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  • 1. 27th Annual International Symposium on Man and His Environment in Health and Disease Special Focus Nutritional & Environmental Aspects Of Cardiovascular Disease SYLLABUS June 25 thru 28, 2009 Sponsored by American Environmental Health Foundation and University of North Texas Health Science CenterReprints are available from American Environmental Health Foundation. This volume is not to be reproduced, all or in part, without the writtenpermission of American Environmental Health Foundation.
  • 2. SYMPOSIUM PURPOSESince 1981, the International Symposium has been recognized as one of the most advanced medical forums in the worldaddressing 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 currentinformation available while providing guidelines to identify, diagnose, treatment and to prevent environmentallytriggered 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 AUDIENCEM.D.=s, D.O.=s, D.D.S.’s medical students, nurses, nutritionists and other health professionals interested in the conceptsand 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 AccreditationCouncil for Continuing Medical Education through the joint sponsorship of the University of North Texas Health ScienceCenter at Fort Worth Office of Professional & Continuing Education and the American Environmental HealthFoundation. The University of North Texas Health Science Center at Fort Worth Office of Professional & ContinuingEducation 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 OsteopathicAssociation to award continuing medical education to physicians.CreditThe University of North Texas Health Science Center at Fort Worth designates this educational activity for a maximumof 24.25 AMA/PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of theirparticipation in the activity.The University of North Texas Health Science Center anticipates this program for 24.25 hours in Category 2A, AOAcredit hours, pending approval by the American Osteopathic Association.
  • 3. Nursing Accreditation/Credit:The University of North Texas Health Science Center at Fort Worth is an approved provider of continuing nursingeducation by the Texas Nurses Association, an accredited approver by the American Nurses Credentialing Center’sCommission on Accreditation.This activity meets Type I criteria for mandatory continuing education requirements toward relicensure as established bythe 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 ofsuccessful completion, participants must attend the activity and complete and return the attendance record/credit requestform and the evaluation form at the end of the activity.EDUCATIONAL FORMATS # Plenary # Panels Discussions # Case Studies # Question & Answer Sessions # SyllabusCONFERENCE 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 answersession. All speakers are encouraged to use any and all appropriate audio/visual aids. (A brief outline of the speech isincluded in this booklet.)FINANCIAL CONSIDERATIONAEHF is a nonprofit organization that was founded in 1975 to provide education and research into EnvironmentalMedicine. This year’s Symposium is our 27th Annual International Symposium and is our major vehicle for educatingthe medical professional.Funding for the symposium is provided by registration fees from physicians and exhibitors. Proceeds from the AEHFstore cover the shortfall between registration fees and expenses for the conference. AEHF does not receive grants or anyoutside financial support for our education. Donations are accepted and used toward research into environmentalmedicine.DISCLAIMERAEHF and the University of North Texas Health Science Center are not responsible for the contents of thesepresentations. AEHF has not altered or modified the contents of the information provided by the speakers.
  • 4. GIVEN IN COOPERATIONWilliam J. Rea, M.D., F.A.C.S. Symposium Chairman, American Environmental Health Foundation, Environmental Health Center – Dallas, Dallas, TXBertie B. Griffiths, Ph.D., American Environmental Health Foundation, Dallas, TXKaye H. Kilburn, M.D. Consultant, President of Neuro-test, Inc. Pasadena, CAWilliam J. Meggs, M.D., Ph.D. Brody School of Medicine, East Carolina University Department of Emergency Medicine Greenville, NCDoug Seba, Ph.D. Independent Marine Scientist Alexandria, VA
  • 5. Schedule of Proceedings, Table of ContentsThursday, June 25, 2009Seba, Ph.D., Doug B. “Environmental Update 2009 With Some Cardiovascular Aspects” ...........................................................9Frustaci, M.D., Andrea “Myocardial Trace Elements Imbalance In Idiopathic Dilated Cardiomyopathy”.....................................20Oschman, Ph.D., James L. “Structure and Properties of the Living Matrix”........................................................................................22Heine, Ph.D., Hartmut “The Structural Principle of the Human Myocardium”..............................................................................30Rea M.D., William J. “Environmental Aspects of Cardiovascular Disease”................................................................................33Coppock, DVM, Robert W. “St. Anthony’s Fire in Veterinary Medicine”............................................................................................41Kilburn, M.D., Kaye H. “Heart Disease 2009 World Trenets and Causes” .....................................................................................51Klinghardt, M.D., Ph.D., Dietrich K. “The Role of Neural Therapy in Modulating the Involvement of the Autonomic Nervous System in Cardiovascular Disease” ...........................................................................................................................61Meggs, M.D., Ph.D., William J. “Diet, Inflammation, and Atherosclerosis” ...............................................................................................64Bhatnagar, Ph.D., Aruni “Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants" - Part I”........................73Hillman, Ph.D., Donald “Cardiovascular Response to Electric and Magnetic Fields”.....................................................................82Schedule of Proceedings, Table of ContentsFriday, June 26, 2009Sinatra, M.D., Stephen T. “Metabolic Cardiolgy-The New Emerging Frontier”.................................................................................95Stark, M.D., Martha “Murmur of the Heart: The Story It Tells When We Listen”...................................................................111Suleman, M.D., Amer “Heart Rate Variability As Predictor of Sudden Death” .........................................................................120
  • 6. Friday, June 26, 2009Monro, M.D., Jean “Fructose Metabolism: A Toxic Challenge”............................................................................................122Simon, M.D., Theodore R “Nuclear Medicine In Cardiac Disease Update 2009”............................................................................136Frampton, M.D., Mark W. “The Cardiovascular Consequences of Particulate Air Pollution”...........................................................142Reiter, Ph.D., Russel, J. “Melatonin: Role in Blood Pressure Regulation”....................................................................................144Overberg, Ph.D., Ron “Nutrition Tips for Cardiovascular Disease” ..........................................................................................150Abou-Donia, Ph.D., Mohamed B. “Splenda Alters Gut Microflora in Male Rats”........................................................................................159Patel, M.D., Kalapana “Role of Heart Rate Variabilityin the Practice of Environmental Medicine”...........................................169Rizzo, M.D., Carmelo “Urticaria and Vasculitis in Patients with HCV”.....................................................................................171Suleman, M.D., Amer “Syndromes of Orthostatic Intolerance”..................................................................................................174Saturday, June 27, 2009Coppock, DVM, Robert W. “Mycotoxins and The Heart”...................................................................................................................179Roberts, Jr., M.D., James “Immunomodulation in Atherosclerosis and Heart Failure”....................................................................196Klinghardt, M.D., Ph.D. Dietrich K. “Cavitation in the Jawbone, the Vagus Nerve, and the Heart.”................................................................220Rea, M.D., William J. “Environmental Aspects in the Treatment of Cardiovascular Disease”...................................................222Meggs, M.D., Ph.D., William J. “Accelerators of Atherosclerosis”............................................................................................................232Sinatra, M.D., Stephen T. “Energy Medicine-Good Vibes vs Bad”.................................................................................................241Patel, M.D., Kalapana “Environmental Aspects of Lyme Disease and Autonomic Deregulation”..............................................254Hillman, Ph.D., Donald “The Electropathic Stress Syndrome--Neuroendocrine Responses to EMF”...........................................256
  • 7. Saturday, June 27, 2009Bhatnagar, Ph.D., Aruni “Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants - Part II”..........................268Abou-Donia, Ph.D., Mohamed B. “Splenda Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Rats”.......................................276Sunday, June 28, 2009Frustaci, M.D., Andrea “Selenium And Zinc Deficient Cardiomyopathy In Human Intestinal Malabsorption”...........................285Monro, M.D. Jean “Aspects of Tissue Oxygenation”............................................................................................................287Heine, Ph.D., Hartmut “Cardiocyte-Fibroblast Coupling. Basis for Myocardial Functioning”....................................................298Kilburn, M.D., Kaye H. “Heart Disease and Rotten Egg Gas”.......................................................................................................300Reiter, Ph.D., Russel J. Melatonin Protects Heart From Free Radical Damage”...........................................................................307Jaeckle, M.D., Richard, “The Crosstalk Between the Central and Autonomic Nervous System”..................................................318
  • 8. THURSDAY, JUNE 25, 2009OBJECTIVES & ABSTRACTS
  • 9. Objectives & NotesDoug B. Seba, Ph.D. Date of talk: Thursday, June 25, 2009, 9:10 a.m.107 S. West Street, #430 Phone: 703/949-1055Alexandria, VA 22314Training: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 notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 10. Global Environmental Update 2009: Aspects of Cardiovascular Disease Douglas B. Seba ObjectivesAt the end of this Presentation, the participant should be able to: 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. AbstractThe earth is both a dry/dusty and a wet/moldy place. Both may be increasing in the natural environment perhaps aidedby climate change. The world is also a geomagnetic water planet under constant solar/cosmic radiation. There is nodoubt that a great deal of man-made items (chemical, physical, biological) are being impressed on these epochalgeologic events. There also appears to be an increase in these man-made moieties in indoor environments as humansspend more time in enclosed structures particularly with air conditioning. For more than a quarter-century thisSymposium 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 subtleand hidden exposures that are paramount in both their diagnosis and treatment. It is central to the theme ofenvironmental illness to correctly realize this relationship to often hidden or under appreciated exposures and theirconnection to chronic disease including the heart.It is the Presenter’s experience that the environmental scientists and physicians at this Symposium are probably themost qualified to help chronically ill patients cope with daily exposures to hidden heart stressors. From thatperspective, this is a very limited review to set the tone for this Symposium. Highly selected examples of the abovenatural and man-made processes are taken from a mix of media, websites, and scientific publications relevant to thecurrent 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 CapeVerde 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)November2008pp 800-807 DOI: 10.1097/EDE.0b013e31818131ef03. 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, March24, 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 07March 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’. NatureChemical 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
  • 11. 12. Brauner EV et al. Indoor Particles Affect Vascular Function in the Aged-An Air Filtration-based InterventionStudy. 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 FibreToxicology 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 Originatingfrom 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 pp1085-1095. 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, AmericanGeophysical 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 16February 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 2008DOI: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 theEnvironment. 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 Press2008 400 p $28 ISBN: 978-0-19-530067-3
  • 12. Objectives & NotesAndrea Frustaci, M.D. Date of talk: Thursday, June 25, 2009, 9:40 a.m.La Sapienza University Phone: 39/0630155231Heart and Great Vessels Department Fax: 39/063055535Viale del Policlinico 155 Email: biocard@inmi.itRome, 00161ItalyTraining: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”At the end of this Presentation, the participant should be able to: 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 entityThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 13. Marked Elevation of Myocardial Trace Elements in Idiopathic Dilated Cardiomyopathy Compared With Secondary Cardiac Dysfunction ANDREA FRUSTACI, MD Department 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 variousforms of cardiac failure.Background: Both myocardial TE accumulation and deficiency have been associated with the development of heart failureindistinguishable 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-freetechnique, 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 andskeletal muscle surgical biopsies from 10 pts with mitral stenosis and normal LV function 3) LV endomyocardial biopsies fromfour normal subjects.Results: A large increase (>10,000 times for Hg and Sb) of TE concentration has been observed in myocardial but not in muscularsamples in all pts with IDCM. Pts with secondary cardiac dysfunction had mild increase (s 5 times) of myocardial TE and normalmuscular 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. 20ng/g) higher than controls.Conclusion: A large, significant increase of myocardial TE is present in IDCM but not in secondary cardiac dysfunction. Theincreased concentration of TE in pts with IDCM may adversely affect mitochondrial activity and myocardial metabolism andworsen cell function.
  • 14. Objectives & NotesRobert W. Coppock, DVM Date of talk: Thursday, June 25, 2009, 10:30 a.m.Toxicologist and Assoc Ltd Phone: 780/632-6122P O Box 2031 Fax: 780/632-4492Vegreville, AB T9C 1T2 Email: rcoppock@toxicologist.caCanadaTraining:Current Job Description: Private practice in toxicologyDisclosure Statement:SPEECH TITLE: “St. Anthony’s Fire in Veterinary Medicine”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 15. St. Anthony’s Fire in Veterinary Medicine Robert W. Coppock, DVM, PhD, DABVT, DABTErgotism is the oldest mycotoxicosis known and historical references to ergotism include the names ignis sacer andSt. Anthony’s Fire. Claviceps and other ergot-producing species invade and replace the ovary in grassesincluding cereal grains. Wet cool weather favors fungal infection of the florets. The initial stage is soft white fungalmass (sphacelium) that produces sugary honeydew and conidia. The sphacelium form a hard dry sclerotium (restingform) that is resistant to degradation and contain the ergot alkaloids. Ergot alkaloids target the vascular system andother organs and systems. In field poisoning, domestic animals are exposed to mixtures of ergot alkaloids. Themixtures 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 peripheralblood arterioles. Vasoconstriction causes necrosis of distal appendages and skin. The pattern of vasoconstriction variesand can be unique to a particular occurrence. Ischemic bowl syndrome can occur. Cattle have been observed toselectively graze the flowering parts of brome grass infected with Claviceps purpura at the honeydew stage ofdevelopment. This pattern of grazing resulted in ergotism in Holstein heifers that caused skin necrosis on the bodytrunk 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 mostcommon infected grass is tall fescue. The endophyte is symbiotic with fescue and improves its tolerance toenvironmental stressors.
