urticaria and vasculitis in patients with hcv and

27th Annual International Symposiumon

Man and His Environment in Health and Disease

Special Focus

Nutritional & Environmental AspectsOf

Cardiovascular Disease

SYLLABUS

June 25 thru 28, 2009

Sponsored by American Environmental Health Foundation

andUniversity of North Texas Health Science Center

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.

SYMPOSIUM PURPOSESince 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 2009 conference will focus on “Nutritional & Environmental Aspects of Cardiovascular Disease.” This Conference presents the most current information available while providing guidelines to identify, diagnose, treatment and to prevent environmentally triggered responses in the body.

GOALS OF THE MEETING! To provide new insights into the mechanisms and the environmental causes behind many problems seen by the

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

patients.! To provide concepts, tools that will enhance the physicians practice.

OBJECTIVES OF THE MEETING! Improve the outcome of treating patients with a thorough understanding of nutritional and environmental aspects

of cardiovascular disease.! Use new concepts and treatments related to nutritional and environmental aspects of cardiovascular disease and

to help better diagnose and manage patients.! Apply the concepts of this conference to your practice by using nutrition and environmental manipulation for the

treatment of cardiovascular disease.! Use the information presented to enhance the effectiveness, cost-efficiency, and competitiveness in relation to

nutritional and environmental aspects of cardiovascular disease.

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

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.

CreditThe University of North Texas Health Science Center at Fort Worth designates this educational activity for a maximum of 24.25 AMA/PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity.

The University of North Texas Health Science Center anticipates this program for 24.25 hours in Category 2A, AOA credit hours, pending approval by the American Osteopathic Association.

Nursing Accreditation/Credit:The University of North Texas Health Science Center at Fort Worth is an 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 I 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 a maximum of 24.25 Type 1 Contact Hours TNA/ANCC. To receive a certificate of successful completion, participants must attend the activity and complete and return the attendance record/credit request form and the evaluation form at the end of the activity.

EDUCATIONAL FORMATS Plenary Panels Discussions Case Studies Question & Answer Sessions Syllabus

CONFERENCE FORMATThe AEHF Committee has selected some of the leading experts in the fields of cardiovascular disease, 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.)

FINANCIAL CONSIDERATIONAEHF is a nonprofit organization that was founded in 1975 to provide education and research into Environmental Medicine. This year’s Symposium is our 27th 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.

DISCLAIMERAEHF and the University of North Texas Health Science Center are not responsible for the contents of these presentations. AEHF has not altered or modified the contents of the information provided by the speakers.

GIVEN IN COOPERATION

William J. Rea, M.D., F.A.C.S.Symposium Chairman,American Environmental Health Foundation,Environmental Health Center – Dallas, Dallas, TX

Bertie B. Griffiths, Ph.D.,American Environmental Health Foundation,Dallas, TX

Kaye H. Kilburn, M.D.Consultant, President of Neuro-test, Inc.Pasadena, CA

William J. Meggs, M.D., Ph.D.Brody School of Medicine, East Carolina UniversityDepartment of Emergency MedicineGreenville, NC

Doug Seba, Ph.D. Independent Marine Scientist

Alexandria, VA

Schedule of Proceedings, Table of Contents

Thursday, June 25, 2009

Seba, Ph.D., Doug B.

“Environmental Update 2009 With Some Cardiovascular Aspects” ............................................................9

Frustaci, M.D., Andrea

“Myocardial Trace Elements Imbalance In Idiopathic Dilated Cardiomyopathy”......................................20

Oschman, Ph.D., James L.

“Structure and Properties of the Living Matrix”..........................................................................................22

Heine, Ph.D., Hartmut

“The Structural Principle of the Human Myocardium”...............................................................................30

Rea M.D., William J.

“Environmental Aspects of Cardiovascular Disease”..................................................................................33

Coppock, DVM, Robert W.

“St. Anthony’s Fire in Veterinary Medicine”..............................................................................................41

Kilburn, M.D., Kaye H.

“Heart Disease 2009 World Trenets and Causes” ......................................................................................51

Klinghardt, M.D., Ph.D., Dietrich K.

“The Role of Neural Therapy in Modulating the Involvement of the Autonomic Nervous System in

Cardiovascular Disease” .............................................................................................................................61

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

“Diet, Inflammation, and Atherosclerosis” .................................................................................................64

Bhatnagar, Ph.D., Aruni

“Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants" - Part I”.........................73

Hillman, Ph.D., Donald

“Cardiovascular Response to Electric and Magnetic Fields”......................................................................82

Schedule of Proceedings, Table of Contents

Friday, June 26, 2009

Sinatra, M.D., Stephen T.

“Metabolic Cardiolgy-The New Emerging Frontier”..................................................................................95

Stark, M.D., Martha

“Murmur of the Heart: The Story It Tells When We Listen”....................................................................111

Suleman, M.D., Amer

“Heart Rate Variability As Predictor of Sudden Death” ...........................................................................120

Friday, June 26, 2009

Monro, M.D., Jean

“Fructose Metabolism: A Toxic Challenge”..............................................................................................122

Simon, M.D., Theodore R

“Nuclear Medicine In Cardiac Disease Update 2009”..............................................................................136

Frampton, M.D., Mark W.

“The Cardiovascular Consequences of Particulate Air Pollution”............................................................142

Reiter, Ph.D., Russel, J.

“Melatonin: Role in Blood Pressure Regulation”......................................................................................144

Overberg, Ph.D., Ron

“Nutrition Tips for Cardiovascular Disease” ............................................................................................150

Abou-Donia, Ph.D., Mohamed B.

“Splenda Alters Gut Microflora in Male Rats”..........................................................................................159

Patel, M.D., Kalapana

“Role of Heart Rate Variabilityin the Practice of Environmental Medicine”............................................169

Rizzo, M.D., Carmelo

“Urticaria and Vasculitis in Patients with HCV”.......................................................................................171

Suleman, M.D., Amer

“Syndromes of Orthostatic Intolerance”....................................................................................................174

Saturday, June 27, 2009

Coppock, DVM, Robert W.

“Mycotoxins and The Heart”.....................................................................................................................179

Roberts, Jr., M.D., James

“Immunomodulation in Atherosclerosis and Heart Failure”.....................................................................196

Klinghardt, M.D., Ph.D. Dietrich K.

“Cavitation in the Jawbone, the Vagus Nerve, and the Heart.”.................................................................220

Rea, M.D., William J.

“Environmental Aspects in the Treatment of Cardiovascular Disease”....................................................222

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

“Accelerators of Atherosclerosis”..............................................................................................................232

Sinatra, M.D., Stephen T.

“Energy Medicine-Good Vibes vs Bad”...................................................................................................241

Patel, M.D., Kalapana

“Environmental Aspects of Lyme Disease and Autonomic Deregulation”...............................................254

Hillman, Ph.D., Donald

“The Electropathic Stress Syndrome--Neuroendocrine Responses to EMF”............................................256

Saturday, June 27, 2009

Bhatnagar, Ph.D., Aruni

“Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants - Part II”...........................268

Abou-Donia, Ph.D., Mohamed B.

“Splenda Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Rats”.......................................276

Sunday, June 28, 2009

Frustaci, M.D., Andrea

“Selenium And Zinc Deficient Cardiomyopathy In Human Intestinal Malabsorption”............................285

Monro, M.D. Jean

“Aspects of Tissue Oxygenation”..............................................................................................................287

Heine, Ph.D., Hartmut

“Cardiocyte-Fibroblast Coupling. Basis for Myocardial Functioning”.....................................................298

Kilburn, M.D., Kaye H.

“Heart Disease and Rotten Egg Gas”.........................................................................................................300

Reiter, Ph.D., Russel J.

Melatonin Protects Heart From Free Radical Damage”............................................................................307

Jaeckle, M.D., Richard,

“The Crosstalk Between the Central and Autonomic Nervous System”...................................................318

THURSDAY, JUNE 25, 2009

OBJECTIVES & ABSTRACTS

Objectives & Notes

Doug B. Seba, Ph.D. Date of talk: Thursday, June 25, 2009, 9:10 a.m.

107 S. West Street, #430Alexandria, VA 22314

Phone: 703/949-1055

Training:Current Job Description: Independent Marine ScientistUniversity Attended University of Miami, Coral Gables, Florida – M.S./Ph.DOther Information: Over 50 years experience in ecology and chemicalsDisclosure Statement:

SPEECH TITLE: “Environmental Update 2009 with Some Cardiovascular Aspects”

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

1. Understanding that for 27 years, the essence of this conference has been to make the connection between environmental stressors (physical, chemical, biologial0 and adverse health effects, particularly cardiovascular.

2. Realize that environmental phenomenon such as electromagnet radiation, atmospheric dust, or xenobiotics combined with fate and transport mechanisms, can have major impacts on cardiovascular function

3. Comprehend that adverse health effects on cardiovascular capabilities can occur at significant time and distance from their environmental loci.

The American Environmental Health Foundation and the University of North Texas Health Science Center is not responsible for the contents of this presentation. AEHF has not altered or modified the contents of the information provided by this speaker.

Global Environmental Update 2009: Aspects of Cardiovascular Disease

Douglas B. Seba

Objectives


1. Appreciate that for over a quarter of a century, the focus of this Symposium has been to elucidate the direct connection between environmental stressors, whether natural, man-made, or a combination, and adverse health effects.

2. Understand that exposure to chemical, physical, and biological incitants along with fate and transport mechanisms, can have major impacts on chronic diseases, especially cardiovascular.

3. Realize that the development of lasting illnesses (including heart) in patients can occur at great time and distance from their environmental origins.

Abstract

The earth is both a dry/dusty and a wet/moldy place. Both may be increasing in the natural environment perhaps aided by climate change. The world is also a geomagnetic water planet under constant solar/cosmic radiation. There is no doubt that a great deal of man-made items (chemical, physical, biological) are being impressed on these epochal geologic events. There also appears to be an increase in these man-made moieties in indoor environments as humans spend more time in enclosed structures particularly with air conditioning. For more than a quarter-century this Symposium and this Presenter have highlighted the fact that for most environmental patients including cardiovascular, whether their illness is from chemical, physical or biological sources, or some combination of them, it is often subtle and hidden exposures that are paramount in both their diagnosis and treatment. It is central to the theme of environmental illness to correctly realize this relationship to often hidden or under appreciated exposures and their connection to chronic disease including the heart.

It is the Presenter’s experience that the environmental scientists and physicians at this Symposium are probably the most qualified to help chronically ill patients cope with daily exposures to hidden heart stressors. From that perspective, this is a very limited review to set the tone for this Symposium. Highly selected examples of the above natural and man-made processes are taken from a mix of media, websites, and scientific publications relevant to the current timeline including some of the Presenter’s own environmental research of interest to attendees.

References01. Mukhopadhyay S and P Kreycik. Dust generation and drought patterns in Africa from helium-4 in a modern Cape Verde coral. Geophysical Research Letters 35, L20820, 2008. DOI:10.1029/2008GL03572202. Perez L,et. al., Coarse Particles From Saharan Dust and Daily Mortality, Epidemiology:Volume 19(6)November 2008pp 800-807 DOI: 10.1097/EDE.0b013e31818131ef 03. Borrell B. They came from above. TheScientist. 22:12 pp.36-44. 2008. www.the-scientist.com04. Paytan A., et.al. Toxicity of atmospheric aerosols on marine phytoplankton. PNAS 106:12 pp. 4601-4605, March 24, 2009. DOI:10.1073/pnas.0811486106.05. Evan AT. A summary of the 2008 dust forecast from the University of Wisconsin News. http:/cimss.ssec.wisc.edu/clavr/amato/Amato_T_Evan/Seasonal_Dust_Products.html06. Ali M. Darwin, Dysox, and Disease. Principles and Practice of Integrative Medicine 11. 3rd. ed. New York: Institute of Integrative Medicine Press; 2008.07. DeBose JL et al. Dimethysulfoniopropionate as a Foraging Cue for Reef Fishes. Science 319:5868 p 1356 07 March 2008 DOI:10.1`126/science.115110908. Borrell B. Baghdad hack. TheScientist. 22:12 pp. 17-18. 2008. www.the-scientist.com09. Christner BC et al. Ubiquity of Biological Ice Nucleators in Snowfall. Science 319:5867 p 1214. February 29, 2008. DOI: 10.1126/science.114975710. Kastrup CJ et al. Spatial localization of bacteria controls coagulation of human blood by ‘quorum acting’. Nature Chemical Biology 4 p742-750. 2008. DOI: 10:1038/nchembio.12411. Deckker PD, et.al. Geochemical and microbiological fingerprinting of airborne dust that fell in Canberra, Australia, in October 2002. G3:GeochemistryGeophysicsGeosystems. 9:12 22pp. 24 December, 2008. DOI: 10.1029/2008GC002091

12. Brauner EV et al. Indoor Particles Affect Vascular Function in the Aged-An Air Filtration-based Intervention Study. American Journal of Respiratory and Critical Care Medicine. 177:4 pp.419-425. March 2008. DOI: 10.1164/reem.200704632oc13. Cruts, B et al. Exposure to diesel exhaust induces changes in EEG in human volunteers. Particle and Fibre Toxicology 5 pp. 4-14. March 2008. DOI: 10.1186/1743-8977-5-414. Morawska L, et al. An Investigation into the Characteristics and Formation Mechanism of Particles Originating from the Operation of Laser Printers. Environmental Science & Technology 43:4 pp 1015-1022. January 23, 2009. DOI: 10.1021/es802193n15. Jerrett M et al. Long-Term Ozone Exposure and Mortality. New England Journal of Medicine 360:11 pp 1085-1095. March 12, 2009.16. http://www.dailytech.com/Sun+Makes+History+First+Spotless+Month+in+a+Century/article12823.htm17. Olsen N and M Mandea. Will the Magnetic North Pole Move to Siberia? Eos, Transactions, American Geophysical Union 88:29 pp 292-293. 17 July 200718. Erickson B. FDA Approves Drug From Transgenic Goat Milk. Chemical & Engineering News 87:07 p 9 16 February 200919. Down J et al. Drugs found in drinking water. AP Archive Story #557240 March 10 200820. Jahren AH and RA Kraft. Carbon and nitrogen stable isotopes in fast food: Signatures of corn and confinement. Proceedings National Academy of Sciences 105:46 pp 17855-17860 November 18 2008 DOI:10.1073/pnas.080987010521. Yin M et al. A Fluorescent Core-Shell Dendritic Macromolecule Specifically Stains The Extracellular Matrix. Journal American Chemical Society 130:25 pp 7806-7807 2008 DOI:10.1021/ja802236222. Scheindlin S. Polluting With Pharmaceuticals. Chemical & Engineering News 86:14 p 4-6 07 April 200823. Busweiler R. Agents shoot EPA fugitive. Keysnews.com p 1 11 March 200824. Engelhaupt E. Happy Birthday, Love Canal. Environmental Science & Technology 42:22 pp. 8179-8186 2008. DOI: 10.1021/ee802376z25. Jjemba PK. Pharma-Ecology: The Occurrence and Fate of Pharmaceuticals and Personal Care Products in the Environment. John Wiley & Sons 2008 314 p $95 hardcover ISBN: 978-0-470-04630-226. Shabecoff P and A Shabecoff. Poisoned Profits: The Toxic Assault on Our Children. Random House 2008 353 p $26 ISBN: 978-1-4000-6430-427. Schapiro M. Exposed: The Toxic Chemistry of Everyday Products and What’s at Stake for American Power. Chelsea Green Publishing 2007 224 p $23 ISBN: 13-978-1-933392-15-828. Michaels D. Doubt Is Their Product: How Industry’s Assault of Science Threatens Your Health. Oxford Press 2008 400 p $28 ISBN: 978-0-19-530067-3

Objectives & Notes

Andrea Frustaci, M.D. Date of talk: Thursday, June 25, 2009, 9:40 a.m.

La Sapienza UniversityHeart and Great Vessels DepartmentViale del Policlinico 155Rome, 00161Italy

Phone: 39/0630155231Fax: 39/063055535Email: [email protected]

Training:Current Job Description: Associate Professor in CardiologyCurrent Faculty Appointments: La Sapienza University, Heart and Great Vessels

Department, Rome ItalyDisclosure Statement:

SPEECH TITLE: “Myocardial Trace Elements Imbalance In Idiopathic Dilated Cardiomyopathy”


1. Know that heavy metals like mercury and antimony are remarkably increased in the myocardium of patients with idiopathic dilated cardiomyopathy.

2. Understand that increased heavy metals can interfere with ca++ activity at actin-myosin junction of myocardiocytes

3. Know that heavy metals accumulation may ultimately concur to the unexplained progressive cardiac dilatation and dysfunction characterizing this entity


Marked Elevation of Myocardial Trace Elements in Idiopathic Dilated Cardiomyopathy Compared With Secondary Cardiac Dysfunction

ANDREA FRUSTACI, MDDepartment of Cardiovascular and Respiratory Sciences, La Sapienza University,

Rome, Italy.

AbstractObjectives: We sought to investigate the possible pathogenetic role of myocardial trace elements (TE) in patients with various forms of cardiac failure.

Background: Both myocardial TE accumulation and deficiency have been associated with the development of heart failure indistinguishable from an idiopathic dilated cardiomyopathy.

Methods: myocardial and muscular content of 32 TE has been assessed in biopsy samples of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current exposure to TE. One muscular and one left ventricular (LV) endomyocardial specimen each patient, drawn with metal contamination-free technique, were analyzed by neutron activation analysis and compared with 1) similar surgical samples from patients with valvular (12 pts) and ischemic (13 pts) heart disease comparable for age and degree of left ventricular (LV) dysfunction, 2) papillary and skeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function 3) LV endomyocardial biopsies from four normal subjects.

Results: A large increase (>10,000 times for Hg and Sb) of TE concentration has been observed in myocardial but not in muscular samples in all pts with IDCM. Pts with secondary cardiac dysfunction had mild increase ( 5 times) of myocardial TE and normal muscular TE. In particular, in pts with IDCM mean Hg concentration was 22,000 times (178,400 ng/g vs. 8 ng/g), Sb 12,000 times (19,260 ng/g vs. 1.5 ng/g), Au 11 times (26 ng/g vs 2.3 ng/g), Cr 13 times (2,300 ng/g vs. 177 ng/g), Co 4 times (86, 5 ng/g vs. 20 ng/g) higher than controls.

Conclusion: A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. The increased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism and worsen cell function.

Objectives & Notes

Robert W. Coppock, DVM Date of talk: Thursday, June 25, 2009, 10:30 a.m.

Toxicologist and Assoc LtdP O Box 2031Vegreville, AB T9C 1T2Canada

Phone: 780/632-6122Fax: 780/632-4492Email: [email protected]

Training:Current Job Description: Private practice in toxicologyDisclosure Statement:

SPEECH TITLE: “St. Anthony’s Fire in Veterinary Medicine”


1. Gain knowledge of ergotism in domestic animals and sources of ergot in livestock feeds stuffs

2. Understand that clinical signs of ergot can be variable and vary from necrosis of the limbs and other appendages, necrosis of the skin to ischemic bowl syndrome. The clinical effects vary with the mixture of ergot alkaloids.

3. Ergotism is the oldest reported mycotoxicosis. Effects in humans include hallucinations.


St. Anthony’s Fire in Veterinary Medicine

Robert W. Coppock, DVM, PhD, DABVT, DABT

Ergotism is the oldest mycotoxicosis known and historical references to ergotism include the names ignis sacer and St. Anthony’s Fire. Claviceps and other ergot-producing species invade and replace the ovary in grasses including cereal grains. Wet cool weather favors fungal infection of the florets. The initial stage is soft white fungal mass (sphacelium) that produces sugary honeydew and conidia. The sphacelium form a hard dry sclerotium (resting form) that is resistant to degradation and contain the ergot alkaloids. Ergot alkaloids target the vascular system and other organs and systems. In field poisoning, domestic animals are exposed to mixtures of ergot alkaloids. The mixtures of ergot alkaloids vary considerably with the strain of the fungus, plant species, climate and other factors. Ergot alkaloids cause constriction of the arterioles and a characteristic hyperplasia of their tunica media in peripheral blood arterioles. Vasoconstriction causes necrosis of distal appendages and skin. The pattern of vasoconstriction varies and can be unique to a particular occurrence. Ischemic bowl syndrome can occur. Cattle have been observed to selectively graze the flowering parts of brome grass infected with Claviceps purpura at the honeydew stage of development. This pattern of grazing resulted in ergotism in Holstein heifers that caused skin necrosis on the body trunk and necrosis of the lamina of the hoof. Myopachynsis of the arterioles of the skin, lungs, kidneys, small intestine, spleen, myocardium and brain were observed. Ergot alkaloids are also present in endophytic fungi (eg Epichloe spp) that infect grasses. The vasoconstriction in addition to causing dry gangrene also can cause heat intolerance. The most common infected grass is tall fescue. The endophyte is symbiotic with fescue and improves its tolerance to environmental stressors.

Objectives & Notes Hartmut Heine, Ph.D. Date of talk: Thursday, June 25, 2009 11:00 a.m. Billerbeckweg 1-3D-75242 Neuhausen, Germany

Phone: 49 (0) 7234 6246Fax: 49 (0) 7234 949109 Email: [email protected]

Training: Current Job Description: Private Scientific Research Institute

Professor emeritus of AnatomyFormally full professor and head of the Department of Anatomy and Clinical Morphology of the University of Witten/Herdecke, Germany

Other Information: Heine H, Schaeg G. Kann die Tumorstammzelle morphologisch charakterisiert werden? Deutsche Zeitschrift für klinische Forschung 2008; 12: 42-45

Disclosure Statement:

SPEECH TITLE: “The Structural Principle of the Human Myocardium” At the end of this Presentation, the participant should be able to:

1. Understanding the determined chaotic functional of the myocardium.

2. Differentiate the structural suppositions of normal and pathological heart functions

3. Realize environmental influences on the determined chaotic myocardial system. The American Environmental Health Foundation and the University of North Texas Health Science Center is not responsible for the contents of this presentation. AEHF has not altered or modified the contents of the information provided by this speaker.

The Structural Principle of the Human Myocardium

Hartmut Heine

Refering to the horizontal oriented basis of the heart, one can distinguish an outer layer of diagonal (ca. 60° angle)

myocard fibers an annular middle layer (0° angle) and opposite to the outer layer an inner diagonal layer (Fig. 1, 2).

This principle peters out in more subtle preparations. A pinnate rhomboidal pattern consisting of muscular and

connective tissue fibers appears in longitudinal and cross sections of the myocardium (Fig. 2). Superimposed

transparent folia with straight lines shifted randomly or in a distinct angle against each other also show rhomboidal

patterns which are analogous to histologically cuts of the myocardium (Fig. 2). The patterns change with every change

in the sectional direction. This means that the myocardium is nowhere structured uniformly. This is the very reason for

the fact that the structural principle of the heart cannot be determined solely from preparations (Heine 1989).

The rhomboidal pattern recognisable in microscopical sections of the myocardium never show any congruency despite

all similarity of the rhombi. These however, are only self-similar exposing the heart function as a non linear determined

chaotic system based on oscillations of mixed (negative and positive) feedback loops.

