
Bimodality
Pain Depression

44. What we thought was…
Depression & Chronic Pain caused:
 Inflammation
 Dysregulation, and
 Degeneration of the brain

45. What we now know is…
 Inflammation
 Dysregulation, and
 Degeneration of the brain
Actually cause Depression & Chronic Pain

46. Chronic pain and Depression are symptoms
of INFLAMMATION in the brain

47. CNS Mediators of Neuroinflammation
67,68,76,77,79,80,81,82

48. So what is the role of Gut-Brain Axis in Neuroinflammation?
https://www.pinterest.com/pin/541135711448157239/?lp=true

49. A New Map of Neuroinflammation
 Central Nervous System
Autonomic Nervous System
 Enteric Nervous System
 Endocrine-Hypothalamic-Pituitary-Adrenal
Immune
 Humoral
Bidirectional communications between the gut and the brain that occurs via:
Mindaltering microorganisms: the impact of the gut microbiota on brain and behaviour © 2012 Nature Publishing Group. Used with permission from Macmillan Publishers Ltd: [Nature Reviews Neuroscience], Cryan, J. F., & Dinan, T. G. (2012, October). Mind-altering
microorganisms: the impact of the gut microbiota on brain and behaviour. Nature Reviews Neuroscience, 13, 701-712. doi:10.1038/nrn3346, copyright 2012.

50. Microbiome-Gut-Brain Axis
 Controls the maturation and development of the Enteric Nervous
System (ENS) and Central Nervous System (CNS)
 Resilience- influences stress activity
71,72

51. Microbiome-Gut-Brain Axis
 Memory via regulation of BDNF
 Cognitive functioning
 Blood brain barrier
Leaky gut= leaky brain Leaky brain = leaky gut
72,73

52. Neuroinflammatory Diseases Associated
with Disruption of the Gut Microbiome
 Anxiety/Depression
 Autism Spectrum Disorders
 Parkinson’s Disease
 Multiple Sclerosis
 Alzheimer’s Disease
 Chronic Fatigue Syndrome
76,90,91,92

53. 93,94,95
Chronic Pain Conditions Associated with
Alteration of Gut Microbiota
 Chronic Prostatitis
 Chronic Pelvic Pain
 Visceral Pain
 Migraine
 Fibromyalgia
 Arthritis

54. A New Map of Neuroinflammation
67,68,76,77,79,80,81,82

55. Phase 1: Identify the Issue Eliminate DAMPs
and PAMPs
Phase 2: Treatment
Treat the Issue
Phase 3: Put out the fire
Quiet the mast cell and microglia
Treatment Strategy

56. Phase 1: Identify the Issue:
Eliminate DAMPs & PAMPs
Identify and eliminate DAMPs, PAMPs and other etiologic and perpetuating agents
Testing for MCAD,
IgG, IgE Testing
Tilt Table Testing
MRI
Hormonal Panel
Genomic Testing
Psychotherapy
Antibodies Testing
AVISE Testing
Patient History
AllergiesIschemiaMetabolismPsychologicalAutoimmune
Testing
• Celiac Disease
• Hashimoto’s
• Sjorgens
• PANS/PANDAS
• Physical abuse
• Emotional abuse
• Grief
• PTSD
• Thyroid
• MTHFR
• Metabolic Syndrome
• POTS
• CVA
• Food
• Environmental
• Medications

57. Phase 1: Identify the Issue:
Eliminate DAMPs & PAMPs
Identify and eliminate DAMPs, PAMPs and other etiologic and perpetuating agents
Genomic TestingSleep StudyGI Health
Organic Acid Testing
Infectious
Disease
Heavy Metals
Mold Toxins
Patient History
MedicationHypoxiaGut DysbiosisPathogensToxins
Testing
• Mold
• Heavy Metals
• Herbicides
• Pesticides
• Spirochetes/Lyme
• Parasites
• Bacteria
• Virus
• Intestinal Permeability
• SIBO
• Sleep Apnea • Opioids
• Antibiotics
• PPI
• NSAIDS

58. Testing
Real Time Labs: Mycotoxin Panel

59. Definition of Mycotoxins
 Secondary metabolites of fungi belonging to Aspergillus, Penicillium, Stachybotrys and Fusarium
 Found in water-damaged homes and buildings, especially Penicillium expansum, Aspergillus
fumigatus and Aspergillus versicolor species
 Common contaminants of human foodstuffs: wine, coffee beans, nuts and animal feed
 Can enter the food chain through contaminated cereals and foodstuffs such as: milk, meat and
eggs, obtained from animals fed mycotoxin-contaminated feedstuffs
 Ingestion of low levels of toxins overtime, may cause an array of metabolic, physiologic and
immunologic disturbances
118, 119, 120,127