  • 16. Objectives & NotesHartmut Heine, Ph.D. Date of talk: Thursday, June 25, 2009 11:00 a.m.Billerbeckweg 1-3 Phone: 49 (0) 7234 6246D-75242 Neuhausen, Fax: 49 (0) 7234 949109Germany Email: hartmutheine@aol.comTraining:Current Job Description: Private Scientific Research Institute Professor emeritus of Anatomy Formally full professor and head of the Department of Anatomy and Clinical Morphology of the University of Witten/Herdecke, GermanyOther Information: Heine H, Schaeg G. Kann die Tumorstammzelle morphologisch charakterisiert werden? Deutsche Zeitschrift für klinische Forschung 2008; 12: 42-45Disclosure 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 notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 17. The Structural Principle of the Human Myocardium Hartmut HeineRefering 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 andconnective tissue fibers appears in longitudinal and cross sections of the myocardium (Fig. 2). Superimposedtransparent folia with straight lines shifted randomly or in a distinct angle against each other also show rhomboidalpatterns which are analogous to histologically cuts of the myocardium (Fig. 2). The patterns change with every changein the sectional direction. This means that the myocardium is nowhere structured uniformly. This is the very reason forthe 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 despiteall similarity of the rhombi. These however, are only self-similar exposing the heart function as a non linear determinedchaotic 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 fibrediameter of approx. 0.5 mm, the ventricular wall consists of approx. 80 layers of muscle fibres. When 80 straight linesare randomly superimposed in a computer simulation, an image of many self-similar little rhombi results in much thesame way as can be seen in the myocardial sections (Fig. 3). By way of spatial reconstruction, a coiled intertwinedhyperboloid 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 energyexpenditure at maximum efficiency (by the way this principle applies to all organs) (Fig. 3). In such a non-linearsystem, any errors, once occurred, are not eliminated, with new errors adding to the previous ones. This can beobserved with all cardiac diseases, because both the muscular and the fibrous hyperboloids may suffer pathologicalstructural alterations separately or jointly, interfereing hyperboloid power transmission. Thus, disturbances of thishyperboloid principle have relations to all cardiac diseases (Heine 1989).ConclusionsThe structural principle of the heart consists of matching muscular and connective tissue hyperboloids pervading eachother. Expressed in simplified terms, there are two forms of hyperboloids in the heart (Fig. 3): one is made up of themuscle fibres, and the complementary one of the interstitial connective tissue, resulting in a hyperboloid joint as isused, for example, in engineering the transmission of rotations from one shaft to another one of any direction. Allcardiac 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 Herzdes 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
  • 18. Objectives & NotesWilliam J. Rea, M.D. Date of talk: Thursday, June 25, 2009, 11:30 a.m.Environmental Health Center - Dallas Phone: 214/368-41328345 Walnut Hill Lane, Ste. 220 Fax: 214/691-8432Dallas, TX 75231 Email: wjr@ehcd.comTraining: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 CenterBoard Certifications: American Board of Surgery, American board of Thoracic Surgery, American Board of Environmental MedicineOther Information: Author of “Chemical Sensitivity I-IV”, “Optimum Environments for Optimum Health”Disclosure Statement:
  • 19. Objectives & NotesJames L. Oschman, Ph.D. Date of talk: Thursday, June 25, 2009 1:30 p.m.Natures Own Research Association Phone: 603/742-3789P.O. Box 1935 Fax: 603/742-4695Dover, NH 03821 Email: joschman@aol.comTraining: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, 2003 About 30 papers in leading scientific journals, and about an equal number in complementary medicine journals.Disclosure Statement:SPEECH TITLE: “Structure and Properties of the Living Matrix”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center isnot responsible for the contents of this presentation. AEHF has not altered or modified the contents of theinformation provided by this speaker.
  • 20. Objectives & NotesKaye H. Kilburn, M.D. Date of talk: Thursday, June 25, 2009, 2:00 p.m.P.O. Box 5374 Phone: 626/798-4299Pasadena, CA 91107 Fax: 626/798-3859 Email: khkilburn@sbcglobal.netTraining: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 2004Disclosure Statement:SPEECH TITLE: “Heart Disease 2009 World Trenets and Causes”At the end of this Presentation, the participant should be able to: 1. Describe the chemical causes of myocardial infarction and differentiate these from the familiar "riskfactors." 2. Track the historical evolution of myocardial infarction in the twentieth century 3. Understand role of nanoparticles in hypertension, vascular disease and thrombosis.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 21. Heart Disease 2009: Trends and Causes By Kaye H. Kilburn, M.D. USC Keck School of Medicine (ret.) Neuro-Test Inc., Pasadena, CA 91107AbstractThree coincidences made me wonder and question: what causes coronary heart disease (CAD) and myocardialinfarction (MI)? The accepted risk factors: cigarette smoking, hypertension and elevated total serum cholesterol wereacknowledged 40 years ago. Missing was the proximate cause. Chemical causation was suggested when Chet who hadan acute coronary occlusion with MI the day he inhaled two or three breaths of chlorine. Barney had severe anginapectoris after less than 5 minutes of exposure to chlorine and showed multi-vessel coronary disease within 3 years. Thethird 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 workersand other men for 20 years. In the 1960’s, the rising rate in the comparison groups that included many cigarettesmokers made the rates nearly identical. Probably increased inhalation of side stream cigarette smoke and fossil fuelcombustion products raised the general population’s deaths from heart disease to wipe put the previous rayon workerdifference. 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 tauntedto react go with the flow, to migrate easily from pulmonary veins first to arteries, the coronaries, the aorta, carotids tothe brain, kidneys, and the other organs and limbs. In the past decade, mankind’s worldwide bane of CAD, killer ofmore than 6 million human beings each year has been identified as an inflammatory cascade in arteries. Myocardialinfarction and stroke responsible for another 4.5 million deaths per year thus are not just plaques, collections of lipidslike grease, but are inflammatory lesions of transmuted cells. Current focus on ‘How can this process be interrupted orpatched 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 theUnited States and Great Britain was accessible with emergency response for chest pain so that untoward delay does notseem a factor. The broad age spectrum of serious coronary events was recognized in the 1950’s although women werediagnosed less frequently than men. None of these factors explains the orders of magnitude jump in the incidence andmortality of CAD and MI.Of the accepted risk factors only inhaled chemicals from smoking cigarettes are a cause. In contrast, hypertensionmeasures vascular over-response. Caloric over-indulgence obesity, and elevated cholesterol levels, are factors in onlyhalf of the CAD patients.The other twentieth century smoke is from fuel burning in cars and trucks. This profligate gas and diesel use pollutesair, water and soil with hydrocarbons and particles. Picture 90 million personal cigarette “smokestacks” in the sea ofexhaust pipe smog. Add to the burdens, the chemicals to make plastics by combining chlorine with hydrocarbons bythe petrochemical industry. Many chlorinated hydrocarbons like tricholoroethylene disorder heart rhythms, inducearrhythmias and may incite CAD.Gasoline and diesel exhaust exposure increased logarithmically after 1945 to be nearly exponential (doubling eachdecade). Air pollution disasters caused deaths from pulmonary disease in New York and London in 1952 and led toregulation. But the adverse effects of cigarette smoking clearly exceeded those of air pollution. Proof of the later isinferred from the increases in background lung cancer rate over this period. Now the rate for men and women whonever 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 isinhaled fossil fuel combustion products which supports their consideration as causal factors for CAD-MI. Burning coalincreased 10 fold, but petroleum (oil) increased more than 3,000 times in the twentieth century. From 1 million tons ofoil production and use in the United States in 1870, it is now over 7,000 million tons.
  • 22. In the 1960’s, the Los Angeles area compared to the rest of California showed that the highly urbanized south coast airbasin exposes nearly 15 million people to smog. This exposure now extends up Cajon Pass to Barstow exposing highdesert people to fossil fuel combustion chemicals from the basin. Similar smog saturation that in 1960 characterizedKern 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 heartdisease of rates in these smog saturated conurbations with wind swept poorly populated areas show adverse healtheffects of air pollution.The development of artificial kidney machines seemed just in time for the epidemic of kidney failure. Large amountsof Medicare funds support biweekly dialysis and selecting candidates for transplantation of someone else’s kidney hasbecome an ethical dilemma adding to its economic impact. Diabetes and interstitial kidney disease related to chemicalexposures, especially to solvents, provide a constantly growing flow of patients to dialysis/transplant centers andpresent 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 andcirrhosis for patients in public hospitals. The obstructed macrovessels cause MI, stroke and blocked peripheral vesselsin 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 betterhealth.ReferencesBedford 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?, EnvironHealth Perspect, 2005; 113: 915-919.Bell DM, Fair MA, Elnicki DM, et al, Characteristics of West Virginians Having Myocardial Infarction, SouthernMedical Journal, 1998; 91: 1042-1045.Chen L, Yokel RA, Henning B, et al, Manufactured aluminum oxide nanoparticles decrease expression of tight junctionproteins 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 Massand 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 courseof 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, JAMA1987; 257: 2318-2324.Fabbri LM, Saetta M, Picotti G and Mapp CE: Late asthmatic reactions, airway inflammation and chronic asthma istoluene-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 retrospectivecohort 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 of187,766 Men, JAMA 1954; 1316-1328,Heart Protection Study Collaborative Group, MRC/BHF Heart Protection Study of cholesterol-lowering withsimvastatin 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.
  • 23. Hennekens CH, Increasing Burden of Cardiovascular Disease: Current Knowledge and Future Directions for Researchon Risk Factors, Circulation. 1998; 97: 1095-1102.Holland WW, Bennett AE, Cameron IR, Florey CV, Leeder SR, Schilling RSF, Swan AV and Waller RE: Healtheffects 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 cellmetaplasia, 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 (AnAnalysis 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 Toxicol1995;4:267-276.Kilburn KH: Leukocyte recruitment to airways by cigarette smoke and particle phase in contrast to cytotoxicity ofvapor. Science 1975;189:634-637.Kilburn KH and McKenzie WN: Leukocyte recruitment to airways by aldehyde-carbon combinations that mimiccigarette 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: isthis 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 RespiratoryCells, Environ. Health Perspect., 2005; 113: 956-963.Peters A, Veronese B, Calderón-Garcidueñas L, et al, Translocation and potential neurological effects of fine andultrafine 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 HeartAssociation, 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. MalePhysicians, Ann Intern Med. 1994; 120: 458-462.Saldana TM, Basso O, Hoppin JA, et al, Pesticide exposure and self-reported gestational diabetes mellitus in theAgricultural 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.
  • 24. Objectives & NotesDietrich K. Klinghardt, M.D., Ph.D. Date of talk: Thursday, June 25, 2009, 2:30 p.m.Institute of Neurobiology Phone: 425/688-8818P.O. Box 5023 Fax: 425/453-7015Bellevue, WA 98007 Email: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 writtenthat 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 inCardiovascular Disease”At the end of this Presentation, the participant should be able to: 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 American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 25. 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 tosuccessfully modulate ANS-regulation, function and neurotransmitter release. The ANS is directly involved innumerous aspects of cardiac function: the dual innervation (sympathetic and parasympathetic) of the SAand AV nodes, up- and down-regulates aspects of the cardiac rhythm. The sympathetic innervation of thecoronary arteries allows for maximum vasodilatation in acute stress situations to maximize flight and fightresponses. The sympathetic fibers and their neurotransmitter release into the cardiac muscle sensitizes theheart 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 ganglia c. 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 ownganglia which communicate with the brain ( Lacey, J. I. and B. C. Lacey (1978). Two-way communicationbetween 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 andefferent neurons (connecting the heart to far away places such as the amygdala). Many systemic healthproblems - such as some cases of chronic depression - can be an expression of a failure of communicationbetween heart and brain rather then a brain problem. The intrinsic system also responds to input from withinthe heart and is capable of regulating virtually any aspect of cardiac function – this made the heart transplantpossible. The heart’s intrinsic nervous system is vital for the maintenance of cardiovascular stability andefficiency. 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 thebrain (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 dopamine 3. oxytocinSegmental therapy, the stellate ganglion block in combination with a sphenopalatine ganglion block, andintravenous 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 EKGsignals on the wrist, ankles etc. These signals seem to have an integrating effect for all our physiologicalsystems 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, gutdysbiosis evaluation (urine organic acids, parasitology) and other localizing tests are helpful to select themost 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
  • 26. • 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 inmany countries as a safe, inexpensive and effective adjuvant in cardiology.
  • 27. Objectives & NotesWilliam J. Meggs, M.D., Ph.D. Date of talk: Thursday, June 25, 2009, 3:30 p.m.Brody School of Medicine, East Carolina University Phone: 252/744-2954600 Moye Blvd., Room 3ED311. Fax: 252/744-3589PCMH, 3ED-311, Department of Emergency Medicine Email: meggsw@ecu.eduGreenville, NC 27834-4354Training: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”Disclosure Statement:SPEECH TITLE: “Diet, Inflammation, and Atherosclerosis”At the end of this Presentation, the participant should be able to: 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 AtherosclerosisThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 28. 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 atherosclerosisAbstractAtherosclerosis is a natural part of the aging process. Inflammation is a major mechanism that the body usesto produce the planned obsolescence mediated by atherosclerosis. The leading causes of death inindustrialized countries are myocardial infarctions and strokes, the end-stage manifestations ofarthrosclerosis. The age at which the manifestations of atherosclerosis become clinically relevant is acomplex blend of genetic and environmental factors. Diet is a major determinant of the rate at whichatherosclerosis progresses. While we cannot at present control a genetic predisposition to early onset ofatherosclerosis, environmental and dietary factors are controllable at an individual’s discretion. Dietary andother interventions that can reduce one’s risk of heart attacks and strokes will be discussed.ReferencesLibby: Braunwalds 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 AgricFood Chem 2004;52:4026-37Wan Y et al. Effects of cocoa powder and dark chocolate on LDL oxidative susceptibility and prostaglandinconcentrations 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.