Given a median wall thickness of the left ventricle of the human heart of 30-40 mm and an average muscle fibre

diameter of approx. 0.5 mm, the ventricular wall consists of approx. 80 layers of muscle fibres. When 80 straight lines

are randomly superimposed in a computer simulation, an image of many self-similar little rhombi results in much the

same way as can be seen in the myocardial sections (Fig. 3). By way of spatial reconstruction, a coiled intertwined

hyperboloid structural principle can be identified (Fig. 3). Since the surface of one hyperboloid, comparable to a saddle,

represents an energetic minimal surface, power transmission from one hyperboloid to another means minimal energy

expenditure at maximum efficiency (by the way this principle applies to all organs) (Fig. 3). In such a non-linear

system, any errors, once occurred, are not eliminated, with new errors adding to the previous ones. This can be

observed with all cardiac diseases, because both the muscular and the fibrous hyperboloids may suffer pathological

structural alterations separately or jointly, interfereing hyperboloid power transmission. Thus, disturbances of this

hyperboloid principle have relations to all cardiac diseases (Heine 1989).

Conclusions

The structural principle of the heart consists of matching muscular and connective tissue hyperboloids pervading each

other. Expressed in simplified terms, there are two forms of hyperboloids in the heart (Fig. 3): one is made up of the

muscle fibres, and the complementary one of the interstitial connective tissue, resulting in a hyperboloid joint as is

used, for example, in engineering the transmission of rotations from one shaft to another one of any direction. All

cardiac diseases seem to have disturbances of this principle.

LiteratureBargmann W, Doerr W (eds.). Das Herz des Menschen. Vol. 1, 2. Stuttgart: Thieme, 1963: 130Doerr W, Schiebler TH. Pathologische Anatomie des Reizleitungssystems. In: Bargmann W, Doerr W (eds.). Das Herz des Menschen. Vol 2. Stuttgart: Thieme, 1963: 805Heine H. Gibt es ein Strukturprinzip des Myokards? Morph Jahrbuch 1989; 135: 463-474Ruthishauser W, Hess O. Herz und Kreislauf. In: Siegenthaler (ed.) Klinische Pathophysiologie. 8. Aufl. Stuttgart: Thieme, 2001: 624Trost U. Analyse eines räumlichen Modells vom Herzmuskel. Doctoral Thesis (MD). Berlin: Free University 1978

Objectives & Notes

William J. Rea, M.D. Date of talk: Thursday, June 25, 2009, 11:30 a.m.

Environmental Health Center - Dallas8345 Walnut Hill Lane, Ste. 220Dallas, TX 75231


Training:Current Job Description: President of the Environmental Health Center – Dallas,

President, American Environmental Health FoundationCurrent Faculty Appointments:Medical School/ University Attended Ohio State University College of Medicine, Columbus,

OHInternship: Parkland Memorial Hospital, Dallas, TXResidency: University of Texas Southwestern Medical School;

Parkland Memorial Hospital, Baylor, Veteran’s Hospital, Children’s Medical Center

Board Certifications: American Board of Surgery, American board of Thoracic Surgery, American Board of Environmental Medicine

Other Information: Author of “Chemical Sensitivity I-IV”, “Optimum Environments for Optimum Health”


Objectives & Notes

James L. Oschman, Ph.D. Date of talk: Thursday, June 25, 2009 1:30 p.m.

Nature's Own Research AssociationP.O. Box 1935Dover, NH 03821


Training:Current Job Description: Author and presenter of lectures and workshops on

energy medicine internationallyUniversity Attended University of PittsburghOther Information: Energy Medicine: the scientific basis, Churchill

Livingstone/Harcourt Brace, Edinburgh, 2000.Energy Medicine in Therapeutics and Human Performance, Butterworth Heinemann, Edinburgh, 2003About 30 papers in leading scientific journals, and about an equal number in complementary medicine journals.


SPEECH TITLE: “Structure and Properties of the Living Matrix”


1. List 4 molecules that are part of the living matrix.

2. List 2 mechanisms of information transfer in the living matrix.

3. List 2 mechanisms of energy transfer in the living matrix.


Objectives & Notes

Kaye H. Kilburn, M.D. Date of talk: Thursday, June 25, 2009, 2:00 p.m.

P.O. Box 5374Pasadena, CA 91107


Training:Current Job Description: Consultant, President of Neuro-test, Inc.Current Faculty Appointments: USC retired 2006Medical School/ University Attended University of Utah 1954Internship: Western Reserve Hospitals – ClevelandResidency: University of Utah: Medicine and pathology, Duke:

cardiopulmonary, London: cardiologyBoard Certifications: Am Board Internal Medicine, Am Board Preventive

Medicine, occupational HealthOther Information: “Chemical Brain Injury,” NY: John Wiley 1998; “Mold

and Mycotoxins,” editor Washington DC: Heldref 2004; “Endangered Brains” Princeton Scientific Press 2004


SPEECH TITLE: “Heart Disease 2009 World Trenets and Causes”


1. Describe the chemical causes of myocardial infarction and differentiate these from the familiar "risk factors."

2. Track the historical evolution of myocardial infarction in the twentieth century

3. Understand role of nanoparticles in hypertension, vascular disease and thrombosis.


Heart Disease 2009: Trends and Causes

By Kaye H. Kilburn, M.D.USC Keck School of Medicine (ret.)

Neuro-Test Inc., Pasadena, CA 91107

Abstract

Three coincidences made me wonder and question: what causes coronary heart disease (CAD) and myocardial infarction (MI)? The accepted risk factors: cigarette smoking, hypertension and elevated total serum cholesterol were acknowledged 40 years ago. Missing was the proximate cause. Chemical causation was suggested when Chet who had an acute coronary occlusion with MI the day he inhaled two or three breaths of chlorine. Barney had severe angina pectoris after less than 5 minutes of exposure to chlorine and showed multi-vessel coronary disease within 3 years. The third was Phil, who had a stroke following severe breathlessness from a few breaths of chlorine.

I was led from chlorine to other chemicals as causes by workers who had inhaled hydrogen sulfide and carbon disulfide, in British and American viscose rayon plants from 1938 to 1962. Their death rates had exceeded other textile workers and other men for 20 years. In the 1960’s, the rising rate in the comparison groups that included many cigarette smokers made the rates nearly identical. Probably increased inhalation of side stream cigarette smoke and fossil fuel combustion products raised the general population’s deaths from heart disease to wipe put the previous rayon worker difference. Many chemicals in smoke inflame coronary arteries.

Inhaled particles that land in the alveoli initiate inflammation that impairs the lungs and its blood vessels. Cells taunted to react go with the flow, to migrate easily from pulmonary veins first to arteries, the coronaries, the aorta, carotids to the brain, kidneys, and the other organs and limbs. In the past decade, mankind’s worldwide bane of CAD, killer of more than 6 million human beings each year has been identified as an inflammatory cascade in arteries. Myocardial infarction and stroke responsible for another 4.5 million deaths per year thus are not just plaques, collections of lipids like grease, but are inflammatory lesions of transmuted cells. Current focus on ‘How can this process be interrupted or patched around must shift to prevent it by avoiding inhaled particles, from smoke.

Although others have suggested that patients saved from infections by antibiotics may have developed CAD and MI. There is no evidence of this and except for advancing age, the risk factors differ. By the 1950’s hospital care in the United States and Great Britain was accessible with emergency response for chest pain so that untoward delay does not seem a factor. The broad age spectrum of serious coronary events was recognized in the 1950’s although women were diagnosed less frequently than men. None of these factors explains the orders of magnitude jump in the incidence and mortality of CAD and MI.

Of the accepted risk factors only inhaled chemicals from smoking cigarettes are a cause. In contrast, hypertension measures vascular over-response. Caloric over-indulgence obesity, and elevated cholesterol levels, are factors in only half of the CAD patients.

The other twentieth century smoke is from fuel burning in cars and trucks. This profligate gas and diesel use pollutes air, water and soil with hydrocarbons and particles. Picture 90 million personal cigarette “smokestacks” in the sea of exhaust pipe smog. Add to the burdens, the chemicals to make plastics by combining chlorine with hydrocarbons by the petrochemical industry. Many chlorinated hydrocarbons like tricholoroethylene disorder heart rhythms, induce arrhythmias and may incite CAD.

Gasoline and diesel exhaust exposure increased logarithmically after 1945 to be nearly exponential (doubling each decade). Air pollution disasters caused deaths from pulmonary disease in New York and London in 1952 and led to regulation. But the adverse effects of cigarette smoking clearly exceeded those of air pollution. Proof of the later is inferred from the increases in background lung cancer rate over this period. Now the rate for men and women who never smoked is higher than it was for cigarette smokers in 1950.

Lung cancer rates in non-smokers in 1980 exceeded that of smokers in the era of 1940-1950. The best explanation is inhaled fossil fuel combustion products which supports their consideration as causal factors for CAD-MI. Burning coal increased 10 fold, but petroleum (oil) increased more than 3,000 times in the twentieth century. From 1 million tons of oil production and use in the United States in 1870, it is now over 7,000 million tons.

In the 1960’s, the Los Angeles area compared to the rest of California showed that the highly urbanized south coast air basin exposes nearly 15 million people to smog. This exposure now extends up Cajon Pass to Barstow exposing high desert people to fossil fuel combustion chemicals from the basin. Similar smog saturation that in 1960 characterized Kern County (Bakersfield), now includes all of California Central Valley. Now affects of exposure are seen in Denver, Colorado; Houston, Texas; Mexico City; Rome; Beijing; Shanghai; Bangkok and many others. Comparisons of heart disease of rates in these smog saturated conurbations with wind swept poorly populated areas show adverse health effects of air pollution.

The development of artificial kidney machines seemed just in time for the epidemic of kidney failure. Large amounts of Medicare funds support biweekly dialysis and selecting candidates for transplantation of someone else’s kidney has become an ethical dilemma adding to its economic impact. Diabetes and interstitial kidney disease related to chemical exposures, especially to solvents, provide a constantly growing flow of patients to dialysis/transplant centers and present further opportunities for prevention by avoidance.

Obesity is a widespread heath problem affecting 31% of American adults in the year 2000, up from 13% in 1960. Obesity, diabetes, hypertension, heart disease, has eclipsed alcoholism and its complication such as fatty liver and cirrhosis for patients in public hospitals. The obstructed macrovessels cause MI, stroke and blocked peripheral vessels in diabetes steals limbs and neuro vascular disease in the eye causes blindness. Obesity must be addressed as a disease, making indignities suffered by the excessively fat people civil rights actions, is not the preventive step needed for better health.

References

Bedford DE, Prognosis – (of Myocardial Infarction), The Lancet, 1935; 223-234.Beggs PJ, Bambrick HJ, Is the Global Rise of Asthma an Early Impact of Anthropogenic Climate Change?, Environ Health Perspect, 2005; 113: 915-919.Bell DM, Fair MA, Elnicki DM, et al, Characteristics of West Virginians Having Myocardial Infarction, Southern Medical Journal, 1998; 91: 1042-1045.Chen L, Yokel RA, Henning B, et al, Manufactured aluminum oxide nanoparticles decrease expression of tight junction proteins in brain vasculature, Journal of Neuroimmune Pharmacology, doi: 10.1007/s11481-008-9131-5y.Cohen S.I., Deane M., Goldsmith J.R., Carbon Monoxide and Survival From Myocardial Infarction, Arch. Environ. Health, Oct. 1969; 19: 510-520.Delfino RJ, Sioutas C, Malik S, Potential Role of Ultrafine Particles in Associations between Airborne Particle Mass and Cardiovascular Health, Environ Health Perspect 2005; 113: 934-946.Doll R, Hill AB, The Mortality of Doctors in Relation to Their Smoking Habits, Brit. Med. J. 1954; 1451-1455.Editorial, From what will we die in 2020?, The Lancet, 1997; 349: 1263.Entman ML, Michael L, Rossen RD, Dreyer WJ, Anderson DC, Taylor AA, and Smith CW Inflammation in the course of early myocardial ischemia, FASEB J. 5: 2529-2537, 1991.Ernst E.; Hammerschmidt DE; Bagge U; Matrai A; Dormandy J; Leukocytes and the Risk of Ischemic Diseases, JAMA 1987; 257: 2318-2324.Fabbri LM, Saetta M, Picotti G and Mapp CE: Late asthmatic reactions, airway inflammation and chronic asthma is toluene-diisocyanate-sensitized subjects. Respiration 1991;58:18-21.Fernandez, Manny, Study Links Truck Exhaust to Schoolchildren’s Asthma, New York Times, Date? 2006.Floyer J: A treatise of the asthma (2nd ed). London: R Wilkin, 1717.Fye WB, Acute Myocardial Infarction: A Historical Summary, Current Topics in Cardiology, 1991.Fye WB, The delayed diagnosis of myocardial infarction: it took half a century!, Circulation: 1985; 72: 262-271.Garshick E, Schenker MB, Munoz A, Segal M, Smith TJ, Woskie SR, Hammond SK and Speizer FE: A retrospective cohort study of lung cancer and diesel exhaust exposure in railroad workers. Am Rev Respir Dis 1988;137:820-825.Grimm Jr. RH, Neaton JD, Ludwig W. Prognostic Importance of the White Blood Cell Count for Coronary, Cancer, and All-Cause Mortality, JAMA, 1985; 254: 1932-1937.Hammond EC, Horn D, The Relationship Between Human Smoking Habits and Death Rates: A Follow-up Study of 187,766 Men, JAMA 1954; 1316-1328,

Heart Protection Study Collaborative Group, MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomized placebo-controlled trial, The Lancet, 2003; 361: 2005-2016.

Henderson AH, Libby P, Fuster V, et al, Coronary Heart Disease, Supplement to The Lancet, 1996.Hennekens CH, Increasing Burden of Cardiovascular Disease: Current Knowledge and Future Directions for Research on Risk Factors, Circulation. 1998; 97: 1095-1102.Holland WW, Bennett AE, Cameron IR, Florey CV, Leeder SR, Schilling RSF, Swan AV and Waller RE: Health effects of particulate pollution: reappraising the evidence. Am J Epidemiol 1979;110:527-659.Karpick RJ, Pratt PC, Asmundsson T and Kilburn KH: Pathological findings in respiratory failure: goblet cell metaplasia, alveolar damage, and myocardial infarction. Ann Intern Med 72:189-197, 1970.Kempner W, Newborg BC, Peschel RL, et al. Treatment of Massive Obesity With Rice/Reduction Diet Program (An Analysis of 106 Patients With at Least a 45-kg Weight Loss, Arch Intern Med. 1975; 135: 1575-1584.Kilburn KH: Evidence that inhaled chlorine is neurotoxic and causes airway obstruction. Int’l J Occup Med Toxicol 1995;4:267-276.Kilburn KH: Leukocyte recruitment to airways by cigarette smoke and particle phase in contrast to cytotoxicity of vapor. Science 1975;189:634-637.Kilburn KH and McKenzie WN: Leukocyte recruitment to airways by aldehyde-carbon combinations that mimic cigarette smoke. Lab Inves 1978;38:134-141.Kilburn KH, Warshaw RH and Thornton JC: Expiratory flows decreased in Los Angeles children from 1984 to 1987: is this evidence of effects of air pollution? Environ Res 1992;59:150-158.Lachocki TM, Church CF and Pryor WA: Persistent free radicals in the smoke of common household materials: biological and clinical implications, Environ Res 1988; 45: 127-139. Lydgate C, Is industrial pollution making America fat? (Studies link pervasive ‘obesogens’ to weight gain in frogs, mice, Portland Tribune, 4-15-08.Mallick NP, Gokal R, Haemodialysis, The Lancet, 1999; 353; 737-742.Meggs WJ, Brewer KL, Weight gain associated with chronic exposure to chlorpyrifos in rats, J Med Toxicol, 2007; 3: 89-93.Parker-Pope T, Diabetes: Underrated, Insidious and Deadly, New York Times, 7-1-08.Penn A, Murphy G, Barker S, et al, Combustion-Derived Ultrafine Transport Organic Toxicants to Target Respiratory Cells, Environ. Health Perspect., 2005; 113: 956-963.Peters A, Veronese B, Calderón-Garcidueñas L, et al, Translocation and potential neurological effects of fine and ultrafine particles a critical update, Particle and Fibre Toxicology, 2006: 3: 13 doi: 10.1186/1743-8977-3-13.Pollack A, The Dialysis Business: Fair Treatment?, New York Times, 9-16-07.Porta M, Persistent organic pollutants and the burden of diabetes, The Lancet, 2006; 368: 558-559.Reddy KS, Yusuf SD, Emerging Epidemic of Cardiovascular Disease in Developing Countries, American Heart Association, Inc. 1998; 97: 596-601. Robbins AS, Manson JE, Lee I, Satterfield S, Hennekens CH, Cigarette Smoking and Stroke in a Cohort of U.S. Male Physicians, Ann Intern Med. 1994; 120: 458-462.Saldana TM, Basso O, Hoppin JA, et al, Pesticide exposure and self-reported gestational diabetes mellitus in the Agricultural Health Study, Diabetes Care, 2007; 3: 529-534.Sample S, High Impact: Cardiologist’s Studies Pump Research on Chronic Heart Failure, Health Sciences Report, 2000: 8-10.Tiller JR, Schilling RSF, Morris JN, Occupational Toxic Factor in Mortality from Coronary Heart Disease, Brit. Med. J., 1968; 4: 407-411.Tuller D, Overshadowed, Kidney Disease Takes a Growing Toll, New York Times, 11-18-08.Wilson, Janet, Study Doubles Estimate of Smog Deaths, Los Angeles Times, 3-25-06.

Objectives & Notes

Dietrich K. Klinghardt, M.D., Ph.D. Date of talk: Thursday, June 25, 2009, 2:30 p.m.

Institute of NeurobiologyP.O. Box 5023Bellevue, WA 98007

Phone: 425/688-8818Fax: 425/453-7015Email:

Training:Current Job Description:Current Faculty Appointments: Capitol University, Washington, DCMedical School Albert-Ludwig University Freiburg, GermanyInternship: Albert Ludwig University, Freiburg, GermanyResidency: Surgery University Clinic, Freiburg, GermanyBoard Certifications: Board certified in General Practice

(Germany) and Pain Management, USOther Information: (books or articles you have written that may be of interest to the attendees)Disclosure Statement:

SPEECH TITLE: “The Role of Neural Therapy in Modulating the Involvement of the Autonomic Nervous System in Cardiovascular Disease”


1. Understand the intrinsic nervous system of the heart.

2. Understand two ways in which the heart communicates with the brain: a. direct ANS projections to the brain b. several neuropeptides.

3. Learn that incomplete healing of the wisdom tooth extraction site is a common cause of supraventricular tachycardia.


The Role of Neural Therapy in Modulating the Involvement of the Autonomic Nervous System in Cardiovascular Disease

Abstract from Dietrich Klinghardt, MD, Ph.D.

Neural Therapy is a targeted treatment of the ANS with injections of Procaine into autonomic ganglia, scars, glands, trigger points and the skin overlying organs and joints (segmental therapy) and has been shown to successfully modulate ANS-regulation, function and neurotransmitter release. The ANS is directly involved in numerous aspects of cardiac function: the dual innervation (sympathetic and parasympathetic) of the SA and AV nodes, up- and down-regulates aspects of the cardiac rhythm. The sympathetic innervation of the coronary arteries allows for maximum vasodilatation in acute stress situations to maximize flight and fight responses. The sympathetic fibers and their neurotransmitter release into the cardiac muscle sensitizes the heart muscle fibers. The vagus nerve can be compromised in several locations:

a. level of the brainstem (toxicity from retrograde transport of toxins from intestinal tract, cross transfer from other cranial nerves – especially 5th bringing into this area mercury from dental amalgam fillings and thioethers from jaw infections)

b. vagal gangliac. during the course of the nerve itself (anterior neck problems such as enlarged thyroid or lymph

nodes, rib subluxation, increased muscle tension and trigger points)

Other aspects of cardiac neurology that must be considered:1. Just as the enteric nervous system of the gut the heart has its own intrinsic nervous system with its own ganglia which communicate with the brain ( Lacey, J. I. and B. C. Lacey (1978). Two-way communication between the heart and the brain: Significance of time within thecardiac cycle. American Psychologist (February): 99-113) and the rest of the body, with both afferent and efferent neurons (connecting the heart to far away places such as the amygdala). Many systemic health problems - such as some cases of chronic depression - can be an expression of a failure of communication between heart and brain rather then a brain problem. The intrinsic system also responds to input from within the heart and is capable of regulating virtually any aspect of cardiac function – this made the heart transplant possible. The heart’s intrinsic nervous system is vital for the maintenance of cardiovascular stability and efficiency. This system responds well to two neural therapy interventions: segmental therapy of the heart, utilizing the viscero-cutaneous reflex, and intravenous procaine injections.

2. The heart also produces neuropeptides which communicate with other organs in the body, especially the brain (Armour, J. A. and J. Ardell, Eds. (1994). Neurocardiology. New York, NY, Oxford University Press).Amongst them are

1. atrial natriuretic factor (ANF) 2. norepinephrine and dopamine3. oxytocin

Segmental therapy, the stellate ganglion block in combination with a sphenopalatine ganglion block, and intravenous procaine are the most effective interventions on this level.

3. The heart is also the most powerful generator of rhythmic patterns as evidenced by picking up EKG signals on the wrist, ankles etc. These signals seem to have an integrating effect for all our physiological systems in the body. Most rhythm disturbances can be positively and lastingly improved by neural therapy.

In neural therapy the patient’s history of injuries, toxic exposures and emotional trauma are most important. Beyond that, careful physical examination, HRV testing, dental x-rays and dental status evaluation, gut dysbiosis evaluation (urine organic acids, parasitology) and other localizing tests are helpful to select the most effective neural therapy intervention for heart related issues.

Typical and common examples:

Episodes of atrial tachycardia: infected lower wisdom tooth extraction site (diagnosis established with procaine injection to suspected area while monitoring heart rate. Treatment with cavitation surgery)

Permanently elevated heart rate: diagnostic procaine injection into the thyroid gland, segmental therapy to the brain (“crown”)

Angina: search for untreated scars ( appendectomy, hernia, tonsillectomy, etc.), diagnostic segmental therapy of the heart region, diagnostic dental injections

Chronic depression with heaviness in the heart: segmental therapy to the heart, thyroid injection and segmental treatment to the brain

Anxiety with heart symptoms: thyroid injection Established coronary artery stenosis, heart failure or other medically urgent heart condition: 1- 2

times weekly stellate ganglion block to downregulate sympathetics, segmental therapy of the heart segment, regular i.v treatment with procaine (alkalkinizing protocol). Direct daily treatment to the heart with NASA infrared device (“health light” from BioTools for Wellness). EECP 30 sessions.

Neural therapy has been practiced since the early part of the 20th century and has established itself in many countries as a safe, inexpensive and effective adjuvant in cardiology.

Objectives & Notes

William J. Meggs, M.D., Ph.D. Date of talk: Thursday, June 25, 2009, 3:30 p.m.

