AEHF - ARTICLES

23rd Annual International Symposium

Man and His Environment in Health and Disease

Special Focus

The Autonomic Nervous System and Its Relationship to Environmental Pollutants Including the Cardiovascular System and Electromagnetic Sensitivity

Sponsored by

American Environmental Health Foundation

and

University of North Texas Health Science Center

Physician Accreditation/Credit:

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of the University of North Texas Health Science Center at Fort Worth Office of Professional & Continuing Education and the American Environmental Health Foundation. The University of North Texas Health Science Center at Fort Worth Office of Professional & Continuing Education is accredited by the ACCME to provide continuing medical education for physicians.

The University of North Texas Health Science Center at Fort Worth is accredited by the American Osteopathic Association to award continuing medical education to physicians.

The University of North Texas Health Science Center at Fort Worth designates this educational activity for a maximum of 24 Category 1 credits toward the AMA Physician’s Recognition Award. Each physician should claim only those credits that he/she actually spent in the activity.

The University of North Texas Health Science Center anticipates this program for 24 hours in Category 2A CME credit hours, pending approval from the American Osteopathic Association.

Nursing Accreditation/Credit:

University of North Texas Health Science Center at Fort Worth Office of Professional & Continuing Education, Provider #02588A, is approved provider of continuing nursing education by the Texas Nurses Association, an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation. This activity meets Type 1 criteria for mandatory continuing education requirements toward relicensure as established by the Board of Nurse Examiners for the State of Texas. This activity is approved for 28.8 Contact Hours.

To receive a certificate of successful completion, participants must attend the activity in its entirety and complete and return the activity evaluation credit request form.

Reprints are available from American Environmental Health Foundation. This volume is not to be reproduced, all or in part, without the written permission of American Environmental Health Foundation.

FINANCIAL CONSIDERATION

AEHF is a nonprofit organization that was founded in 1975 to provide education and research into Environmental Medicine. This year’s Symposium is our 23^rd Annual International Symposium and is our major vehicle for educating the medical professional.

Funding for the symposium is provided by registration fees from physicians and exhibitors. Proceeds from the AEHF store cover the shortfall between registration fees and expenses for the conference. AEHF does not receive grants or any outside financial support for our education. Donations are accepted and used toward research into environmental medicine.

INTRODUCTION

SYMPOSIUM PURPOSE

Since 1981, the International Symposium has been recognized as one of the most advanced medical forums in the world addressing the research and treatment of environmental effects on health and disease. The 2005 conference will focus on â€œThe Autonomic Nervous System and Its Relationship to Environmental Pollutants Including the Cardiovascular System and Electromagnetic Sensitivityâ€?. This Conference presents the most current information available while providing guidelines to identify, diagnose, treat and to prevent environmentally triggered responses in the body.

GOALS OF THE MEETING

! To provide new insights in The Autonomic Nervous System and Its Relationship to Environmental Pollutants and the environmental causes behind many problems you see.

! To present new diagnostic and treatment modalities to help you improve the quality of care for your complex patients.

! To provide concepts, tools that will enhance your practice.

OBJECTIVES OF THE MEETING

! Improve the outcome of treating patients with sensitivities to The Autonomic Nervous System and Its Relationship to Environmental Pollutants.

! Use new concepts and treatments to help better diagnose and manage many patients with environmentally triggered problems and sensitivities to The Autonomic Nervous System and Its Relationship to Environmental Pollutants.

! Apply the concepts of this conference to your practice by using nutrition and environmental manipulation for the treatment of sensitivities to The Autonomic Nervous System and Its Relationship to Environmental Pollutants.

! Use the information presented to enhance the effectiveness, cost-efficiency, and competitiveness of the physician in relation to The Autonomic Nervous System and Its Relationship to Environmental Pollutants.

INTENDED AUDIENCE

M.D.=s, D.O.=s, medical students, nurses, nutritionists and other health professionals interested in the concepts and practice of Environmental Medicine, Occupational Medicine and Toxicology.

EDUCATIONAL FORMATS

# Plenary

# Panels Discussions

# Case Studies

# Question & Answer Sessions.

CONFERENCE FORMAT

The AEHF Committee has selected some of the leading experts in the fields of chronic disease, nutrition and chemical sensitivity.

Each speaker=s presentation will last approximately 20 minutes and will be followed by a 10 minute question and answer session. All speakers are encouraged to use any and all appropriate audio/visual aids. (A brief outline of the speech is included in this booklet.)

GIVEN IN COOPERATION

William J. Rea, M.D., F.A.C.S.

Symposium Chairman,

American Environmental Health Foundation,

Environmental Health Center – Dallas,

Dallas, Texas

Bertie B. Griffiths, Ph.D.,

Environmental Health Center – Dallas

Dallas, Texas

Kaye H. Kilburn, M. D.

University of Southern California Medical Center

Keck School of Medicine

Los Angeles, CA

William J. Meggs, M.D., Ph.D.

Brody School of Medicine, East Carolina University

Department of Emergency Medicine

Greenville, NC

23^rd Annual International Symposium

on Man and His Environment

Schedule

Saturday, June 11, 2005

9:00 ANNOUNCEMENTS/MODERATOR: Bertie Griffiths, Ph.D.

9:05 â€œModulation of Enteric Nervous System by Intestinal Contentsâ€?, Javier Santos, M.D.

9:25 Q & A

9:35 â€œGroup A Strep and Neuro Psychiatric Disordersâ€?, Richard Jaeckle, M.D.

9:55 Q & A

10:05 MORNING BREAK WITH EXHIBITORS

10:30 â€œManifestations and Management of Mold Allergiesâ€?, David Hurst, M.D., Ph.D.

10:50 Q & A

11:00 â€œTreatment of the Damaged Autonomic Nervous System in Environmentally Damaged Patientsâ€?,

William J. Rea, M.D., FACS

11:20 Q & A

11:30 â€œIntervention with Glutathione-Galavit; Realities of Delivery to Neuronsâ€?, Kaye Kilburn, M.D.

11:50 Q & A

12:00n BUFFET LUNCH WITH EXHIBITORS

MODERATOR: Richard Jaeckle, M.D.

1:30 â€œRecent Developments in Functional Imagingâ€?, Theodore R. Simon, M.D.

1:50 Q & A

2:00 â€œMan’s Sense of Awarenessâ€?, Jean Monro, M.D.

2:20 Q & A

2:30 â€œControlled Inhalational Challenge in Multiple Chemical Sensitivityâ€?, Roy Fox, M.D.

2:50 Q & A

3:00 AFTERNOON BREAK WITH EXHIBITORS

3:30 â€œThe Sphenopalatine Ganglion and Environmental Sensitivityâ€?, Dietrich Klinghardt, M.D., Ph.D.

3:50 Q & A

4:00 â€œAllergy as a Cause of Sleep Apnea Syndromeâ€?, Jorge A. Ayala Moran, M.D.

4:20 Q & A

4:30 â€œEffect of EMF on Male Reproductive Organsâ€?, Kou Sakabe, M.D.

4:50 Q& A

5:00 PANEL DISCUSSION/CASE STUDIES: Aristo Vojdani Ph.D.

â€œNeuroimmune Abnormalities in a Patient Exposed to a Combination of Mercury and Chemicals Used in Fumigationâ€?