  • 29. Objectives & NotesAruni Bhatnagar, Ph.D. Date of talk: Thursday, June 25, 2009, 4:00 p.m.University of Louisville Phone: 502/852-5724580 S. Preston St. Fax:The Baxter II, Room 421 Email:Louisville, KY 40202Training: Post-doctoral training in cellular cardiac electrophysiologyCurrent 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 IAt the end of this Presentation, the participant should be able to:These talks are to discuss the contribution of exposure to environmental pollutants to heart disease. Specific issues thatwill be discussed include evidence implicating that exposure to particulate air pollutants and gaseous co-pollutantsincreases CVD risk. Data relating to an increase in both acute and chronic risk will be examined. The effects of otherpollutants such as metals and aldehydes will also be discussed. 1. Estimate risk due to exposure to particulate air pollution 2. Understand the impact of the environment of cardiovascular disease 3. Understand the pathophysiological mechanisms that impart and mediate the effects of the environment on acute cardiovascular events as well as chronic atherosclerotic diseaseThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 30. Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants Aruni Bhatnagar, Ph.D., FAHA, Division of Cardiology, Department of Medicine, University of Louisville, Louisville, KYHeart disease is the leading cause of death in the industrialized world. The rates of heart disease, however, vary fromone country to another. Geographic variations in CVD mortality probably reflect genetic, social, and cultural factors aswell as disparities in health care. Nevertheless, epidemiological data suggest a strong influence of environmentalfactors, since rates of CVD incidence and mortality could be markedly altered within a generation, indicating that CVDrisk is in large part derived from environmental factors.How the environment influences heart disease is not well understood. Multiple studies suggest that environmentalfactors such as smoking, nutrition, and physical activity are key factors that determine CVD risk. Nevertheless, itremains unclear how these factors contribute to the incidence and the severity of heart disease. In addition, thepathologic mechanisms by which environmental factors influence specific features of heart disease remain largelyunknown. Epidemiological evidence indicates that CVD risk is derived from several variant and invariant “riskfactors” such as high cholesterol, blood pressure, diabetes and smoking. In addition, exposure to environmentalpollutants has also emerged as a new risk factor for the development of heart disease. Extant literature provides ampleevidence 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 fora significant association between particulate air pollution levels and short-term mortality as well as increased mortalityrisk due to long-term exposure.Over 100 epidemiological studies report a link with daily fluctuations in air pollutants at relatively low commonlyencountered levels of air pollutants in several urban areas throughout the world events. Consistent positive relationshipsbetween daily PM10 levels and mortality counts have been reported by studies using either time series modeling or acase-cross over design. The strength of association appears to be stronger for PM 2.5 than PM10, indicating that PM2.5may 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 changingcovariants. Nevertheless, consistent associations have been reported for risk of death from all causes, but particularlyfrom cardiopulmonary disease. In some studies significant associations have also been reported for sulfur oxideconcentrations, while others have found no association with common copollutants (NO2, SO2, CO, and O3). For obviousreasons, no controlled toxicological studies with mortality as an end point have been conducted to experimentally verifythe 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 - theHarvard six cities and the American Cancer Society cohort studies report a significant positive association betweencardiopulmonary mortality and PM2.5 and sulfate concentrations. No excessive mortality risk was associated withexposure 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 %) thanobserved 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 inflammationresults in an increase in atherogenesis, thrombosis and endothelial dysfunction. Environmental effects on atherogenesisare poorly understood. Data from Watanbe heritable hyperlipidemic rabbits show that repeated intrapharyngealinstillation of PM10 (twice a week for 4 weeks) stimulates progression of atherosclerotic plaques and increases lipidaccumulation in aortic lesions as well as plaque cell turnover. These observations suggest exposure to PM 10 couldaccelerate atherogenesis and potentially enhance the vulnerability of atherosclerotic plaques to rupture. In addition toair pollution and tobacco smoke, there is extensive evidence suggesting that exposure to metals also acceleratesatherogenesis.Exposure to arsenic in particular has been linked to an increase in atherosclerotic disease. Studies with humanpopulations exposed to arsenic in well water in Taiwan suggest that the incidence of CVD depends upon the level ofexposure to arsenic Epidemiological studies of regions with high arsenic levels in the ground water show a markedincrease in several forms of CVD including carotid atherosclerosis, hypertension, and ischemic heart disease. Arsenicexposure is also associated with peripheral atherosclerosis, which severely decreases blood flow to extremities and
  • 31. result in gangrene. In Taiwan and Bangladesh, gangrene is most commonly present on feet leading to the characteristicblackfoot disease. Consumption of arsenic contaminated drinking water is also associated with an increase incardiovascular mortality in the U.S.Exposure to pollutants could also increase thrombosis. Platelets from smokers demonstrate an increase in spontaneousas well as agonist (ADP, thrombin) stimulated aggregation. In addition, PM can contribute to the development andmaintenance of a pro-thrombotic state. This is supported by studies demonstrating a positive correlation between PM10exposure, plasma levels of fibrinogen and an increase in blood viscosity. Similarly, ultrafine particles increase plateletnumber, 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 demonstratingassociations between exposure and hospitalizations for ischemic heart disease. Most prominent among theseatmospheric gases include ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen oxides (NO2). Ozoneexposure, 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 concentrationsin cigarette, cotton, wood, and coal smoke. The specific contribution of aldehydes to the cardiovascular effects of trafficair pollution, however, remains to be fully assessed. In a recent study on the cardiovascular effects of traffic exposureon highway patrol troopers, aldehydes were strongly correlated with an increase in plasma von Willebrand factor andchanges in heart rate variability. Cardiovascular toxicity of environmental aldehydes is also underscored by studiesshowing increased risk of atherosclerotic disease in plant workers producing formaldehyde and a higher incidence ofheart disease in undertakers, embalmers and perfumery workers who are exposed to high levels of aldehydes during thecourse of their work. Nevertheless, it remains unclear whether exposure to ambient levels of aldehydes is associatedwith an excessive CVD risk and whether long-term repeated exposures to aldehydes has broad impact on cardiovascularfunction 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 contributeprogressively to disease and dysfunction. Although some cardiovascular diseases (such as familialhypercholesterolemia or the long Q-T syndrome) have clear, well-defined genetic origins, the most common forms ofCVD develop in response to environmental injury. This injury might result from excessive consumption of saturatedfat, lack of exercise or from continuous exposure to environmental pollutants. In each case, disease appears to developfrom failed responses to repair injury and to restore normal function rather than from common genetic flaws thatmanifests to greater severity with increasing age. During disease development genetic factors undoubtedly play animportant role in modulating environmental influences. As a result, individuals with different genetic makeup displaydifferent susceptibilities to environmental insults. Nevertheless, given its high prevalence, CVD is unlikely to beentirely or even substantially regulated by genetics. For the same reasons, it is also unlikely that the environment playsa secondary role in the etiology of CVD. Migrant population studies and studies within the same population withchanging environment (lifestyle choice, nutrition, etc) have shown that significant changes in the environment couldsubstantially alter CVD risk. Both population-based cohort studies and animal experiments have provided ample datato 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 andthrombosis. This evidence suggests that environments that induce systemic inflammation or increase oxidative stressexacerbate atherogenesis, because both inflammation and oxidative stress are key contributors to atherosclerotic lesionformation. Nevertheless, it is not clear whether there are common sets of mechanisms by which environmental agentsimpair 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.
  • 32. Objectives & NotesDonald Hillman, Ph.D. Date of talk: Thursday, June 25, 2009, 4:30 p.m.Michigan State University Phone: 517/351-9561750 Berkshire Lane Fax: 517/351-1944East Lansing, MI 48823 Email: donag1@aol.comTraining: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.Disclosure Statement:SPEECH TITLE: “Cardiovascular Response to Electric and Magnetic Fields”At the end of this Presentation, the participant should be able to: 1. Recognize sources of EMF exposure in the living environment 2. Understand common neural pathways of electrical exposure 3. Measure cardiovascular response to EMFThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 33. 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 EastLansing and on a farm near Leslie, Michigan. The utility’s primary neutral-to-ground wire (PN-G) connected to agrounded-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) potentialbetween 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 andhypertension after nine 46-kiloVolt (kV) transmission lines were built over his workspace and radiated 2.5-6.5 mG athead height near his grain-storage building. A challenge exposure to 2-4 mG EMF in a medical laboratory confirmedthe patient’s cardiovascular symptoms and sensitivity to EMF. The findings help to explain the increase ofhypertension observed by the American Heart Association (AHA), and concur with cardiovascular changes of workersin 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 aHigh School Teacher of Vocational Agriculture and County Extension Agent 1951-55. He studied environmentaleffects on dairy cattle performance and investigated effects of electric and magnetic fields on behaviour, health, andproductivity of dairy cattle in some 110 herds assisting farmers, veterinarians, electricians, and engineers in problemcases. He is a member of The American Dairy Science Association-Am..Soc.of Animal.Science, and the AmericanSociety of Agricultural and Biological Engineers. He has investigated EMF effects on humans and other species andserves as a private consultant regarding EMF effects on dairy cattle.Selected Digital References: http://www.powerwatch.org.uk/science/studies.asp http://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/ EMF-Cardiovascular Disease ReferencesAdey, W. R., F. M. Bawin, and A. F. Lawrence, 1982. Effects of weak amplitude-modulated fields in calcium efflux from awake cat cerebral cortex. J. Bioelectromagnetics Soc. 3:295-308.Bawin, S. M., L. K. Kaczmarek, and W. R. Adey. 1975. Effects of modulated VHF fields on the central nervous system. Space Biol. Lab, Braqin Research Institute, U. CA, Los Angeles, Annals NY Academy of Science 247:74-81.Becker, Robert O. 1990. Cross Currents , The Perils of Electropollution– the Promise of Electromedicine. Jeromy P. Tarcher/Perigee Books, The Putnam Publishers, New York, NY.Berne, Robert M., Mathew N. Levy, Bruce M. Koeppen, and Bruce A. Stanton. 1998. Physiology. Fifth Edition, Mosby, Elsevier Inc., Philadelphia. PA, USA.Blackman, C. F., S. G. Benane, D. J. Elliot, et al. 1988. Influence of electromagnetic fields on the efflux of calcium ions from brain tissue in vitro: a three model analysis consistent with the frequency response up to 510 Hz. Bioelectromagnetics 9:215-227.Bortkiewicz, A., Zmyslony, H., Gadricke, E. 1998. Exposure to electromagnetic fields with frequencies of 50 Hz and changes in the circulatory system in workers at electrical power stations. 1:med Pr. 49(3):261-274 (In Polish: Zakladu Fizjologii Pracy Ergonomii). PubMed.