Brody School of Medicine, East Carolina University600 Moye Blvd., Room 3ED311.PCMH, 3ED-311, Department of Emergency MedicineGreenville, NC 27834-4354


Training:Current Job Description: Chief of Toxicology, Professor of Emergency MedicineCurrent Faculty Appointments: Professor, Brody School of MedicineMedical School/ University Attended University of Miami, Miami, FloridaInternship: Rochester General HospitalResidency: Rochester General Hospital, Fellowships at NIH and

NYUBoard Certifications: Medical Toxicology, Allergy and Immunology, Internal

Medicine, Emergency MedicineOther Information: Author of “The Inflammation Cure”, over 50 research

publications, Co-editor of “Health and Safety in Farming, Forestry, & Fisheries”; Co-author of “Biomarkers of Immunotoxicology”


SPEECH TITLE: “Diet, Inflammation, and Atherosclerosis”


1. To know the role of Inflammation in Atherosclerosis

2. To know how diet modulates inflammation

3. To know diets that reduce the risk of Atherosclerosis


Diet, Inflammation, and Athrosclerosis

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

Objectives• To know the role of inflammation in atherosclerosis

• To know how diet modulates inflammation

• To know diets that reduce the risk of atherosclerosis

Abstract

Atherosclerosis is a natural part of the aging process. Inflammation is a major mechanism that the body uses to produce the planned obsolescence mediated by atherosclerosis. The leading causes of death in industrialized countries are myocardial infarctions and strokes, the end-stage manifestations of arthrosclerosis. The age at which the manifestations of atherosclerosis become clinically relevant is a complex blend of genetic and environmental factors. Diet is a major determinant of the rate at which atherosclerosis progresses. While we cannot at present control a genetic predisposition to early onset of atherosclerosis, environmental and dietary factors are controllable at an individual’s discretion. Dietary and other interventions that can reduce one’s risk of heart attacks and strokes will be discussed.

References

Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.Gu L, et al. Procyanidin (PC) content and total antioxidant capacity (TAC) of chocolate and cocoa products. FASEB J 2005;19:A1032:Abstract#598.20. Wu X, et al. Lipophilic and hydrophilic antioxidant capacities of common foods in the United States. J Agric Food Chem 2004;52:4026-37Wan Y et al. Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandin concentrations in humans. Am J Clin Nutr 2001 74 :596-602.Grassi D, et al. 2005a. Cocoa reduces blood pressure and insulin resistance and improves endothelium-dependent vasodilation in hypertensives. Hypertension 2005 46: 1-8.Waterhouse AL et al. Antioxidants in chocolate, Lancet, Sept.1996; 348(1):834.Inhibition of LDL oxidation by cocoa, Lancet, November 1996; 348(2):1514.Meggs WJ, Svec C. The inflammation Cure. McGraw Hill, 2003Meggs WJ, Heidal K, Escott-Stumpf S. the Inflammation Cure Cookbook. To be published.

Objectives & Notes

Aruni Bhatnagar, Ph.D. Date of talk: Thursday, June 25, 2009, 4:00 p.m.

University of Louisville580 S. Preston St.The Baxter II, Room 421Louisville, KY 40202

Phone: 502/852-5724Fax:Email:

Training: Post-doctoral training in cellular cardiac electrophysiology

Current Job Description: Professor of Medicine - Teaching and ResearchCurrent Faculty Appointments: Department of Medicine, Physiology and Biophysics, and

Pharmacology and ToxicologyMedical School University of Kanpur, UP, India (Ph.D) and University of

Texas Medical Branch Galveston, TXDisclosure Statement:

SPEECH TITLE: “Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants"- Part I


These talks are to discuss the contribution of exposure to environmental pollutants to heart disease. Specific issues that will be discussed include evidence implicating that exposure to particulate air pollutants and gaseous co-pollutants increases CVD risk. Data relating to an increase in both acute and chronic risk will be examined. The effects of other pollutants such as metals and aldehydes will also be discussed.

1. Estimate risk due to exposure to particulate air pollution2. Understand the impact of the environment of cardiovascular disease3. Understand the pathophysiological mechanisms that impart and mediate the effects of the environment on

acute cardiovascular events as well as chronic atherosclerotic disease


Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants

Aruni Bhatnagar, Ph.D., FAHA, Division of Cardiology, Department of Medicine, University of Louisville, Louisville, KY

Heart disease is the leading cause of death in the industrialized world. The rates of heart disease, however, vary from one country to another. Geographic variations in CVD mortality probably reflect genetic, social, and cultural factors as well as disparities in health care. Nevertheless, epidemiological data suggest a strong influence of environmental factors, since rates of CVD incidence and mortality could be markedly altered within a generation, indicating that CVD risk is in large part derived from environmental factors.

How the environment influences heart disease is not well understood. Multiple studies suggest that environmental factors such as smoking, nutrition, and physical activity are key factors that determine CVD risk. Nevertheless, it remains unclear how these factors contribute to the incidence and the severity of heart disease. In addition, the pathologic mechanisms by which environmental factors influence specific features of heart disease remain largely unknown. Epidemiological evidence indicates that CVD risk is derived from several variant and invariant “risk factors” such as high cholesterol, blood pressure, diabetes and smoking. In addition, exposure to environmental pollutants has also emerged as a new risk factor for the development of heart disease. Extant literature provides ample evidence linking most common pollutants to heart disease. Several pollutants ranging from tobacco smoke, particulates, metals, and pollutant gases have been reported to either exacerbate CVD or precipitate acute clinical. Multiple studies reporting health effects of ambient particles have been published. These studies provide evidence for a significant association between particulate air pollution levels and short-term mortality as well as increased mortality risk due to long-term exposure.

Over 100 epidemiological studies report a link with daily fluctuations in air pollutants at relatively low commonly encountered levels of air pollutants in several urban areas throughout the world events. Consistent positive relationships between daily PM10 levels and mortality counts have been reported by studies using either time series modeling or a case-cross over design. The strength of association appears to be stronger for PM2.5 than PM10, indicating that PM2.5

may be the more responsible for the observed association. The magnitude of the effect (about 1%) is small, variable, and dependent upon several statistical considerations including controlling for seasonality and slowly changing covariants. Nevertheless, consistent associations have been reported for risk of death from all causes, but particularly from cardiopulmonary disease. In some studies significant associations have also been reported for sulfur oxide concentrations, while others have found no association with common copollutants (NO2, SO2, CO, and O3). For obvious reasons, no controlled toxicological studies with mortality as an end point have been conducted to experimentally verify the link between short time exposure to air pollutants and increased mortality counts.

The effects of long-term exposure to air pollution on mortality have also been examined. Two major studies - the Harvard six cities and the American Cancer Society cohort studies report a significant positive association between cardiopulmonary mortality and PM2.5 and sulfate concentrations. No excessive mortality risk was associated with exposure to coarse PM or other gaseous pollutants. Similar associations have also been reported by several other long-term exposure studies. Notably, increases in mortality risks were much larger (generally more than 10 %) than observed with daily time-series studies. The magnitude of the reported effect is, however, variable.

Animals studies with particulate air pollution show that exposure can lead to an increase in cardiovascular inflammation results in an increase in atherogenesis, thrombosis and endothelial dysfunction. Environmental effects on atherogenesis are poorly understood. Data from Watanbe heritable hyperlipidemic rabbits show that repeated intrapharyngeal instillation of PM10 (twice a week for 4 weeks) stimulates progression of atherosclerotic plaques and increases lipid accumulation in aortic lesions as well as plaque cell turnover. These observations suggest exposure to PM 10 could accelerate atherogenesis and potentially enhance the vulnerability of atherosclerotic plaques to rupture. In addition to air pollution and tobacco smoke, there is extensive evidence suggesting that exposure to metals also accelerates atherogenesis.

Exposure to arsenic in particular has been linked to an increase in atherosclerotic disease. Studies with human populations exposed to arsenic in well water in Taiwan suggest that the incidence of CVD depends upon the level of exposure to arsenic Epidemiological studies of regions with high arsenic levels in the ground water show a marked

increase in several forms of CVD including carotid atherosclerosis, hypertension, and ischemic heart disease. Arsenic exposure is also associated with peripheral atherosclerosis, which severely decreases blood flow to extremities and result in gangrene. In Taiwan and Bangladesh, gangrene is most commonly present on feet leading to the characteristic blackfoot disease. Consumption of arsenic contaminated drinking water is also associated with an increase in cardiovascular mortality in the U.S. Exposure to pollutants could also increase thrombosis. Platelets from smokers demonstrate an increase in spontaneous as well as agonist (ADP, thrombin) stimulated aggregation. In addition, PM can contribute to the development and maintenance of a pro-thrombotic state. This is supported by studies demonstrating a positive correlation between PM10

exposure, plasma levels of fibrinogen and an increase in blood viscosity. Similarly, ultrafine particles increase platelet number, reduce bleeding times and increase levels of soluble P-selectin, a marker of platelet activation Aside from PM, component gases of ambient air have been linked to thrombosis through epidemiological studies demonstrating associations between exposure and hospitalizations for ischemic heart disease. Most prominent among these atmospheric gases include ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen oxides (NO2). Ozone exposure, in particular demonstrates a particularly strong association with enhanced platelet aggregation and acute MI. In contrast this association was lacking with NO2 and SO2.

Reactive aldehydes are another constituent of ambient air pollution that might be linked to cardiovascular disease. Aldehydes are a significant component of automobile exhaust and smog and have been detected in high concentrations in cigarette, cotton, wood, and coal smoke. The specific contribution of aldehydes to the cardiovascular effects of traffic air pollution, however, remains to be fully assessed. In a recent study on the cardiovascular effects of traffic exposure on highway patrol troopers, aldehydes were strongly correlated with an increase in plasma von Willebrand factor and changes in heart rate variability. Cardiovascular toxicity of environmental aldehydes is also underscored by studies showing increased risk of atherosclerotic disease in plant workers producing formaldehyde and a higher incidence of heart disease in undertakers, embalmers and perfumery workers who are exposed to high levels of aldehydes during the course of their work. Nevertheless, it remains unclear whether exposure to ambient levels of aldehydes is associated with an excessive CVD risk and whether long-term repeated exposures to aldehydes has broad impact on cardiovascular function and CVD disease or susceptibility.

In the absence of injury, the cardiovascular system does not directly interact with the environment. It is, however, highly sensitive to environmental changes. These responses could promote cardiovascular health or could contribute progressively to disease and dysfunction. Although some cardiovascular diseases (such as familial hypercholesterolemia or the long Q-T syndrome) have clear, well-defined genetic origins, the most common forms of CVD develop in response to environmental injury. This injury might result from excessive consumption of saturated fat, lack of exercise or from continuous exposure to environmental pollutants. In each case, disease appears to develop from failed responses to repair injury and to restore normal function rather than from common genetic flaws that manifests to greater severity with increasing age. During disease development genetic factors undoubtedly play an important role in modulating environmental influences. As a result, individuals with different genetic makeup display different susceptibilities to environmental insults. Nevertheless, given its high prevalence, CVD is unlikely to be entirely or even substantially regulated by genetics. For the same reasons, it is also unlikely that the environment plays a secondary role in the etiology of CVD. Migrant population studies and studies within the same population with changing environment (lifestyle choice, nutrition, etc) have shown that significant changes in the environment could substantially alter CVD risk. Both population-based cohort studies and animal experiments have provided ample data to support the view that exposure to environmental pollutants (ambient air particulates, tobacco smoke, metals, aldehydes, etc) can induce endothelial dysfunction and significantly accelerate and exacerbate atherogenesis and thrombosis. This evidence suggests that environments that induce systemic inflammation or increase oxidative stress exacerbate atherogenesis, because both inflammation and oxidative stress are key contributors to atherosclerotic lesion formation. Nevertheless, it is not clear whether there are common sets of mechanisms by which environmental agents impair vascular function and promote atherogenesis and to what extent primary interfaces with the environment (e.g., lung, gut, skin, etc) modify the external insult or orchestrate the cardiovascular response.

References: 1.Brook, R. D., Franklin, B., Cascio, W., Hong, Y., Howard, G., Lipsett, M., et al. Air pollution and cardiovascular

disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation 6-1-2004; 109: 2655-2671

2. Bhatnagar, A. Cardiovascular pathophysiology of environmental pollutants. Am.J.Physiol Heart Circ.Physiol 2004; 286: H479-H485.

3. Bhatnagar, A. Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ.Res. 9-29-2006; 99: 692-705. 4. Pope, C. A., III and Dockery, D. W. Health effects of fine particulate air pollution: lines that connect. J.Air Waste Manag.Assoc. 2006; 56: 709-742.

Objectives & Notes

Donald Hillman, Ph.D. Date of talk: Thursday, June 25, 2009, 4:30 p.m.

Michigan State University750 Berkshire LaneEast Lansing, MI 48823


Training:Current Job Description: ConsultantCurrent Faculty Appointments: Professor EmeritusMedical School/ University Attended Michigan State University, East Lansing Dairy Nutrition

MajorInternship:Residency:Board Certifications:Other Information: Problem solving on farms and have documented and

published work on Electropathic Stress Syndrome and on Chronic Fluoride and Iodine Toxicity.


SPEECH TITLE: “Cardiovascular Response to Electric and Magnetic Fields”


1. Recognize sources of EMF exposure in the living environment

2. Understand common neural pathways of electrical exposure

3. Measure cardiovascular response to EMF


Cardiovascular Response to Electric and Magnetic Fields

Donald Hillman¹, PhD., Professor Emeritus, Department of Animal Science, Michigan State University, East Lansing, MI 48823

Abstract

Sources of electric and magnetic fields (EMF) and effects on human health were studied in homes in East Lansing and on a farm near Leslie, Michigan. The utility’s primary neutral-to-ground wire (PN-G) connected to a grounded-Y distribution system was a major source of EMF radiation into the living environment of homes, schools, and workplaces. Exposure to 2-50 milliGauss (mG) magnetic field in the living environment increased heart rate +29% and diastolic blood pressure +48% in direct proportion to the flux density of the magnetic field. Induced current (mA) exposure measured with oscilloscope leads attached to the human body was proportional to milliVolt (mV) potential between right-leg and left-arm and to mG EMF at floor level in the living room above the ground wire in five trials. Installation of a dielectric union in the water pipe mitigated EMF radiation. A farmer developed arrhythmia and hypertension after nine 46-kiloVolt (kV) transmission lines were built over his workspace and radiated 2.5-6.5 mG at head height near his grain-storage building. A challenge exposure to 2-4 mG EMF in a medical laboratory confirmed the patient’s cardiovascular symptoms and sensitivity to EMF. The findings help to explain the increase of hypertension observed by the American Heart Association (AHA), and concur with cardiovascular changes of workers in electrical industries.

¹Donald Hillman, PhD., Professor Emeritus, Department of Animal Science, Michigan State University, East Lansing, MI 48823. Hillman served as Extension Specialist in Dairy Nutrition and Management from 1955-1982. He was a High School Teacher of Vocational Agriculture and County Extension Agent 1951-55. He studied environmental effects on dairy cattle performance and investigated effects of electric and magnetic fields on behaviour, health, and productivity of dairy cattle in some 110 herds assisting farmers, veterinarians, electricians, and engineers in problem cases. He is a member of The American Dairy Science Association-Am..Soc.of Animal.Science, and the American Society of Agricultural and Biological Engineers. He has investigated EMF effects on humans and other species and serves as a private consultant regarding EMF effects on dairy cattle.

Selected Digital References:

http://www.powerwatch.org.uk/science/studies.asphttp://www.bioinitiative.org/

http://www.microwavenews.com/ http://omega.twoday.net/stories/3642285/

http://electricalpollution.com/Shocking_News.html http://www.weepinitiative.org/

http://electricalpollution.com/

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FRIDAY, JUNE 26, 2009


Objectives & Notes

Stephen T. Sinatra, M.D. Date of talk: Friday, June 26, 2009, 8:05 a.m.

Optimum Health257 E. Center StreetManchester, CT 06040


Training:Current Job Description: Cardiologist, Lecturer, WriterCurrent Faculty Appointments: Assistant Clinical Professor of Medicine, University of

ConnecticutMedical School/ University Attended Albany Medical SchoolInternship: Albany Medical Center HospitalResidency: St. Francis Hospital, Hartford CTBoard Certifications: 1975 American Board of Internal medicine, 1977

American Board of Cardiovascular DiseaseOther Information: Author of “Metabolic Cardiology-The Sinatra Solution”,

revised 2008, “Reverse Heart Disease Now”, articles Metabolic Cardiology-The Missing Link in Cardiovascular Disease, Congestive heart Failure—The Metabolic Cardiology Solution accepted by Alternative Therapies—not published.


SPEECH TITLE: “Metabolic Cardiolgy-The New Emerging Frontier”


1. Learn how the new triad of bioenergetic energy in cardiac health, Coenzyme Q10, L-carnitine and D- ribose, can help prevent and overcome heart disease, and the important contribution these energy-supplying nutrients make in people’s lives.

2. Describe why ATP supporting nutrients can improve symptoms of fibromyalgia and chronic fatigue.

3. Define the complex role of energy and the heart.

4. Learn how targeted nutraceuticals can help people survive heart disease.

5. Learn how mitochondrial defense is a cardinal factor in cardiac dysfunction and age management


Metabolic CardiologyA New Paradigm for the Prevention and Treatment of Heart Disease

Metabolic therapy involves the administration of a substance normally found in the body to enhance a metabolic reaction within the cell. Such therapy may be achieved in two ways. A substance can be given to achieve greater than normal levels in the body to drive an enzymatic reaction in a preferential direction, or a substance can be given to correct a deficiency of a cellular component. Metabolic therapy differs from standard pharmaceutical therapies in that metabolic therapy supports enzymatic reactions, whereby multiple standard pharmaceutical therapies block, rather than enhance cellular processes. Beta blockers, calcium channel blockers, ACE inhibitors, and even statins are pharmaceutical drugs that inhibit pathways to achieve a physiologic response. Simply stated, metabolic cardiology involves an energy gain rather than an energy drain.

The importance of supporting energy production in heart cells and the preservation of the mitochondria in these cells will be the focus of a new frontier in cardiovascular prevention, treatment and management. Many physicians are not trained to look at heart disease in terms of cellular biochemistry; therefore, the challenge in any metabolic cardiology discussion is in taking the conversation from the “bench to the bedside”. An understanding of the vital role that adenosine triphosphate (ATP) plays in the heart is critical for any physician or clinician considering therapeutic options that support ATP production and turnover in jeopardized cardiac muscle cells.

Metabolic therapies that help cardiomyocytes meet their absolute need for ATP fulfill a major clinical challenge of preserving pulsatile cardiac function while maintaining cell and tissue viability. D-ribose, L-carnitine and coenzyme Q10 work in synergy to help the ischemic or hypoxic heart preserves its energy charge. This lecture introduces how ATP, diastolic heart function and metabolic support help maintain cardiac energy by preserving ATP substrates.

Coenzyme Q10, L-carnitine and D-ribose support energy cellular production. Coenzyme Q10 is a lipid soluble antioxidant that plays a vital role in cellular ATP production. L-carnitine supports beta-oxidation of fatty acids in the mitochondria and enhances turnover of ATP. D-ribose is the energy-limiting substrate that supports the production of ATP in the mitochondria.

The energy-starved heart is poorly understood by physicians who treat cardiac disease on a day-to-day basis. Metabolic support with D-ribose, L-carnitine and coenzyme Q10 is critical for the maintenance of contractile reserve and energy charge in minimally oxidative ischemic or hypoxic hearts. Preservation of cellular energy provides the chemical driving force required to complete ATPase reactions needed to maintain cell and tissue viability and function. D-ribose, coenzyme Q10 and L-carnitine exert a physiological benefit that has a positive impact on cardiac function. The use of such nutraceutical support for the heart will be of particular importance for physicians who treat cardiovascular disease in their practices. A new, emerging field in metabolic cardiology will be realized as clinicians choose to treat the energy-starved heart at the level of basic energy metabolism.

Goals and Objectives:

1. Define the complex role of energy and the heart.2. Learn how the new triad of bioenergetic energy in cardiac health, i.e., coenzyme Q10, L-carnitine and

D-ribose, can help prevent and overcome heart disease and the important contribution these energy-supporting nutrients make in people’s lives.

3. Discover how ATP supporting nutrients will improve symptoms of fibromyalgia, chronic fatigue and congestive heart failure.

4. Learn how mitochondrial defense is a cardinal factor to understanding the nature of heart disease. 5. Explore how targeted nutraceuticals can help people survive heart disease.

Objectives & Notes

Martha Stark, M.D. Date of talk: Friday, June 26, 2009, 8:35 a.m.

Harvard Medical School3 Ripley StreetNewton, MA 02459

Phone: 617/244-7188Fax:Email: [email protected]

Training:Current Job Description: Teaching/lecture circuit and full-time private practice in

psychiatric medicine and psychoanalysisCurrent Faculty Appointments: The Center for Psychoanalytic Studies, Massachusetts

General Hospital, Harvard Medical School; Beth Israel Deaconess Medical Center, Harvard Medical School; Massachusetts Institute for Psychoanalysis

Medical School/ University Attended Harvard Medical SchoolResidency: Adult Psychiatry Residency – The Cambridge Hospital,

Cambridge, MA; Child Psychiatry Fellowship – Massachusetts Mental Health Center, Boston, MA; Psychoanalytic Training – Boston Psychoanalytic Institute, Boston, MA

Board Certifications: American Association of Psychiatric MedicineOther Information: Stark M (1994). Working with Resistance. Northvale, NJ:

Jason Aronson; Stark M (1994). A Primer on Working with Resistance. Northvale, NJ Jason Aronson; Stark M (1999). Modes of Therapeutic Action: Enhancement of Knowledge, Provision of Experience, and Engagement in Relationship. Northvale, NJ: Jason Aronson


SPEECH TITLE: “Murmur of the Heart: The Story It Tells When We Listen”


1. Recognize the ways in which environmental stressors (both toxicities and deficiencies) impact the heart

2. Appreciate that coronary collateralization serves both a defensive and an adaptive function

3. Understand the importance of "orderedness" and "ease of flow" of the coronary circulation in the maintenance of optimal heart health and the prevention of "dis-order" and "dis-ease" within the body


MURMUR OF THE HEART: The Story It Tells If We Listen

Martha Stark, MD27th Annual International Symposium – June 25 – 28, 2009

"And now here's my secret, a very simple secret:It is only with the heart that one can see rightly;

what is essential is invisible to the eye."The Little Prince by Antoine de Saint-Exupery

Cardiovascular disease is the leading cause of death in the United States, killing one person every 34 sec-onds and taking even more lives than does cancer. Furthermore, it accounts for 30% of deaths worldwide.

Stressful stuff happens. But whatever the primary target, the critical issue will be the ability of the system (in this instance, the cardiovascular system) to adapt to the impact of the environmental perturbation. Too much stress, traumatic stress, will be too overwhelming for the system to process and integrate, prompting instead defense, disorder, and disease. Too little stress will provide no impetus for transformation and growth, serving instead simply to reinforce the status quo of the system. But just the right amount of stress, optimal stress, will provide the challenge needed to prompt adaptation and reconstitution of the system at a higher level of order, complexity, integration, and coherence.

Stressful stuff happens. But it’s how well the system is able to process and integrate its impact that will make of it either a growth – disrupting event or a growth – promoting opportunity, either one that overwhelms or one that prompts transformation and growth, either one that further challenges an already – compromised system or one that further supports an early – resilient system.

The villain in our piece will be traumatic stress, stress that overwhelms and disrupts, stress that the system cannot process and must therefore defend against. The heroine in our piece will be optimal (or nontrau-matic) stress, stress that provides the impetus for transformation and growth, stress that the system can process, integrate, and ultimately adapt to – although always at some cost to the system. Importantly, not only does optimal stress not overwhelm but it prompts the system adaptively to reconstitute at a higher level.

In other words, it’s how well the system is able to manage the cumulative impact of the myriad of environ-mental stressors to which it’s being continuously exposed that will make of them either traumatic events or growth opportunities – and that ability to manage stress will be a story about the system’s ability to process, integrate, and adapt to the impact of environmental challenge, input from the outside that either threatens to overwhelm the system or prompts the system to mobilize its ability to heal itself. Environmental stressors will take the form of both “presence of bad” (toxicity) and “absence of good” (deficiency).