6:00 ADJOURN

SATURDAY, JUNE 11, 2005

ABSTRACTS

AND

HANDOUTS

Objectives & Notes

Javier Santos, M.D.	Date of talk: Saturday, June 11, 2005, 9:05am

Hospital General Valle Hebron Institut Fundacio Recerca, Digestive Diseases Research Unit Paseo Valle Hebron 119-129 Barcelona, Barcelona 08035 Spain	Phone: 93/489-4035
	Fax: 93/489-4456
	Email: [email protected]

Training:
Current Job Description:	Principal Investigator, Digestive Diseases Research Unit, Hospital Valle de Hebron, Barcelona, Spain
Medical School/University Attended:	University of Navarra, Spain
Internship:	Hospital Valle de Hebron, Barcelona, Spain
Residency:	Hospital Valle de Hebron, Barcelona, Spain
Board Certifications:	Not applicable

SPEECH TITLE: “Modulation of Enteric Nervous System by Intestinal Contentsâ€?

At the end of this Presentation, the participant should be able to:

1. To acknowledge that intestinal contents, particularly microbial products, may influence the activity and responses of enteric, autonomic and central nervous systems and innate and acquired immunity.

2. To preview how this influence could be relevant to the development of human inflammatory disorders.

The above information was provided by the Speaker.

Modulation of Enteric Nervous System by Intestinal Contents. Javier Santos, M.D., Ph.D. Hospital Universitario Valle de Hebron. Digestive System Research Unit. Barcelona, Spain.

Goals and Objectives

2. To preview how this influence could be relevant to the development of human inflammatory disorders.

Outline

The intestinal epithelium is a single columnar layer with a surface area of about 400 m2 where besides the enterocytes other cell types are present: goblet cells, endocrine cells, stem cells and intraepithelial immunocytes. Epithelial cells are bound together by junctional complexes in the apical surface that restrict the passage of even very small (2-kDa) molecules but and it is relatively impermeant to macromolecules or bacteria. The intestinal epithelium also boasts a number of specialized protective adaptations that are not found in other sites including anti-microbial peptides, secretory immunoglobulin A, mucins and Trefoil peptides. The apical surface of the enterocyt faces the intestinal lumen which homes a huge number of microorganisms, up to 100 trillion in distal segments, exceeding by far the number of all other microbial communities associated with the body’s surfaces. The gut contains more than 100 million neurons with innervation extending through all layers of the tract, suggesting that this specific interface of nerves, microorganisms and immune cells might be crucial to normal homeostasis and to the prevention of uncontrolled inflammation

The gut-associated lymphoid tissue Peyer’s patches is covered by a specialized follicle-associated epithelium containing M cells, a subepithelial dome rich in dendritic cells (DCs) and B-cell follicles that contain germinal centres. Transport of soluble proteins and microbes across the epithelium occurs through both specialized M cells and by DCs. Bacteria that penetrate the enterocyte epithelial layer are rapidly killed by the macrophages in the lamina propria. M cells use transepithelial vesicular transport to carry microbes to antigen presenting cells in the underlying gut-associated lymhoid tissue. The DC might extend its dendrite-like processes through epithelial tight junctions and sample and uptake luminal antigen directly. This process is uptake is regulated by CX3CL1, a chemokine produced by intestinal epithelial cells. TGF-β and other factors derived from stromal cells prompt resident intestinal macrophages to profound anergy. These macrophages do not express innate response receptors and do not release inflammatory cytokines in response to bacteria—but they retain phagocytic and bactericidal activity. Factors derived from epithelial cells condition intestinal dendritic cells to become nonresponsive although these cells are still able to open the tight junctions and sense of commensal bacteria. During infection, invasive bacteria activate epithelial cells to produce proinflammatory mediators that recruit additional immune cells.

A small number of bacteria can survive inside enabling the interaction of DCs with T and B cells in the Peyer’s patches and/or the migration of DCs to the draining mesenteric lymph nodes. Although DCs loaded with commensal bacteria can traffic to the mesenteric lymph nodes, the lymph nodes function as a barrier, and the loaded DCs cannot penetrate farther to reach the systemic secondary-lymphoid tissues. The result is that the induction of immune responses by live bacteria is confined to the mucosa itself. Following activation, B- and T-cell blasts can leave the mesenteric lymph nodes through the efferent lymph, enter the bloodstream at the thoracic duct and home back to the intestinal mucosa.

The signalling loop that mediates the epithelial response to microorganisms is based on sensing of structural motifs known as pathogen-associated molecular patterns that are specific for prokaryotic components. The motifs are recognized by pattern-recognition receptors such as the Toll-like receptors or the nucleotide-binding oligomerization domain family of proteins. Although there are differences in the signalling pathways, activation of pattern-recognition receptors induces the expression of pro-inflammatory genes. This leads epithelial cells to produce an array of pro-inflammatory cytokines and chemokines, among which CXCL8 is most abundant.

The presence or absence of intestinal bacteria has a large impact on lymphoid structures of both the intestine and systemic tissues. The intestines of germ-free mice have low numbers of lamina propria CD4+ cells, greatly reduced numbers of IgA-producing cells and hypoplastic Peyer’s patches. These abnormalities reverse within weeks of colonization. On the other hand, the hygiene hypothesis states that a leading cause of the increased incidence of allergy and inflammatory conditions in Western world is the decrease exposure to common infections during life. Two theories, immune deviation and counter regulation, offer explanations to simultaneous increase in autoimmunity and inflammatory disorders (Th1 mediated) and allergies (Th2 mediated) immune deviation and counter regulation although neither explanation is likely to account entirely for the long-term consequences of altered hygiene conditions

Finally, microbial endocrinology considers the possibility that eukaryotic and procariotic cells share common chemical messengers and receptors. If true, this may help to understand how a hormone could directly influence bacterial growth and also how the production of hormone-like compounds by microorganisms modulate host neuro-immune-cell responses.

Conclusion

Gut microflora actively communicates with the enteric and central nervous systems and the immune system to tightly regulate intestinal function

References

1.Science 2005;307:1915-1920.

2.Curr Op Immunol 2004, 16:277–283.

3.Nature Rev Immunol 2001;1:59-66.

4.Nature Rev Immunol 2004;4:481.

5.Nature Med 2005;11:254

6.Nat Rev Immunol 2004;4:962

7.Science 2002;296;4:

8. Gut 2005;54;317-320.

9.Trends Microbiol 2004;12:14

9.Trends Immunol 2004;25:505.

10.JPET 2005;312:417

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Objectives & Notes

Richard Jaeckle, M.D.	Date of talk: Saturday, June 11, 2005, 9:35am

8220 Walnut Hill Lane, Suite 404 Dallas, TX 75231	Phone: 214/696-0964
	Fax: 214/696-1094
	Email: [email protected]

Training:
Current Job Description:	Private Practice of Psychiatry and Environmental Medicine
Medical School/ University Attended	University of Texas Southwestern Medical School
Internship:	Veterans Administration Hospital, Dallas, TX
Residency:	Psychiatry: St Louis Univ Hospitals & Child Psychiatry: Washington Univ Child Guidance Clinic
Board Certifications:	AmerBdPsyNeurol:Psychiatry; AmerBdPsyNeurol: Child Psychiatry; AmerBdEnvironMed

SPEECH TITLE: “Group A Strep and Neuro Psychiatric Disordersâ€?

At the end of this Presentation, the participant should be able to:

1. Know the definition and pathogenicity of PANDAS.

2. Anticipate the incidence of GAS in mood/behavior disorders

3. Associate certain psychiatric disorders to medical problems

The above information was provided by the Speaker.