  • 34. Bortkiewicz, A., E. Gadzicka, M. Zmyslony. 2003. Biological effects and health risks of electromagnetic fields at levels classified by INCRIP as admissible among occupationally exposed workers: a study of the Nofer Institute of Occupational Medicine, Lodz, Poland. 1Med Pr:54(3):291-7.Braune, S., C. Wrocklage, J. Raczek, T. Gailus, and C. H. Lucking. 1998. Resting blood pressure increased during exposure to a radio-frequency electromagnetic field. Lancet 351:1857-1858.Carlo, George, and Martin Schram. 2001. Cell phones invisible hazards in the wireless age. Libr. of Congress ISBN 0-7867-0818-2. Carol and Graf Publishers, Inc., New York, NY.Cook, M., C. Graham, H. D. Cohen, and M. M. Gerkovich. 1994. A replication study of human exposure to 60 Hz fields: effects on neurobehavioral measures. Bioelectromagnetics 13:261-285.Craine, L. B., E. M. Ehlers, and D. K. Nelson. 1969. Effects of distribution system ground voltages appearing on domestic water lines. Paper No. 69-184, ASAE, St. Joseph, MI 49085.Easterly, C. E.. 1982. Cardiovascular risk from exposure to static magnetic fields. J. Am. Ind. Hyg. Assoc. 43:533-539.Funk, Richard H. W., and Thomas Monsees. 2006. Effects of electromagnetic fields on cells: physiological and therapeutic approaches and molecular mechanisms of interaction. Review. Cells Tissues Organs 182:59-78.Gadricka, E., A. Bortkiewicz, M. Zmyslony, and C. Palcznski. 1997. Evaluation of selected functional circulation parameters of workers from various occupational groups exposed to electromagnetic fields of high frequency. III. 24-h monitoring of arterial blood pressure (ABP). Med Pr. 48:15-24. In Polish: Zakladu fizjologii Pracy I Ergonomii, Instytutu Medycyny Prac, Lodzi.Ghione, S., C. Del Seppia, L. Mezzasalma, M. Emdin, and P. Luschi. 2004. Human head exposure to a 37 Hz electromagnetic field: effects on blood pressure, somatosensory perception, and related parameters. Bioelectromagnetics 25(3):167-175.Gorewit, R. C., D.V., Henke Drenkerd, and N. R. Scott. 1984. Physiological Effects of Electrical Current on Dairy Cows. Stray Voltage: Proceedings of the National Stray Voltage Symposium. American Soc. of Agricultural Engineers, ASAE, St. Joseph, MI.Graham, C., M. R. Cook, H, d. Cohen, D. W. Riffle, S. Hoffman, and N. M. Gerkovich. 1999. Human exposure to 60 Hz magnetic fields: neurophysiological effects. Int. J. Psychophysiol 33(2):169-175.Graham, C., M. R. Cook, and M. M. Gerkovich. 1994. A dose response study of human exposure to 60 Hz electric and magnetic fields. Bioelectromagnetics 15:477-463.Havas, Magda, and David Stetzer. 2004. Dirty electricity and electrical sensitivity: five case studies. WHO Workshop on Electrical Hypersensitivity. October 24-25, Czech Republic, Prague. mhavas@trentu.ca.Hillman, Donald. 2005. Magnetic Fields in Homes and School: Source and mitigation in our home. Shocking News #7, 750 Berkshire Lane, East Lansing, MI 48823, donag1@aol.com.Hillman, Donald, Dave Stetzer, William O. English, Martin Graham, Edward Rothwell. 2008. Electromagnetic Fields in Homes, Schools, and Workplaces: 1. Sources of electropathic stress syndrome. Bioelectromagnetics In Press.Hillman1, Donald, Dave Stetzer, William O. English, Martin Graham, Edward Rothwell. 2008. Electromagnetic Fields in Homes, Schools, and Workplaces: 2. Induced Voltage and Current near 46-kV Transmission Lines. (In press).Hillman, D., D.L. Hillman W. J. Rea, Yaqin Pan. Martin Graham, D. Stetzer, W.O. English, and E. Rothwell. 2008. Electric and magnetic fields in homes, schools, and workplaces. 3. The electropathic stress syndrome: cardiac and neuroendocrine responses. (In press).Horowitz, L. N., J. F. Spear, M. E. Josephson, J. A. Kastor, and E. N. Moore. 1979. The effects of coronary artery disease on the ventricular fibrillation threshold in man. Circulation Res. 60: 792-797.Huber, Reto, Jurgen Schudererm, Thomas Graf, Katherine Jutz, Alexander A. Borbely, Niels Kuster, and Peter Acherman. 2003. Radio frequency electromagnetic field exposure in humans: estimation of SAR distribution in the brain, effects on sleep, and heart rate. Bioelectromagnetics 24:262-276Huber, R., T. Graf, A. Cote, L. Wittman, E. Gallman, D. Matter, et al. 2000. Exposure to pulsed high frequency electromagnetic field during waking affects human sleep EEG. NeuroReport 11:3321-3325.Imaida, K., M. Taki, T. Yamaguchi, T. Ito, S-I Watanabi, K. Wake, A. Aimoto, Y. Kamimuri, N. Ito, T. Shirai. 1998. Lack of promoting effects of the electromagnetic near-field used for cellular phones (929.2 MHz) on rat liver carcinogenesis in a medium-term liver bioassay. Carcinogenesis 19:311-314.Johansson, Ollie. 2006. Electrohypersensitivy: state-of-the-art of a fundamental impairment. Electromagnetic Biology and Medicine 25:245-258.Kaune, W. T., T. Dovan, R. J. Kavet, D. A. Savitz, and R. R. Neutra. 2002. Study of high- and low-current- configuration homes from the 1988 Denver childhood cancer study. Bioelectromagnetics 23:177-188.Kennedy, Barry W. 2000. Power Quality Primer, McGraw-Hill, New York, NY.Korpinen, L. and A. Uusitalo. 1993. Influence of 50 Hz electric and magnetic fields on the human heart. Bioelectromagnetics 14:329-340.
  • 35. Lefcourt, Alan M., Stanislaw Kahl, and Michael Akers. 1986. Correlation of Indices of Stress with Intensity of Electric Shock, J. Dairy Sci. 69:833.842.Lyskov, E. B., J. M. Juultilainen, V. Jousmaki, J. Partanen, S. Medvedev, and O. Hanninen. 1993. Effects of 45 Hz magnetic fields on the functional state of the human brain. Bioelectromagnetics 14:87-95.Marino, Andrew A., Erik Nilsen, and Clifton Frilot. 2003. Nonlinear changes in brain electrical activity due to cell phone radiation. Bioelectromagnetics 24:339-336.Marino, Andrew, Thomas J. Berger, B. Peter Austin, Robert O. Becker, and Francis X. Hart. 1977. In Vivo Bioelectrochemical changes associated with exposure to extremely low frequency electric fields. Physiological Chemistry and Physics, Vol 9 (4&5).Montano, N., C. Cogliati, V. J. Dias da Silva, T. Gnecchi-Ruscone, and A. Malliani. 2001. Sympathetic rhythms and cardiovascular oscillations. Auton Neurosci 90:29-34.OSHA. 1997. Directives CPL 2-1.18A - Enforcement of the electrical power generation, transmission, and distribution standard. Effective Date: October 20, 1997. Occupational Safety and Health Administration. U. S. Department of Labor, Washington, D. C.Pakhomov, Andrei G., Satnam P. Mathur, Joanne Doyle, Bruce E Stuck, Jonathan L. Kiel, and Michael R. Murphy. 2000. Comparative effects of extremely high power microwave pulses and a brief CW irradiation on pacemaker function in isolated frog heart slices. Bioelectromagnetics 21:245-254.Rea, William J., Yagan Pan, Ervin J. Fenyves, Tehiko Sujisawa, Hideo Suyama, Nasroli Samadi, and Gerald H. Ross. 1991. Electromagnetic Field Sensitivity. Bioelectricity 10(1&2):241-256.Reilly, J. Patrick. 1998. Applied electricity from electrical stimulation to electropathology. Springer-Verlog, NY, adapted from the same title, Cambridge University Press, 1992.Richardson, Alfred W. 1959. Blood Coagulation Changes Due to Electromagnetic Microwave Irradiations. Office of Naval Research and St. Louis University School of Medicine, St. Louis, Mo.Robinson, C. F., M. Peterson, and S. Palu. 1999. Mortality patterns among electrical workers in the U.S. construction industry. Amer J Industrial Med. 36:630-637.Sage, Cindy. 2007. BioInitiative: A Rationale for a Biologically-based Exposure Standard for Electromagnetic Radiation. Compiled reviews of research by 14 noted scientists. Available on line: www.bioinitiative.org.Sait, M. L., et al. 1999. A study of heart rate and heart rate variability in human subjects exposed to occupational levels of 50 Hz circular polarized magnetic fields. Med Eng Phys 21:(5):361-369.Sastre, A., C. Graham, and M. R. Cook. 2000. Brain frequency magnetic fields alter cardiac autonomic control mechanisms. Clin Neurophysiol 111:1942-1948.Sastre, A., M. R. Cook, and C. Graham. 1998. Nocturnal exposure to intermittent 60 Hz magnetic fields alters human cardiac rhythm. Bioelectromagnetics 19:98-106.Shirakawa, S., W. J. Rea, S. Ishikawa, and A. R. Johnson. 1986. Evaluation of the autonomic nervous system by pupillographical study in the chemically sensitive. Microwave News 10:5-14.Smith, C. W., R. V. S. Choy, and J. A. Monro. 1989. The diagnosis and therapy of electrical hypersensitivity. J. Clin Ecol 6:119-128.Smith, C. W. and S. Best. 1989. Electromagnetic Man. St. Martins Press, New York.Stetzer, Dave. 1999. Effects of low-level nonlinear voltage applied to cows. Video tape of cattle and horse movements in relation to oscilloscope record of transients. Stetzer Electric Inc., Blair, Wisconsin, USA. Dave@stetzerelectric.com.Szmigielski, S., A. Bortkiewicz, E. Gadzicka, M. Zmyslony, and R. Kubacki. 1998. Alteration of diurnal rhythms of blood pressure and heart rate to workers exposed to radiofrequency electromagnetic fields. Blood Press Monit 3(6):323-330.Thaker, Jay. 2007. Okemos high school science project shows ipods interfere with pacemaker function. Presented at American Arrhythmia Association, Annual Meeting, Denver, Colorado. Lansing State Journal, May 2007.Tikhonova, G. I. 2003. Heart Disease of personnel of the civil aircraft radio-tracking system in Russia. Radiatsionnaia biologiia, radio-cologiia/Rossiiskaia akademia nauk. Sept-Oct., 433(5):559-564. Research Institute of Occupational Health, Moscow, 105275 Russia.Van Wijngaarden, Edwin, David A. Savitz, Robert C. Kleckner, Jainwen Cai, and Dana Loomis. 2000. Exposure to electromagnetic fields and suicide rate among utility workers: a nested case-control study. Occu Environ Med 57:258-263.Varani, Katia, Stefania Gessi, Stefania Merighi, Valeria Iannotta, Elena Cattsbriga, Susanna Spissani, Rugerro Cadossi, and Pier Andrea Bores. 2000. Effect of Pulsed EMF on A2 a Adenosine Receptors in Human Neutrophils. British Journal of Pharmacology, 136:57-66.Weaver, R. A. 1973. Human circadian rhythms under the influence of weak electric fields and the different aspects of these studies, Int. J. Biometeor. 17:227-237.
  • 36. Zaffanella, L. E. 1993. Survey of residential magnetic field sources. Electric Power Research Institute, TR-102759, Vol 1-2, Palo Alto, CAZhao, M., H. Bai, E. Wang, J. V. Forrester, and C. D. McCaig. 2004. Electrical stimulation directly induces pre- angiogenic responses in vascular endothelial cells by signaling VEGA receptors. J. Cell Sci 117:397-405.Zipse, Donald. 2002. The hazardous multigrounded neutral distribution system and dangerous stray currents. Zipse Electrical Engineering, Inc., Wilmington, Delaware.
  • 37. FRIDAY, JUNE 26, 2009OBJECTIVES & ABSTRACTS
  • 38. Objectives & NotesStephen T. Sinatra, M.D. Date of talk: Friday, June 26, 2009, 8:05 a.m.Optimum Health Phone: 860/645-3825257 E. Center Street Fax: 860/643-2531Manchester, CT 06040 Email: stsinatra@msn.comTraining: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.Disclosure Statement:SPEECH TITLE: “Metabolic Cardiolgy-The New Emerging Frontier”At the end of this Presentation, the participant should be able to: 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 managementThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 39. Metabolic Cardiology A New Paradigm for the Prevention and Treatment of Heart DiseaseMetabolic therapy involves the administration of a substance normally found in the body to enhance ametabolic reaction within the cell. Such therapy may be achieved in two ways. A substance can be given toachieve greater than normal levels in the body to drive an enzymatic reaction in a preferential direction, or asubstance can be given to correct a deficiency of a cellular component. Metabolic therapy differs fromstandard pharmaceutical therapies in that metabolic therapy supports enzymatic reactions, whereby multiplestandard pharmaceutical therapies block, rather than enhance cellular processes. Beta blockers, calciumchannel blockers, ACE inhibitors, and even statins are pharmaceutical drugs that inhibit pathways to achievea physiologic response. Simply stated, metabolic cardiology involves an energy gain rather than an energydrain.The importance of supporting energy production in heart cells and the preservation of the mitochondria inthese 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, thechallenge in any metabolic cardiology discussion is in taking the conversation from the “bench to thebedside”. An understanding of the vital role that adenosine triphosphate (ATP) plays in the heart is criticalfor any physician or clinician considering therapeutic options that support ATP production and turnover injeopardized cardiac muscle cells.Metabolic therapies that help cardiomyocytes meet their absolute need for ATP fulfill a major clinicalchallenge 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 energycharge. This lecture introduces how ATP, diastolic heart function and metabolic support help maintaincardiac energy by preserving ATP substrates.Coenzyme Q10, L-carnitine and D-ribose support energy cellular production. Coenzyme Q10 is a lipidsoluble antioxidant that plays a vital role in cellular ATP production. L-carnitine supports beta-oxidation offatty acids in the mitochondria and enhances turnover of ATP. D-ribose is the energy-limiting substrate thatsupports the production of ATP in the mitochondria.The energy-starved heart is poorly understood by physicians who treat cardiac disease on a day-to-daybasis. Metabolic support with D-ribose, L-carnitine and coenzyme Q10 is critical for the maintenance ofcontractile reserve and energy charge in minimally oxidative ischemic or hypoxic hearts. Preservation ofcellular energy provides the chemical driving force required to complete ATPase reactions needed tomaintain cell and tissue viability and function. D-ribose, coenzyme Q10 and L-carnitine exert a physiologicalbenefit that has a positive impact on cardiac function. The use of such nutraceutical support for the heart willbe 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 heartat 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.