With respect to the heart, environmental stressors will include the various risk factors for cardiac disease, in-cluding smoking; high blood pressure; uncontrolled diabetes; a sedentary life system / physical inactivity; obesity / excess weight; too much alcohol; elevated cholesterol (especially high LDL and low HDL); elevated C-reactive protein; increased age; male sex; and a family history of heart disease; to name a few – some of which factors are uncontrollable, some of which are controllable and reversible.

The cumulative impact of these risk factors may indeed challenge the cardiovascular system in such a way that there is an initial disruption to its underlying orderedness and the ease therefore with which information and energy can be propagated throughout its expanse. This disruption will activate defenses, which will, in turn, give rise to symptoms. Both the defenses and the symptoms must be recognized as signals of underly-ing dysfunction, imbalance, lack of harmony, and dysregulation within the system. Defenses, symptoms, disorders, and diseases include the following: chest pain or discomfort (angina); neck, jaw, or arm pain; pal-pitations / skipped beats; tachycardia / rapid heart beat; shortness of breath / dyspnea – at rest or on exer-tion; cyanosis; edema / swelling; intermittent claudication; myocardial ischemia; vascular insufficiency; coro-

nary artery disease / atherosclerotic heart disease; valvular heart disease (leaky / incompetent / stenotic valves); cardiac arrhythmias; cardiomyopathy; or pericarditis.

But if the system receives enough support (in the form of therapeutic interventions that lighten the total body load and replenish the total body reserves), then the cardiovascular system’s orderedness can be restored and the ease of flow of information and energy throughout the system revitalized. Once order and ease of flow are restored, the underlying dysfunction, imbalance, and dysregulation can be reversed – such that the system will once again be able to process and integrate the impact of environmental stressors and reconsti-tute at a higher level of organization.

Lightening the load and replenishing the reserves can be accomplished through a heart – healthy diet (low in sodium, saturated fat, trans fat, cholesterol, refined sugars, processed foods); less animal food, more plant food (fruits, vegetables, nuts, whole grains): increased intake of foods rich in vitamins, minerals, antioxi-dants; nutrient supplementation; regular vigorous aerobic exercise; cessation of smoking; control of blood sugar levels; donation of blood to lower the hematocrit (and reduce the blood viscosity); adoption of a more active and healthy lifestyle; fish oil; nattokinase; l-arginine; CoQ10; magnesium; vitamin C; l-carnitine; d-ri-bose; low-dose aspirin; garlic; and alpha lipoic acid.

Lightening the load and replenishing the reserves will be the support necessary to trigger / jump start the body’s self – healing, adaptive (homeostatic) mechanisms. With this support, the system will be able adap-tively to reconstitute at a higher level of order, complexity, integration, and coherence and the flow of infor-mation and energy throughout the cardiovascular system can be revitalized – thereby restoring the heart’s ability to process and integrate the myriad of environmental stressors to which it is being continuously ex-posed as a part of daily life.

Particularly important adaptations will include the development of new blood vessels in the coronary circula-tion – variously described as neovascularization, angiogenesis, vasculogenesis, development of collateral coronary vessels, and development of anastomoses. Collateral circulation provides alternate routes of blood flow to the heart in cases where the heart isn’t getting the blood supply it needs, as, for example, with my-ocardial ischemia.

The coronary arteries that run on the surface of the heart are called epicardial coronary arteries. These ar-teries, when healthy, are capable of autoregulation to maintain coronary blood flow at levels appropriate to the demands of the heart muscle – in other words, if perfusion pressure to the heart is suddenly decreased, compensatory vasodilatation of the arterioles will occur to maintain a constant flow. New blood vessels may be formed (angiogenesis) or blood vessels that are already present may be remodeled (vascular remodel-ing).

Similarly, those individuals who engage in a long – term aerobic training program have larger hearts, greater end – diastolic ventricular volume, and a lower heart rate (both at rest and during exercise). The body’s wis-dom is such that it is able to adapt to the demands of a constantly changing environment.

LEARNING OBJECTIVES

1. recognize the ways in which environmental stressors (both toxicities and deficiencies) impact the car-diovascular system

2. appreciate that coronary collateralization serves both a defensive and an adaptive function3. understand the importance of “orderedness” and “ease of flow” of the coronary circulation in the

maintenance of optimal heart health and the prevention of “dis-order” and “dis-ease” within the body

REFERENCES

Kingma JG. Cardiac adaptation to ischemia – reperfusion injury. Ann N Y Acad Sci 1999;874:83-99.

Mack PJ, et al. Biomechanical regulation of endothelial – dependent events critical for adaptive remodeling.

The Journal of Biological Chemistry 2008.

Meerson FZ, Breger AM. The common mechanism of the heart’s adaptation and deadaptation: hypertrophy and atrophy of the heart muscle. Basic Res Cardiol 1977 Mar-Jun;72(2-3):228-234.

Moir TW. Study of luminal coronary collateral circulation in the beating canine heart. Circulation Research 1969;24:735-744.

Moir TW. Coronary vascular adjustments to acute myocardial ischemia. Arch Intern Med 1972;129(5):799-807.

Semenza GL. Surviving ischemia: adaptive responses mediated by hypoxia – inducible factor 1. J Clin In-vest 2000 October 1;106(7):809-812.

Tyagi SC. Vasculogenesis and angiogenesis: extracellular matrix remodeling in coronary collateral arteries and the ischemic heart. Journal of Cellular Biochemistry 1998;65(3):388-394.

Objectives & Notes

Amer Suleman, M.D. Date of talk: Friday, June 26, 2009, 9:05 a.m.

The Heartbeat Clinic7777 Forest LaneSte A236Dallas, TX 75230


Training:Current Job Description: President of The Heartbeat ClinicCurrent Faculty Appointments: Consultant in cardiovascular medicine and

electrophysiology medical City Hospitals DallasMedical School/ University Attended King Edward Medical CollegeInternship: SUNY Buffalo NYResidency: SUNY Buffalo NYBoard Certifications: Internal medicine, cardiology, cardiac electrophysiology,

Hyertension, echocardiography, pacemaker and defibrillators, echocardiography, neurosonology

Other Information: CME editor cardiology for WEBMDDisclosure Statement:

SPEECH TITLE: “Heart Rate Variability As Predictor of Sudden Death”


1. Understand meaning of vagal and sympathetic tone

2. Able to identify the risk factors for sudden death

3. Able to understand different methods employed for assessment of heart rate variability


Objectives & Notes

Jean Monro, M.D. Date of talk: Friday, June 26, 2009, 9:35 a.m.

Breakspear HospitalHertfordshire HouseWood Lane, Paradise EstateHemel Hempstead, Herts HP2 4FDEngland

Phone: 011/44-1442-231333Fax: 011/44-1442-266388Email: [email protected]

Training:Current Job Description: Medical Director of The Breakspear Hospital, EnglandCurrent Faculty Appointments: Medical Director of The Breakspear Hospital, EnglandMedical School/ University Attended London Hospital Medical School, EnglandInternship:Residency: London HospitalBoard Certifications: MB BS, MRCS, LRCP, FAAEM, DipIBEM, MACOEMDisclosure Statement:

SPEECH TITLE: “Fructose Metabolism: A Toxic Challenge”


1. Consider fructose in relation to vascular and metabolic disease and obesity.

2. Its relationship to gout and chronic fatigue syndrome

3. The sociological and economic implications of these


Objectives & Notes

Theodore R. Simon, M.D. Date of talk: Friday, June 26, 2009, 10:30 a.m.

North Texas Imaging Center8345 Walnut Hill Lane, Ste. 210Dallas, TX 75231


Training:Current Job Description: PhysicianCurrent Faculty Appointments:Medical School/ University Attended Yale UniversityInternship: University of RochesterResidency: University of California at San Francisco; Yale

UniversityBoard Certifications: ABNMOther Information: See CV at www.theodorersimon.com; Editorial Board:

Journal of Nuclear MedicineDisclosure Statement:

SPEECH TITLE: “Nuclear Medicine In Cardiac Disease Update 2009”


1. Use plasma volume determinations as a tool for evaluating syncope

2. Determine appropriate nuclear medicine testing for cardiac patients.

3. Understand the limitations and risks of nuclear medicine options.


Thalamic Activity Seen by Scintigraphy of the Brain on Neurotoxic Patients

byTheodore R. Simon, M.D.

ForTwenty-seventh Annual AEHF International Symposium

June 2009

Abstract

Introduction We have described a pattern present in patients with clinical evidence of neurotoxicity and compared the incidence of this pattern with normal controls. In reviewing our experience, we have now recognized that an additional finding should be included in that pattern, increased thalamic activity.

The original findings were described as: Mismatch between the early (predominately flow) and late (predominately functional)

image sets (MISMATCH),

Failure of the brain to maintain a normal sequestration of the tracer (SHUNTING),

Multiple hot and cold foci distributed throughout the cortex without regard to lobar distribution (SALT & PEPPER), and

Asymmetric temporal activity.

MISMATCH is caused by a decoupling of blood flow versus the competency of a glutathione-mediated functional system that normally sequesters the tracer. SHUNTING is part of that same process which results in less tracer located in the brain and, hence, more in the soft tissues. The cause of SALT & PEPPER is not established, although we believe it is due to vascular effects—most likely vasculitis. Asymmetric temporal activity is a frequent abnormal finding described in other processes such as memory loss difficulties.

On reviewing our experience, we noticed a high incidence of abnormally increased tracer activity in the thalamus. The thalamus is part of the diencephalon. It is concerned with relaying sensory, pain, temperature, and visceral sensations. Abnormalities, including regional cerebral blood flow abnormalities, have been described in patients with fibromyalgia.

MethodsWe studied consecutive brain scintigraphic examinations referred for possible

neurotoxicity. Each examination was evaluated in terms of the four classic criteria for neurotoxicity as well as an overall impression of the degree of neurotoxicity. In addition, thalamic activity was evaluated. The usual five-point scale was used for evaluation where “normal” and “minimal” were considered normal while “mild”, “moderate”, and “severe” were considered abnormal. The incidence and degree of each criteria were then tabulated.

MaterialsWe planned to study the last 52 consecutive brain scintigraphic examinations performed at the Environmental Health Center—Dallas. Five data sets from the Fincher normal series were found. These were reanalyzed in terms of thalamic activity.

ResultsThe patients were aged 6 to 64 with a mean ± SEM of 43.2 ± 2.01. Thirteen males

(25%) and 38 females (75%) were included. An additional female was excluded due to lack of clinical information. Exposures were: mold, 13 (25%); chronic, 25 (49%); and other, 13 (25%).

Overall impressions were: normal, 1 (2%); mild, 30 (59%); moderate, 16 (31%); and severe, 4 (8%). Abnormalities by criteria were: MISMATCH, 20 (39%); salt & pepper, 38 (75%);, SHUNTING, 37 (73%); and increased thalamus, 38 (75%).

Concomitant signs were seen in all cases of increased thalamic activity. The number of concomitant signs were: one, 9 (24%); two, 5 (13%); three, 13 (34%); four, 11 (29%).

The number of abnormal criteria present in these examinations respectively including and excluding the thalamus increase were: no criteria, 0, 0; one criterion 10 (20%), 12 (24%); two criteria, 8 (16%), 12 (24%); three criteria, 21 (41%), 13 (25%); and four criteria, 12 (24%), 14 (27%). All five criteria were present in 11 (22%) cases.

One of the five (20%) normal data sets had abnormal thalamic activity. That activity was only on the right side.

DiscussionIncreased thalamic activity provides a valid addition to the criteria used to evaluate

neurotoxicity by dual phase triple-head single photon emission computed tomographic techniques. Right-sided abnormal thalamic activity in a normal patient establishes that this finding is not exclusive to the neurotoxic patient.

ReferencesApkarian AV et al. Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neuroscience 2004; 24:10410-10415.Blomqvist A et al. Cytoarchitectonic and immunohistochemical characterization of a specific pain and temperature relay, the posterior portion of the ventral medial nucleus, in the human thalamus. Brain 2000; 123:601-619.Chen JJH et al. Regional cerebral blood flow between primary and concomitant fibromyalgia patients: a possible way to differentiate concomitant fibromyalgia from the primary disease. Scand J Rheumatol 2007;36:226-232.Dougherty DD et al. A combined [11C]diprenorphine PET study and fMRI study of acupuncture analgesia. Behavioural Brain Research 2008; 193:63-68Fulbright RK et al. Functional MR imaging of regional brain activation associated with the affective experience of pain. AJR 2001;177:1205-1210.Guedj E et al. 99mTc-ECD brain perfusion SPECT in hyperalgesic fibromyalgia. Eur J Nucl Med Mol Imaging 2007; 34:130-134.Kwiatek R et al. Regional cerebral blood flow in Fibromyalgia: Single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis & Rheumatism 2000;43:2823-2833.Peyron R et al. Functional imaging of brain responses to pain. A review and meta-analysis. Neurophysiol Clin 2000;30:263-288.

Objectives & Notes

MarkW. Frampton, M.D. Date of talk: Friday, June 26, 2009, 11:00 a.m.

University of Rochester601 Elmwood Ave,Rochester, NY 14642

Phone: 585-275-4861Fax:Email: [email protected]

Training:Current Job Description: Clinical research studies of respiratory and cardiovascular

effects of air pollutionCurrent Faculty Appointments: Professor of Medicine and Environmental MedicineMedical School/ University Attended New York University School of MedicineInternship: State University of NY at Buffalo, Buffalo General HospitalResidency: State University of NY at Buffalo, Buffalo General HospitalBoard Certifications: Internal Medicine, PulmonaryOther Information: Frampton MW, Utell MJ, eds. Exposure to Airborne

Particles: Health Effects and Mechanisms. Clin Occup Environ Med vol. 5, 2006.

Frampton MW, Stewart J, Oberdörster G, Morrow PE, Chalupa D, Frasier LM, Speers DM, Cox C, Huang L-S, Utell MJ. Inhalation of ultrafine particles alters blood leukocyte expression of adhesion molecules in humans. Environ Health Perspect 114:51-58, 2006.

Shah AP, Pietropaoli AP, Frasier LM, Speers DM, Chalupa DC, Delehanty JM, Huang L-S, Utell MJ, Frampton MW. Effect of inhaled ultrafine particles on endothelial function in healthy human subjects. Environ Health Perspect. 116:375-380, 2008.

Zareba W, Couderc JP, Oberdörster G, Chalupa D, Cox C, Huang L-S, Peters A, Utell MJ, Frampton MW. 2008. ECG Parameters and exposure to carbon ultrafine particles in young healthy subjects. Inhal Toxicol, In press.


SPEECH TITLE: “The Cardiovascular Consequences of Particulate Air Pollution”


1. Understand the evidence linking air pollution with cardiovascular disease

2. Understand the role of human clinical studies in investigating the health effects of air pollution

3. Understand ultrafine particles and their pulmonary and cardiovascular health effects


The Cardiovascular Consequences of Particulate Air PollutionMark W. Frampton MD

University of Rochester Medical Center

Research conducted over the past 15 years has made it clear that exposure to particulate matter (PM) air pollution is a major public health issue. Worldwide, outdoor PM pollution is estimated to cause 500,000 excess deaths annually. In the US, recent epidemiological studies suggest that chronic PM exposure shortens life on the order of one or two years (1). Conversely, reducing exposure to particulate air pollution appears to extend life. A recent study suggests that, for every 10 µg/m3 reduction in ambient levels of fine particles in US cities, life expectancy is extended by more than half a year (2).

Exposure to particulate matter is associated with increased risk for both respiratory and cardiovascular morbidity and mortality. Because cardiovascular disease is a more frequent cause of morbidity and mortality than respiratory disease, the majority of deaths related to air pollution exposure are cardiovascular. Therefore, understanding the toxicological mechanisms is an important priority.

Our laboratory studies human clinical responses to air pollution exposure. We initiated a series of studies of respiratory and cardiovascular responses to inhalation of elemental carbon ultrafine particles (3, 4). Ultrafine particles (< 100 nm) behave differently than larger particles because they have a very large surface area, but very little mass. They tend to evade typical pulmonary clearance mechanisms, and have the ability to diffuse across cell membranes and enter cell organelles. It is possible that they have direct effects on vascular structures, and may enter the circulation via the pulmonary capillaries.

Our studies suggest that exposure to carbon ultrafine particles, at concentrations that can be experienced on a busy highway, may induce subtle acute changes in both the pulmonary (5) and systemic (6) vascular beds, possibly induced by injury or activation of vascular endothelial cells. We have now extended our studies by using a system which concentrates outdoor ultrafine particles for use in human clinical studies. Preliminary findings suggest that outdoor concentrated ultrafine particles may have pulmonary vascular as well as systemic vascular effects. These human studies provide insights into mechanisms by which PM may contribute to the burden of pulmonary and cardiovascular disease, and provide data to inform efforts in improving air quality.

1. U.S. EPA. Air quality criteria for particulate matter. U.S. Environmental Protection Agency, Washington, D.C.; 2005.2. Pope CA, 3rd, Ezzati M, Dockery DW. Fine-particulate air pollution and life expectancy in the United States. N Engl J Med 2009;360:376-386.3. Frampton MW, Pietropaoli AP, Morrow PE, Utell MJ. Human clinical studies of airborne pollutants. In: Gardner DE, editor. Toxicology of the lung, Fourth ed. Boca Raton: Taylor & Francis; 2006. p. 29-82.

4. Frampton MW. Does inhalation of ultrafine particles cause pulmonary vascular effects in humans? Inhal Toxicol 2007;19(Suppl. 1):75-80.5. Frampton MW, Stewart JC, Oberdörster G, Morrow PE, Chalupa D, Pietropaoli AP, Frasier LM, Speers DM, Cox C, Huang L-S, et al. Inhalation of carbon ultrafine particles alters blood leukocyte expression of adhesion molecules in humans. Environ Health Perspect 2006;114:51-58.6. Shah AP, Pietropaoli AP, Frasier LM, Speers DM, Chalupa DC, Delehanty JM, Huang L-S, Utell MJ, Frampton MW. Effect of inhaled carbon ultrafine particles on reactive hyperemia in healthy human subjects. Environ Health Perspect 2008;116:375-380.

Objectives & Notes

Russel J. Reiter, Ph.D. Date of talk: Friday, June 26, 2009, 1:30 p.m.

University of Texas Health Science Center7703 Floyd Curl DriveSan Antonio, TX 78229-3900


Training:Current Job Description: Biomedical Research and TeachingCurrent Faculty Appointments: ProfessorMedical School/ University Attended Bowman Gray School of Medicine, Winston-

Salem, NCOther Information: Written in excess 1,200 scientific research articles for

medical journals, 10 books and edited 34 books; Editor-in-chief of Journal of Pineal Research


SPEECH TITLE: “Melatonin: Role in Blood Pressure Regulation”


1. Understanding the importance of the circadian melatonin rhythm.

2. Explain the importance of the nocturnal melatonin reduction.

3. Apply the information in the clinical setting.

The American Environmental Health Foundation and the University of North Texas Health Science Center is not responsible for the contents of this presentation. AEHF has not altered or modified the contents of the information

provided by this speaker.

Melatonin: Role in Blood Pressure RegulationRussel J. Reiter

Department of Cellular and Structural Biology,

University of Texas Health Science Center, San Antonio, Texas, USA

AbstractIn experimental rodents, surgical removal of the pineal gland, the major source of circulating melatonin, causes

a gradual and sustained rise in blood pressure (BP). Conversely, when melatonin is chronically administered to pinealectomized rodents the increment in BP is ameliorated. In humans as well, the nighttime rise in endogenous circulating melatonin levels may be inversely related to the reduction in nighttime blood pressure. Among hypertensive patients, some exhibit a much greater reduction in BP at night (the so-called extreme dippers and dippers) while others exhibit only a slight nighttime reduction in systolic and diastolic pressure (non-dippers and inverted dippers). Longitudinal studies of these patients show that inverted dippers and non-dippers die at a faster rate than do dippers and extreme dippers. The chronic administration of melatonin to individuals with hypertension induces a measurable drop in nighttime systolic and diastolic BP. Moreover, the higher the nighttime level of endogenous melatonin (estimated from urinary metabolite of melatonin, 6-hydroxymelatonin sulfate), the greater the reduction in arterial BP at night. The implication of these findings is that melatonin may have utility as an antihypertensive agent.

IntroductionAn experimentally documented association between the pineal gland, the major source of circulating melatonin,

and elevated blood pressure has a long history. In 1967, Zanoboni and Zanoboni-Muciaccia [1] observed that surgical removal of the pineal gland from rats caused a gradual and sustained rise in arterial blood pressure, a finding that has been duplicated in a variety of subsequent investigations. Moreover, the hypertensive response associated with pinealectomy is reversed by the chronic administration of melatonin in the drinking water [2]. In addition, pinealectomy also abolishes the nocturnal depression in blood pressure [3]. The nighttime reduction in arterial pressure is usual in diurnal species such as humans. Mechanistically, the development of hypertension in pinealectomized rats is hypothesized to involve an elevated activity of neural vasomotor centers [4] and/or alterations in the renin-angiotension-aldosterone pathway [5]; neither mechanism has been proven, however.

The Human Melatonin Rhythm: Photoperiodic ModulationAs with every mammalian species, blood melatonin levels in humans exhibit a circadian rhythm with peak

levels occurring exclusively during the night. Melatonin is not produced during the day since light detected by specialized photoreceptive cells in the retinas suppresses its production [6]. Artificial light exposure after darkness onset also compromises the ability of the pineal gland to produce and secrete melatonin [7]. Continuous light exposure, like pinealectomy, totally abolishes the circadian melatonin rhythm with the levels being maintained at low daytime values.

The widespread use of artificial light sources has greatly compromised the ability of the human pineal gland to produce melatonin. In both humans and animals maintained under naturally occurring periods of light and dark, the duration of elevated melatonin is proportional to the length of the dark period. For humans, however, the normal period of environmental darkness is typically truncated by the use of artificial light after sunset and before sun rise. This likewise limits the total amount of melatonin produced as shown by the abbreviated nocturnal elevation of this indoleamine per 24 hour period [8]. Additionally, brief intermittent exposure to bright light after darkness onset rapidly suppresses circulating endogenous melatonin levels [9]. Finally, the ubiquitous light pollution common in urban areas, which accounts for what is referred to as trespass light (i.e., light that an individual cannot control), also may reduce endogenous melatonin levels [10].

The ability to impose light after darkness onset clearly reduces the total quantity of melatonin humans are capable of generating. Thus, compared to species that experience only regularly alternating periods of environmental day and night, humans are relatively melatonin deficient. Besides suppressing melatonin levels, light after darkness onset provides the biological clock with misinformation which leads to disturbances in biological rhythmicity, i.e., chronodisruption [11]. The combination of a relative melatonin deficient state and altered circadian rhythmicity may have a variety of pathophysiologicial consequences including an elevation in blood pressure.

Melatonin: Modulation of Blood PressureTo reduce blood pressure, the pharmaceutical industry has developed a wide range of drugs, e.g.,angiotensin

converting enzyme inhibitors, beta-adrenergic blockers, alpha-adrenergic blockers, calcium channel blockers, diuretics, vasodilators, etc., and more recently viper venom is being tested and a vaccine is under consideration. Despite the large number of drugs available, the percentage of hypertensive patients who have well-controlled blood pressure is much lower than desired. Additionally, each of the agents mentioned has some untoward side effects. One of these negative actions is the inhibition of the nighttime synthesis and secretion (due to the use of beta-adrenergic blockers) of melatonin, a potential endogenous antihypertensive molecule [12, 13].