Richard G Jaeckle, MD

8220 Walnut Hill #404

Dallas, TX 75231

Group A Strep and NeuroPsychiatric Disorders

Objectives of Presentation:

1) Know the Definition and Pathogenicity of PANDAS.

2) Anticipate the Incidence of Group A Strep (GAS) in NeuroPsychiatric Disorders.

3) Associate Certain Psychiatric disorders to Medical Problems.

Outline:

The initial description and definition of PANDAS in 1994 is followed by the case presentation of a teenager with depression and schizophrenia whose illness was associated with GAS. An interest in the association of GAS and mood disorders led to the study of 100 healthy psychiatric patients for indications of persistent colonization with GAS and elevations of the anti-streptolysin O antibody (ASO). The PANDAS profile was used in some patients. When possible, tonsillar size, rapid ID throat swabs and skin test with the Group A Strep antigen was also performed. The incidence of positive index patients is 29% and 10% of the cohort received tonsillectomy and adenoidectomy.

Conclusions:

• There appears to be a high incidence of GAS colonization in these psychiatric patients.

• Rapid Strep ID is not an effective tool for detecting GAS colonization.

• Tonsillar size is not an reliable tool for detecting colonization

• ASO titer is a simple and effective tool for detecting GAS colonization.

• Skin test with GAS vaccine is not commercially available, but is quite sensitive and useful.

• Significant medical problems are not being recognized and treated.

• The PANDAS panel provides useful additional parameters for evaluation of GAS pathogenicity

References:

• Bowers M, Will Immunotherapy succeed whether others have failed Neuropsychiatry reviews, v2#2, Mar 2001

• http://www.nimh.nih.gov/research.pandassumary.cfm

– Aug18, 2001; NIMH Roundtable

• Arch Pediatr Adol Med 2002:156(4)356-361

• http://intramural.nimh.nih.gov/research/pdn/web.htm

• Leonard HL, Swede SE, PANDAS; Int J Neuropsychopharm 4:191, 2001

• Vojdani A et al, Antibodies to Neuron-specific Antigens in children with autism: Possible cross-reaction with encephalitogenic proteins from milk, chlamydia pneumoniae and GAS; Neuroimmun 129:168, 2002

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Objectives & Notes

David Hurst, M.D., Ph.D.	Date of talk: Saturday, June 11, 2005, 10:30am

23 Spring St., Suite D Gorham, ME 04074	Phone: 207/883-6464
	Fax:
	Email: [email protected]

Training:
Current Job Description:	Private Practice – Otolaryngic Allergy
Current Faculty Appointments:	Tufts University, Boston, Massachusetts
Medical School/University Attended:	Indiana University
Internship:	Portland, ME
Residency:	Tufts – B.U. – Boston, Massachusetts
Board Certifications:	AAO-UNS, AAOA
Other Information:	Ph.D. – Uppgala, Sweden

SPEECH TITLE: “Manifestations and Management of Mold Allergiesâ€?

At the end of this Presentation, the participant should be able to:

1. Recognize the unusual symptoms of confusion and fatigue and chronic external otitis which may be signs of mold allergy.

2. Understand how mold allergy affects sinusitis and asthma.

3. Be comfortable in knowing how to manage patients with multiple mold inhalant and food allergies.

The above information was provided by the Speaker.

Manifestation and Management of Mold Allergies

David S. Hurst, M.D., Ph.D.

Portland, ME

Abstract:

This course will briefly survey the emerging concepts regarding parasympathetic manifestations in allergy. Discussion will center on the diverse spectrum of symptoms encountered in patients with mold allergy including classic rhinitis, chronic otitis externa, asthma, eczema and complaints of bizarre mood and behavior disorders among both children and adults. The efficacy of mold immunotherapy and mold food elimination diets will be reviewed.

References: (PMID = Pub Med ID)

General Allergy

Hurst DS, Gordon BR, Fornadley JA, Hunsaker DH.

Safety of home-based and office allergy immunotherapy: A multicenter prospective study.

Otolaryngol Head Neck Surg. 1999 Nov;121(5):553-61. PMID: 10547469

Passalacqua G, Canonica GW. *****

Long-lasting clinical efficacy of allergen specific immunotherapy.

Allergy. 2002 Apr;57(4):275-6.

PMID: 11906355

Passalacqua G, Canonica GW. ***

Treating the allergic patient: think globally, treat globally.

Allergy. 2002 Oct;57(10):876-83. â€œUnified Airway Diseaseâ€?

PMID: 12269932

Smith GC, Pell JP. (A great spoof on evidenced based medicine) *****

Parachute use to prevent death and major trauma related to gravitational challenge: Systematic review of randomised controlled trials.

BMJ. 2003 Dec 20;327(7429):1459-61. Review.

PMID: 14684649

General Sinusitis/Asthma

Nomenclature

Johansson SG, Bieber T, Dahl R, Friedmann PS, Lanier BQ, Lockey RF, Motala C, Ortega Martell JA, Platts-Mills TA, Ring J, Thien F, Van Cauwenberge P, Williams HC.

Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003.

J Allergy Clin Immunol. 2004 May;113(5):832-6. PMID: 15131563

A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force.

Allergy. 2001 Sep;56(9):813-24. Review.

PMID: 11551246

David Hurst, MD, PhD

207-883-6464

Mold Allergy

Hossain MA, Ahmed MS, Ghannoum MA.

Attributes of Stachybotrys chartarum and its association with human disease.

J Allergy Clin Immunol. 2004 Feb;113(2):200-8; quiz 209. Review. PMID: 14767429

Fungal Allergy and Pathogenicity; ed: Adorini, Arai, Berek, Schmitt-Verhulst

In: Chem Immunol. 2002;81:5-9. Review.

PMID: 12102005

Mold allergy: some progress made, more needed.
J Allergy Clin Immunol. 2004 Feb;113(2):216-8. No abstract available. PMID: 14767432

Are indoor molds causing a new disease?
J Allergy Clin Immunol. 2004 Feb;113(2):221-6. Epub 2004 Jan 09. Review.
PMID: 14722497

Campbell AW, Thrasher JD, Madison RA, Vojdani A, Gray MR, Johnson A.

Neural autoantibodies and neurophysiologic abnormalities in patients exposed to molds in water-damaged buildings.

Arch Environ Health. 2003 Aug;58(8):464-74.

PMID: 15259425

Dennis DP.

Chronic sinusitis: defective T-cells responding to superantigens, treated by reduction of fungi in the nose and air.

Arch Environ Health. 2003 Jul;58(7):433-41.

PMID: 15143856

Johanning E.

Indoor moisture and mold-related health problems.

Allerg Immunol (Paris). 2004 May;36(5):182-5. Review. PMID: 15206571

Bush RK, Portnoy JM.

The role and abatement of fungal allergens in allergic diseases.

J Allergy Clin Immunol. 2001 Mar;107(3 Suppl):S430-40. Review. PMID: 11242604

more info and handouts: http://home.earthlink.net/~meear/drdavidhurst/

Objectives & Notes

William J. Rea, M.D., FACS	Date of talk: Saturday, June 11, 2005, 11:00am

Environmental Health Center – Dallas 8345 Walnut Hill Lane, Ste. 220 Dallas, TX 75231	Phone: 214/368-4132
	Fax: 214/691-8432
	Email: [email protected]

Training:
Current Job Description:	M.D., President – Environmental Health Center – Dallas
Current Faculty Appointments:	Professor of Medicine, Capital University of Integrative Medicine, Washington, D.C.
Medical School/University Attended:	Ohio State University College of Medicine, Columbus, OH
Internship:	Parkland Memorial Hospital, Dallas, TX
Residency:	University of Texas SW Medical School, Dallas, TX
Board Certifications:	American Board of Surgery; American Board of Thoracic Surgery; American Board of Environmental Medicine
Other Information:	â€œOptimum Environments for Optimum Health and Creativityâ€?