60. Classification of Mycotoxins
• Mycotoxins are challenging to classify, due to their diverse chemical structures and
biosynthetic origins. Thus, they can be classified as:
 Hepatotoxins
 Nephrotoxins
 Neurotoxins
 Immunotoxins
 Teratogens
 Mutagens,
 Carcinogens
 Allergens…
119, 121

61. Mycotoxin Transmission Health Impact
Aflatoxins: B1, B2, G1, G2, M1, M2 • Peanuts and peanut products, corn, wheat,
rice, cottonseed, nuts, eggs, dairy products,
figs
• Water-damaged buildings
Hepatotoxicity, bile duct hyperplasia, hemorrhage of intestinal tract and
kidneys, carcinogenesis (liver tumors), immunotoxin, mutagenic, neurotoxic.
Ochratoxins A • Cereal grains (wheat, barley, oats, corn), dry
beans, moldy peanuts, cheese, coffee,
raisins, grapes, dried fruits, wine
• Water-damaged buildings
Nephrotoxic, liver damage, teratogenesis, kidney tumors, neurotoxic,
immunotoxin, class 2B possible human carcinogen
Trichothecenes (T-2, Deoxynivalenol,
diacetoxyscirpenol (DON),Satratoxin)
• Corn, wheat
• Water-damaged buildings
• Biologic warfare
Neurotoxins, Immunotoxin, Digestive disorders, oral lesions, hemorrhage of
stomach, heart, intestines, lungs, bladder, kidney, edema
Gliotoxin • Water-damaged buildings
• GI Tract infections
Immunotoxin, cytotoxic, genotoxic, apoptotic cell death inducer
Patulin Apples, apple juice, wheat, moldy feed Brain and lung edema, lung hemorrhage, paralysis of motor nerves,
convulsions, carcinogenesis
Zearalenone Corn, hay Estrogenic effects (edema of vulva, uterine enlargement), testicular atrophy,
enlargement o mammary glands, abortion
119, 121, 127, 128

62. Routes of Exposure
Human exposure to mycotoxins can occur through different routes:
 Gastrointestinal: through ingestion of contaminated food, beverages and water
 Respiratory: inhalation of aerosolized particles
 Mucous
 Cutaneous
119, 120, 121

63. Routes of Exposure
Experiments studying effects of acute inhalation of T2 mycotoxins in both young and mature mice
showed that inhalation of T2 mycotoxins is:
• At least 10 times more toxic than systemic administrations
• At least 20 times more toxic than dermal administration
120

64. Aflatoxin B1 in the Brain
 Brain autopsies of children living in areas with high aflatoxin exposure revealed its presence in
81% of the cases studied
 At low doses, Aflatoxin B1 compromises the integrity of the blood brain barrier, studies suggest
that lipophilic nature of aflatoxins allow their storage in the brain tissue.
 Oxidative metabolism of AFB1 is active even at very low doses of exposure in neutrophils,
dendritic cells, lymphocytes and monocytes. This may be due to an isoform of cytochrome 450
(CYP1A1)
124, 130

65. Aflatoxins and Microglia
• In murine CNS-derived cells, AFB1 treatment caused microglia to express proinflammatory genes especially TLR2,
MyD88, Ikβ, TNF-α, CXCR4 and iNOS at early hours of exposure
• Overexpression of iNOS mRNA remained high even after 48 hours of exposure
• AFB1 exposure triggers the overexpression of TLR2 with the activation of NF-kB pathway, leading to an increase in
secretion of TNFα in microglial cells.
• The secretion of IL-1β could be an indicator of an inflammatory condition in both astrocytes and microglia
• Up-regulation of iNOS mRNA gene could be an indicator of ongoing oxidative stress on both cell types
• Over-expression of p53 gene in microglia indicates the activation of pro-apoptotic pathways and cytotoxic activity of
low dose AFB1 in these cells
130

66. Aflatoxins and Astrocytes
 Treatment of astrocytes with AFB1 induced higher secretion of IL-1, IL-6,
TNFα, and IL-10
 Simultaneously, AFB1 exposure triggers the overexpression of pro-apoptotic
genes in astrocytes (p21, p53), and genes related to apoptosis occurrence
(caspace 3 and 8)
130

67. 130

68. Ochratoxin A in the Brain
 OTA compromises the cytoskeletal integrity of astrocytes
 OTA affect gene expression pertaining to the brain inflammatory response system
 OTA decreses the neuroprotective capacity of glial cells
 OTA causes acute depletion of striatal dopamine
 Increased oxidative stress triggers high lipid peroxidation and oxidative DNA damage
 Inhibition od oxidative DNA repair activity
 Evidence of apoptosis in the substantia nigra, striatum and hippocampus and other brain
regions
 These brain regions, especially the hippocampus are primary sites for neurodegeneration
123