Of particular interest for the current review is the failure of some patients to experience a reduction in mean arterial blood pressure at night, when endogenous melatonin levels are normally at a maximum. Typically, blood pressure oscillates over a 24 hour period with the values during the day being high and with the nocturnal pressure exhibiting a drop, i.e., a dip. Those individuals who experience a reduced arterial blood pressure at night are, therefore, referred to as dippers [14]. Conversely, there are a number of patients who either totally lack or exhibit only a slight reduction in blood pressure at night, the so-called non-dippers. Presumably, the increased strain on the cardiovascular system imposed by a lack of reduction in arterial pressure on a nightly basis contributes to the higher risk of cardiovascular mortality in non-dippers than in dippers [15].

The most comprehensive study designed to investigate the association between mortality and nocturnal blood pressure in humans is that of Ohkubo and colleagues [16]. This group measured the ambulatory blood pressure of 1,542 rural Japanese patients (>40 years of age) and subsequently followed them for a minimum of 5.1 years to determine the frequency of death. Based on the blood pressure measures, patients were initially categorized into one of the following four groups: 1) extreme dippers, who exhibited a ≥ 20% drop in nocturnal blood pressure; 2) dippers with a nocturnal decline of ≥ 10% to < 20%; 3) non-dippers, a drop of ≥ 0% to < 10%; and 4), inverted dippers with no reduction in nocturnal blood pressure. The frequency of mortality during the follow-up period was analyzed using the Cox proportional hazards regression model adjusted for age, sex, smoking status, previous history of cardiovascular disease and the use of antihypertensive medications.

The results of this longitudinal study revealed a highly significant correlation between nocturnal blood pressure and mortality rate. The individuals who lacked a nighttime decline in blood pressure (inverted dippers) had the highest death rate while the extreme dippers and dippers died at a much lower frequency.

The results of Ohkubo and co-workers [16] are consistent with the findings of other cross-sectional studies in which cardiovascular tissue damage was reported to be more pronounced in non-dippers than in dippers [17, 18]; likewise, in mild to moderately hypertensive individuals, the frequency of cardiovascular morbidity was significantly greater in non-dippers than in dippers [19]. Collectively, the results of studies from a variety of sources document that a drop in nocturnal blood pressure is beneficial in reducing structural tissue damage and limiting cardiovascular pathophysiology. The physiological basis for the drop in nocturnal blood pressure in some individuals and not in others remains unknown.

In a search to potentially provide an explanation for the variable reduction in arterial blood pressure at night, Jonas et al [20] compared the nighttime rise in blood melatonin levels in 8 age-matched dippers and non-dippers, all of whom were elderly and suffering with essential hypertension. To estimate the amount of melatonin produced, the urinary surrogate of melatonin, i.e., 6-hydoxymelatonin sulfate (6-MTs), was measured in two urine samples, one collected during the day and the other at night. The results revealed nearly a three-fold difference in the quantity of urinary 6-MTs excreted by the two groups, with the dippers having the higher levels of the melatonin surrogate. The findings are consistent with the nighttime rise in melatonin possibly accounting for the reduction in arterial blood pressure in hypertensive patients. The two major shortcomings of this report are that the number of patients was small and a melatonin surrogate, urinary 6-MTs, was used as an indirect index of melatonin production.

In view of the obvious inverse relationships between the nighttime rise in circulating melatonin and the decline in blood pressure, Scheer et al [24] conducted a randomized, double-blind, placebo-controlled, cross-over study in 16 men with essential hypertension who were given oral melatonin (2.5 mg) either acutely (one night) or chronically (for 3 weeks) one hour before sleep. Blood pressure was monitored by means of a 24-hour ambulatory unit and actigraphy

was used to access sleep quality. While a single melatonin dose was ineffective, chronic administration reduced both nocturnal systolic and diastolic blood pressure by 6 and 4 mm Hg, respectively, without influencing heart rate. The day-night amplitudes of the rhythms in systolic and diastolic pressures in the chronically melatonin-treated patients were elevated by 15% and 25%, respectively. While melatonin also improved sleep quality, this was unrelated to the blood pressure changes. Again, the implications of this study are consistent with the higher nocturnal melatonin being directly involved in reducing blood pressure at night or that melatonin has effects on the circadian pacemaker which secondarily depresses hypertension.

As with hypertensive men, normotensive and hypertensive women (aged 47-63 years) also respond to chronic melatonin therapy with a reduction in nighttime blood pressure. In a randomized, double-blind, cross-over study, Cagnaccia and colleagues [22] reported that 3 mg melatonin nightly for 3 weeks significantly decreased nocturnal systolic, diastolic, and mean blood pressure without influencing heart rate. Like Scheer et al [21], Cagnacci and co-workers [22] concluded that the improvement in sleep quality resulting from melatonin administration did not explain the nighttime depressive effect of melatonin on blood pressure. Also, the latter group seemed to favor the direct inhibitory effect of melatonin on blood pressure rather than involving its chronobiotic actions which then secondarily reduced blood pressure [22, 23].

The findings of a single experimental study in animals is also suggestive that melatonin may be of benefit for reducing systolic blood pressure in metabolic syndrome as well. When rats were fed a high fructose diet for 5 weeks, daytime systolic pressure rose while nighttime melatonin levels fell (estimated using urinary 6-MTs) [24]. When the animals were given melatonin (30 mg/kg/day) in the drinking water, the rise in blood pressure in the fructose-fed rats was significantly attenuated.

Perspectives and ConclusionsThe findings summarized herein regarding the amplitude of the endogenous nocturnal melatonin peak and its

correlation with the drop in nighttime blood pressure coupled with evidence showing that melatonin administration in pharmacological doses reduces systolic and diastolic pressure is suggestive that the normal circadian rhythm of melatonin is a modulator of blood pressure in man. If these inverse rhythms are in fact functionally associated, then it follows that any factor that compromises nighttime melatonin production would also cause a rise in blood pressure or possibly convert dippers to non-dippers

As summarized in this brief review, it is obvious that nighttime light exposure is particularly detrimental to the nighttime production of melatonin. Thus, truncating the duration of nocturnal darkness (by sleeping only 5-6 hours nightly) or bright light exposure after darkness onset severely reduces the amount of melatonin available to potentially reduce blood pressure. Depressed melatonin is also a major factor in night shift workers and in individuals engaged in frequent, long-haul, transmeridian travel. Finally, drug administration (e.g., beta-blockers, benzodiazepines, etc.) and increased age markedly reduce the ability of the pineal gland to synthesize and secrete melatonin. Hence, any of these conditions may contribute to a rise in systolic and diastolic pressure. Of particular interest may be the gradual elevation in systemic blood pressure during aging, given the persistent reduction in melatonin in the elderly.

Besides physiological levels of melatonin possibly influencing the circadian blood pressure rhythm, it seems logical that this non-toxic molecule should find utility as a pharmacological agent to control blood pressure in non-dippers and in hypertensive subjects especially in conjunction with conventional blood pressure medications [12]. Mechanistically, melatonin has a variety of actions whereby it may function to lower blood pressure/hypertension. Hence, melatonin has endothelium-relaxing effects, it is a potent scavenger of free radicals (which negatively influence blood pressure) and it may work via epigenetic mechanisms at the level of the area postrema to regulate blood pressure.

References1. Zanoboni A, Zanoboni-Muciaccia W. Experimental hypertension in pinealectomized rats. Life Sci 1967; 6:2327-2331.2. Holmes SW, Sugden D. The effect of melatonin on pinealectomy-induced hypertension in the rat. Br J Pharmacol 1976; 56:360P-361P.3. Hisada T, Ozono S, Sato K, Watanabe Y, Watanabe M. Relationship between metabolic rhythm in the pineal body and the systemic blood pressure. IRCS J Med Sci 1976; 4:142-143.4. Karppanen H, Airaksinen MM, Särkimäki I. Effects in rats of pinealectomy and oxypertine on spontaneous locomotor activity and blood pressure during various light schedules. Am Med Exp Fenn 1973; 51:93-103.

5. Karppanen H, Vapaatalo H. Effects of an aldosterone antagonist, spironolactone on pinealectomized rats. Pharmacology 1971; 3:76-84.6. Reiter RJ. Melatonin: The chemical expression of darkness. Mol Cell Endocrinol 1991; C153-C158.7. Brainard GC, Lewy AJ, Menaker M, Fredericksin RH, Miller LS, Weleber RG, Cassone V, Hudson D. Dose-response relationship between light irradiance and suppression of melatonin in human volunteers. Brain Res 1988; 454:213-218.8. Wehr TA. The durations of human melatonin secretion and sleep respond to changes in daylength (photoperiod). J Clin Endocrinol Metab 1991;73:1276-1280.9. Lewy AJ, Wehr TA, Goodwin FK, Newsome DA, Markey SP. Light suppresses melatonin secretion in humans. Science 1980;210:1267-126910. Reiter RJ, Tan DX, Korkmaz A, Erren TC, Piekarski C, Tamura H, Manchester LC. Light at night, chronodisruption, melatonin suppression, and cancer risk: a review. Crit Rev Oncogen 2007; 13:303-328.11. Erren TC, Pape HG, Reiter RJ, Piekarski C. Chronodisruption and cancer. Naturwissenschaften 2008; 95:367-382.12. Simko F, Paulis L. Melatonin as a potential antihypertensive treatment. J Pineal Res 2007;42:319-322.13. Simko F, Paulis L. Blood pressure modulation and cardiovascular protection by melatonin: potential mechanisms behind. Physiol Res 2007; 56:671-684.14. O’Brien E, Scheridan J, O’Malley K. Dippers and non-dippers. Lancet 1988; 2:397.15. Mansoor GA. Sleep artigraphy in hypertensive patients with the “non-dipper” blood pressure prolife. J Hum Hyperten 2002;16:237-242.16. Ohkubo T, Imai Y, Tsuji I, Nagai K, Watanabe N, Minami N, Kato J, Kikuchi N, Nishiyama A, Aihara A, Sekino M, Satoh H, Hisamichi S. Relation between nocturnal decline in blood pressure and mortality: the Ohasama study. Am J Hyperten 1997; 10:1201-1207.17. Rizzoni D, Muiesan ML, Montani G, Zulli R, Calebich S, Agabiti-Rosei E. Relationship between initial cardiovascular structural changes and daytime and night-time blood pressure monitoring. Am J Hyperten 1992; 5:180-186.18. Shimada K, Kawamoto I, Matsubayashi K, Nishinaga M, Kimura S, Ozawa T. Diurnal blood variation and silent cardiovascular damage in elderly patients with hypertension. J Hyperten 1992; 10:875-878.19. Verdecchia P, Porcellati C, Schillaci G, Borgioni C, Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I. Ambulatory blood pressure: an independent predictor of prognosis in essential hypertension. Hypertension 1994; 24:793-801.20. Jonas M, Garfinkel D, Zisapel N, Laudon M, Grossman E. Impaired nocturnal melatonin secretion in non-dipper hypertensive patients. Blood Press 2003; 12:19-24.21. Scheer FAJL, van Montfrans GA, Van Someren EJW, Mairuhu G, Buijs RM. Daily nighttime melatonin reduces blood pressure in male patients with essential hypertension. Hypertension 2004; 43:192-197.22. Cagnacci A, Cannoletta M, Renzi A, Baldassari F, Arangino S, Volpe A. Prolonged melatonin administration decreases nocturnal blood pressure in women. Am J Hypertens 2005; 18:1614-1618.23. Scheer FAJL. Potential use of melatonin as adjunct antihypertensive therapy. Am J Hypertens 2005; 18:1619-1620.24. Liebowitz A, Peleg E, Sharabi Y, Shabatai Z, Shamiss A, Grossman E. The role of melatonin in the pathogenesis of hypertension in rats with metabolic syndrome. Am J Hypertens 2008; 21:348-351.

Objectives & Notes

Ron Overberg, Ph.D., C.C.N., R.D. Date of talk: Friday, June 26, 2009, 2:00 p.m.



Training:Current Job Description: Nutritionist at Envrionmental Health Center - Dallas and

Nutriwellness in DallasUniversity Attended University of Texas, Dallas, TexasInternship: Texas Woman’s University, Denton, TexasBoard Certifications: Clinical NutritionistOther Information: Registered Dietitian, licensed in TexasDisclosure Statement:

SPEECH TITLE: “Nutrition Tips for Cardiovascular Disease”


1. Explain the importance of fat in the diet of chemically sensitive patients.

2. Decide which tests would be most beneficial.

3. instruct the patient on the various supplements.


Nutrition Tips for Cardiovascular DiseaseRon Overberg, Ph.D.

Abstract.

Most Cardiovascular disease can be explained by poor health choices or simply living too long. Some CVD is due to bad genetics but most of those can be overcome by good health promoting habits.

What helps in general is to consume less food. Clients are encouraged to consume enough calories to maintain their ideal weight. It helps to exercise - few do; and the majority of those who exercise pay no attention to diet. Having cold water fish at least once a week has been shown to be heart protective. So is the consumption of at least 5-9 servings of fruits and vegetables day in order to get sufficient minerals, flavonoids and carotenoids. Suggested serving sizes are really small by “American standards” or should we call it “American appetite”: Half a cup of something mashed or 1 cup of something leafy. Still, only 25 % of the population achieves 5 servings per day. Most people only get 2-3 servings of fruits and vegetables daily and most of the top ten fruits and vegetables are poor sources of carotenoids, which are heart protective.

Then we have our hectic lifestyles, trying to keep up with the Jones and always perceiving that the grass is greener on the other side. We don’t take time to relax, or get enough sleep. Around 1900, sleep was estimated to be about 9 hours per night; in 1963 it was 5.5 hours a night; and more recently it is estimated to be 6.9 hours Sundays through Thursdays and 8 hours on Friday and Saturday. I don’t think that we evolved enough to do with less sleep in just 100 years. Overall it is no surprise that much CVD disease was not as prevalent 100 years ago.

This presentation shows information and tools used to educate patients about dietary fats, supplemental fats and supplements that can be incorporated in a daily diet to prevent or improve cardiovascular disease.

Referenceswww.cdc.gov/nccdphp/dnpa/5Aday/index.htm http://www.ncbi.nlm.nih.gov/pubmed/10524389 http://efaeducation.nih.gov/sig/ods.html Brain fats: http://www.fi.edu/brain/fats.htm#brainblockers “Fats that Heal and Fats that Kill” by Udo Erasmus ISBN 0-920470-38-6 “Smart Fats“ by Michael A. Schmidt ISBN 1-883319-62-5 Fat content an fatty acid composition of seeds and seed oils by Guy Inchbald 9/29/00 Judd et al 2002 Lipids 37: 23-131 Plasma Lipid and lipoprotein levels following a 5 week dietary intervention.http://www.queenhill.demon.co.uk/seedoils/index.htm http://www.foodsafety.gov/~dms/qatrans2.html http://www.innovatewithdairy.com/InnovateWithDairy/Articles/DBV_TransFat_032404.html “What your Doctor may NOT tell you about HYPERTENSION” by Mark Houston, M.D. ISBN 0-446-69084-8Berkley Heart Lab www.bhlinc.com 800-432-7889 particle size and number NMR Lipoprofile www.liposcience.com 877 547-6837 particle size and numberSpectracell www.spectracell.com 800 227-5227 particle size and number VAP by Atherotech www.thevaptest.com 877 901-8510 particle sizehttp://www.cfsan.fda.gov/label.html

“Effects of Trace Components of Dietary Fat on Cholesterol Metabolism: Phytosterols, Oxysterols, and Squalene.” Richard E. Ostlund, Jr, M.D., Susan B. Racette, Ph.D., and William F. Stenson, M.D. Nutrition Reviews Vol. 60, No. 12 November 2002: 349-359Vit D and CVD: Atherosclerosis. 2008 Nov 11 Vit. D level at 32.4 ng/ml: J Am Coll Nutr. 2003; 22:142-146Human Vitamin and Mineral Requirements, Chapter 10, by WHO/FOA http://www.fao.org/docrep/004/Y2809E/y2809e00.HTM

Objectives & Notes

Mohamed B. Abou-Donia, Ph.D. Date of talk: Friday, June 26, 2009, 2:30 p.m.

Duke University Medical CenterLaboratory of NeurotoxicologyDept. of Pharmacology and Cancer Biology,Box 3813Durham, NC 27710


Training:Current Job Description: Teaching, Research, Member of the Executive

Committee for Admission of Medical StudentsCurrent Faculty Appointments: Professor of Pharmacology and cancer Biology and of

NeurobiologyMedical School/ University Attended University of California, BerkeleyBoard Certifications: American Board of Toxicology, Academy of

Toxicological SciencesOther Information: Neurotoxicology, editor, CRC Press, inc., 329 published

papers, Areas of Researched Funded: Health Effects of Pesticides, Combined Chemical Exposure, Persian Gulf War Illness, Nicotine, Artificial Sweeteners and Biomarkers for Chemical Exposure


SPEECH TITLE: “Splenda Alters Gut Microflora in Male Rats”


1. The role of gut microflora in body function

2. The effect of Splenda on the composition and number of gut microflora

3. The consequence of Splenda-altered gut microflora on health


Splenda Increases Body Weight and Alters Gut Microflora in Male Rats

Mohamed B. Abou-Donia1, Eman M. El-Masry1, Ali A. Abdel-Rahman1, Roger E. McLendon2, and Susan S.

Schiffman3, 1Departments of Pharmacology and Cancer Biology, 2Pathology and 3Psychiatry, Duke University Medical

Center, Durham, NC 27710, USA

Splenda is comprised of the high-potency artificial sweetener sucralose (1.1%) and the fillers, maltodextrin and glucose.

Splenda was administered by oral gavage at 100, 300, 500, or 1000 mg/kg to adult male Sprague-Dawley rats for 12

wk, during which fecal samples were collected weekly for bacterial analysis and measurement of fecal pH and body

weight was determined. After 12 wk, half of the animals from control and each treatment group were sacrificed, and

the remaining animals were allowed to recover for an additional 12-wk period, and further assessments of fecal

microflora, fecal pH and body weight. At the end of the 12-week treatment period, the numbers of total anaerobes,

bifidobacteria, lactobacilli, Bacteroides, clostridia, and total aerobic bacteria were significantly decreased; however,

there was no significant treatment effect on enterobacteria. Splenda also significantly increased fecal pH and body

weight. Following the 12-wk recovery period, only the total anaerobes and bifidobacteria remained significantly

depressed whereas pH values and body weight gain remained elevated. These changes occurred at Splenda dosages

that contained sucralose at 1.1 – 11 mg/kg (the US FDA Acceptable Daily Intake for sucralose is 5 mg/kg). In

conclusion, 12-wk administration of Splenda caused numerous adverse effects that continued for another 12-wk period,

including: (1) increased body weight, (2) reduction in beneficial fecal microflora and (3) elevated fecal pH.

Abou-Donia, MB, El-Masry EM, Abdel-Rahman, AA, McLendon, RE, and Schiffman, SS (2008). Splenda alters gut

microflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ, Health 71:

1415-1429.

Objectives & Notes

Kalpana Patel, M.D. Date of talk: Friday, June 26, 2009, 3:30 p.m.

Allergy and Environmental Health Center - Buffalo65 Wehrle Dr.Buffalo, NY 14225


Training:Current Job Description: Director/President of Allergy and Environmental Health

Center BuffaloCurrent Faculty Appointments: Assistant Professor of pediatrics Suny BuffaloMedical School/ University Attended B.J. Medical SchoolInternship: Bexar County Hospital, San Antonio TXResidency: Bexar County Hospital, San Antonio TXBoard Certifications: American Board of Pediatrics, American Board of

Environmental MedicineOther Information: Comprehensive approach to Treating Autism and ADHD.

Pre Pilot Study. Journal of Alternative and Complementary Medicine, October 2007. 2) Nutritional and Environmental Approaches to Preventing and Treating Autism and ADHD Review


SPEECH TITLE: “Role of Heart Rate Variabilityin the Practice of Environmental Medicine”


1. Understand what heart rate variability is.

2. Demonstrate different patterns in 100 consecutive patients to understand sick patterns.

3. Role of sympathetic dominance in different diseases.


Carmelo Rizzo, M.D. Date of talk: Friday, June 26, 2009, 4:00 p.m.

Via Tor Sant’Antonio, 3400013 – Fonte Nuova (RM) Italy


Training:Current Job Description: Clinical Nutrition and AllergyCurrent Faculty Appointments: University Unicampus-RomeMedical School/ University Attended University of Rome La SapienzaInternship: University of Rome La SapienzaResidency: University of Rome La SapienzaOther Information: Professor Master in Foot Surgery at Campus Biomedico

Univ. Hospital – Rome, Prof. of Clinical Ecology, Nutrition and Allergology at Scuola di Specializzazione in Biotipologia e Metodologia Omeopatica – University of Urbino from 1992 to 2005. Prof. of Olistic Nutrition at Scuola di Naturopatia di Anguillara (RM). Prof. and Director of Master “Scuola di Nutrizione Clinica” (Clinical Nutrition), Rome, Milan,Palermo and Ascoli Piceno from 2004 to 2008. Prof. and scientific commitee member by “Centre International d’informations, recherches et ètudes sue les troubles du mètabolisme et du comportement” in Geneve up to 2007. Prof. of Clinical Nutrition and Environmental Medicine for A.I.Nu.C. (International Academy of Clinical Nutrition).


SPEECH TITLE: “Urticaria and Vasculitis in Patient with HCV”


1. Vasculitis and Urticaria as spy of Chronic Heapatopathy


Objectives & Notes

Amer Suleman, M.D. Date of talk: Friday, June 26, 2009, 4:30 p.m.

The Heartbeat Clinic7777 Forest LaneSte A236Dallas, TX 75230


Training:Current Job Description: President of The Heartbeat ClinicCurrent Faculty Appointments: Consultant in cardiovascular medicine and

electrophysiology medical City Hospitals DallasMedical School/ University Attended King Edward Medical CollegeInternship: SUNY Buffalo NYResidency: SUNY Buffalo NYBoard Certifications: Internal medicine, cardiology, cardiac electrophysiology,

Hyertension, echocardiography, pacemaker and defibrillators, echocardiography, neurosonology

Other Information: CME editor cardiology for WEBMDDisclosure Statement:

SPEECH TITLE: “Syndromes of Orthostatic Intolerance”


1. Understand the definition of orthostatic tolerance

2. Understand different types of orthostatic tolerance

3. Identify major diagnostic and treatments modalities


SATURDAY, JUNE 27, 2009


Objectives & Notes

Robert W. Coppock, DVM Date of talk: Saturday, June 27, 2009, 8:05 a.m.

Toxicologist and Assoc LtdP O Box 2031Vegreville, AB T9C 1T2 Canada


Training:Current Job Description: Private practice in toxicologyCurrent Faculty Appointments: Adjunct Professor: Faculty of Medicine and School of

Public Health, University of Alberta; Concordia University College

University Attended: BS – Chemistry – Andrews University, DVM – Michigan State University, MS – Animal Pathology – Oklahoma State University, PhD – Toxicology – University of Illinois at Urbana

Residency: Veterinary Toxicology at Oklahoma State University, College of Veterinary Medicine, Oklahoma Animal Disease Diagnostic Laboratory

Board Certifications: American Board of Veterinary Toxicology, American Board of Toxicology

Other Information: Coppock, RW. Threats to by wildlife chemical warfare agents. In: Gupta, RC. Handbook of the Toxicology of Chemical Warfare Agents. San Francisco: Elsevier, pp 1200; 2009.

Coppock, RW. Potential Agents That Can Cause Contamination of Animal Feedstuffs and Terror. In: Gupta, RC. Handbook of the Toxicology of Chemical Warfare Agents. San Francisco: Elsevier, pp 1200; 2009.