  • 40. Objectives & NotesMartha Stark, M.D. Date of talk: Friday, June 26, 2009, 8:35 a.m.Harvard Medical School Phone: 617/244-71883 Ripley Street Fax:Newton, MA 02459 Email: marthastarkmd@hms.harvard.eduTraining: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 PsychoanalysisMedical 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, MABoard 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 AronsonDisclosure Statement:SPEECH TITLE: “Murmur of the Heart: The Story It Tells When We Listen”At the end of this Presentation, the participant should be able to: 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 bodyThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 41. MURMUR OF THE HEART: The Story It Tells If We Listen Martha Stark, MD 27th Annual International Symposium – June 25 – 28, 2009 "And now heres 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-ExuperyCardiovascular 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 (inthis instance, the cardiovascular system) to adapt to the impact of the environmental perturbation. Toomuch stress, traumatic stress, will be too overwhelming for the system to process and integrate, promptinginstead defense, disorder, and disease. Too little stress will provide no impetus for transformation andgrowth, 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 ahigher 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 willmake of it either a growth – disrupting event or a growth – promoting opportunity, either one that overwhelmsor one that prompts transformation and growth, either one that further challenges an already – compromisedsystem 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 systemcannot process and must therefore defend against. The heroine in our piece will be optimal (or nontraumat-ic) stress, stress that provides the impetus for transformation and growth, stress that the system can pro-cess, integrate, and ultimately adapt to – although always at some cost to the system. Importantly, not onlydoes 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 orgrowth 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 tooverwhelm the system or prompts the system to mobilize its ability to heal itself. Environmental stressorswill 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); elevatedC-reactive protein; increased age; male sex; and a family history of heart disease; to name a few – some ofwhich 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 waythat there is an initial disruption to its underlying orderedness and the ease therefore with which informationand energy can be propagated throughout its expanse. This disruption will activate defenses, which will, inturn, 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 / stenoticvalves); cardiac arrhythmias; cardiomyopathy; or pericarditis.But if the system receives enough support (in the form of therapeutic interventions that lighten the total body
  • 42. load and replenish the total body reserves), then the cardiovascular system’s orderedness can be restoredand the ease of flow of information and energy throughout the system revitalized. Once order and ease offlow are restored, the underlying dysfunction, imbalance, and dysregulation can be reversed – such that thesystem 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 insodium, saturated fat, trans fat, cholesterol, refined sugars, processed foods); less animal food, more plantfood (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 bloodsugar levels; donation of blood to lower the hematocrit (and reduce the blood viscosity); adoption of a moreactive 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 thebody’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’sability 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 collateralcoronary vessels, and development of anastomoses. Collateral circulation provides alternate routes of bloodflow 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 tothe 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 maybe 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, greaterend – 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 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 REFERENCESKingma 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: hypertrophyand 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
  • 43. 1969;24:735-744.Moir TW. Coronary vascular adjustments to acute myocardial ischemia. Arch Intern Med1972;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 arteriesand the ischemic heart. Journal of Cellular Biochemistry 1998;65(3):388-394.
  • 44. Objectives & NotesAmer Suleman, M.D. Date of talk: Friday, June 26, 2009, 9:05 a.m.The Heartbeat Clinic Phone: 972/566-43277777 Forest Lane Fax: 972/566-4532Ste A236 Email: asuleman@theheartbeatclinic.comDallas, TX 75230Training: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, neurosonologyOther Information: CME editor cardiology for WEBMDDisclosure Statement:SPEECH TITLE: “Heart Rate Variability As Predictor of Sudden Death”At the end of this Presentation, the participant should be able to: 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 variabilityThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 45. Objectives & NotesJean Monro, M.D. Date of talk: Friday, June 26, 2009, 9:35 a.m.Breakspear Hospital Phone: 011/44-1442-231333Hertfordshire House Fax: 011/44-1442-266388Wood Lane, Paradise Estate Email: jmonro@breakspearmedical.comHemel Hempstead, Herts HP2 4FDEnglandTraining: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”At the end of this Presentation, the participant should be able to: 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 theseThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 46. Objectives & NotesTheodore R. Simon, M.D. Date of talk: Friday, June 26, 2009, 10:30 a.m.North Texas Imaging Center Phone: 214/459-00528345 Walnut Hill Lane, Ste. 210 Fax: 214/459-0054Dallas, TX 75231 Email: ted@aya.yale.eduTraining: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”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center isnot responsible for the contents of this presentation. AEHF has not altered or modified the contents of theinformation provided by this speaker.
  • 47. Thalamic Activity Seen by Scintigraphy of the Brain on Neurotoxic Patients by Theodore R. Simon, M.D. For Twenty-seventh Annual AEHF International Symposium June 2009 Abstract Introduction We have described a pattern present in patients with clinical evidence of neurotoxicity and compared theincidence of this pattern with normal controls. In reviewing our experience, we have now recognized that anadditional 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-mediatedfunctional system that normally sequesters the tracer. SHUNTING is part of that same process which results inless tracer located in the brain and, hence, more in the soft tissues. The cause of SALT & PEPPER is notestablished, although we believe it is due to vascular effects—most likely vasculitis. Asymmetric temporal activityis 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 thethalamus. 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 describedin patients with fibromyalgia. Methods We studied consecutive brain scintigraphic examinations referred for possible neurotoxicity. Eachexamination was evaluated in terms of the four classic criteria for neurotoxicity as well as an overall impression ofthe degree of neurotoxicity. In addition, thalamic activity was evaluated. The usual five-point scale was used forevaluation where “normal” and “minimal” were considered normal while “mild”, “moderate”, and “severe” wereconsidered 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 EnvironmentalHealth Center—Dallas. Five data sets from the Fincher normal series were found. These were reanalyzed in termsof thalamic activity. Results The 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%); andincreased thalamus, 38 (75%). Concomitant signs were seen in all cases of increased thalamic activity. The number of concomitant signswere: 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 thethalamus increase were: no criteria, 0, 0; one criterion 10 (20%), 12 (24%); two criteria, 8 (16%), 12 (24%); threecriteria, 21 (41%), 13 (25%); and four criteria, 12 (24%), 14 (27%). All five criteria were present in 11 (22%)cases.
  • 48. One of the five (20%) normal data sets had abnormal thalamic activity. That activity was only on the rightside. Discussion Increased thalamic activity provides a valid addition to the criteria used to evaluate neurotoxicity by dualphase triple-head single photon emission computed tomographic techniques. Right-sided abnormal thalamicactivity 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. JNeuroscience 2004; 24:10410-10415.Blomqvist A et al. Cytoarchitectonic and immunohistochemical characterization of a specific pain and temperaturerelay, 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 possibleway 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 ofpain. 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 tomographyevidence 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 Clin2000;30:263-288.
  • 49. Objectives & NotesMarkW. Frampton, M.D. Date of talk: Friday, June 26, 2009, 11:00 a.m.University of Rochester Phone: 585-275-4861601 Elmwood Ave, Fax:Rochester, NY 14642 Email: mark_frampton@urmc.rochester.eduTraining: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.Disclosure Statement:SPEECH TITLE: “The Cardiovascular Consequences of Particulate Air Pollution”At the end of this Presentation, the participant should be able to: 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 effectsThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 50. The Cardiovascular Consequences of Particulate Air Pollution Mark W. Frampton MD University of Rochester Medical CenterResearch conducted over the past 15 years has made it clear that exposure to particulate matter (PM) air pollution is amajor public health issue. Worldwide, outdoor PM pollution is estimated to cause 500,000 excess deaths annually. Inthe 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, forevery 10 µg/m3 reduction in ambient levels of fine particles in US cities, life expectancy is extended by more than half ayear (2).Exposure to particulate matter is associated with increased risk for both respiratory and cardiovascular morbidity andmortality. 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 toxicologicalmechanisms is an important priority.Our laboratory studies human clinical responses to air pollution exposure. We initiated a series of studies of respiratoryand 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 toevade typical pulmonary clearance mechanisms, and have the ability to diffuse across cell membranes and enter cellorganelles. It is possible that they have direct effects on vascular structures, and may enter the circulation via thepulmonary capillaries.Our studies suggest that exposure to carbon ultrafine particles, at concentrations that can be experienced on a busyhighway, may induce subtle acute changes in both the pulmonary (5) and systemic (6) vascular beds, possibly inducedby injury or activation of vascular endothelial cells. We have now extended our studies by using a system whichconcentrates outdoor ultrafine particles for use in human clinical studies. Preliminary findings suggest that outdoorconcentrated ultrafine particles may have pulmonary vascular as well as systemic vascular effects. These humanstudies provide insights into mechanisms by which PM may contribute to the burden of pulmonary and cardiovasculardisease, 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? InhalToxicol 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 adhesionmolecules 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. EnvironHealth Perspect 2008;116:375-380.
  • 51. Objectives & NotesRussel J. Reiter, Ph.D. Date of talk: Friday, June 26, 2009, 1:30 p.m.University of Texas Health Science Center Phone: 210/567-38597703 Floyd Curl Drive Fax: 210/567-6948San Antonio, TX 78229-3900 Email: reiter@uthscsa.eduTraining: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 ResearchDisclosure Statement:SPEECH TITLE: “Melatonin: Role in Blood Pressure Regulation”At the end of this Presentation, the participant should be able to: 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 notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 52. Melatonin: Role in Blood Pressure Regulation Russel J. Reiter Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, Texas, USAAbstract In experimental rodents, surgical removal of the pineal gland, the major source of circulating melatonin, causesa gradual and sustained rise in blood pressure (BP). Conversely, when melatonin is chronically administered topinealectomized rodents the increment in BP is ameliorated. In humans as well, the nighttime rise in endogenouscirculating melatonin levels may be inversely related to the reduction in nighttime blood pressure. Among hypertensivepatients, some exhibit a much greater reduction in BP at night (the so-called extreme dippers and dippers) while othersexhibit 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 andextreme dippers. The chronic administration of melatonin to individuals with hypertension induces a measurable dropin nighttime systolic and diastolic BP. Moreover, the higher the nighttime level of endogenous melatonin (estimatedfrom 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.Introduction An 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 surgicalremoval of the pineal gland from rats caused a gradual and sustained rise in arterial blood pressure, a finding that hasbeen duplicated in a variety of subsequent investigations. Moreover, the hypertensive response associated withpinealectomy 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 pressureis usual in diurnal species such as humans. Mechanistically, the development of hypertension in pinealectomized rats ishypothesized 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 Modulation As with every mammalian species, blood melatonin levels in humans exhibit a circadian rhythm with peaklevels occurring exclusively during the night. Melatonin is not produced during the day since light detected byspecialized photoreceptive cells in the retinas suppresses its production [6]. Artificial light exposure after darknessonset 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 daytimevalues. The widespread use of artificial light sources has greatly compromised the ability of the human pineal gland toproduce melatonin. In both humans and animals maintained under naturally occurring periods of light and dark, theduration of elevated melatonin is proportional to the length of the dark period. For humans, however, the normal periodof environmental darkness is typically truncated by the use of artificial light after sunset and before sun rise. Thislikewise limits the total amount of melatonin produced as shown by the abbreviated nocturnal elevation of thisindoleamine per 24 hour period [8]. Additionally, brief intermittent exposure to bright light after darkness onset rapidlysuppresses 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 reduceendogenous melatonin levels [10]. The ability to impose light after darkness onset clearly reduces the total quantity of melatonin humans arecapable of generating. Thus, compared to species that experience only regularly alternating periods of environmentalday and night, humans are relatively melatonin deficient. Besides suppressing melatonin levels, light after darknessonset 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 mayhave a variety of pathophysiologicial consequences including an elevation in blood pressure.
  • 53. Melatonin: Modulation of Blood Pressure To reduce blood pressure, the pharmaceutical industry has developed a wide range of drugs, e.g.,angiotensinconverting 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 largenumber of drugs available, the percentage of hypertensive patients who have well-controlled blood pressure is muchlower than desired. Additionally, each of the agents mentioned has some untoward side effects. One of these negativeactions is the inhibition of the nighttime synthesis and secretion (due to the use of beta-adrenergic blockers) ofmelatonin, 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 meanarterial blood pressure at night, when endogenous melatonin levels are normally at a maximum. Typically, bloodpressure oscillates over a 24 hour period with the values during the day being high and with the nocturnal pressureexhibiting 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 slightreduction in blood pressure at night, the so-called non-dippers. Presumably, the increased strain on the cardiovascularsystem imposed by a lack of reduction in arterial pressure on a nightly basis contributes to the higher risk ofcardiovascular mortality in non-dippers than in dippers [15]. The most comprehensive study designed to investigate the association between mortality and nocturnal bloodpressure in humans is that of Ohkubo and colleagues [16]. This group measured the ambulatory blood pressure of1,542 rural Japanese patients (>40 years of age) and subsequently followed them for a minimum of 5.1 years todetermine the frequency of death. Based on the blood pressure measures, patients were initially categorized into one ofthe following four groups: 1) extreme dippers, who exhibited a ≥ 20% drop in nocturnal blood pressure; 2) dippers witha nocturnal decline of ≥ 10% to < 20%; 3) non-dippers, a drop of ≥ 0% to < 10%; and 4), inverted dippers with noreduction in nocturnal blood pressure. The frequency of mortality during the follow-up period was analyzed using theCox proportional hazards regression model adjusted for age, sex, smoking status, previous history of cardiovasculardisease and the use of antihypertensive medications. The results of this longitudinal study revealed a highly significant correlation between nocturnal blood pressureand mortality rate. The individuals who lacked a nighttime decline in blood pressure (inverted dippers) had the highestdeath 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 inwhich 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 significantlygreater in non-dippers than in dippers [19]. Collectively, the results of studies from a variety of sources document thata drop in nocturnal blood pressure is beneficial in reducing structural tissue damage and limiting cardiovascularpathophysiology. The physiological basis for the drop in nocturnal blood pressure in some individuals and not in othersremains 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 ofwhom were elderly and suffering with essential hypertension. To estimate the amount of melatonin produced, theurinary surrogate of melatonin, i.e., 6-hydoxymelatonin sulfate (6-MTs), was measured in two urine samples, onecollected during the day and the other at night. The results revealed nearly a three-fold difference in the quantity ofurinary 6-MTs excreted by the two groups, with the dippers having the higher levels of the melatonin surrogate. Thefindings are consistent with the nighttime rise in melatonin possibly accounting for the reduction in arterial bloodpressure in hypertensive patients. The two major shortcomings of this report are that the number of patients was smalland 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 declinein blood pressure, Scheer et al [24] conducted a randomized, double-blind, placebo-controlled, cross-over study in 16men with essential hypertension who were given oral melatonin (2.5 mg) either acutely (one night) or chronically (for 3weeks) one hour before sleep. Blood pressure was monitored by means of a 24-hour ambulatory unit and actigraphywas used to access sleep quality. While a single melatonin dose was ineffective, chronic administration reduced bothnocturnal systolic and diastolic blood pressure by 6 and 4 mm Hg, respectively, without influencing heart rate. Theday-night amplitudes of the rhythms in systolic and diastolic pressures in the chronically melatonin-treated patientswere elevated by 15% and 25%, respectively. While melatonin also improved sleep quality, this was unrelated to the
  • 54. blood pressure changes. Again, the implications of this study are consistent with the higher nocturnal melatonin beingdirectly involved in reducing blood pressure at night or that melatonin has effects on the circadian pacemaker whichsecondarily depresses hypertension. As with hypertensive men, normotensive and hypertensive women (aged 47-63 years) also respond to chronicmelatonin 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 nocturnalsystolic, 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 explainthe nighttime depressive effect of melatonin on blood pressure. Also, the latter group seemed to favor the directinhibitory effect of melatonin on blood pressure rather than involving its chronobiotic actions which then secondarilyreduced blood pressure [22, 23]. The findings of a single experimental study in animals is also suggestive that melatonin may be of benefit forreducing 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 theanimals were given melatonin (30 mg/kg/day) in the drinking water, the rise in blood pressure in the fructose-fed ratswas significantly attenuated.Perspectives and Conclusions The findings summarized herein regarding the amplitude of the endogenous nocturnal melatonin peak and itscorrelation with the drop in nighttime blood pressure coupled with evidence showing that melatonin administration inpharmacological doses reduces systolic and diastolic pressure is suggestive that the normal circadian rhythm ofmelatonin is a modulator of blood pressure in man. If these inverse rhythms are in fact functionally associated, then itfollows that any factor that compromises nighttime melatonin production would also cause a rise in blood pressure orpossibly convert dippers to non-dippers As summarized in this brief review, it is obvious that nighttime light exposure is particularly detrimental to thenighttime production of melatonin. Thus, truncating the duration of nocturnal darkness (by sleeping only 5-6 hoursnightly) or bright light exposure after darkness onset severely reduces the amount of melatonin available to potentiallyreduce blood pressure. Depressed melatonin is also a major factor in night shift workers and in individuals engaged infrequent, long-haul, transmeridian travel. Finally, drug administration (e.g., beta-blockers, benzodiazepines, etc.) andincreased age markedly reduce the ability of the pineal gland to synthesize and secrete melatonin. Hence, any of theseconditions may contribute to a rise in systolic and diastolic pressure. Of particular interest may be the gradual elevationin 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 seemslogical 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 influenceblood 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 Pharmacol1976; 56:360P-361P.3. Hisada T, Ozono S, Sato K, Watanabe Y, Watanabe M. Relationship between metabolic rhythm in the pineal bodyand 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 spontaneouslocomotor 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.