69. Trichothecenes: T2 Toxin in the Brain
 Low levels of T2 toxin are responsible for the changes in the metabolism of brain
biogenic amines, leading to changes in the amino acid permeability across the
BBB
 T2 is easily distributed to the fetal and adult brain inducing apoptosis in the CNS
125

70.  Lymphocytes show maximum sensitivity to T-2 toxins, Macrophages and B
cells are also targets
 T-2 has immunomodulatory and immunosuppressive activity in the immune
system
 Oral, parenteral and cutaneous exposure produces lesions in hematopoietic,
lymphoid and gastrointestinal tissues and functional suppression of
reproductive organs
Trichothecenes: T-2 Toxin
121, 124

71. Gliotoxins
 Aspergillus fumigatus is frequently found in moldy houses, especially from dust produces
gliotoxin and other toxins.
 Candida Albicans is another source of gliotoxins
 Gliotoxin is known to possess a number of cytotoxic and immunosuppressive activities
such as:
 Inhibition of superoxide release, migration and microbicidal activity
 Cytokine release by leukocytes
 T-lymphocyte mediated cytotoxicity and genotoxicity
 Inducer of apoptotic cell death in different cell types
126, 129

72. Code Test Specimen Value Result Not Present if less than Equivocal if between Present if greater or
equal
E8501 Ochratoxin A Urine 0.29000 ppb Not Present 1.8 ppb 1.8-2.0 ppb 2.0 ppb
E8502 Aflatoxin Group (B1,B2,G1,G2) Urine 0.14000 ppb Not Present 0.8 ppb 0.8-1.0 ppb 1.0 ppb
E8503 Trichothecene Group (Macrocyclic) Urine 0.12000 ppb Not Present 0.18 ppb 0.18-0.2 ppb 0.2 ppb
E8510 Gliotoxin Derivative Urine 2.71000 ppb Present 0.5 ppb 0.5-1.0 ppb 1.0 ppb

73. Fumonisin B1 (FB1)
May be responsible for disruption of sphingolipid metabolism inducing lipid
peroxidation, which may affect DNA integrity leading to DNA oxidized bases,
altering cell membrane and causing cytotoxicity
119, 123

74. Fumonisin B1 (FB1) in the Brain
 FB1 toxicity is implicated in the etiology of neuronal tubule defects in children
 Reports indicate a potential for direct neurotoxicity
 FB1 induces oxidative stress in human, rat and mouse neural cell cultures
 Inhibits axonal growth in cultured hippocampal neurons
 Disrupts myelination in glial cells
 Causes changes in neurotransmitter metabolite levels in different brain regions
119, 123

75. Neurocognitive Symptoms
Measured IQ scores in children exposed to indoor mold for more than 2 years showed
statistically significant IQ deficits of approximately 10 points using the WISC-R scale of
intelligence.
• Longer exposure tripled the risk of low IQ scores
• Depression in increased in people exposed to damp indoor environments
• Patients present with other classic neurologic disorders including:
1. Pain syndromes
2. Movement disorders
3. Delirium
4. Dementia
5. Disorders of balance and coordination
120, 122

76. Mycotoxins and Depression
 Patients with mold exposure history report moderate to severe levels of cognitive,
physical and emotional symptoms, mainly Depression
 Electroencephalography results showed hypoactivation in the frontal cortex
 Neuropsychological testing indicated impairments similar to those seen in mild
traumatic brain injury
 Studies demonstrated presence of OTA, AF M1, FB1 in urine and serum of children
diagnosed with Autism compared to healthy
120, 122

77. Mycotoxins and the gastrointestinal
tract
 Gut microbiota impacts the permeability of the intestines thus the absorption
and bioavailability of mycotoxins
 Mycotoxins can disrupt the gut microbiome
 Mycotoxins have direct toxicity of the intestinal barrier
 Mycotoxins can impair the local immune response in the intestines
 Gut microbiota can detoxify mycotoxins
119

78. Mycotoxin Interaction in Hepatic
and Intestinal Epithelial Cells
119
“Tissues with high rates of cell turnover, are very susceptible to mycotoxins, due
to their ability to strongly compromise the homeostasis of self-renewing
capacities of cells causing the impairment of epithelial barrier increasing
membrane permeability”

79. Mycotoxin Interaction in Hepatic
and Intestinal Epithelial Cells
119, 123
 Intestinal and hepatic cells are more sensitive to DON alone than other mycotoxins
 OTA-DON is the most toxic combination for intestinal cells
 AFB1-DON is the most toxic combination for hepatic cells
 DON alone is believed to cause various chronic intestinal inflammatory diseases, including
Crohn’s disease and Ulcerative Colitis
 AFB1-DON combination in hepatic cells showed a strong synergism, in addition to their high
individual toxicities, leading to DNA damage and high oxidative stress