Disclosure Statement: None

SPEECH TITLE: “Mycotoxins and The Heart”


1. Understand that the heart can be a target for mycotoxins.

2. Gain knowledge of the mechanisms of effects of certain mycotoxins on the heart.

3. Understand that heart lesions associated with mycotoxins generally are not considered in differential diagnosis.



Mycotoxins and The HeartRobert W. Coppock, DVM, PhD, DABVT, DABT

Mycotoxins have been shown to target the heart. Moniliformin has been shown to cause cardiac myopathy in chickens, turkeys, ducklings and rats. There may be links with moniliformin in the diet and the multifocal myocardial necrosis observed in Keshan disease. Cyclopiazonic acid causes myocardial degeneration in chickens, turkeys, rats and vervet monkeys. Fumonisin B1 (FB1) causes acute pulmonary edema in pigs due to negative cardiac inotropism, but cardiac lesions are not a consistent finding in pigs poisoned with FB1. The mycotoxin fusaric acid induces hypotension in cats, dogs, rats and humans. Citreoviridin producing species of Penicillium are associated with cardiac beriberi. Heart failure is associated with the neurological effects of citreoviridin. The mechanisms of actions will be discussed.

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Uraguchi, K. 1969. Mycotoxic Origin of Cardiac Beriberi. J Stored Prod Res 5 (3):227-236.van Rensburg, S. J. 1984. Subacute toxicity of the mycotoxin cyclopiazonic acid. Food Chem Toxicol 22 (12):993-8.

Voss, K. A., J. K. Porter, C. W. Bacon, F. I. Meredith, and W. P. Norred. 1999. Fusaric acid and modification of the subchronic toxicity to rats of fumonisins in F. moniliforme culture material. Food Chem Toxicol 37 (8):853-861.

Wicklow, D. T., R. D. Stubblefield, B. W. Horn, and O. L. Shotwell. 1988. Citreoviridin levels in Eupenicillium ochrosalmoneum-infested maize kernels at harvest. Appl Environ Microbiol 54 (5):1096-8.

Yarom, R., R. More, S. Raz, Y. Shimoni, O. Sarel, and B. Yagen. 1983. T-2 toxin effect on isolated perfused rat hearts. Basic Res Cardiol 78 (6):623-30.

Yarom, R., R. More, Y. Sherman, and B. Yagen. 1983. T-2 toxin-induced pathology in the hearts of rats. Br J Exp Pathol 64 (5):570-7.

Yutani, C., M. Imakita, H. Ishibashi-Ueda, S. Okubo, M. Naito, and T. Kunieda. 1988. Nodular regenerative hyperplasia of the liver associated with primary pulmonary hypertension. Hum Pathol 19 (6):726-31.

Zhao, D. 1990. [Ultrastructural study of moniliformin-induced lesions on the myocardium of rats and mice]. Zhonghua Yi Xue Za Zhi 70 (11):618-620.

Zhao, D., Q. Feng, X. Yan, C. Li, Y. Pan, and Q. Cui. 1993. Ultrastructural study of moniliformin induced lesions of myocardium in rats and mice. Biomed Environ Sci 6 (1):37-44.

Objectives & Notes

James Roberts, Jr., M.D., F.A.C.C. Date of talk: Saturday, June 27, 2009, 8:35 a.m.

3110 West Central AvenueToledo, OH 43606


Training:Current Job Description: Private Practice - Invasive and Complementary

CardiologyCurrent Faculty Appointments: NoneMedical School Medical College of OhioInternship: University of CincinnatiResidency: University of CincinnatiBoard Certifications: Internal Medicine, Cardiovascular Medicine,

Diplomat Candidate, American Board of Chelation Therapy, Interim Diplomat, American Board of Oxidative Medicine

Other Information: Co-Author of Reverse Heart Disease NowDisclosure Statement: None

SPEECH TITLE: “Immune Mechanisms in Atherosclerosis”


1. Recall the basics of immune system function.2. Understand the immune mechanisms underlying atherosclerosis and CHF. 3. Appreciate the role of metals as catalysts of an abnormal immune response.


Immune Mechanisms in Atherosclerosis – Abstract

Atherosclerosis is a chronic, maladaptive, Th1 (macrophage and CD4+ lymphocyte) driven immune response to perceived intimal infection with oxidized lipids. Nutritional and pharmacologic therapies designed to prevent or treat atherosclerosis can be seen to work within this framework. Apo-B100 containing lipids at above nutritional levels are trapped within the intima and later oxidized (the latter event favored by tissue metals and low levels of antioxidants and HDL). oxLDL, an entity not present in cavemen or within the thymus gland of modern man during T cell maturation, is perceived by the immune system as a threat. An inflammatory response is initiated. Endothelial function is compromised; adhesion molecules are displayed and chemokines elaborated. Mononuclear cells are drawn into the intima. Monocyte-derived macrophages recognize oxLDL not via nutritional LDL receptors, but rather via scavenger and CD36 receptors that mediate microbe phagocytosis. oxLDL blocks reverse cholesterol transport within the macrophages and other intimal cells. Lipid accumulation leads to the formation of foam cells, the precursor lesion of plaque. The next wave of macrophages, now armed with up regulated toll-like receptors, phagocytose oxLDL, degrade the apo-B100 protein, and present on MHC II molecules snippets of this protein to infiltrating T lymphocytes.

T lymphocytes are taught in the thymus to recognize non-self protein fragments as a threat and to initiate a humoral (Th2) or macrophage (Th1) mediated immune response. If by chance a T lymphocyte bearing a T cell receptor specific for an ox-apo-B100 fragment encounters an intimal macrophage bearing this 12-20 amino acid antigenic determinant, then the T cell activates, elaborates interferon-gamma (IFN-), and begins to proliferate. IFN- increases macrophage oxidant and phagocytic function. Additional ox-apoB100 is presented to the growing clone of reactive T cells, and more IFN- is elaborated. A chemokine trail pulls additional T cells, bearing different T cell receptors, and monocytes that have ingested microbes elsewhere, into this “under perceived attack” region of the vessel wall. The monocytes differentiate into macrophages, and then present to the T cells protein fragments derived from the microbes ingested elsewhere. Expansion of these activated T cell lines soon follows. Free radical stress compromises the endothelium and allows smooth muscle cells to proliferate, thickening the plaque but also providing it with tensile strength. IFN-, however, blocks smooth muscle proliferation and TNF-, produced in response to IFN-, leads to the release of nascent degradative enzymes (matrix metalloproteinases) from intimal macrophages. The MMPs are then activated by tryptase released from activated mast cells, which are found within the adventitia and shoulder region of the active plaque. As this process evolves, 5-10 clones of lesional activated T cells, some specific for oxLDL protein, and others specific for beta2-microglobulin, hsp, or a microbial determinant, escape from regulatory control. They now proliferate autonomously. They no longer require macrophage co-stimulation, and they release prodigious quantities of IFN-, within the lesion, and later within the circulation. The plaque shoulder region, rich in mononuclear cells and no longer strengthened by smooth muscle, can fissure, throwing off platelet clots, or rupture, releasing thrombogenic atheroma into the lumen – an acute coronary syndrome (ACS) follows.

Adverse outcome or recurrence of ACS is predicted by high levels of autonomous (CD4+28null) T cells, toll-like receptor up regulation on circulating monocytes, and other markers of immune system activation (maladaptive for the patient but appropriate from the perspective of the immune system, which thinks it is protecting the intima from a serious, chronic infection).

Urgent therapy might include a stent impregnated with a drug that blocks lymphocyte proliferation and a statin. Statins down regulate immune function. Macrophage radical generating, phagocytic, and antigen presenting function is down regulated, endothelial activation is lessened, and CD40-CD40-ligand signaling between immune effector cells is blunted. Out-of-control CD4+28null T cell levels fall and levels of anti-inflammatory regulatory T cells rise (this is all a great idea in a 75 year old with recurrent ACS but perhaps not so great an idea in a 25 year old with high but non-oxidized cholesterol and a lifetime ahead of infectious and immune challenges). Angiotensin I is converted into angiotensin II by ACE, 90% of which is located within the intima, a process that can be blocked by lipophilic ACEI. Chymase released by activated mast cells can also cleave angiotensin I, and here ARB therapy comes into play, as Ang II activates NF-KB in intimal cells, furthering the inflammatory response. Il-6 is elaborated and released into the circulation, stimulating the liver to synthesize more angiotensinogen, creating an inflammatory forward feedback loop. Pentoxifylline blunts transcription of TNF- and shifts T cell function away from plaque forming and destabilizing Th1 and towards non-atherosclerotic Th2, and has been shown to be helpful in ACS, CHF of any cause (another condition characterized and driven by Th1 activation), and presumably will help prevent and stabilize atherosclerosis (it does so in animal studies). Metals (toxic, copper, and iron) promote LDL oxidation, while anti-oxidants (especially Vitamin C and selenium) block this process that mutates a nutritional substance into the atherosclerosis initiator. 1,2-Dilinolenylphosphatidylcholine stimulates the antioxidant and reverse cholesterol transport function of HDL. Pomegranate juice stimulates paroxonase, the key antioxidant enzyme of HDL, leading to oxLDL reduction. Both have been shown to improve functional status and reverse atherosclerosis is symptomatic humans. Other HDL raising and/or stimulating therapies will likely do the same. Measures designed to lower circulating levels of apoB-100 containing particles will lessen the quantity of LDL that can be oxidized within the inflamed, now oxidant rich and antioxidant poor intima (why extreme LDL reduction is recommended in advanced disease vs. mild to moderate reduction in prevention). Metal overload increases CV risk. Metal detoxification is employed by physiologically oriented physicians in the prevention and treatment of atherosclerosis. Its primary mechanism of benefit is likely an attenuation of LDL oxidation within the intima. Fish oil, Vitamin D, Co-Enzyme Q-10, Carnitine, and many other nutritional agents, amongst their many benefits, down regulate or temper an over active immune response. To prevent atherosclerosis or slow its progression we need to prevent LDL, remnant particle, and Lp (a) trapping and oxidation within the intima. To prevent the consequences of atherosclerosis we need to down regulate or temper the overactive and eventually autonomous immune response that oxLDL initiates. Heart failure, coronary or non-coronary in etiology, is also associated with a deleterious Th1 immune response, explaining the benefit of immune modulators including statins, ACEI, Pentoxifylline, and even Methotrexate (Yes, statins deplete Co-Q10, and this aggravates CHF, but by blunting an overactive Th1 response, statin therapy will improve functional status and increase ejection fraction – thus low dose statin therapy with Co-Q10 coverage is rationale). Atherosclerosis is an inappropriate immune response to intimal oxidation of LDL. Prevention of LDL oxidation and down regulation of the consequent immune activation characterizes our preventative and therapeutic measures. Novel anti-LDL oxidation or immune modulating therapies are anticipated and eagerly awaited by the physiologically oriented health care practitioner. James C. Roberts MD FACC 4/10/09

Objectives & Notes

Dietrich K. Klinghardt, M.D., Ph.D. Date of talk: Saturday, June27, 2009, 9:35 a.m.

Institute of NeurobiologyP.O. Box 5023Bellevue, WA 98007

Phone: 425/688-8818Fax: 425/453-7015

Training:Current Job Description: Founder of the American Academy of Neural Therapy,

now the Klinghardt Academy of Neurobiology, and lead clinician at the Comprehensive Medical Center

Current Faculty Appointments: Capitol University, Washington, DCMedical School/ University Attended Albert-Ludwig University Freiburg, GermanyInternship: Albert Ludwig University, Freiburg, GermanyResidency: Surgery University Clinic, Freiburg, GermanyBoard Certifications: Board certified in General Practice

(Germany) and Pain Management, USDisclosure Statement: None

SPEECH TITLE: “Cavitation in the Jawbone, the Vagus Nerve, and the Heart.”


1. Understand the lymphatic drainage of the jaw bone and the proximity of lymph vessels and vagus nerve

2. Have a working idea of diagnostic local anesthesia in the oral cavity for heart rhythm problems

3. Have a working idea of three major treatment options for cardiac arrhythmias: a. Repeated local anaesthetic injections b. The x-tip procedure (intraosseous injections) c. Cavitation surgery


Abstract from Dietrich Klinghardt, MD, Ph.D.

Cavitations in the Jawbone, the Vagus Nerve and the Heart

Practitioners in Europe have for over 100 years observed a frequent connection between chronic infections in the jaw bone and problems with the rhythm of the heart (supraventricular tachycardia, chronically elevated heart rate, ventricular arythmias and asystole, heart palpitations, etc.). Successful treatment strategies involved

a. establishing a solid diagnosis with diagnostic procaine injections in the oral cavityb. treating the cavitation or infected jaw bone with surgery

The vagus nerve is the largest contributor to slowing down the heart rhythm in times of rest, relaxation or sleep. Most of the vagal fibers to the heart originate in the right vagus (behind and deep to the right ear).The anatomy of the jaw and the vagus nerve are related: lymphatic vessels and lymphatic drainage from the jaw bone parallel the course of the vagus nerve in the anterior neck region. This could explain how the nerve which is so involved in downregulating the heart rhythm and the oxygen consumption of the heart can become toxic and dysfunctional. Infected jaw bone creates potent neurotoxins, thioethers and mercaptans, which can easily disrupt normal neural transmission.

In this paper we will present a major new diagnostic tool and a new treatment option: Intraosseous neural therapy (the injection of procaine into the suspected jaw bone area using the x-

tip or stabident equipment - rather then injecting just next to it into the gum) Intraosseous and para-lymphatic ozone injections – rather then cavitation surgery

Most commonly a chronic low grade infection in the lower wisdom tooth extraction site is responsible for the patients vagus nerve and/or heart condition. The misfiring vagus nerve can also disturb any major other organ: the lungs, the intestines, the liver, the pancreas, the kidneys. In this case the illness caused by the jaw issue may be an inability to detox (liver, kidneys are compromised), chronic constipation, asthma, therapy resistant gut dysbiosis and many other conditions.

The new procedures are less invasive then existing other approaches, often more precise and more effective, and the learning curve to master them is much faster.

Any cardiac condition may be caused – or contributed to – by pathology in the jaw bone. Neural Therapy is a valuable tool for both diagnosis and treatment.

Objectives & Notes

William J. Rea, M.D. Date of talk: Saturday, June 27, 2009, 10:30 a.m.



Training:Current Job Description: Founder and President of the Environmental Health

Center - DallasCurrent Faculty Appointments:Medical School Ohio State University College of Medicine, Columbus,

OHInternship: Parkland Memorial Hospital, Dallas, TXResidency: University of Texas Southwestern Medical School;

Parkland Memorial Hospital, Baylor, Veteran’s Hospital, Children’s Medical Center

Board Certifications: American Board of Surgery, American board of Thoracic Surgery, American Board of Environmental Medicine

Other Information: Author of “Chemical Sensitivity I-IV”, “Optimum Environments for Optimum Health”


SPEECH TITLE: “Environmental Aspects in the Treatment of Cardiovascular Disease”


1. Recognize the severity of the disease so they can identify those patients early on.

2. Inform the physicians of the severity of the disease.

3. Help physicians treat the environmental aspects of cardiovascular disease.


ENVIRONMENTAL TREATMENTOF CARDIOVASCULAR DISEASE

William J. Rea, M.D., F.A.C.S., F.A.A.E.M.Bertie Griffiths, Ph.D.

Yaqin Pan, M.D.Ron Overberg, Ph.D.

The acute and long term treatment of environmentally triggered cardiovascular disease involves massive avoidance of pollutants in air, food and water, treatment of hypersensitivities to water contaminants, food and food contaminants, pollens, molds, terpenes, dust mites, animal dander and chemicals (natural gas, phenols, alcohols, perfumes, etc.), nutritional supplementation and replacement (intravenous, oral), heat depuration (sauna), physical therapy and exercise, immune modulators, oxygen therapy, autogenous vaccines, and a type of cranial and sacral manipulation, chiropractic manipulation, acupuncture, and energy balancing. Each of the first six treatments will be discussed separately:

Avoidance1. Air – ECU-like conditions (clinic, motel, home)2. Water – spring, distilled, filtered, glass bottles3. Organic food – rotary diet

Intradermal Neutralization, Subcutaneous Treatment, and Sublingual Treatment1. Molds, foods, chemicals2. Metals in the body – pacemaker, defibrillator, artificial valves, other implants (Dacron, Teflon,

Silicone)

Nutrient Treatment1. Vitamins – C, D, E, B-Complex2. Minerals – Potassium, magnesium, selenium3. Amino acids – glutathione, taurine4. Fatty acids

Heat Depuration1. Sauna2. Massage3. Exercise

Oxygen Therapy1. Pictures

Immune Modulators1. Gammaglobulins2. ALF3. Autogenous vaccine

Objectives & Notes

William J. Meggs, M.D., Ph.D. Date of talk: Saturday, June 27, 2009, 11:00 a.m.

Brody School of Medicine, East Carolina University600 Moye Blvd., Room 3ED311.PCMH, 3ED-311, Department of Emergency MedicineGreenville, NC 27834-4354


Training:Current Job Description: Chief of Toxicology, Professor of Emergency MedicineCurrent Faculty Appointments: Professor, Brody School of MedicineMedical School University of Miami, Miami, FloridaInternship: Rochester General HospitalResidency: Rochester General Hospital, Fellowships at NIH and

NYUBoard Certifications: Medical Toxicology, Allergy and Immunology, Internal

Medicine, Emergency MedicineOther Information: Author of “The Inflammation Cure”, over 50 research

publications, Co-editor of “Health and Safety in Farming, Forestry, & Fisheries”; Co-author of “Biomarkers of Immunotoxicology”


SPEECH TITLE: “Accelerators of Atherosclerosis”


1. To understand Atherosclerosis as a universal ingrained mechanism that can be accelerated or delayed.

2. To know the major accelerators of Atherosclerosis.

3. To know lifestyle choices that can delay one’s risk of Atherosclerotic diseases.


Accelerators of Atherosclerosis

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

Objectives• To understand atherosclerosis as a natural, universal process• To understand environmental and exposure factors that can accelerate the process of atherosclerosis• To know other cardio toxic effects that can occur with exposures

Abstract

Atherosclerosis is a natural process that is part of the planned obsolescence that is built into the mammalian genome. There are interventions that can forestall or push the process forward in time, and interventions that can accelerate the onset of atherosclerosis. In addition to the well known accelerators such as hypertension, hyperlipidemia, and hyperglycemia, toxic exposures such as cocaine, amphetamines, and inhalants can accelerate atherosclerosis. Phamaceuticals with cardiotoxicity include corticosteroids, protease inhibitors, chemotherapeutic agents, transplant rejection medications, ergotamine, and metals. Occupational exposure to carbon disulfide among rayon workers has been associated with increases in both all cause mortality and deaths from ischemic heart disease.

ReferencesKulasekaram R et al. Curr Med Res Opin 2005; 21:1717Libby: Braunwald’s Heart Disease, 8th EditionMyint PK et al, BMJ 2009;338:b349 Steinhart CE et al. AIDS Read 2004; 14:86Sudano I et al: Cardiovascular disease in HIV infection. Am Heart J 2006; 151:1147. P M Sweetnam, S W Taylor, and P C Elwood. Exposure to carbon disulphide and ischaemic heart disease in a viscose rayon factory. Br J Ind Med. 1987 April; 44(4): 220–227.

Objectives & Notes

Stephen T. Sinatra, M.D. Date of talk: Saturday, June 27, 2009, 1:30 p.m.

Optimum Health257 E. Center StreetManchester, CT 06040

Phone: 860/645-3825Fax: 860/643-2531

Training:Current Job Description: Cardiologist, Lecturer, WriterCurrent Faculty Appointments: Assistant Clinical Professor of Medicine, University of

ConnecticutMedical School Albany Medical SchoolInternship: Albany Medical Center HospitalResidency: St. Francis Hospital, Hartford CTBoard Certifications: 1975 American Board of Internal medicine, 1977

American Board of Cardiovascular DiseaseOther Information: Author of “Metabolic Cardiology-The Sinatra Solution”,

revised 2008, “Reverse Heart Disease Now”, articles Metabolic Cardiology-The Missing Link in Cardiovascular Disease, Congestive heart Failure—The Metabolic Cardiology Solution accepted by Alternative Therapies—not published.


SPEECH TITLE: “Energy Medicine-Good Vibes vs Bad”


1. Discuss the role of energy medicine in optimum health

2. List five nutraceuticals that promote favorable vibrational frequencies in the body

3. Discuss how electrical medicine assists in optimizing cellular function


Energy MedicineGood Vibes vs Bad

AbstractThe essence of disease originates from nutrient depletion in the context of physical and emotional trauma and environmental and electrical toxicity. At the essence of this triad are the compromised receptor sites on the cellular membrane. As the cellular membrane becomes vulnerable and dysfunctional, vital nutrients such as oxygen, vitamins, minerals, and hormones are not able to enter and nourish the cell in sufficient amounts. Toxic waste is not adequately flushed out of the cell. This scenario accelerates the development of microbial enhancement. Eventually the cells become toxic, unable to regenerate and malfunction occurs.

This lecture will discuss how vibrational frequencies hold the key to optimum health. Bioenergetic-supporting nutrients as well as avoidance of toxic EMF and wireless technologies, grounding the body, FIR sauna and the utilization of very low frequency pulsed electromagnetic waves are just a few of the exciting discoveries that assist the quantum energy of the body. This is the new wisdom that will assist us in the good vibe/bad vibe technological age.

Our technological age continually serves up wired and wireless wonders to make life more convenient. I have a persistent gnawing sense that something potentially disastrous is going on.

Illnesses like multiple sclerosis, autoimmune disorders, fibromyalgia, chronic fatigue, and autism have been proliferating in recent years. The incidence of cancer is up, particularly among young people.

The standard reasons for the staggering rise in these, and other manifestations of unwellness, certainly hold true: poor diet, physical inactivity, stress, and environmental toxicity. All combine to weaken the human immune system and open the door for inflammation and microbial mayhem. But there’s another factor—largely overlooked—which I think will attract more and more attention in coming years: the knockdown effect on bodily operating systems delivered by “electropollution.” By that I mean the chaotic, unseen, and unfelt environmental electrical fields we humans are increasingly exposed to from all the electronics, appliances, and telecommunications in our lives.

The potential for these electromagnetic (EMF) fields to stoke heart rhythm abnormalities and interfere with sleep patterns is well-documented. Electro medicine is a very dynamic field, but the science is far from conclusive as yet. There’s much still unknown and a lot of debate over whether common man-made electrical fields, generated by everything from high tension wires, office and home wiring, wireless networks, and cell phone proliferation makes a significant impact on health.

Electro technology is everywhere these days and has to have some effect—major or minor—on our bodies. After all, we are highly tuned and highly sensitive bioelectrical creatures. Every process in the body is regulated by dynamic electrical currents, most obvious, of course, the pumping action of the heart and the exquisitely complex circuitry of the brain.

All beings are conglomerations of electromagnetic energy. In essence, our bodies function—for better or for worse—as dynamic electrical circuits. Cells transmit and receive energy, and each has its own range of frequency within which it operates. Healthy cells, for instance, oscillate at higher frequencies than do unhealthy cells, such as cancer cells. James Oschman, Ph.D., a top expert and author of Energy Medicine in Therapeutics and Human Performance (Butterworth-Heinemann) says all “organisms (are) poised to respond to minute ‘whispers’ in the electromagnetic environment,” whether those fluctuations come from afar or near.