  • 55. 8. Wehr TA. The durations of human melatonin secretion and sleep respond to changes in daylength (photoperiod). JClin 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 mechanismsbehind. 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 HumHyperten 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, SekinoM, Satoh H, Hisamichi S. Relation between nocturnal decline in blood pressure and mortality: the Ohasama study. AmJ Hyperten 1997; 10:1201-1207.17. Rizzoni D, Muiesan ML, Montani G, Zulli R, Calebich S, Agabiti-Rosei E. Relationship between initialcardiovascular 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 silentcardiovascular 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-dipperhypertensive patients. Blood Press 2003; 12:19-24.21. Scheer FAJL, van Montfrans GA, Van Someren EJW, Mairuhu G, Buijs RM. Daily nighttime melatonin reducesblood 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 administrationdecreases 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 pathogenesisof hypertension in rats with metabolic syndrome. Am J Hypertens 2008; 21:348-351.
  • 56. Objectives & NotesRon Overberg, Ph.D., C.C.N., R.D. Date of talk: Friday, June 26, 2009, 2:00 p.m.Environmental Health Center - Dallas Phone: 214/373-51448345 Walnut Hill Lane, Ste. 220 Fax: 214/691-8432Dallas, TX 75231 Email: drron@ehcd.comTraining: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”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 57. Nutrition Tips for Cardiovascular Disease Ron Overberg, Ph.D.Abstract. Most Cardiovascular disease can be explained by poor health choices or simply living too long. Some CVD isdue 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 maintaintheir ideal weight. It helps to exercise - few do; and the majority of those who exercise pay no attention to diet. Havingcold water fish at least once a week has been shown to be heart protective. So is the consumption of at least 5-9servings of fruits and vegetables day in order to get sufficient minerals, flavonoids and carotenoids. Suggested servingsizes are really small by “American standards” or should we call it “American appetite”: Half a cup of somethingmashed or 1 cup of something leafy. Still, only 25 % of the population achieves 5 servings per day. Most people onlyget 2-3 servings of fruits and vegetables daily and most of the top ten fruits and vegetables are poor sources ofcarotenoids, which are heart protective. Then we have our hectic lifestyles, trying to keep up with the Jones and always perceiving that the grass isgreener on the other side. We don’t take time to relax, or get enough sleep. Around 1900, sleep was estimated to beabout 9 hours per night; in 1963 it was 5.5 hours a night; and more recently it is estimated to be 6.9 hours Sundaysthrough Thursdays and 8 hours on Friday and Saturday. I don’t think that we evolved enough to do with less sleep injust 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 andsupplements 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/10524389http://efaeducation.nih.gov/sig/ods.htmlBrain 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 1-883319-62-5Fat content an fatty acid composition of seeds and seed oils by Guy Inchbald 9/29/00Judd 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.htmhttp://www.foodsafety.gov/~dms/qatrans2.htmlhttp://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 numberNMR Lipoprofile www.liposcience.com 877 547-6837 particle size and numberSpectracell www.spectracell.com 800 227-5227 particle size and numberVAP 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 11Vit. 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
  • 58. Objectives & NotesMohamed B. Abou-Donia, Ph.D. Date of talk: Friday, June 26, 2009, 2:30 p.m.Duke University Medical Center Phone: 919/684-2221Laboratory of Neurotoxicology Fax: 919/681-8224Dept. of Pharmacology and Cancer Biology, Email: donia@duke.eduBox 3813Durham, NC 27710Training: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 ExposureDisclosure Statement:SPEECH TITLE: “Splenda Alters Gut Microflora in Male Rats”At the end of this Presentation, the participant should be able to: 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 healthThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 59. Splenda Increases Body Weight and Alters Gut Microflora in Male RatsMohamed 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 MedicalCenter, Durham, NC 27710, USASplenda 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 12wk, during which fecal samples were collected weekly for bacterial analysis and measurement of fecal pH and bodyweight was determined. After 12 wk, half of the animals from control and each treatment group were sacrificed, andthe remaining animals were allowed to recover for an additional 12-wk period, and further assessments of fecalmicroflora, 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 bodyweight. Following the 12-wk recovery period, only the total anaerobes and bifidobacteria remained significantlydepressed whereas pH values and body weight gain remained elevated. These changes occurred at Splenda dosagesthat contained sucralose at 1.1 – 11 mg/kg (the US FDA Acceptable Daily Intake for sucralose is 5 mg/kg). Inconclusion, 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 gutmicroflora and increases intestinal P-glycoprotein and cytochrome P-450 in male rats. J. Toxicol. Environ, Health 71:1415-1429.
  • 60. Objectives & NotesKalpana Patel, M.D. Date of talk: Friday, June 26, 2009, 3:30 p.m.Allergy and Environmental Health Center - Buffalo Phone: 716/833-221365 Wehrle Dr. Fax: 716/833-2244Buffalo, NY 14225 Email: aehcwny@juno.comTraining: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 ReviewDisclosure Statement:SPEECH TITLE: “Role of Heart Rate Variabilityin the Practice of Environmental Medicine”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 61. Carmelo Rizzo, M.D. Date of talk: Friday, June 26, 2009, 4:00 p.m.Via Tor Sant’Antonio, 34 Phone: 011/39-347941192400013 – Fonte Nuova (RM) Fax: 011/39-064465874Italy Email: info@carmelorizzo.itTraining: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).Disclosure Statement:SPEECH TITLE: “Urticaria and Vasculitis in Patient with HCV”At the end of this Presentation, the participant should be able to: 1. Vasculitis and Urticaria as spy of Chronic HeapatopathyThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 62. Objectives & NotesAmer Suleman, M.D. Date of talk: Friday, June 26, 2009, 4:30 p.m.The Heartbeat Clinic Phone: 972/566-43277777 Forest Lane Fax: 972/566-4532Ste A236 Email: asuleman@theheartbeatclinic.comDallas, TX 75230Training: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, neurosonologyOther Information: CME editor cardiology for WEBMDDisclosure Statement:SPEECH TITLE: “Syndromes of Orthostatic Intolerance”At the end of this Presentation, the participant should be able to: 1. Understand the definition of orthostatic tolerance 2. Understand different types of orthostatic tolerance 3. Identify major diagnostic and treatments modalitiesThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 63. SATURDAY, JUNE 27, 2009OBJECTIVES & ABSTRACTS
  • 64. Objectives & NotesRobert W. Coppock, DVM Date of talk: Saturday, June 27, 2009, 8:05 a.m.Toxicologist and Assoc Ltd Phone: 780/632-6122P O Box 2031 Fax: 780/632-4492Vegreville, AB T9C 1T2 Canada Email: rcoppock@toxicologist.caTraining:Current Job Description: Private practice in toxicologyCurrent Faculty Appointments: Adjunct Professor: Faculty of Medicine and School of Public Health, University of Alberta; Concordia University CollegeUniversity Attended: BS – Chemistry – Andrews University, DVM – Michigan State University, MS – Animal Pathology – Oklahoma State University, PhD – Toxicology – University of Illinois at UrbanaResidency: Veterinary Toxicology at Oklahoma State University, College of Veterinary Medicine, Oklahoma Animal Disease Diagnostic LaboratoryBoard Certifications: American Board of Veterinary Toxicology, American Board of ToxicologyOther 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: NoneSPEECH TITLE: “Mycotoxins and The Heart”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker. Mycotoxins and The Heart Robert W. Coppock, DVM, PhD, DABVT, DABT
  • 65. Mycotoxins have been shown to target the heart. Moniliformin has been shown to cause cardiac myopathy inchickens, turkeys, ducklings and rats. There may be links with moniliformin in the diet and the multifocal myocardialnecrosis observed in Keshan disease. Cyclopiazonic acid causes myocardial degeneration in chickens, turkeys, rats andvervet monkeys. Fumonisin B1 (FB1) causes acute pulmonary edema in pigs due to negative cardiac inotropism, butcardiac lesions are not a consistent finding in pigs poisoned with FB1. The mycotoxin fusaric acid induces hypotensionin 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. References for Mycotoxins and The HeartAbdelhamid, A. M., I. el-Shawaf, S. A. el-Ayoty, M. M. Ali, and T. Gamil. 1990. Effect of low level of dietaryaflatoxins on baladi rabbits. Arch Tierernahr 40 (5-6):517-537.Abdel-Haq, H., M. Palmery, M. G. Leone, L. Saso, and B. Silvestrini. 2000. Stimulation of guinea pig isolated atria byaflatoxins. Toxicol In Vitro 14 (3):193-197.Agata, N., H. Tanaka, and K. Shigenobu. 1993. Possible action of cyclopiazonic acid on myocardial sarcoplasmicreticulum: inotropic effects on neonatal and adult rat heart. Br J Pharmacol 108 (3):571-572.Angsubhakorn, S., P. Poomvises, K. Romruen, and P. M. Newberne. 1981. Aflatoxicosis in horses. J Am Vet MedAssoc 178 (3):274-8.Balachandran, C., and K. R. Parthasarathy. 1996. Occurrence of cyclopiazonic acid in feeds and feedstuffs in TamilNadu, India. Mycopathologia 133 (3):159-162.Baudet, S., R. Shaoulian, and D. M. Bers. 1993. Effects of thapsigargin and cyclopiazonic acid on twitch force andsarcoplasmic reticulum Ca2+ content of rabbit ventricular muscle. Circ Res 73 (5):813-819.Bermudez, A. J., D. R. Ledoux, and G. E. Rottinghaus. 1995. Effects of Fusarium moniliforme culture materialcontaining known levels of fumonisin B1 in ducklings. Avian Dis 39 (4):879-886.Bermudez, A. J., D. R. Ledoux, G. E. Rottinghaus, and G. A. Bennett. 1997. The individual and combined effects of theFusarium mycotoxins moniliformin and fumonisin B1 in turkeys. Avian Dis 41 (2):304-311.Borison, H. L., and M. L. Goodheart. 1989. Neural factors in acute emetic, cardiovascular, and respiratory effects ofT-2 toxin in cats. Toxicol Appl Pharmacol 101 (3):399-413.Broomhead, J. N., D. R. Ledoux, A. J. Bermudez, and G. E. Rottinghaus. 2002. Chronic effects of moniliformin inbroiler and turkeys fed dietary treatments to market age. Avian Dis 46 (4):901-908.Bukatina, A. E., and F. Fuchs. 1994. Effect of phalloidin on the ATPase activity of striated muscle myofibrils. J MuscleRes Cell Motil 15 (1):29-36.Burdock, G. A., and W. G. Flamm. 2000. Review Article: Safety Assessment of the Mycotoxin Cyclopiazonic Acid.Intern J Toxicol 19 (3):195-218.Byrem, T. M., A. M. Booren, G. M. Hill, F. S. Chu, and G. M. Strasburg. 1999. The effect of cyclopiazonic acid on thedevelopment of pale, soft, and exudative pork from pigs of defined malignant hyperthermia genotype. J Anim Sci 77(1):166-172.Casteel, S. W., J. R. Turk, and G. E. Rottinghaus. 1994. Chronic effects of dietary fumonisin on the heart andpulmonary vasculature of swine. Fundam Appl Toxicol 23 (4):518-524.Castella, G., M. R. Bragulat, and F. J. Cabanes. 1999. Fumonisin production by Fusarium species isolated from cerealsand feeds in Spain. J Food Prot 62 (7):811-813.