80. Mycotoxin Interaction in Hepatic and
Intestinal Epithelial Cells
119

81. “Despite the distinct mechanistic pathways of mycotoxins, once
combined these may lead to additive, synergistic and antagonistic toxic
effects after mixed exposure originated from different environmental
sources via gastrointestinal and inhalation routes”
119

82. Presence of Mycotoxins in the Body
ELISA techniques have detected the presence of mycotoxins in a number of tissues including:
• Urine
• Nasal polyps and secretions
• Cancerous breast tissue
• Spinal fluid
• Breast milk
• Gastric and colon tissue
• Bladder and transitional cell carcinomas
• Brain astrocytoma
• Lung
• Lymph nodes especially those with granulomatous diseases
• Renal cell tumors

83. Remediation
 The most important component of treatment is complete avoidance of
further exposure to the water-damaged environment
 In addition to all items contaminated by these environments
120

84. • Shoemaker Protocol
• Sequestering Agents:
 Cholestyramine
 Clay
 Chlorella
 Charcoal
• Glutathione
• Amphotericin B Nasal spray: 5mg capsule in 24cc distilled water with LoxaSperse & EDTA 1%.
Irrigate nostrils BID
• Antioxidants
• Probiotics
• Dietary Interventions
• Saunas and Exercise
Treatment
120

85. Dietary Interventions
1. Anti-candida/ Anti-fungal Diet, exclude
 Dairy and all aged cheeses
 Dried fruits
 Processed foods, cold cuts, processed
meats
 Legumes
 Peanuts, pistachios, chestnuts
 Vinegars, pickles
 Sugar, and sweeteners
 Fruits
 Coffee, alcohol
 Farm raised fish and seafood
 All grains/ gluten
2. Detox Food Plan:
 Gluten free
 Dairy free
 No farmed fish and seafood
 No processed meats and sugars

86. Phase 3: Put out the fire
Quiet the mast cell and microglia

87. Sauna and Exercise
 Infrared saunas have the advantage of inducing sweating at a lower body temperature
 Induced sweating reduces the total overall body burden of toxins and support recovery
in persons exposed to water-damaged buildings
 Ochratoxin A has been found in human sweat
 Studies have found that a number of toxins appear to preferably excrete in sweat
 Exercise prevents oxidative stress and memory deficits
116

88. 7,15,19,21,28,30,31

89. 1,2,3,4,5,6,8,9,10,11,12,13,14,16,17,18,20,22,23,24,25,26,27,29,32,33,34,35,36

90. My Recommendations
 Omega-3 fatty acids: 1.5 gms – 9 gms per day
 Vitamin D blood level: 50 - 60ng/ml
 Liposomal Glutathione: Readisorb .5 -1tsp twice a day
 NAC: 600 mg TID
 CoQ10: 100 mg – 300 mg TID
 Ginkgo Extract: 240 mg – 600 mg
 Curcumin: 200 mg QD-BID
 Resveratrol: 500-1,000 mg
 Melatonin: .1 mg – 9 mg a day

91. MEDICATIONS
H1 BLOCKERS
H2 BLOCKERS
CROMOLYN SODIUM
Mast Cell Activation Syndrome Treatment

92. H1 Blockers
Ketotifen Mast Cell Stabilizer Compound 1mg BID
Loratadina
Cetirizine
Fexofenadine
2-4 times normal- spread over 2-3 times a day
Cromolyn SodiumLeukotriene Receptor
Blockers
H2 Blockers
Ranitidine
Famotidine
Nizatidine
Montekulast Sodium Gastrocrom: 2 vials/
4 times a day
Mast Cell Activation Syndrome Treatment

93. Mast Cell Activation Syndrome Treatment
Palmitoylethaolamide (PEA)
Dosage
 Endogenous fatty acid amide, also found in: soybeans, egg yolks, peanuts
 Down regulates mas cell activity and controls microglia cell behaviors
 May play a role in maintaining cellular homeostasis, acting as mediator of resolution of
inflammatory processes
 Frist 2 months: 1 capsule TID
 3rd and 4th month: 1 capsule BID
 Then 1-2 a day

94. Mast Cell Activation Syndrome Treatment
 Quercetin: 500mg-1000mg
 Luteol: 100mg/10kg
 Rutin: 30mg/10kg
112,113,114,115

96. Phase 2
Treat the issue
Phase 3
Put out the fire!
Phase 1
Identify the issue
BRAIN ON FIRE!

97. I kindly thank you
for your attention.
Dr. Gary Kaplan, D.O. DABFM, DABPM, FAAMA
Medical Director, Kaplan Center for Integrative Medicine
Clinical Associate Professor, Georgetown University School of Medicine
Author, Total Recovery: Breaking the Cycle of Chronic Pain and Depression