“The fields within the human body are inevitably affected by the larger fields of the planet and other celestial bodies,” he says. “For example, sunspots and the cycles of the moon cause changes in ionospheric currents and geophysical fields which in turn influence the fields within us.” Geomagnetic storms generated by turmoil on the sun can be so intense that they damage its satellites, power lines, telephone cables and disrupt radio communications. Not surprising, that these disturbances can and do affect physiology, creating cardiovascular problems and seizures.

Closer to home, man-made electromagnetic fields can have influences on our bodies as well. Perhaps the most documented influence is that of leukemia among children living near high voltage power lines. Of course, our modern array of electric devices such as hair dryers, computers, televisions, cell phones, and radios all produce a variety of signals and energy, some of which radiate directly into the tissue of nearby organisms. Some people are more vulnerable than others to “electropollution.” Many of them are often sensitive to many different environmental substances, and have “allergies” to the 50 or 60 Hz electromagnetic fields. This means they can develop headaches, arthritic pain, insomnia, chest discomfort and arrhythmia, anxiety, and depression from exposure to transformers, fluorescent lights, microwave ovens, and other appliances. Unfortunately, the connection with electropollution is rarely diagnosed and although these individuals may take medication, their symptoms rarely go away.

Electropollution has the potential to reduce heart rate variability (HRV), a term referring to the imperceptible variations in the heart’s beat-to-beat interval governed by breathing and other physiological rhythms. HRV is currently regarded both as an extremely accurate predictor of sudden death and an indicator of stress.

A few years ago, researchers in Germany suggested that signals from cell phones and microwave masts were contributing to a disturbing disappearance of honeybees, essential players in plant pollination. “Colony collapse disorder,” as it is called, was first observed in the United States but has spread to Europe. Tower signals are thought to disrupt the natural navigational bearings of bees returning to their home hives from pollen-hunting sorties. EMF interference leaves them wandering aimlessly and they die. If sensitive honeybees can be affected, why not us?

Researchers report that children, the elderly, and anyone with a lowered immune system are most at risk. One team of researchers at UCLA studied the association between prenatal and postnatal exposure to cell phones and behavioral problems in young children. They reviewed the answers to a questionnaire filled out by more than 13,000 mothers and concluded that exposure to cell phones during pregnancy (and to a lesser degree after birth) suggests a link to emotional and hyperactivity problems in young kids. “If real,” the researchers said, the associations rise to the level of public health concern given the widespread use of the technology.

Recently I read a long-term Swedish study finding that the use of cell phones for 2,000 plus hours during a lifetime could substantially increase the risk of developing a malignant cranial tumor. One summary of studies on long-term heavy users indicates a 20 percent increased risk of a tumor, and particularly on the same side of your head that you use to talk on the phone. I’ve also learned that excessive cell phone use may generate a feeling of fullness and warmth in the ears, as well as a ringing sensation like tinnitus. Such symptoms could foretell an early auditory abnormality. How can you discharge electropollution from your body? One simple, costless way is just walking barefoot on dirt, sand, grass, and unpainted cement. The more time you can spend directly connected—flesh to earth—the better. You are literally, figuratively, and electrically grounding yourself. Try sitting and reading

for 15 minutes or a half hour in your backyard, weather allowing of course, with your bare feet on the ground. When it comes to shoes, leather serves the purpose as a conductor but not rubber and plastic.

Connected to the earth, either walking or sitting, you are not only discharging electropollution but also getting an infusion of activated electrons produced on the surface of the earth from solar radiation. The moment your foot touches the earth your physiology changes. In essence, grounding the body balances the autonomic nervous system by attenuating sympathetic overdrive.

I encourage you to take stock of your phone systems. Consider using the speakerphone feature on your phones in order to protect your head and all its vital contents. Be mindful of the exposure that kids in your family may be getting. So many youngsters chat idly for hours with their friends on cell phones. Researchers believe younger cell phone users may face a higher risk of developing tumors because their nervous systems are not fully developed and their skulls are not as thick as those of adults.

You might want to consider buying an electropollution detector, devices that can tell you how strong these potentially upsetting waves are, and how far they extend out from their source. You will be surprised, as I have been, at their intensity and range. I was surprised, for instance, when I checked the radiation emanating from a baby monitor. It was really high. Could the frequencies coming out of those monitors affect sleeping toddlers?

This paper has been modified and taken from Dr. Sinatra’s Heart Health and Nutrition newsletter.

ReferencesAkerstedt T, Arnetz B, Ficca G, Paulson LE, Kallner A. A 50-Hz electromagnetic field impairs sleep. J Sleep Res 1999;8:77-81.

Baris D, Armstrong BG, Deadman J, Theriault G. A case cohort study of suicide in relation to exposure to electric and magnetic fields among electrical utility workers. Occup Environ Med 1996;53:17-24.

Bjorntorp P. Do stress reactions cause abdominal obesity and co-morbidities? Obes Rev 2001;2:73-86.

Borbely AA, Huber R, Graf T, Fuchs B, Gallmann E, Achermann P. Pulsed high-frequency electromagnetic field affects human sleep and sleep electroencephalogram. Neurosci Lett 1999;275:207-210.

Brown RP, Kocsis JH, Caroff S, Amsterdam J, Winokur A, Stokes P, Frazer A. Depressed mood and reality disturbance correlate with decreased nocturnal melatonin depressed patients. Acta Psychiatr Scand 1987;76:272-275.

Coghill RW, Steward J, Philips A. Extra low frequency electric and magnetic fields in the bedplace of children diagnosed with leukaemia: A case-controlled study. Eur J Cancer Prev 1996;5:153-158.

Divan HA, Kheifets L, Obel C, et al. Prenatal and postnatal exposure to cell phone use and behavioral problems in children. Epidemiology, 2008;19(4):523-9.

Genuis SJ. Fielding a current idea: exploring the public health impact of electromagnetic radiation. Public Health. 2008 Feb;122(2):113-24. Epub 2007 Jun 18.

Ghaly Teplitz D. Biologic effects of grounding the human body during sleep as measured by cortisol levels and subjective reporting of sleep, pain and stress. J Altern Complement Med. 2004 Oct;10(5):767-776.

Harrell L, Carlberg M, Mild KH. Pooled analysis of two case-control studies on use of cellular and cordless telephones and the risk for malignant brain tumors diagnosed in 1997-2003. Int Arch Occup Environ Health. 2006;79(8):630-39.

Havas M, Stetzer D. Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes and multiple sclerosis. Electromag Biol Med 2006;25(4):259-68.

Havas M, Stetzer D. Dirty electricity and electrical hypersensitivity: five case studies. World Health Org Workshop on Elec Hypersensitivity, Oct 2004, Prague, Czech Republic.Mann K, Wagner P, Brunn G, Hassan F, Hiemke C, Roschke J. Effects of pulsed high-frequency electromagnetic fields on the neuroendocrine system. Neuroendocrinology 1998a;67:139-144.

Milham S, Morgan LL. A new electromagnetic exposure metric: high frequency voltage transients associated with increased cancer incidence in teachers in California school. Am J Ind Med. 2008 Aug;51(8):579-86.

Oschman JL. Energy Medicine in Therapeutics and Human Performance, Can Electrons Act as Antioxidants? A Review and Commentary J Alt Comp Med, 2007;13(9):955-67, 2000 Energy Medicine: The scientific basis. Harcourt/Churchill Livingston, Edinburgh.

Salford LG, Brun AE, Eberhardt JL, Malmgren L, Persson BRR. Nerve cell damage in mammalian brain after exposure to microwaves from GSM mobile phones. Environ Health Perspect 2003 June;111(7):881-883.

Savitz DA, Checkoway H, Loomis DP. Magnetic field exposure and neurodegenerative disease mortality among electric utility workers. Epidemiology 1998 July;9(4):398-404.Sinatra 1-8, 48 slides 6 per page

Objectives & Notes

Kalpana Patel, M.D. Date of talk: Saturday, June 27, 2009, 2:00 p.m.

Allergy and Environmental Health Center - Buffalo65 Wehrle Dr.Buffalo, NY 14225


Training:Current Job Description: Director/President of Allergy and Environmental Health

Center BuffaloCurrent Faculty Appointments: Assistant Professor of pediatrics Suny BuffaloMedical School B.J. Medical SchoolInternship: Bexar County Hospital, San Antonio TXResidency: Bexar County Hospital, San Antonio TXBoard Certifications: American Board of Pediatrics, American Board of

Environmental MedicineOther Information: Comprehensive approach to Treating Autism and ADHD.

Pre Pilot Study. Journal of Alternative and Complementary Medicine, October 2007. 2) Nutritional and Environmental Approaches to Preventing and Treating Autism and ADHD Review


SPEECH TITLE: “Environmental Aspects of Lyme Disease and Autonomic Deregulation”


1. Presentation of different patterns of Lyme Disease.

2. Similarities between Lyme disease and environmentally triggered diseases.

3. Role of medication in reversibility of deregulation.


Dr Patel’s presentation was not available at time of printing of this abstract.

Objectives & Notes

Donald Hillman, Ph.D. Date of talk: Saturday, June 27, 2009, 2:30 p.m.

Michigan State University750 Berkshire LaneEast Lansing, MI 48823


Training:Current Job Description: ConsultantCurrent Faculty Appointments: Professor EmeritusMedical School/ University Attended Michigan State University, East Lansing Dairy Nutrition

MajorOther Information: Problem solving on farms and have documented and

published work on Electropathic Stress Syndrome and on Chronic Fluoride and Iodine Toxicity.


SPEECH TITLE: “The Electropathic Stress Syndrome--Neuroendocrine Responses to EMF”


1. Recognize signs of Electropathic Stress Syndrome

2. Understand autonomic nervous system responses to EMF

3. Recommend Electropathic Stress therapy


The Electropathic Stress Syndrome in Animals and Humans

Donald Hillman¹, PhD., Professor Emeritus, Department of Animal Science, Michigan State University, East Lansing, MI 48823

Abstract

Excessive exposure to electric and magnetic fields (EMF) affects the central nervous system of man and animals via stimulation of peripheral sensors similar to responses to severe environmental temperatures, noise, and atomic radiation. EMF produces a neuroendocrine stress that interferes with normal homeostasis of the autonomic nervous system (ANS). The syndrome is manifested in hypothalamic, pituitary, and pineal gland secretions that influence the performance of other endocrine glands and most organs of the body. Both sympathetic and parasympathetic responses to EMF have been reported to be partially dependent on the body exposure site, the intensity and the frequency of electrical signals. Biological permeability tends to increase as the intensity and frequency of electrical signals increases. Radiofrequency current has direct effects on adrenal gland release of corticostearoids, epinephrine, norepinephrine and dopamine and indirect effects on the immune response causing changes in concentrations of blood proteins, i.e., immunoglobulins, cytokinins, blood viscosity, lymphocytes, erythrocytes, and electrolytes. Such interference results in proliferation of certain cancers, allergies, cardiovascular disease, impairment of cell membrane transfer of AMP-ATP energy, Ca++, K+, enzymes, and glucose/fat metabolism of diabetics. Numerous examples of electropathic stress syndrome regarding human and animal behaviour, reproduction, and productivity are cited in credible medical and bioelectric scientific journals. Some of the references are listed below.

¹Donald Hillman, PhD., Professor Emeritus, Department of Animal Science, Michigan State University, East Lansing, MI 48823. Hillman served as Extension Specialist in Dairy Nutrition and Management from 1955-1982. He was a High School Teacher of Vocational Agriculture and County Extension Agent 1951-55. He studied environmental effects on dairy cattle performance and investigated effects of electric and magnetic fields on behaviour, health, and productivity of dairy cattle in some 110 herds assisting farmers, veterinarians, electricians, and engineers in problem cases. He is a member of The American Dairy Science Association-Am..Soc.of Animal.Science, and the American Society of Agricultural and Biological Engineers. He has investigated EMF effects on humans and other species and serves as a private consultant regarding EMF effects on dairy cattle.

Selected Digital References:

http://www.powerwatch.org.uk/science/studies.asphttp://www.bioinitiative.org/

http://www.microwavenews.com/ http://omega.twoday.net/stories/3642285/

http://electricalpollution.com/Shocking_News.html http://www.weepinitiative.org/

http://electricalpollution.com/

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Objectives & Notes

Aruni Bhatnagar, Ph.D. Date of talk: Saturday, June 27, 2009, 3:30 p.m.

University of Louisville580 S. Preston St.The Baxter II, Room 421Louisville, KY 40202

Phone: 502/852-5724

Training: Post-doctoral training in cellular cardiac electrophysiology

Current Job Description: Professor of Medicine - Teaching and ResearchCurrent Faculty Appointments: Department of Medicine, Physiology and Biophysics, and

Pharmacology and ToxicologyMedical School University of Kanpur, UP, India (Ph.D) and University of

Texas Medical Branch Galveston, TXDisclosure Statement: None

SPEECH TITLE: “Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants"- Part II


These talks are to discuss the contribution of exposure to environmental pollutants to heart disease. Specific issues that will be discussed include evidence implicating that exposure to particulate air pollutants and gaseous co-pollutants increases CVD risk. Data relating to an increase in both acute and chronic risk will be examined. The effects of other pollutants such as metals and aldehydes will also be discussed.

1. Estimate risk due to exposure to particulate air pollution2. Understand the impact of the environment of cardiovascular disease3. Understand the pathophysiological mechanisms that impart and mediate the effects of the environment on

acute cardiovascular events as well as chronic atherosclerotic disease


Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants

Aruni Bhatnagar, Ph.D., FAHA, Division of Cardiology, Department of Medicine, University of Louisville, Louisville, KY

Heart disease is the leading cause of death in the industrialized world. The rates of heart disease, however, vary from one country to another. Geographic variations in CVD mortality probably reflect genetic, social, and cultural factors as well as disparities in health care. Nevertheless, epidemiological data suggest a strong influence of environmental factors, since rates of CVD incidence and mortality could be markedly altered within a generation, indicating that CVD risk is in large part derived from environmental factors.

How the environment influences heart disease is not well understood. Multiple studies suggest that environmental factors such as smoking, nutrition, and physical activity are key factors that determine CVD risk. Nevertheless, it remains unclear how these factors contribute to the incidence and the severity of heart disease. In addition, the pathologic mechanisms by which environmental factors influence specific features of heart disease remain largely unknown. Epidemiological evidence indicates that CVD risk is derived from several variant and invariant “risk factors” such as high cholesterol, blood pressure, diabetes and smoking. In addition, exposure to environmental pollutants has also emerged as a new risk factor for the development of heart disease. Extant literature provides ample evidence linking most common pollutants to heart disease. Several pollutants ranging from tobacco smoke, particulates, metals, and pollutant gases have been reported to either exacerbate CVD or precipitate acute clinical. Multiple studies reporting health effects of ambient particles have been published. These studies provide evidence for a significant association between particulate air pollution levels and short-term mortality as well as increased mortality risk due to long-term exposure.

Over 100 epidemiological studies report a link with daily fluctuations in air pollutants at relatively low commonly encountered levels of air pollutants in several urban areas throughout the world events. Consistent positive relationships between daily PM10 levels and mortality counts have been reported by studies using either time series modeling or a case-cross over design. The strength of association appears to be stronger for PM2.5 than PM10, indicating that PM2.5 may be the more responsible for the observed association. The magnitude of the effect (about 1%) is small, variable, and dependent upon several statistical considerations including controlling for seasonality and slowly changing covariants. Nevertheless, consistent associations have been reported for risk of death from all causes, but particularly from cardiopulmonary disease. In some studies significant associations have also been reported for sulfur oxide concentrations, while others have found no association with common copollutants (NO2, SO2, CO, and O3). For obvious reasons, no controlled toxicological studies with mortality as an end point have been conducted to experimentally verify the link between short time exposure to air pollutants and increased mortality counts.

The effects of long-term exposure to air pollution on mortality have also been examined. Two major studies - the Harvard six cities and the American Cancer Society cohort studies report a significant positive association between cardiopulmonary mortality and PM2.5 and sulfate concentrations. No excessive mortality risk was associated with exposure to coarse PM or other gaseous pollutants. Similar associations have also been reported by several other long-term exposure studies. Notably, increases in mortality risks were much larger (generally more than 10 %) than observed with daily time-series studies. The magnitude of the reported effect is, however, variable.

Animals studies with particulate air pollution show that exposure can lead to an increase in cardiovascular inflammation results in an increase in atherogenesis, thrombosis and endothelial dysfunction. Environmental effects on atherogenesis are poorly understood. Data from Watanbe heritable hyperlipidemic rabbits show that repeated intrapharyngeal instillation of PM10 (twice a week for 4 weeks) stimulates progression of atherosclerotic plaques and increases lipid accumulation in aortic lesions as well as plaque cell turnover. These observations suggest exposure to PM10 could accelerate atherogenesis and potentially enhance the vulnerability of atherosclerotic plaques to rupture. In addition to air pollution and tobacco smoke, there is extensive evidence suggesting that exposure to metals also accelerates atherogenesis.

Exposure to arsenic in particular has been linked to an increase in atherosclerotic disease. Studies with human populations exposed to arsenic in well water in Taiwan suggest that the incidence of CVD depends upon the level of exposure to arsenic Epidemiological studies of regions with high arsenic levels in the ground water show a marked increase in several forms of CVD including carotid atherosclerosis, hypertension, and ischemic heart disease. Arsenic exposure is also associated with peripheral atherosclerosis, which severely decreases blood flow to extremities and result in gangrene. In Taiwan and Bangladesh, gangrene is most commonly present on feet leading to the characteristic blackfoot disease. Consumption of arsenic contaminated drinking water is also associated with an increase in cardiovascular mortality in the U.S.

Exposure to pollutants could also increase thrombosis. Platelets from smokers demonstrate an increase in spontaneous as well as agonist (ADP, thrombin) stimulated aggregation. In addition, PM can contribute to the development and maintenance of a pro-thrombotic state. This is supported by studies demonstrating a positive correlation between PM10 exposure, plasma levels of fibrinogen and an increase in blood viscosity. Similarly, ultrafine particles increase platelet number, reduce bleeding times and increase levels of soluble P-selectin, a marker of platelet activation Aside from PM, component gases of ambient air have been linked to thrombosis through epidemiological studies demonstrating associations between exposure and hospitalizations for ischemic heart disease. Most prominent among these atmospheric gases include ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen oxides (NO2). Ozone exposure, in particular demonstrates a particularly strong association with enhanced platelet aggregation and acute MI. In contrast this association was lacking with NO2 and SO2.

Reactive aldehydes are another constituent of ambient air pollution that might be linked to cardiovascular disease. Aldehydes are a significant component of automobile exhaust and smog and have been detected in high concentrations in cigarette, cotton, wood, and coal smoke. The specific contribution of aldehydes to the cardiovascular effects of traffic air pollution, however, remains to be fully assessed. In a recent study on the cardiovascular effects of traffic exposure on highway patrol troopers, aldehydes were strongly correlated with an increase in plasma von Willebrand factor and changes in heart rate variability. Cardiovascular toxicity of environmental aldehydes is also underscored by studies showing increased risk of atherosclerotic disease in plant workers producing formaldehyde and a higher incidence of heart disease in undertakers, embalmers and perfumery workers who are exposed to high levels of aldehydes during the course of their work. Nevertheless, it remains unclear whether exposure to ambient levels of aldehydes is associated with an excessive CVD risk and whether long-term repeated exposures to aldehydes has broad impact on cardiovascular function and CVD disease or susceptibility.

In the absence of injury, the cardiovascular system does not directly interact with the environment. It is, however, highly sensitive to environmental changes. These responses could promote cardiovascular health or could contribute progressively to disease and dysfunction. Although some cardiovascular diseases (such as familial hypercholesterolemia or the long Q-T syndrome) have clear, well-defined genetic origins, the most common forms of CVD develop in response to environmental injury. This injury might result from

excessive consumption of saturated fat, lack of exercise or from continuous exposure to environmental pollutants. In each case, disease appears to develop from failed responses to repair injury and to restore normal function rather than from common genetic flaws that manifests to greater severity with increasing age. During disease development genetic factors undoubtedly play an important role in modulating environmental influences. As a result, individuals with different genetic makeup display different susceptibilities to environmental insults. Nevertheless, given its high prevalence, CVD is unlikely to be entirely or even substantially regulated by genetics. For the same reasons, it is also unlikely that the environment plays a secondary role in the etiology of CVD. Migrant population studies and studies within the same population with changing environment (lifestyle choice, nutrition, etc) have shown that significant changes in the environment could substantially alter CVD risk. Both population-based cohort studies and animal experiments have provided ample data to support the view that exposure to environmental pollutants (ambient air particulates, tobacco smoke, metals, aldehydes, etc) can induce endothelial dysfunction and significantly accelerate and exacerbate atherogenesis and thrombosis. This evidence suggests that environments that induce systemic inflammation or increase oxidative stress exacerbate atherogenesis, because both inflammation and oxidative stress are key contributors to atherosclerotic lesion formation. Nevertheless, it is not clear whether there are common sets of mechanisms by which environmental agents impair vascular function and promote atherogenesis and to what extent primary interfaces with the environment (e.g., lung, gut, skin, etc) modify the external insult or orchestrate the cardiovascular response.

References:

1. Brook, R. D., Franklin, B., Cascio, W., Hong, Y., Howard, G., Lipsett, M., et al. Air pollution and cardiovascular disease: a statement for healthcare professionals from the Expert Panel on Population and Prevention Science of the American Heart Association. Circulation 6-1-2004; 109: 2655-2671

2. Bhatnagar, A. Cardiovascular pathophysiology of environmental pollutants. Am.J.Physiol Heart Circ.Physiol 2004; 286: H479-H485.

3. Bhatnagar, A. Environmental cardiology: studying mechanistic links between pollution and heart disease. Circ.Res. 9-29-2006; 99: 692-705.

4. Pope, C. A., III and Dockery, D. W. Health effects of fine particulate air pollution: lines that connect. J.Air Waste Manag.Assoc. 2006; 56: 709-742.

Objectives & Notes

Mohamed B. Abou-Donia, Ph.D. Date of talk: Saturday, June 27, 2009, 4:00 p.m.

Duke University Medical CenterLaboratory of NeurotoxicologyDept. of Pharmacology and Cancer Biology,Box 3813Durham, NC 27710


Training:

Current Job Description: Teaching, Research, Member of the Executive Committee for Admission of Medical Students

Current Faculty Appointments: Professor of Pharmacology and cancer Biology and of Neurobiology

Medical School University of California, BerkeleyBoard Certifications: American Board of Toxicology, Academy of

Toxicological SciencesOther Information: Neurotoxicology, editor, CRC Press, inc., 329 published

papers, Areas of Researched Funded: Health Effects of Pesticides, Combined Chemical Exposure, Persian Gulf War Illness, Nicotine, Artificial Sweeteners and Biomarkers for Chemical Exposure


SPEECH TITLE: “Splenda Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Rats”


1. The function of P-glycoprotein and Cytochrome P-450 in the bioavailability of drugs and nutrients

2. The effect Splenda on the expression of the gut P-glycoprotein and Cytochrome P-450

3. The consequences of increased P-glycoprotein and Cytochrome P-450 on bioavailability of drugs


Splenda Increases Intestinal P-Glycoprotein (P-gp) & Cytochrome P450 in Male Rats

Mohamed B. Abou-Donia1, Eman M. El-Masry1, Ali A. Abdel-Rahman1, Roger E. McLendon2, and Susan S. Schiffman3, 1Departments of Pharmacology and Cancer Biology, 2Pathology and 3Psychiatry, Duke University Medical Center, Durham, NC 27710 USA

Splenda is comprised of the high-potency artificial sweetener sucralose (1.1%) and the fillers, maltodextrin and glucose. Splenda was administered by oral gavage at 100, 300, 500, or 1000 mg/kg to male Sprague-Dawley rats for 12 wk. After 12 weeks, half of the animals from each control and treatment group were sacrificed to determine the intestinal expression of the membrane efflux transporter P-glycoprotein (P-gp) and metabolism enzymes, the cytochrome P450 isozymes, CYP3A4 and CYP2D1 by Western blot. The remaining animals were allowed to recover for an additional 12-wk period, and further assessments of expression of P-gp and CYP isozymes. At the end of the 12-wk treatment period, there was an enhanced the expression of P-gp up to 2.43-fold, CYP3A4 up to 2.51-fold, and CYP2D1 up to 3.49-fold. Following the 12-week recovery period, P-gp and CYP3A4 and CYP2D1 remained elevated. These changes occurred at Splenda dosages that contained sucralose at 1.1 – 11 mg/kg (the US FDA Acceptable Daily Intake for sucralose is 5 mg/kg). Evidence indicates that a 12-wk administration of Splenda caused several adverse effects, including (1) an enhanced P-gp and (2) CYP3A4 and CYP2D1 expression at levels known to limit the bioavailability of orally-administered drugs.