SPEECH TITLE: “Autonomic Nervous System Changes with Treatment in 100 Chemically Sensitvite Patientsâ€?

At the end of this Presentation, the participant should be able to:

1. Treat the nutritional aspects of ANS dysfunction

2. Treat the toxic aspects of ANS dysfunction

3. Treat the hypersensitivity aspects of ANS dysfunction

The above information was provided by the Speaker.

Objectives & Notes

Kaye H. Kilburn, M.D.	Date of talk: Saturday, June11, 2005, 11:30am

University of Southern California Medical Center, Keck School of Medicine Bldg 7/7401 1000 So. Fremont St. Alhambra, CA 91803	Phone: 626/457-4202
	Fax: 626/457-4203
	Email: [email protected]

Training:
Current Job Description:	Ralph Edgington Professor of Internal Medicine, University of Southern California Keck School of Medicine
Medical School/University Attended:	University of Utah College of Medicine
Internship:	Western Reserve, University Hospitals Cleveland, Internal Medicine
Residency:	University of Utah Medicine, Pathology; Duke, Cardiopulmonary Physiology; University of London Cardiology
Board Certifications:	Diplomat American Board of Internal Medicine, American Board of Preventive Medicine Occupational Health
Other Information:	Books: Chemical Brain Injury and Endangered Brains Mold and Mycotoxins, (Kilburn, KH ed) Written several articles

SPEECH TITLE: “Intervention with Glutathione-Galavit; Realities of Delivery to Neuronsâ€?

At the end of this Presentation, the participant should be able to:

1. Understand the rational basis for redox regulation of brain cells.

2. See the need for measurement of brain functions before and intervention.

3. Have basis for evaluating therapy directed to brain impairment and chemical intolerance.

The above information was provided by the Speaker.

Intervention in CBI-MCS with Glutathione–Galavit

Realities in Delivery to Neurons

¹Kaye H. Kilburn, M.D.

²William S. Lynn, Ph.D.

University of Southern California¹

Keck School of Medicine

Laboratory for Environmental Sciences

Bldg A7 #7401

1000 S. Fremont Ave/ Unit #2

Alhambra, CA 91803

CATO Research ²

4364 S.Alston Ave.

Durham, NC 27713

Phone: 626-457-4202¹

Fax: 626-457-4203

Email: [email protected]

Background

Empirical treatment for chemical brain injury especially that due to molds and mycotoxins and multiple chemical sensitivity beyond â€œto avoidâ€? includes body burden reduction by purging, sweating, exercise and desensitization. Many nutritional supplements and anti oxidants, statins, antifungal agents and immune enhancers have been given to patients. Often patients â€œfeel betterâ€? during or after these ministrations but there are no measurements of neurobehavioral function to appraise efficacy. Furthermore glutathione (50 to 100 mg/ml) to provide suflhydral SH groups has a logical promise and has been administered without adverse effects to many patients with multiple chemical sensitivity.

The initial objective was to determine the effect of intranasal glutathione (G_l) on neurobehavioral (NB) function in patients with chemical intolerance and chemical brain injury. Several physicians had described improvement in patients’ feelings and decreased symptoms from 1 or 2 squirts of glutathione, 100 mg/ml in each nostril 3 times a day. The procedure adopted after finding only one of 30 patients reacted adversely was to obtain baseline measurements of 26 NB functions, teach patients to self administer G_l and repeat measurements after intervals of one month after that (TW, JL, MC, JM). Four patients returned at monthly or bimonthly intervals for 4 to 12 months. Some functions improved, but rarely to predicted (normal) levels but subjective recall, memory, mood, and alertness improved and symptom frequencies decreased. There was no toxicity, but no additional improvements after 30 days, in fact none after 14 days so a shorter interval of 3 days was adopted for evaluation of G_l. The second step was to add an oxidation-reduction regulating, redox, agent Galavit (G_a) 10 mg/ml and continue G_l at 50 mg/ml for 3 days (G_l / G_a). All 4 patients decreased their neurobehavioral abnormalities and feelings and symptoms improved after 3 days. The third step was to measure quickness of response and then fourth to see whether G_a alone improved functions.

Objective

This study was designed .to test whether functions changed during or after IN glutathione and compare effects with an IN redox agent ∝–luminol (Galavit).

Methods

Patients were evaluated for 26 neurobehavioral functions including balance, reaction time, color determination, visual field performance and score, hearing, vibration and grip strength.

Cognitive tests included problem solving in Culture Fair, digit symbol vocabulary, recall of stories (memory), peg placement, trailmaking A and B and information similarities and picture completion, Profile of Mood States, assessed feeling supplemental by Beck’s Depression Scale and the McLean Limbic System Inventory. A well seasoned machine readable constrained data base facilitated data handling and comparisons.

Glutathione was initially given by aerosol but as equivalent effects on symptoms followed the intranasal administration, 27 patients received approximately 50 or 100 mg per day intranasal via sniffing that delivered 1.0 to 1.20 ml per day to the nose. The efficiency of nasal absorption to the brain is unknown but insulin, oxytoxin and peptides have been measured in cerebrospinal fluid after sniffing them. Baseline measurements of 26 functions provide the baseline for effects of aerosol – intranasal glutathione. Patients returned for testing after 4 or 6 weeks.

Results: In a year’s interval since first evaluation, two patients of 27 had returned to normal function. Interval function of the other 25 was unchanged or worse. IN glutathione improved function, reduced abnormality score by 2-3 with greater effect on psychological than physiological performance with no effect on balance and reaction time. One subject who had been exposed to organophosphate insecticides became nauseated and vomited after the first dose of IN glutathione at 50 mg/ml and could not tolerate a reduced dose.

The second step was to add a redox regulator to IN glutathione. We chose ∝-luminol, manufactured to drug purity in Russia as Galavit that has been used to treat inflammation and cancer by injections into tissue and intravenously. No toxic effects were seen when it was taken by the investigators and given to two patients. Ten patients were in this search for efficacy testing. They mixed Galavit 20 mg/ml with Glutathione 100 mg/ml and 6 subjects administered it intra nasally 3 times per day. Four patients showed decreased neurobehavioral abnormalities after 3 days with improved feeling state (POMS score) and decreased symptoms.

The third step, four new patients, 2 untreated and 2 who received G_l without improvement earlier were given G_a alone and were measured at 24 and 48 hours. Three improved at 24 hours and improved further at 48 hours. Total abnormalities decreased in DM from base of 8 to 5 and 5; JK from base of 14 to 10 and 3.5 and TT from base of 6.5 to 5.5 to 6 but balance and reaction time improved. Further improvement was seen in 2 after glutathione (G_l) was added for 24 and 48 hours, DM after G_l/ G_a was 1 and remained 1 and TT from base of 6.5, to 5.5 and 6.0, and after G_l/ G_a was 6.0. DM had normal function and no mood or symptom problems and remained normal after 2 weeks at home. TT had improved balance that remained abnormal. The fourth, SM, was unchanged so returned for a second course. The third, JK who could not take glutathione, was almost functionally normal after 48 hours of Galavit. Abnormalities decreased for baseline of 14 to 3.5.