  • 66. Chen, L. Y., X. L. Tian, and B. Yang. 1990. A study on the inhibition of rat myocardium glutathione peroxidase andglutathione reductase by moniliformin. Mycopathologia 110 (2):119-124.Cole, R. J., J. W. Dorner, R. H. Cox, R. A. Hill, H. G. Cluter, and J. M. Wells. 1981. Isolation of Citreoviridin fromPenicillium charlesii Cultures and Molded Pecan Fragments. Appl Environ Microbiol 42 (4):677-681.Colvin, B. M., A. J. Cooley, and R. W. Beaver. 1993. Fumonisin toxicosis in swine: clinical and pathologic findings. JVet Diagn Invest 5 (2):232-241.Constable, P. D., G. W. Smith, G. E. Rottinghaus, M. E. Tumbleson, and W. M. Haschek. 2003. Fumonisin-inducedblockade of ceramide synthase in sphingolipid biosynthetic pathway alters aortic input impedance spectrum of pigs. AmJ Physiol Heart Circ Physiol 284 (6):H2034-2044.Cullen, J. M., M. Wilson, W. M. Hagler, Jr., J. F. Ort, and R. J. Cole. 1988. Histologic lesions in broiler chicks givencyclopiazonic acid orally. Am J Vet Res 49 (5):728-731.Datta, S. C., and J. J. Ghosh. 1981. Production and purification of Penicillium citreoviride toxin and its effect on TPP-dependent liver transketolase. Folia Microbiol (Praha) 26 (5):408-412.Datta, S. C., and J. J. Ghosh. 1981. Effect of citreoviridin, a mycotoxin from Penicillium citreoviride, on kineticconstants of acetylcholinesterase and ATPase in synaptosomes and microsomes from rat brain. Toxicon 19 (4):555-562.Dorner, J. W., R. J. Cole, L. G. Lomax, H. S. Gosser, and U. L. Diener. 1983. Cyclopiazonic acid production byAspergillus flavus and its effects on broiler chickens. Appl Environ Microbiol 46 (3):698-703.Dwyer, M. R., L. F. Kubena, R. B. Harvey, K. Mayura, A. B. Sarr, S. Buckley, R. H. Bailey, and T. D. Phillips. 1997.Effects of inorganic adsorbents and cyclopiazonic acid in broiler chickens. Poult Sci 76 (8):1141-1149.Engelhardt, J. A., W. W. Carlton, and J. F. Tuite. 1989. Toxicity of Fusarium moniliforme var. subglutinans for chicks,ducklings, and turkey poults. Avian Dis 33 (2):357-360.Fan, L. L., J. Li, and L. H. Sun. 1991. Effect of moniliformin on myocardial contractility in rats. Biomed Environ Sci 4(3):290-294.Fuyu, Y. 2006. Keshan disease and mitochondrial cardiomyopathy. Sci China C Life Sci 49 (6):513-518.Gbodi, T. A., N. Nwude, Y. O. Aliu, C. O. Ikediobi, and C. O. Chineme. 1991. Acute toxicity of crude extracts ofAspergillus quadrilineatus isolated from acha (Digitaria exilis Stapf). Vet Hum Toxicol 33 (1):27-31.Gelderblom, W. C., N. P. Kriek, W. F. Marasas, and P. G. Thiel. 1991. Toxicity and carcinogenicity of the Fusariummoniliforme metabolite, fumonisin B1, in rats. Carcinogenesis 12 (7):1247-1251.Gomez, J. P., and D. Potreau. 1996. Effects of thapsigargin and cyclopiazonic acid on intracellular calcium activity innewborn rat cardiomyocytes during their development in primary culture. J Cardiovasc Pharmacol 27 (3):335-346.Gumprecht, L. A., G. W. Smith, P. C. Constable, and W. M. Haschek. 2001. Species and organ specificity offumonisin-induced endothelial alterations: potential role in porcine pulmonary edema. Toxicology 160 (1-3):71-9.Harvey, B., T. S. Edrington, L. F. Kubena, G. E. Rottinghaus, J. R. Turk, K. J. Genovese, R. L. Ziprin, and D. J. Nisbet.2002. Toxicity of fumonisin from Fusarium verticillioides culture material and moniliformin from Fusarium fujikuroiculture material when fed singly and in combination to growing barrows. J Food Prot 65 (2):373-377.Harvey, R. B., T. S. Edrington, L. F. Kubena, G. E. Rottinghaus, J. R. Turk, K. J. Genovese, and D. J. Nisbet. 2001.Toxicity of moniliformin from Fusarium fujikuroi culture material to growing barrows. J Food Prot 64 (11):1780-1784.Haschek, W. M., L. A. Gumprecht, G. Smith, M. E. Tumbleson, and P. D. Constable. 2001. Fumonisin toxicosis inswine: an overview of porcine pulmonary edema and current perspectives. Environ Health Perspect 109 Suppl
  • 67. 2:251-257.Haschek, W. M., G. Motelin, D. K. Ness, K. S. Harlin, W. F. Hall, R. F. Vesonder, R. E. Peterson, and V. R. Beasley.1992. Characterization of fumonisin toxicity in orally and intravenously dosed swine. Mycopathologia 117 (1-2):83-96.He, Q., N. Bhandari, and R. P. Sharma. 2002. Fumonisin B1 alters sphingolipid metabolism and tumor necrosis factoralpha expression in heart and lung of mice. Life Sci 71 (17):2015-23.Jaskiewicz, K., P. M. Close, P. G. Thiel, and R. J. Cole. 1988. Preliminary studies on toxic effects of cyclopiazonic acidalone and in combination with aflatoxin B1 in non-human primates. Toxicology 52 (3):297-307.Javed, T., G. A. Bennett, J. L. Richard, M. A. Dombrink-Kurtzman, L. M. Cote, and W. B. Buck. 1993. Mortality inbroiler chicks on feed amended with Fusarium proliferatum culture material or with purified fumonisin B1 andmoniliformin. Mycopathologia 123 (3):171-184.Jestoi, M. 2008. Emerging fusarium-mycotoxins fusaproliferin, beauvericin, enniatins, and moniliformin: a review. CritRev Food Sci Nutr 48 (1):21-249.Jestoi, M., M. C. Somma, M. Kouva, P. Veijalainen, A. Rizzo, A. Ritieni, and K. Peltonen. 2004. Levels of mycotoxinsand sample cytotoxicity of selected organic and conventional grain-based products purchased from Finnish and Italianmarkets. Mol Nutr Food Res 48 (4):299-307.Kriek, N. P., W. F. Marasas, P. S. Steyn, S. J. van Rensburg, and M. Steyn. 1977. Toxicity of a moniliformin-producingstrain of Fusarium moniliforme var. subglutinans isolated from maize. Food Cosmet Toxicol 15 (6):579-587.Kubena, L. F., R. B. Harvey, S. A. Buckley, T. S. Edrington, and G. E. Rottinghaus. 1997. Individual and combinedeffects of moniliformin present in Fusarium fujikuroi culture material and aflatoxin in broiler chicks. Poult Sci 76(2):265-270.Ledoux, D. R., J. N. Broomhead, A. J. Bermudez, and G. E. Rottinghaus. 2003. Individual and combined effects of theFusarium mycotoxins fumonisin B1 and moniliformin in broiler chicks. Avian Dis 47 (4):1368-1375.Lemmens-Gruber, R., B. Rachoy, E. Steininger, K. Kouri, P. Saleh, R. Krska, R. Josephs, and M. Lemmens. 2000. Theeffect of the Fusarium metabolite beauvericin on electromechanical and -physiological properties in isolated smoothand heart muscle preparations of guinea pigs. Mycopathologia 149 (1):5-12.Liu, J. B., Y. M. Wang, S. Q. Peng, G. Han, Y. S. Dong, H. Y. Yang, C. H. Yan, and G. Q. Wang. 2007. Toxic effectsof Fusarium mycotoxin butenolide on rat myocardium and primary culture of cardiac myocytes. Toxicon 50(3):357-364.Lundeen, G. R., R. H. Poppenga, V. R. Beasley, W. B. Buck, W. J. Tranquilli, and R. J. Lambert. 1986. Systemicdistribution of blood flow during T-2 toxin induced shock in swine. Fundam Appl Toxicol 7 (2):309-23.MacDonald, E. J., K. R. Cavan, and T. K. Smith. 1988. Effect of acute oral doses of T-2 toxin on tissue concentrationsof biogenic amines in the rat. J Anim Sci 66 (2):434-41.Morgan, M. K., S. J. Bursian, G. E. Rottinghaus, G. A. Bennett, J. A. Render, and R. J. Aulerich. 1998. Subacute andreproductive effects in mink from exposure to Fusarium fujikuroi culture material (M-1214) containing knownconcentrations of moniliformin. Arch Environ Contam Toxicol 35 (3):513-7.Morgan, M. K., S. D. Fitzgerald, G. E. Rottinghaus, S. J. Bursian, and R. J. Aulerich. 1999. Toxic effects to mink ofmoniliformin extracted from Fusarium fujikuroi culture material. Vet Hum Toxicol 41 (1):1-5.Morris, C. M., Y. C. Li, D. R. Ledoux, A. J. Bermudez, and G. E. Rottinghaus. 1999. The individual and combinedeffects of feeding moniliformin, supplied by Fusarium fujikuroi culture material, and deoxynivalenol in young turkeypoults. Poult Sci 78 (8):1110-1115.Nagaraj, R. Y., W. Wu, J. A. Will, and R. F. Vesonder. 1996. Acute cardiotoxicity of moniliformin in broiler chickensas measured by electrocardiography. Avian Dis 40 (1):223-227.
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  • 70. Contam 21 (6):598-606.Unitt, M. D., and D. Lloyd. 1981. Effects of inhibitors on mitochondrial adenosine triphosphatase of Tetrahymenapyriformis ST. J Gen Microbiol 126 (2):261-266.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 thesubchronic 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 Eupenicilliumochrosalmoneum-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 ExpPathol 64 (5):570-7.Yutani, C., M. Imakita, H. Ishibashi-Ueda, S. Okubo, M. Naito, and T. Kunieda. 1988. Nodular regenerativehyperplasia 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]. ZhonghuaYi 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 ofmyocardium in rats and mice. Biomed Environ Sci 6 (1):37-44.
  • 71. Objectives & NotesJames Roberts, Jr., M.D., F.A.C.C. Date of talk: Saturday, June 27, 2009, 8:35 a.m.3110 West Central Avenue Phone: 419/531-4235Toledo, OH 43606 Fax: 419/531-6236 Email: jimroberts@glasscity.netTraining: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 MedicineOther Information: Co-Author of Reverse Heart Disease NowDisclosure Statement: NoneSPEECH TITLE: “Immune Mechanisms in Atherosclerosis”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 72. Immune Mechanisms in Atherosclerosis – AbstractAtherosclerosis is a chronic, maladaptive, Th1 (macrophage and CD4+ lymphocyte) driven immune responseto perceived intimal infection with oxidized lipids. Nutritional and pharmacologic therapies designed toprevent or treat atherosclerosis can be seen to work within this framework. Apo-B100 containing lipids atabove nutritional levels are trapped within the intima and later oxidized (the latter event favored by tissuemetals and low levels of antioxidants and HDL). oxLDL, an entity not present in cavemen or within thethymus gland of modern man during T cell maturation, is perceived by the immune system as a threat. Aninflammatory response is initiated. Endothelial function is compromised; adhesion molecules are displayedand chemokines elaborated. Mononuclear cells are drawn into the intima. Monocyte-derived macrophagesrecognize oxLDL not via nutritional LDL receptors, but rather via scavenger and CD36 receptors that mediatemicrobe phagocytosis. oxLDL blocks reverse cholesterol transport within the macrophages and other intimalcells. Lipid accumulation leads to the formation of foam cells, the precursor lesion of plaque. The next waveof macrophages, now armed with up regulated toll-like receptors, phagocytose oxLDL, degrade the apo-B100protein, 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 ahumoral (Th2) or macrophage (Th1) mediated immune response. If by chance a T lymphocyte bearing a Tcell receptor specific for an ox-apo-B100 fragment encounters an intimal macrophage bearing this 12-20amino acid antigenic determinant, then the T cell activates, elaborates interferon-gamma (IFN-γ), and beginsto proliferate. IFN-γ increases macrophage oxidant and phagocytic function. Additional ox-apoB100 ispresented to the growing clone of reactive T cells, and more IFN-γ is elaborated. A chemokine trail pullsadditional 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 ofthese activated T cell lines soon follows.Free radical stress compromises the endothelium and allows smooth muscle cells to proliferate, thickening theplaque but also providing it with tensile strength. IFN-γ, however, blocks smooth muscle proliferation andTNF-α, produced in response to IFN-γ, leads to the release of nascent degradative enzymes (matrixmetalloproteinases) from intimal macrophages. The MMPs are then activated by tryptase released fromactivated mast cells, which are found within the adventitia and shoulder region of the active plaque. As thisprocess evolves, 5-10 clones of lesional activated T cells, some specific for oxLDL protein, and othersspecific for beta2-microglobulin, hsp, or a microbial determinant, escape from regulatory control. They nowproliferate autonomously. They no longer require macrophage co-stimulation, and they release prodigiousquantities of IFN-γ, within the lesion, and later within the circulation. The plaque shoulder region, rich inmononuclear cells and no longer strengthened by smooth muscle, can fissure, throwing off platelet clots, orrupture, 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 isprotecting the intima from a serious, chronic infection).