Abou-Donia, MB, El-Masry EM, Abdel-Rahman, AA, McLendon, RE, and Schiffman, SS (2008). Splenda alters gut microflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ, Health 71: 1415-1429.

SUNDAY, JUNE 28, 2009


Objectives & Notes

Andrea Frustaci, M.D. Date of talk: Sunday, June 28, 2009, 8:30 a.m.

La Sapienza UniversityHeart and Great Vessels DepartmentViale del Policlinico 155Rome, 00161Italy

Phone: 39/0630155231Fax: 39/063055535Email: [email protected]

Training:Current Job Description: Associate Professor in CardiologyCurrent Faculty Appointments: La Sapienza University, Heart and Great Vessels

Department, Rome ItalyMedical School/ University AttendedInternship:Residency:Board Certifications:Other Information:Disclosure Statement: None

SPEECH TITLE: “Selenium And Zinc Deficient Cardiomyopathy In Human Intestinal Malabsorption ”


1. Know that patients with chronic intestinal malabsorption may develop cardiac arrhythmias and/or dysfunction due to myocardial deprivation of selenium and zinc

2. Recognize that selenium and zinc loss determine a reduction of glutathione peroxidase and superoxide dismutase activity with consequent decline of anti-oxidant property of the heart

3. That this reflects in a oxidative damage of cell membranes with enhanced cell autophagy and decreased cardiac contractility


SELENIUM AND ZINC DEFICIENT CARDIOMYOPATHY IN HUMAN INTESTINAL MALABSORPTION

ANDREA FRUSTACI , MD

Department of Cardiovascular and Respiratory Sciences . La Sapienza University, Rome , Italy.

ABSTRACT

Background :Patients with intestinal malabsorption may develop cardiac arrhythmias and/or dysfunction which origin is often elusive. Methods : Five patients (5F, mean age 23± 7 ys) with Celiac disease and 3 patients with intestinal bypass because of severe obesity (2M , 1F mean age 57±3 ys, time from intervention 15±3 ys) presenting unexplained left ventricular (LV) dilatation (LVEDD 68±5 mm) and dysfunction (LVEF 28±5%) , underwent LV endomyocardial biopsy . Biopsy samples were processed for histology , electron-microscopy , polymerase chain reaction for cardiotropic viruses and instrumental neutron activation analysis (INAA) of myocardial trace elements Myocardial anti-oxidant reserve and cell autophagy were evaluated by assessment of glutathione peroxidase activity and of LC3-II, respectively . Controls were surgical samples from patients with mitral stenosis and biopsy samples from patients with idiopathic dilated cardiomyopathy.Results : Histology and electronmicroscopy showed in malabsorption population hypertrophy/degeneration of myocardiocytes with pronounced cell autophagy and increased LC3-II . PCR was negative for viral genomes . INAA showed severe myocardial deficiency of Se and Zn ( p<0.001)and reduced myocardial Glutathione peroxidase activity (p<0.001) vs both idiopathic dilated cardiomyopathy and normal controls .Se and Zn infusion was followed at 6 months by a significant recovery of LV function (LVEF 42± 4.0 %) .Conclusions:A Se and Zn deficient Cardiomyopathy may occur in patients with chronic intestinal malabsorption .It is characterized by decline of myocardial anti-oxidant reserve ,oxidative damage of cell membrane and enhanced myocyte autophagy .

Objectives & Notes

Jean Monro, M.D. Date of talk: Sunday, June 28, 2009, 9:00 a.m.

Breakspear HospitalHertfordshire HouseWood Lane, Paradise EstateHemel Hempstead, Herts HP2 4FDEngland

Phone: 011/44-1442-231333Fax: 011/44-1442-266388Email: [email protected]

Training:Current Job Description: Medical Director of The Breakspear Hospital, EnglandCurrent Faculty Appointments: Medical Director of The Breakspear Hospital, EnglandMedical School London Hospital Medical School, EnglandResidency: London HospitalBoard Certifications: MB BS, MRCS, LRCP, FAAEM, DipIBEM, MACOEMDisclosure Statement: None

SPEECH TITLE: “Aspects Of Tissue Oxygenation”


1. Delivery of oxygen to the tissues depends on oxygen provision through the respiratory system, transport through the capillaries, its transfer from the capillaries to the tissue and its utilisation there.

2. All these will be discussed with data on: transcutaneous gases and the autonomic nervous system – control of breathing and circulation Vascular Endothelial Growth Factor (VEGF) 2,3 Bisphosphoglycerate (BPG) and BPG mutase Coagulation factors Redox

3. The implications of these findings in metabolic disease, infections, post (chronic) infectious states and their treatments will be discussed.


Breakspear Hospital

Title: “ASPECTS OF TISSUE OXYGENATION”

Author: JEAN A MONROMB BS MRCS LRCP FAAEM DIBEM MACOEMMedical Director, Breakspear Hospital, Wood LaneHemel Hempstead, Herts, HP2 4FD, UK

ABSTRACT FOR PRESENTATION FOR 27 TH ANNUAL MEETING (AEHF) 25 – 28 JUNE 2009

2,3-bisphosphoglycerate (2,3-BPG), also known as 2,3-diphosphoglycerate (2,3 BPG/DPG) is the carrier of oxygen from haemoglobin to the tissues.

As muscles contract, the presence of hydrogen ions in the muscles allows oxygen to be separated from the haemoglobin. Equally, as the red blood cells, which are 8 or more microns in diameter, go through capillaries, which might be as small as 4 microns in diameter, they have to twist and be wrung out to release the oxygen. The chemical and physical means of extraction of oxygen from the bloodstream allow its dispersal into the tissues. There, however, it requires to be carried to the cells and the mitochondria within them: the carrier is 2,3-BPG/2,3-DPG.

low 2,3-BPG - the enzyme 2,3-BPG mutase maybe inefficient and anoxia will be present because there is no transport for the oxygen

high 2,3-BPG - there has been tissue anoxia for some time and the body is attempting to compensate. 2,3-BPG is therefore induced

when 2,3-BPG mutase is high, the body has recognised the need for more oxygen and its 2,3-BPG transport

When glucose is broken down to form pyruvate and lactate, 1,3-bisphosphoglycerate is on the pathway. It can continue to 3-phosphoglycerate directly, but a shunt pathway allows the formation of 2,3-bisphosphoglycerate.

Increased red cell 2,3-BPG is high in smokers, because they have a diminished oxygen supply due to their chronic exposure to carbon monoxide. People with chronic anaemia and carbon monoxide poisoning will have an increase in 2,3-BPG and anyone who lives in high altitudes will also have a raised concentration of 2,3-BPG.

Vascular Endothelial Growth Factor (VEGF)The utilisation of oxygen is required by a cycle known as the Krebs cycle. An “e” indicates the point at which energy is released. However, if oxygen is not available then the alternative pathway, which uses carbohydrates for metabolism, is used. This is anaerobic metabolism.

The state of poor aerobic metabolism in the tissues results in fatigue and pain, and the (capillaries) can “bud” to produce extra capillary circulation in order to ensure that oxygen is taken to the tissues.

The endothelial linings of the capillaries can make extra nitric oxide (NO), which creates peroxynitrite (ONOO).

High VEGF levels indicate tissue anoxia. /Cont’d… 2

© Breakspear Medical Group Ltd, 2009Breakspear Medical Group Ltd. Registered in England 2035350

Registered office: Hertfordshire House, Wood Lane, Hemel Hempstead, Hertfordshire HP2 4FD UK

- 2 -

The Krebs Cycle

Transcutaneous Blood Gases The balance between carbon dioxide and oxygen in the soft tissues is crucial to normal functioning at a cellular level. Some people have been found to have too high levels of carbon dioxide. This contributes to a state of acidosis in the cells, and would contribute to fatigue. Some people have too low levels of carbon dioxide, which can lead to abnormal responses by the brainstem. Some people have been found to be hypoxic with very low levels of oxygen. The gases are assessed to see if the abnormalities can be corrected by deep breathing, or by other breathing techniques.

Breakspear Medical Group Ltd. Registered in England 2035350

Food

Protein

FatCarbohydrates

Amino acids Glucose Fatty acids and glycerole

Pyruvatee

Acetyl CoA

citrate

isocitrate

succinylCoA

a-ketoglutarate

e

oxalocetate

malate

Citric acid cyclefumarate

succinate

e

ee

ee e eEnergyWater

Waste products

Aerobic =

Anaerobic =

Registered office: Hertfordshire House, Wood Lane, Hemel Hempstead, Hertfordshire HP2 4FD UK

- 3 -

Transcutaneous Blood Gases (Cont’d):The transcutaneous gases are measured by two different methods and combined together into one sensor. The sensor has two membranes. One is sensitive to carbon dioxide only and the other membrane is sensitive to oxygen only. A small plastic cup is applied to the skin next to the liver, where the skin is warm. The cup is filled with a special fluid that dissolves both oxygen and carbon dioxide. The sensor with the two membranes is then screwed tightly into the cup. Oxygen and carbon dioxide escape through the skin and dissolve into the special fluid. The dissolved gases are then detected by the sensor.

Carbon dioxide is detected by the change in the pH (hydrogen ion concentration). Meanwhile oxygen is detected by its magnetic property which increases with its concentration. In that way, both oxygen and carbon dioxide concentrations can be measured simultaneously in real-time and these concentrations mirror the concentration in the capillaries. This concentration is similar to mixed arterial and venous blood.

The results of these evaluations will be presented and the association between tissue asphyxia and high VEGF and the carrier protein for oxygen from the capillaries to the tissues.

The correlation between VEGF measurements and transcutaneous gases will be presented.

Jean A MonroMedical Director GMC No: 0552174

Objectives & Notes Hartmut Heine, Ph.D. Date of talk: Sunday, June 28, 2009, 9:30 a.m.

Billerbeckweg 1-3D-75242 Neuhausen, Germany

Phone: 49 (0) 7234 6246Fax: 49 (0) 7234 949109Email: [email protected]

Training: Current Job Description: Private Scientific Research Institute

Professor emeritus of AnatomyFormally full professor and head of the Department of Anatomy and Clinical Morphology of the University of Witten/Herdecke, Germany

Other Information: Heine H, Schaeg G. Kann die Tumorstammzelle morphologisch charakterisiert werden? Deutsche Zeitschrift für klinische Forschung 2008; 12: 42-45


SPEECH TITLE: “Cardiocyte-Fibroblast Coupling. Basis for Myocardial Functioning” At the end of this Presentation, the participant should be able to:

1. Realize the functional importance of special connections between cardiocytes and fibroblasts.

2. Understand the fine structural basis of heart function.

3. Have new look on acquired heart diseases. The American Environmental Health Foundation and the University of North Texas Health Science Center is not responsible for the contents of this presentation. AEHF has not altered or modified the contents of the information provided by this speaker.

Objectives & Notes

Kaye H. Kilburn, M.D. Date of talk: Sunday, June 28, 2009, 10:15 a.m.

P.O. Box 5374Pasadena, CA 91107


Training:Current Job Description: Consultant, President of Neuro-test, Inc.Current Faculty Appointments: USC retired 2006Medical School: University of Utah 1954Internship: Western Reserve Hospitals – ClevelandResidency: University of Utah: Medicine and pathology, Duke:

cardiopulmonary, London: cardiologyBoard Certifications: Am Board Internal Medicine, Am Board Preventive

Medicine, occupational HealthOther Information: “Chemical Brain Injury,” NY: John Wiley 1998; “Mold

and Mycotoxins,” editor Washington DC: Heldref 2004; “Endangered Brains” Princeton Scientific Press 2004


SPEECH TITLE: “Heart Disease and Rotten Egg Gas”


1. Describe the connection between hydrogen sulfide and carbon disulfide exposures, and coronary insufficiency vs. cardiomyopathy congestive heart failure.

2. Be able to predict which workers and bystanders will have cardiomyopathy from chemicals.

3. Understand and apply criteria for associating chemicals with heart and vacular disease, including hypotension (Shy-Druger Syndrome).



Heart Disease and Rotten Egg Gas

By Professor Kaye H. Kilburn, M.D.USC Keck School of Medicine (ret.)

Neuro-Test Inc., Pasadena, CA 91107

Dennis thought his job smelled to high heaven, but he liked the pay. He worked at the wastewater treatment plant in Las Vegas for Nevada Power Company from 1983 to 1994. Beginning in 1990, he was treating wastewater at what was described as “all comes and nothing leaves” sewage plant, but he knew that rotten egg gas and water passed into the air. Prior to 1983, Dennis experienced no health problems while working 18 years making gypsum board, which is composed of calcium sulfate.

Four of the 13 workers at the wastewater plant developed palpitations, rapid, irregular heart activity and showed disorders of heart muscle. Dennis was unable to scuba dive, to ski or to run, that were previously his fun and delight. His heart was excessively large and it pumped inefficiently, as shown by a low ejection fraction. The coronary angiograms showed normal vessels and blood pressure was not elevated so his heart disease was diagnosed as cardiomyopathy. A biopsy confirmed a heart muscle fault. He was not an alcoholic or a cocaine user and had none of the other “usual causes of cardiomyopathy.” An extensive search pointed to sewer gas rich in hydrogen sulfide, mercaptans and other reduced sulfur gases as the probable cause. One fellow worker died of heart failure at 28 years of age and another age 32 years had a heart transplant. Shifting concerns to his brain, Dennis’ testing showed he could not discriminate between the pale colors in a spectrum. He had impaired problem solving, but other mind-brain functions were normal. A year later and without further exposure, color discrimination and potential of H2S problem solving were normal and other functions remained intact, but he remained crippled by his heart’s low output of blood, it pumped badly.

Tragic exposure is exemplified by eight sewer workers (aged 23 to 42 years), four killed at the scene and four admitted to the intensive care unit in Athens Greece. One died of pulmonary edema and circulatory failure, three recovered from the acute poisoning and were discharged, one needed a cardiac pacemaker. The others died later of myocardial infarctions. The most important feature of this report is that autopsies of five dead men showed pulmonary edema, pneumonia and pin- point bleeding from the stomachs gastric linings and in all parts of the brain. A New Mexico community and others in Ohio and Hawaii have furnished additional examples of cardiopulmonary disorders from rotten egg gas.

The impression that damage to the brain and lung from H2S always went away when they awakened from coma, waited until 1990 to be disproved. But in 1951, shale oil workers were reported having headaches, lethargy, dizziness, poor memory, fatigue, irritability, insomnia and depression from long term low dose H2S exposures. In the Alberta province of Canada from 1969 to 1973, 221 workers were exposed to H2S and 14 died. One of every 400 oil and gas workers was poisoned in that period. Lungs of those who died from high doses of H2S were heavy and wet from pulmonary edema and red froth poured from cut surfaces. Based on deaths and symptoms of distress of the brain, 10 states have set ambient air pollution limits for H2S of 0.01 to 0.24 ppm.

The potential of H2S to cause cardiovascular disease was explored using the observations provided from exposure to the related compound carbon disulfide (CS2) in the rayon (synthetic cloth) industry in the 1930’s. A pound of CS2 was needed to produce 3 pounds of rayon. Serious brain disability – dementia in workers was observed in Italy, Britain, and in Pennsylvania, where it triggered two public health investigations. The survey of 120 workers found psychiatric symptoms, peripheral neuropathy, losses of cranial nerve functions, and a Parkinson’s disease disorder. Of the 120, 30

workers had peripheral vascular disease, hypertension, and elevated cholesterol. Also, 43 Italian rayon workers had vertigo, painful muscles, (myopathy) and inflamed blood vessels. Those groups are a form fuste of the coronary artery disease epidemics later in the century. Use of carbon disulfide to fumigate grain elevators and corn bins exposed workers in the American Midwest who showed hypertension, peripheral vascular insufficiency, and coronary ischemia.

Humane and scientific interventions (experiments) are required . After measuring neurobehavioral, pulmonary and cardiovascular functions of H2S exposed people, they must reduce their exposure to the, presumed to be safe levels, that are monitored and have functions be re-measured. When people become their own “controls,” matched comparisons provide answers to prevent progressive damage to the heart and brain.

Summary

1. Acute exposures to H2S spills, pits, sewers cause deaths from pulmonary edema.2. A few years of exposure to lower levels 1-20 ppm caused cardiomyopathy in 4/13 workers – not CAD-MI.3. Carbon disulfide (CS2) CAD-MI deaths appeared increased from 1928 to 1964, but may be explained by the

emerging epidemic of cigarette smoking CAD-MI.4. Oil and gas well drilling, collection and refinery exposed many workers in the U.S., Canada and elsewhere. 5. Confined Animal Feeding Operations (CAFO) and sewers expose others.6. Many opportunities should be exploited to answer questions about neurobehavioral, pulmonary and

cardiovascular disease.

Conclusions Evidence of adverse effects of H2S on the myocardium and large arteries of the heart and brain

recommend additional studies. As old enigmas about effects of reduced sulfur gases are examined, new questions arise. The sources

of H2S remain. Avoidance of rotten egg gas should be practiced at work and at home. Flee when you smell rotten egg gas.

ReferencesArnold MF, Dufresne RM, Alleyne BC, et al. Health Implication of Occupational Exposures to Hydrogen Sulfide, Journal of Occupational Medicine, 1985; 27: 373-376.

Beauchamp Jr. RO, Bus JS, Popp JA, et al, A Critical Review of the Literature on Hydrogen Sulfide Toxicity, CRC Critical Reviews in Toxicology, 13: 25-97

Bhambhani Y, Burnham R, Snydmiller G, MacLean L, Effects of 10-ppm Hydrogen Sulfide Inhalation in Exercising Men and Women – Cardiovascular, Metabolic, and Biochemical Responses, J. Occup. Environ. Med., 1997, 39: 122-129.

Brieger H, Chronic Carbon Disulfide Poisoning, J Occup Med, 1961; 3:302-308.

Chapman LJ, Sauter SL, Henning RA, et al, Finger Tremor After Carbon Disulfide-Based Pesticide Exposures, Arch. Neurol. 1991; 48: 866-870.

Cohen AE, Scheel LD, Kopp J.F., et al, Biochemical Mechanisms in Chronic Carbon Disulfide Poisoning, Indust. Hygiene J., 1959; 20: 303-323.

Davidson M, Feinleib M, Carbon disulfide poisoning: A review, Am Heart J. 1972, 83: 100-114.

Editorial, Sulphur and Heart Disease, Brit. Med. J. 1968; 4: 412-413.

Elliott P, Diagnosis and management of dilated cardiomyopathy, Heart 2000; 84: 106.

Gordy ST, Trumper M, Carbon Disulfide Poisoning, JAMA 1938; 110:1543-1549.

Gregorakos I, Dimopoulos G, Liberi S, Antipas G, Hydrogen Sulfide Poisoning: Management and Complications, Angiology, 1995, 45: 1123-1131.

Hänninen H, Psychological picture of manifest and latent carbon disulphide poisoning, Brit. J. Industr. Med., 1971; 28: 374-381.

Inserra, SG Phifer BL Anger WK Lewin M Hilsdon R White MC Neurobehavioral evaluation for a community with chronic exposure to hydrogen sulfide gas Environ Res 2004, 95: 53-61

Lewey FH, Neurological, Medical and Biochemical Signs and Symptoms Indicating Chronic Industrial Carbon Disulphide Absorption, Ann. Intern. Med., 1941, 15: 869-883.

Lowicha, E Beltowski J, Hydrogen sulfide(H2S)—the third gas of interest for pharmacologists Pharmacological Reports 2007,59:4-24.

Nurminen M, Survival Experience of a Cohort of Carbon Disulphide Exposed Workers from an Eight-Year Prospective Follow-up Period, Intern J Epi; 1976; 179-185.

Peters HA, Levine RL, Matthews CG, et al. Carbon Disulfide-Induced Neuropsychiatric Changes in Grain Storage Workers, Am J. Industr. Med. 1982; 3: 373-391.

Snyder JW, Safir EF, Summerville GP, et al. Occupational Fatality and Persistent Neurological Sequelae After Mass Exposure to Hydrogen Sulfide, Amer Journal of Emergency Medicine, 1995; 13: 199-202.

Tiller JR, Schilling RSF, Morris JN, Occupational Toxic Factor in Mortality from Coronary Heart Disease, Brit. Med. J., 1968; 4, 407-411.

Tolonen M, Hernberg S, Nurminen M, et al, A follow-up study of coronary heart disease in viscose rayon workers exposed to carbon disulphide, Brit. J. Industr. Med., 1975; 32: 1-10.

Vigliani EC, Carbon Disulphide Poisoning in Viscose Rayon Factories, Brit. J. Industr. Med., 1954; 11: 235-241.

Yang G, Sun X, Wang R, Hydrogen sulfide-induced apoptosis of human aorta smooth muscle cells via the activation of mitogen-activated protein kinases and caspase-3, The FASEB J 2004; 18: 1782-1784.

Objectives & Notes

Russel J. Reiter, Ph.D. Date of talk: Sunday, June 28, 2009, 10:45 a.m.

University of Texas Health Science Center7703 Floyd Curl DriveSan Antonio, TX 78229-3900


Training:Current Job Description: Biomedical Research and TeachingCurrent Faculty Appointments: ProfessorMedical School: Bowman Gray School of Medicine, Winston-

Salem, NCOther Information: Written in excess 1,200 scientific research articles for

medical journals, 10 books and edited 34 books; Editor-in-chief of Journal of Pineal Research


SPEECH TITLE: “Melatonin Protects Heart From Free Radical Damage”


1. Understanding the mechanism of action of melatonin on free radicals in the heart.

2. Identify situations in which free radical damage occurs in the heart.

3. Apply the information in the clinical setting.


Objectives & Notes

Richard G. Jaeckle, M.D. Date of talk: Sunday, June 28, 2009, 11:45 a.m.

8220 Walnut HIll Lane, Ste. 404Dallas, TX 75231


Training:Current Job Description: Private Practice of Psychiatry & Environmental MedicineCurrent Faculty Appointments:Medical School/ University AttendedInternship:Residency:Board Certifications:Other Information:Disclosure Statement: None

SPEECH TITLE: “The Crosstalk Between the Central and Autonomic Nervous System”


1. Understand the dual branches of the Sypathic Nervous System

2. The two branches function separately or together.

3. Medications/precursors affect the two branches


urticaria and vasculitis in patients with hcv and

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