Summary:

a. Neurobehavioral improvement after Galavit (G_a) occurred in 24 to 48 hours in 4/4 (DM, TW, JK, TT)

b. Intranasal glutathione added to Galavit (G_l/G_a) increased effect in 6 of 6 (JL, MC, DM, TW, JB, FB). Two patients, FB and JB, had least improvement. JB, age 19 years had had brain surgery twice to remove seizure foci that were attributed to mold/mycotoxin impairment.

c. Two of 3 patients with balance disorders improved markedly (TW, and JM) while TT, the most abnormal, had some improvement in extremely abnormal balance but greatly improved cognitive mood and feeling state.

d. After stopping Galavit, DM remained rehabilitated, TW crashed, but was restored with G_l/ G_a. and JM improved again with G_l/ G_a.

e. One patient, SM, had no improvement on G_l alone, G_aalone, or for 48 hours following the combination of G_l/ G_a. but after Glutathione for 2 weeks took Galavit for 4 days with improvement almost to normal. This defined him as a slow responder.

Conclusion:

1. Galavit (∝–luminol) given intranasally improved functions including balance.

2. Glutathione is synergistic with Galavit

3. Balance is a key function for evaluating therapy.

4. Redox regulators combined with SH or NO agents deserve further investigation.

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Objectives & Notes

Richard Jaeckle, M.D.	Date of talk: Saturday, June 11, 2005, 1:00pm

8220 Walnut Hill Lane, Suite 404 Dallas, TX 75231	Phone: 214/696-0964
	Fax: 214/696-1094
	Email: [email protected]

Training:
Current Job Description:	Private Practice of Psychiatry and Environmental Medicine
Medical School/ University Attended	University of Texas Southwestern Medical School
Internship:	Veterans Administration Hospital, Dallas, TX
Residency:	Psychiatry: St Louis Univ Hospitals & Child Psychiatry: Washington Univ Child Guidance Clinic
Board Certifications:	AmerBdPsyNeurol:Psychiatry; AmerBdPsyNeurol: Child Psychiatry; AmerBdEnvironMed

SPEECH TITLE: “Group A Strep and Neuro Psychiatric Disordersâ€?

At the end of this Presentation, the participant should be able to:

1. Know the definition and pathogenicity of PANDAS.

2. Anticipate the incidence of GAS in mood/behavior disorders

3. Associate certain psychiatric disorders to medical problems

The above information was provided by the Speaker.

Richard G Jaeckle, MD

8220 Walnut Hill #404

Dallas, TX 75231

Group A Strep and NeuroPsychiatric Disorders

Objectives of Presentation:

1) Know the Definition and Pathogenicity of PANDAS.

2) Anticipate the Incidence of Group A Strep (GAS) in NeuroPsychiatric Disorders.

3) Associate Certain Psychiatric disorders to Medical Problems.

Outline:

Conclusions:

• There appears to be a high incidence of GAS colonization in these psychiatric patients.

• Rapid Strep ID is not an effective tool for detecting GAS colonization.

• Tonsillar size is not an reliable tool for detecting colonization

• ASO titer is a simple and effective tool for detecting GAS colonization.

• Skin test with GAS vaccine is not commercially available, but is quite sensitive and useful.

• Significant medical problems are not being recognized and treated.

• The PANDAS panel provides useful additional parameters for evaluation of GAS pathogenicity

References:

• Bowers M, Will Immunotherapy succeed whether others have failed Neuropsychiatry reviews, v2#2, Mar 2001

• http://www.nimh.nih.gov/research.pandassumary.cfm

– Aug18, 2001; NIMH Roundtable

• Arch Pediatr Adol Med 2002:156(4)356-361

• http://intramural.nimh.nih.gov/research/pdn/web.htm

• Leonard HL, Swede SE, PANDAS; Int J Neuropsychopharm 4:191, 2001

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Objectives & Notes

Theodore R. Simon, M.D.	Date of talk: Saturday, June 11, 2005, 1:30pm

Functional Imaging of Texas, PA 3209 Drexel Drive Dallas, TX 75205	Phone: 214/435-2866
	Fax: 972/759-5176
	Email: [email protected]

Training:
Current Job Description:	Physician
Current Faculty Appointments:	Associate Professor of Clinical Radiology, SWMS
Medical School/ University Attended	Yale University, School of Medicine
Internship:	University of Rochester
Residency:	University of California at San Francisco; Yale
Board Certifications:	American Board of nuclear Medicine

SPEECH TITLE: “Recent Developments in Functional Imagingâ€?

At the end of this Presentation, the participant should be able to:

1. Identify new diagnostic options with functional imaging.

2. Understand the requirements imposed on patients for functional imaging.

3. Understand ordering issues for obtaining functional imaging.

The above information was provided by the Speaker.

Recent Developments in Functional Imaging

by Theodore R. Simon, M.D.

Goals and Objectives

The participant should understand the strategic implications of functional imaging. These strategies will be explored to allow the participant to become familiar with how to use them to effectively develop diagnostic assessments and objective measures of therapeutic efficacy.

Outline

We will examine available functional imaging techniques to identify and quantitate various attributes of cell function. Specifically we will address central and autonomic neurotransmitters, effects on cell behavior, kinetics, receptors, and metabolism. Case studies of these modalities will be provided, to describe the clinical milieu in which the practitioner can obtain valuable information.

Attention will be directed toward the types of examinations that are available. The tracers, imaging devices, and data analyses will be covered in detail. Tracers currently available will be emphasized, but a peek at likely imminent developments will also be provided. Imaging devices will be explained, especially in light of current widespread confusion regarding PET/CT and SPECT/CT. Examples of one-, two-, three-, and four-dimensional image analyses will be explained as they relate to gathering functional information.

Special consideration will be given to explaining the likely experience of the patient in order to provide the practitioner with a sense of the implications of orders for these tests.

Conclusions

Efficient use of functional imaging can provide both highly sensitive and highly specific information that can target a diagnosis. Moreover, having made the diagnosis and embarked on the therapeutic regimen, functional imaging can objectively assess the success of the strategy and provide prognostic data to provide the patient with reasonable expectations of the likelihood of improvement.

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Objectives & Notes

Jean Monro, M.D.	Date of talk: Saturday, June 11, 2005, 2:00pm

Breakspear Hospital Hertfordshire House Wood Lane, Paradise Hemel Hempstead, Herts HP2 4FD England	Phone: 011/44-1442-261333
	Fax: 011/44-1442-266388
	Email: [email protected]

Training:
Current Job Description:	Medical Director of Breakspear Hospital, England
Medical School/ University Attended	London Hospital Medical School, England
Residency:	London Hospital
Board Certifications:	MB, BS, MRCS, LRCP, FAAEM, DipIBEM, MACOEM
Other Information:	Treatment of cancer with mushroom products. Arch environ Health 2003; 58:533-7

SPEECH TITLE: “Man’s Sense of Awarenessâ€?

At the end of this Presentation, the participant should be able to:

1. Appreciate that particles and frequencies are perceived by man;

2. Realize that the pathway for these is neural;

3. Understand the interaction between sensitivities and allergies and why neutralization therapy works for both.

The above information was provided by the Speaker.

Breakspear Hospital

MAN’S SENSE OF AWARENESS

In any individual with a disease, there are 3 main categories which are amenable to treatment:

· infectious agents

· nutritional state

· pollutants

These have to be considered for each individual in the light of their own immunology, their own encounters and their own nutritional intake.

With regard to our state of health, this is primarily dependent on an individual’s discrimination between self and non-self, which is learned in utero. Thereafter, what is non-self, and which we need to be incorporated into the body, we tag with a piece of self (Secretory IgA). This is then accepted in the body without reaction.

Secretory IgA is a non-inflammatory antibody and reduces the body’s other reactions to any foods that are admitted with it. If there is inadequate Secretory IgA and a food gains access to the system, then the body will react with reactive antibodies to disperse a possible threat. If, however, the substance is not required by the body, but still has IgA attached to it, it can be broken down in the liver and many bacteria and bacterial products are dispersed without untoward effect.

The pathways for foreign material, regarded as â€œsuspiciousâ€? by the immune system and not required for sustenance, are two-fold:

1 Cell-mediated immunity

2 Humoral immunity

These two pathways are antagonistic towards each other, as resources have to be carefully directed and husbanded when there is a threat to the body. If, for example, there is a massive bacterial infection or viral infection, this can be targeted by cell-mediated immunity and antibody production. If, however, there is a very large parasite, such as a worm, infecting the body, then clearly cells are not going to be able to encompass this and antibodies are made, which is the fluid (humoral) immunity. The protein messengers, which perpetuate this type of reaction, are called cytokines. They work in groups to direct the reactions; cytokine groups are known as Th1 and Th2. The group producing cell-mediated immunity are called Th1 cytokines. The group producing humoral immunity are called Th2 cytokines; these induce humoral/fluid/antibody reaction. We know that in people who have long-term viral infections there is a cytokine shift from Th1 to Th2. When this happens, we have to be aware that excessive antibody production results in allergies.

There is a distinction between allergy and sensitivity. The pathway for allergy is subject to many reactions with cells. The pathway for sensitivity is also involved in allergic states, but is the neural pathway for both allergy and sensitivity.

The universal means of perceiving identity is to recognise things which are not self. We do this through our perception of weak electromagnetic fields. If we were to be bombarded by magnetic fields which were intense, this would be the equivalent of being overwhelmed by information. It is not how perception works. We have the means of identifying very weak electromagnetic fields and assessing these as part of our non-self environment. Every item with which we are in touch has a weak electromagnetic field. To be able to sense this and discern what is appropriate for us and what is dangerous is a universal phenomenon of mankind, as basic as the sense of smell or hearing in higher animals. Where there is disequilibrium in our means of assessment of this, people require help. This is the point at which foods, chemicals, inhalants and electromagnetic frequencies, beyond those which can be tolerated, disturb the individual and this is why we use neutralising vaccines for our patients. The amplification of this follows.

Just as light frequencies are converted into chemicals in the eye, then transmitted through ionic exchange via the optic nerve to the ophthalmic area of the cortex, so our electromagnetic perception is similarly mediated.

The other special senses have receptors, physical information which becomes transformed through chemical intervention then through swift ionic exchanges to recognition in the cortex. Sound, touch, vibration, position, temperature are all perceived thus. Another aspect of physics and chemistry co-operating in perception is that melatonin is formed in the pineal gland in the dark. Its production can be switched off by light whether in the sighted or the blind. The blind cannot perceive through sightless eyes or through the reception of frequencies through the eyes. However, it is very likely that they can react to frequencies perceived through the skin.

It is known that the supra-optic nuclei are involved in this perception and jetlag can be overcome by their response to light through a non-optic nerve channel. Our sense of smell is said to be recognition of molecules at the molecular level. However, pheromones are perceived by animals without such a major organisation as the nose; for example, creatures with antennae can appreciate these.

We receive information through perception of the whole range of electromagnetic frequencies through the skin and mucous membranes by the dendritic cells, thence via the C-fibres to the autonomic nervous system, the cord, the hypothalamus and cortex.

We have proved that people who have sensitivities are able to perceive foods, chemicals, inhalants and electromagnetic frequencies similarly. All the first three, if diluted, exhibit the phenomenon of hormesis. This is the stimulatory effect of small doses of substances which, in larger doses, are inhibitory.

With our neutralising vaccines, hormesis is exhibited. We have demonstrated that symptoms produced by a series of doses of a sequence of decreasing dilutions can be negated at one point in the series. Another bipolar response curve will then occur with further dilutions. These continue through a range of dilutions beyond Avogadro’s number. The weaker the range of dilutions, the greater the induction of symptoms and the greater the interval between the provocation and the nullification of symptoms.

This series of provocation and neutralisation strengths can be applied to the individual either by:

1) subcutaneous injection 5) application with a phial against the skin

2) intradermal injection 6) application by a phial held away from

3) sublingual administration the skin at varying distances

4) cutaneous application 7) a weak electromagnetic frequency

The explanation of all of these means of inducing and nullifying symptoms is that the receptor is receiving not a chemical, but a physical initiation of response. Patients exposed to frequencies through the entire frequency range from 1 Hz to 2 GHz in a Faraday cage have shown exactly the same provocation and neutralisation of symptoms.

The receptor is the dendritic cell. It is connected to a C-fibre, then to the autonomic nervous system, the spinal cord, hypothalamus and cortex, where the appreciation of the frequency is that of awareness of self and awareness of non-self, in that the frequencies of all objects outside the body are distinct. We see symptoms induced in patients at any of these intersections.

We see:

1 Cutaneous reactions equivalent to a histamine response.

2 C-fibre transmission, which can be demonstrated. It can be blocked by transcutaneous field applications.

3 Effects on the autonomic nervous system – we know that anaphylaxis can occur with autonomic system inhibition of response (how else can a peanut in someone’s pocket at a doorway to a room be perceived by a highly sensitive patient within that room, as we have observed?). The standard view is an antigen antibody response, which could be mitigated through reception of frequencies. We can demonstrate any autonomic nervous system effect, either sympathetic or parasympathetic, with dilutions of vaccines, including changes in pulse rate, asthmatic effects or rhinitis which can be switched on and off and abdominal distension, due to parasympathetic effects.

4 Effects on the spinal cord – we have observed instant weakness of a limb, with difficulty in walking, or weakness of an arm, for example.

5 Changes in emotional states – because hypothalamic effects can be switched on and off very swiftly.

6 Reception of the information of the whole electromagnetic perception system by the cortex allows awareness of self and non-self.

All of these have been demonstrated in varying degrees in 12,000 patients. We have captured many of these effects on video film. The effects can be replicated and demonstrated independently to any observer and are therefore valid. For any individual, the symptoms produced may be identical with different antigenic stimuli. We can observe these responses in any individual with a degree of sensitivity, because the responses are the universal property of mankind. Sensitivity is heightened in the ill. This is, therefore, our electromagnetic perception system and is responsible for awareness of foreign material.

Jean A Monro

Medical Director

SELF

(Inside the Body)

Acceptable

(by the immune system)

Can be incorporated

into the body without

reaction

Causes inhibition

of further IgA production by IgG antibodies and a reaction occurs

If the If the particles particles

are are

Small Big

Mutually

Inhibitory

Th1 Th2

______

Cell Humoral

Mediated Immunity

Immunity(CMI) with

(and sometimes antibodies

antibodies)

If CMI is inadequate

More antibodies

Cytokine

Shift

(Excessive Th2) Allergy

NON-SELF

(Outside the Body)

e g in the gut, nasal passage

To be questioned

(by the immune system)

Tagged with IgA

Not tagged with IgA

Interactive

Between

These

NON-SELF

(Outside the Body)

skin, gut and mucosa

To be questioned

(by the immune system

neural pathway)

Interactive

Between

These

SELF

(Inside the Body)

Acceptable

(by the immune system)

Neural Pathway

Dendritic cell sensor

‘C’ Fibre

Autonomic Nervous System

Spinal Cord

Hypothalamus

Brain

Perception

Heightened Sensitivity

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Objectives & Notes

Roy Fox, M.D.	Date of talk: Saturday, June 11, 2005, 2:30pm

Nova Scotia Environmental Health Centre P.O. Box 2130, 3064 Highway #2 Fall River, Nova Scotia B2T 1K6 Canada	Phone: 902/860-0551
	Fax: 902/860-2046
	Email: [email protected]

Training:
Current Job Description:	Director, Nova Scotia Environmental Health Centre
Current Faculty Appointments:	Professor of Medicine; Dalhousie University; N.S., Canada
Medical School/University Attended:	Newcastle Upon Tyne, UK
Internship:	Newcastle Teaching Hospitals
Residency:	Royal Free Hospital, London, England
Board Certifications:	FRCP (U.K. – Int. Medicine); FRCPC (Gastroenterology)
Other Information:	Master of Environmental Studies (Dalhousie) 2001 – Thesis “Multiple Chemical Sensitivity and the Environmentâ€?: â€œEnv. Sensitivities in Dialysis Unitâ€? Indoor Air 1999. â€˜Environment & MCSâ€™ Indoor Air 2002: â€œAdaptation in Individuals with Heightened Sensitivity to Combined Environmental Factorsâ€? Archives of Complex Env. Studies 2003.

SPEECH TITLE: “Controlled Inhalational Challenge in Multiple Chemical Sensitivityâ€?

At the end of this Presentation, the participant should be able to:

1. Experimental set up to identify reaction to chemicals in MCS.

2. Problems with adaptation to changes in environment in patients with MCS

3. Complexity of reactivity to environmental triggers.

The above information was provided by the Speaker.

CONTROLLED INHALATIONAL CHALLENGE IN MULTIPLE CHEMICAL SENSITIVITY (MCS)

Roy Fox ¹, Michel Joffres ^{1, 2}, Tara Sampalli ¹

¹ Nova Scotia Environmental Health Centre, Fall River, Nova Scotia, Canada

² Community Health and Epidemiology, Faculty of Medicine, Dalhousie University, Halifax, Canada

Reactivity to environmental triggers in patients with MCS is complex, and it is clear that the reactivity is not usually allergic in nature or due to classical toxic damage. Much discussion has centered on the role of other factors, such as fear, societal fear of chemicals and anxiety.

Patients with MCS have been challenged with chemicals in various studies, but most such studies have not accounted for the autonomic dysfunction and compounding factors such as anxiety and fear. A challenge booth was constructed at the Nova Scotia Environmental Health Centre, a very clean and specially constructed building. The design allows common chemicals to be introduced into the air supply, and for the patient or observing nurse to be unaware of the introduction of a chemical or placebo. In a pilot study of 12 patients with MCS and 7 control subjects it was found that all the control subjects readily adapted to the baseline experimental protocol within 1 or 2 sessions, with 86% adapting in 1 session. After 4 sessions, 2 of the patients could not adapt and still showed random changes in skin conductance and electromyography measured at the upper trapezius. Of the remaining 10 subjects, the number of sessions required for adaptation varied between 2 to 4 sessions with 25% requiring up to 4 sessions and 50% requiring 2 sessions. Placebo or chemical introduction occurred in a randomized sequence post adaptation. Skin conductance, skin temperature, surface electromyography, heart rate and respiratory rate were used to measure response to challenge substances along with symptoms and environmental scores. Skin conductance seemed to be the obvious indicator of a response to the challenge substances. All patients reacted to the introduction of an antistatic fabric softener. 90% reacted to the glue and 80% reacted to the body wash solution in the patient group. While none of the controls reacted to the fabric softener or glue, one control reacted to the body wash solution. Symptom scores were higher for all substances in the patient group.

This study has now been confirmed in a formal study with a larger sample size showing a clear difference in the adaptation between the patients and the control group. The reactivity to the challenge substance as indicated by the skin conductance is still higher in the patient group compared to the controls. The formal study has also revealed the complexity of the reactivity in individuals with MCS. The MCS patient reacts to the presence of chemical triggers, without conscious awareness as all the subjects wore nose plugs and could not smell the substance. Although there is correlation with symptoms, it is not possible to rely upon the conscious interpretation to establish an exposure. Further studies are planned to explore the role of conscious-unconscious awareness and correlation between physiological and symptomatic response.

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Objectives & Notes

Dietrich K. Klinghardt, M.D., Ph.D.	Date of talk: Saturday, June 11, 2005, 3:30pm

Institute of Neurobiology P.O. Box 5023 Bellevue, WA 98007	Phone: 425/822-2509
	Fax: 425/828-3588
	Email: [email protected]

Training:
Current Faculty Appointments:	Capitol University, Washington, DC
Medical School/University Attended:	Albert-Ludwig University Freiburg, Germany
Internship:	Albert Ludwig University, Freiburg, Germany
Residency:	Surgery University Clinic, Freiburg, Germany
Board Certifications:	Board certified in General Practice (Germany) and Pain Management, US

SPEECH TITLE: “The Sphenopalatine Ganglion and Environmental Sensitivityâ€?

At the end of this Presentation, the participant should be able to:

1. Understand the anatomy and physiology of this ganglion.

2. Understand the pathophysiology of this ganglion: toxicity, infection, allergic ganglionitis, descending emotional influences, structural injury from poor occlusion and electric dysfunction from oral electrogalvanic currents (electrogalvanism).

3. Be aware of 3 techniques to restore health in this ganglion: injection, electric stimulation, psychoemotional techniques.

The above information was provided by the Speaker.

The Sphenopalatine Ganglion (SPG) and Environmental Sensitivity

Symptoms of MCS and related disorders often include chronic sinusitis, rhinitis, cognitive problems of the brain and inappropriate emotional states. Often there are related digestive problems, fatigue and the exaggerated reactions to inhalants, foods and odors. Besides the more known innervation of the saliva producing glands and the mucous producing cells of the sinus epithelium and tear glands, projections of the SPG have been found in the middle cerebral artery. The gaglion is mostly parasympathetic, but also has sympathetic connections. The superficial location in the pharynx explains the extraordinary sensitivity of this ganglion to odors and particles in the air. The neighborhood to the teeth suggests a vulnerability to mercury fumes escaping from dental amalgam fillings. The intricate connection to the vagus nerve and the innervation of the saliva producing glands predicts many of the digestive symptoms observed in dysfunctional states. The little explored access of the SPG to the deep cerebral arterial supply can explain many of the brain/limbic system related observations in MCS. Both the literature and clinical experience demonstrate that treating this ganglion can be a rewarding intervention in the treatment of environmental sensitivity.

Objectives & Notes

Jorge A. Ayala Moran, M.D.	Date of talk: Saturday, June 11, 2005, 4:00pm

Clinica Medisur Prol. Av. Las Americas # 1808-7 Fracc. El Dorado 1a Seccion Aguascalientes, Ags. Mexico	Phone: 011-52-449-978-5353
	Fax: 011-52-449-978-5232
	Email: [email protected]

Training:
Current Job Description:	Private Practice, Clinica Medisun Aguascalientes, Mexico
Medical School/ University Attended	Facultad de Medicina â€œMiguel AlemÃ¡nâ€? Universidad Veracruzana
Internship:	Instituto Mexicano del Seguro Social Veracruz México
Residency:	Instituto Nacional de Pediatria, México Cyti
Board Certifications:	Consejo Mexicano de Otorrinolaringologia, Soc. Mexicana de Alergia en ORL
Other Information:	Guia Clinica de Rinosinusitis, Academia Mexicana de Cirugia 2004 Are you looking the cause of disease? Boletin de la Soc. Mexicana de Otorrinolaringology

SPEECH TITLE: “Allergy as a Cause of Sleep Apnea Syndromeâ€?

At the end of this Presentation, the participant should be able to:

The above information was provided by the Speaker.

Objectives & Notes

Kou Sakabe, M.D.	Date of talk: Saturday, June 11, 2005, 4:30pm

Environmental Medical Center The Kitasato Institute, Kitasato University 4-3-18 Seijo Setagaya, Tokyo 157-0066 Japan	Phone: 81-3-5490-2366
	Fax: 81-3-5490-2366
	Email: [email protected]

Training:
Current Job Description:	Clinical Ecologist, Environmental Toxicologist
Current Faculty Appointments:	Professor of Public Health and Clinical Ecology
Medical School/ University Attended	Tokai University School of Medicine
Internship:	Tokai University Hospital
Residency:	Tokai University Hospital
Board Certifications:	Japanese Society of Industrial and Occupational Medicine, Japaneses Association of Physical Medicine, Balneology and Climatology

SPEECH TITLE: “Effect of EMF on Male Reproductive Organsâ€?

At the end of this Presentation, the participant should be able to:

1. Understand the cellular effects of an extremely-low frequency magnetic field (EMF) on spermatogenesis.

2. Understand the endocrine disruptive effect of EMF on male reproductive organs.

3. Understand the effect of EMF on male reproductive organs for health risk assessment.

The above information was provided by the Speaker.

Effect of EMF on Male Reproductive Organs

Kou Sakabe, M.D., Ph.D.

Department of Public Health, Molecular Toxicology and Clinical Ecology,

Kitasato University School of Pharmaceutical Sciences, Tokyo

Professor, Graduate School of Pharmaceutical Sciences, Kitasato University

Director, Environmental Medical Center-Tokyo, The Kitasato Institute

5-9-1 Shirokane, Minatoku, Tokyo 108-8641, Japan

E-mail: [email protected]

The cellular effects of an extremely-low-frequency electromagnetic field (EMF) on mouse spermatogenesis were assessed by DNA flow cytometry and serum testosterone. Seven week old male ICR misce were exposed to a 50 Hz EMF the strength of which was 1.0 m Tesla. Seven mice per treatment group were exposed for 13, 26, 39 or 52 days. For each experimental point, an equal number of mice per sham-treated group were used as a control and were exposed only to the background field below 1μ Tesla in the same room as the treatment group.

In the control mice, the testis cellular DNA content distribution by flow cytometory was characterized by four quantifiable populations; round spermatids (1C), spermatogonia and other diploid cells (2C), spermatogonial cells synthesizing DNA (S-phase) and primary spermatocytes (4C).

In animals exposed for 26 days the number of cells in the 4C and the 4C:2C ratio was significantly lower, the 1C:4C ratio (meiotic transformation) was significantly higher than the corresponding control groups. In animals exposed for 52 days the cell population in 1C and the 1C:2C ratio (total germ-cell transformation) was significantly higher, and the cell population in 2C was significantly lower than the corresponding control groups.

The concentration of serum testosterone in animals exposed for 13 days was significantly higher than in the corresponding control group.

These changes suggest that long-term exposure to an extremely-low-frequency EMF had a possible effect on the proliferation and differentiation of spermatogonia. Moreover, the results of the present study suggest that we must recognize the possibility that EMF can affect the various testicular functions in the capacity of endocrine-disrupting factors.

Finally, the precise mechanism of EMF action on spermatogenesis is still unclear. Further efforts to resolve this question are underway in our laboratory.

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Objectives & Notes

Aristo Vojdani, Ph.D.	Date of talk: Saturday, June 11, 2005, 5:00pm

Immunosciences Lab, Inc. 8693 Wilshire Blvd., Ste. 200 Beverly Hills, CA 90211	Phone: 310/657-1077
	Fax: 310/657-1053
	Email: [email protected]

Training:
Current Job Description:	CEO of Immunosciences Lab., Inc., Beverly Hills, CA
Current Faculty Appointments:	Dept. of Neurobiology, UCLA
Medical School/ University Attended	Bar Ilan University, Ramat Gan, Israel
Residency:	Post-Doctoral study at UCLA
Board Certifications:	Clinical Laboratory Scientist, State of California

CASE STUDY: â€œNeuroimmune Abnormalities in a Patient Exposed to a Combination of Mercury and Chemicals Used in Fumigationâ€?

At the end of this Presentation, the participant should be able to:

1. Understand that chemicals can induce immune deficiency on the one hand, and autoimmunity on the other hand.

2. Observe that cellular immune abnormalities are detected side by side with humoral immune abnormalities in patients exposed to mercury and dursban.

3. Understand that these abnormalities cannot be detected by normal laboratory testing but can be documented by immunotoxicological and neurotoxicological evaluations.

The above information was provided by the Speaker.

Neuroimmune Abnormalities in a Patient Exposed to a Combination of Mercury and Chemicals Used in Fumigation.

Aristo Vojdani, Ph.D., M.T.
Immunosciences Lab., Inc.
8693 Wilshire Blvd., Ste. 200, Beverly Hills, California 90211

Phone (310) 657-1077 (800) 950-4686 Fax (310) 657-1053
E-mail: [email protected] www.immunoscienceslab.com

Abstract

A 53-year-old female practicing dentistry more than 20 years. Loved to eat fish, (mainly salmon), 2-4 times per week. Bought a new house and moved in immediately after fumigation. Three days later, she developed severe headache, dizziness, fatigue, and fibromyalgia.

After being unable to work for five days she decided to go to the emergency room. All physical exams and routine lab tests were found to be normal. During a period of 12 months she visited over 14 doctors; in most cases she was prescribed anti-depressants that did not ease symptoms.

After visiting 14 clinics the patient was referred to one of the AAEM members, who based on medical history and a physical exam, connected the patient’s conditions to either mercury exposure or to Dursban used for fumigation. Blood samples were sent for immunotoxicological evaluations and the following abnormalities were detected: low % T-helper cells, high % T-suppressor cells, low T-helper/suppressor ratio, high % memory lymphocytes, low natural killer cell activity, and low lymphocyte response to T-cell mitogens and very high % of cells going through apoptosis. ANA titer was 1:640 with speckled pattern, elevated total immune complexes, elevated IgG antibodies against mercury bound to human serum albumin, fibrillarin, chromatin, myelin basic protein, neurofilaments, and tubulin were detected.

These results indicated that the patient is having cellular immune deficiency and humoral immune activation resulting in autoimmunity. Analysis of the data may assist in finding mercury or Dursban as being responsible for the detection of immunodysregulation.

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