  • 73. Urgent therapy might include a stent impregnated with a drug that blocks lymphocyte proliferation and astatin. Statins down regulate immune function. Macrophage radical generating, phagocytic, and antigenpresenting function is down regulated, endothelial activation is lessened, and CD40-CD40-ligand signalingbetween 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 perhapsnot so great an idea in a 25 year old with high but non-oxidized cholesterol and a lifetime ahead of infectiousand immune challenges). Angiotensin I is converted into angiotensin II by ACE, 90% of which is locatedwithin the intima, a process that can be blocked by lipophilic ACEI. Chymase released by activated mastcells can also cleave angiotensin I, and here ARB therapy comes into play, as Ang II activates NF-KB inintimal 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-α and shifts T cell function away from plaque forming anddestabilizing Th1 and towards non-atherosclerotic Th2, and has been shown to be helpful in ACS, CHF ofany cause (another condition characterized and driven by Th1 activation), and presumably will help preventand stabilize atherosclerosis (it does so in animal studies). Metals (toxic, copper, and iron) promote LDLoxidation, while anti-oxidants (especially Vitamin C and selenium) block this process that mutates anutritional substance into the atherosclerosis initiator. 1,2-Dilinolenylphosphatidylcholine stimulates theantioxidant and reverse cholesterol transport function of HDL. Pomegranate juice stimulates paroxonase, thekey antioxidant enzyme of HDL, leading to oxLDL reduction. Both have been shown to improve functionalstatus and reverse atherosclerosis is symptomatic humans. Other HDL raising and/or stimulating therapieswill likely do the same. Measures designed to lower circulating levels of apoB-100 containing particles willlessen the quantity of LDL that can be oxidized within the inflamed, now oxidant rich and antioxidant poorintima (why extreme LDL reduction is recommended in advanced disease vs. mild to moderate reduction inprevention). Metal overload increases CV risk. Metal detoxification is employed by physiologically orientedphysicians in the prevention and treatment of atherosclerosis. Its primary mechanism of benefit is likely anattenuation of LDL oxidation within the intima. Fish oil, Vitamin D, Co-Enzyme Q-10, Carnitine, and manyother nutritional agents, amongst their many benefits, down regulate or temper an over active immuneresponse. To prevent atherosclerosis or slow its progression we need to prevent LDL, remnant particle, andLp (a) trapping and oxidation within the intima. To prevent the consequences of atherosclerosis we need todown 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 immuneresponse, explaining the benefit of immune modulators including statins, ACEI, Pentoxifylline, and evenMethotrexate (Yes, statins deplete Co-Q10, and this aggravates CHF, but by blunting an overactive Th1response, statin therapy will improve functional status and increase ejection fraction – thus low dose statintherapy with Co-Q10 coverage is rationale).Atherosclerosis is an inappropriate immune response to intimal oxidation of LDL. Prevention of LDLoxidation and down regulation of the consequent immune activation characterizes our preventative andtherapeutic measures. Novel anti-LDL oxidation or immune modulating therapies are anticipated and eagerlyawaited by the physiologically oriented health care practitioner. James C. Roberts MD FACC 4/10/09
  • 74. Objectives & NotesDietrich K. Klinghardt, M.D., Ph.D. Date of talk: Saturday, June27, 2009, 9:35 a.m.Institute of Neurobiology Phone: 425/688-8818P.O. Box 5023 Fax: 425/453-7015Bellevue, WA 98007Training:Current Job Description: Founder of the American Academy of Neural Therapy, now the Klinghardt Academy of Neurobiology, and lead clinician at the Comprehensive Medical CenterCurrent 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: NoneSPEECH TITLE: “Cavitation in the Jawbone, the Vagus Nerve, and the Heart.”At the end of this Presentation, the participant should be able to: 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 surgeryThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 75. Abstract from Dietrich Klinghardt, MD, Ph.D.Cavitations in the Jawbone, the Vagus Nerve and the HeartPractitioners in Europe have for over 100 years observed a frequent connection between chronic infectionsin the jaw bone and problems with the rhythm of the heart (supraventricular tachycardia, chronically elevatedheart rate, ventricular arythmias and asystole, heart palpitations, etc.).Successful treatment strategies involved a. establishing a solid diagnosis with diagnostic procaine injections in the oral cavity b. treating the cavitation or infected jaw bone with surgeryThe vagus nerve is the largest contributor to slowing down the heart rhythm in times of rest, relaxation orsleep. Most of the vagal fibers to the heart originate in the right vagus (behind and deep to the right ear).Theanatomy of the jaw and the vagus nerve are related: lymphatic vessels and lymphatic drainage from the jawbone parallel the course of the vagus nerve in the anterior neck region. This could explain how the nervewhich is so involved in downregulating the heart rhythm and the oxygen consumption of the heart canbecome 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 surgeryMost commonly a chronic low grade infection in the lower wisdom tooth extraction site is responsible for thepatients vagus nerve and/or heart condition. The misfiring vagus nerve can also disturb any major otherorgan: the lungs, the intestines, the liver, the pancreas, the kidneys. In this case the illness caused by thejaw 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 moreeffective, 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 avaluable tool for both diagnosis and treatment.
  • 76. Objectives & NotesWilliam J. Rea, M.D. Date of talk: Saturday, June 27, 2009, 10:30 a.m.Environmental Health Center - Dallas Phone: 214/368-41328345 Walnut Hill Lane, Ste. 220 Fax: 214/691-8432Dallas, TX 75231 Email: wjr@ehcd.comTraining: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 CenterBoard Certifications: American Board of Surgery, American board of Thoracic Surgery, American Board of Environmental MedicineOther Information: Author of “Chemical Sensitivity I-IV”, “Optimum Environments for Optimum Health”Disclosure Statement: NoneSPEECH TITLE: “Environmental Aspects in the Treatment of Cardiovascular Disease”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 77. ENVIRONMENTAL TREATMENT OF 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 ofpollutants 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, chiropracticmanipulation, acupuncture, and energy balancing. Each of the first six treatments will be discussed separately: Avoidance 1. Air – ECU-like conditions (clinic, motel, home) 2. Water – spring, distilled, filtered, glass bottles 3. Organic food – rotary diet Intradermal Neutralization, Subcutaneous Treatment, and Sublingual Treatment 1. Molds, foods, chemicals 2. Metals in the body – pacemaker, defibrillator, artificial valves, other implants (Dacron, Teflon, Silicone) Nutrient Treatment 1. Vitamins – C, D, E, B-Complex 2. Minerals – Potassium, magnesium, selenium 3. Amino acids – glutathione, taurine 4. Fatty acids Heat Depuration 1. Sauna 2. Massage 3. Exercise Oxygen Therapy 1. Pictures Immune Modulators 1. Gammaglobulins 2. ALF 3. Autogenous vaccine
  • 78. Objectives & NotesWilliam J. Meggs, M.D., Ph.D. Date of talk: Saturday, June 27, 2009, 11:00 a.m.Brody School of Medicine, East Carolina University Phone: 252/744-2954600 Moye Blvd., Room 3ED311. Fax: 252/744-3589PCMH, 3ED-311, Department of Emergency Medicine Email: meggsw@ecu.eduGreenville, NC 27834-4354Training: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”Disclosure Statement: NoneSPEECH TITLE: “Accelerators of Atherosclerosis”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 79. 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 exposuresAbstractAtherosclerosis 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 theonset of atherosclerosis. In addition to the well known accelerators such as hypertension, hyperlipidemia, andhyperglycemia, toxic exposures such as cocaine, amphetamines, and inhalants can accelerate atherosclerosis.Phamaceuticals with cardiotoxicity include corticosteroids, protease inhibitors, chemotherapeutic agents, transplantrejection medications, ergotamine, and metals. Occupational exposure to carbon disulfide among rayon workers hasbeen 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:b349Steinhart 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 viscoserayon factory. Br J Ind Med. 1987 April; 44(4): 220–227.
  • 80. Objectives & NotesStephen T. Sinatra, M.D. Date of talk: Saturday, June 27, 2009, 1:30 p.m.Optimum Health Phone: 860/645-3825257 E. Center Street Fax: 860/643-2531Manchester, CT 06040Training: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.Disclosure Statement: NoneSPEECH TITLE: “Energy Medicine-Good Vibes vs Bad”At the end of this Presentation, the participant should be able to: 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 functionThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 81. Energy Medicine Good Vibes vs BadAbstractThe essence of disease originates from nutrient depletion in the context of physical and emotional traumaand environmental and electrical toxicity. At the essence of this triad are the compromised receptor sites onthe cellular membrane. As the cellular membrane becomes vulnerable and dysfunctional, vital nutrientssuch as oxygen, vitamins, minerals, and hormones are not able to enter and nourish the cell in sufficientamounts. Toxic waste is not adequately flushed out of the cell. This scenario accelerates the developmentof 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, FIRsauna and the utilization of very low frequency pulsed electromagnetic waves are just a few of the excitingdiscoveries that assist the quantum energy of the body. This is the new wisdom that will assist us in thegood vibe/bad vibe technological age.Our technological age continually serves up wired and wireless wonders to make life more convenient. Ihave a persistent gnawing sense that something potentially disastrous is going on.Illnesses like multiple sclerosis, autoimmune disorders, fibromyalgia, chronic fatigue, and autism have beenproliferating 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 holdtrue: poor diet, physical inactivity, stress, and environmental toxicity. All combine to weaken the humanimmune 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 effecton bodily operating systems delivered by “electropollution.” By that I mean the chaotic, unseen, and unfeltenvironmental 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 withsleep patterns is well-documented. Electro medicine is a very dynamic field, but the science is far fromconclusive as yet. There’s much still unknown and a lot of debate over whether common man-madeelectrical 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 isregulated by dynamic electrical currents, most obvious, of course, the pumping action of the heart and theexquisitely complex circuitry of the brain.All beings are conglomerations of electromagnetic energy. In essence, our bodies function—for better or forworse—as dynamic electrical circuits. Cells transmit and receive energy, and each has its own range offrequency within which it operates. Healthy cells, for instance, oscillate at higher frequencies than dounhealthy cells, such as cancer cells. James Oschman, Ph.D., a top expert and author of Energy Medicinein Therapeutics and Human Performance (Butterworth-Heinemann) says all “organisms (are) poised torespond to minute ‘whispers’ in the electromagnetic environment,” whether those fluctuations come from afaror near.
  • 82. “The fields within the human body are inevitably affected by the larger fields of the planet and other celestialbodies,” he says. “For example, sunspots and the cycles of the moon cause changes in ionosphericcurrents and geophysical fields which in turn influence the fields within us.” Geomagnetic storms generatedby turmoil on the sun can be so intense that they damage its satellites, power lines, telephone cables anddisrupt radio communications. Not surprising, that these disturbances can and do affect physiology, creatingcardiovascular problems and seizures.Closer to home, man-made electromagnetic fields can have influences on our bodies as well. Perhaps themost documented influence is that of leukemia among children living near high voltage power lines. Ofcourse, our modern array of electric devices such as hair dryers, computers, televisions, cell phones, andradios all produce a variety of signals and energy, some of which radiate directly into the tissue of nearbyorganisms.Some people are more vulnerable than others to “electropollution.” Many of them are often sensitive tomany 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 maytake medication, their symptoms rarely go away.Electropollution has the potential to reduce heart rate variability (HRV), a term referring to the imperceptiblevariations in the heart’s beat-to-beat interval governed by breathing and other physiological rhythms. HRV iscurrently 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 mastswere contributing to a disturbing disappearance of honeybees, essential players in plant pollination. “Colonycollapse disorder,” as it is called, was first observed in the United States but has spread to Europe. Towersignals are thought to disrupt the natural navigational bearings of bees returning to their home hives frompollen-hunting sorties. EMF interference leaves them wandering aimlessly and they die. If sensitivehoneybees 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 cellphones and behavioral problems in young children. They reviewed the answers to a questionnaire filled outby more than 13,000 mothers and concluded that exposure to cell phones during pregnancy (and to a lesserdegree after birth) suggests a link to emotional and hyperactivity problems in young kids. “If real,” theresearchers said, the associations rise to the level of public health concern given the widespread use of thetechnology.Recently I read a long-term Swedish study finding that the use of cell phones for 2,000 plus hours during alifetime could substantially increase the risk of developing a malignant cranial tumor. One summary ofstudies on long-term heavy users indicates a 20 percent increased risk of a tumor, and particularly on thesame side of your head that you use to talk on the phone. I’ve also learned that excessive cell phone usemay generate a feeling of fullness and warmth in the ears, as well as a ringing sensation like tinnitus. Suchsymptoms could foretell an early auditory abnormality.How can you discharge electropollution from your body? One simple, costless way is just walking barefooton dirt, sand, grass, and unpainted cement. The more time you can spend directly connected—flesh toearth—the better. You are literally, figuratively, and electrically grounding yourself. Try sitting and readingfor 15 minutes or a half hour in your backyard, weather allowing of course, with your bare feet on theground. When it comes to shoes, leather serves the purpose as a conductor but not rubber and plastic.
  • 83. Connected to the earth, either walking or sitting, you are not only discharging electropollution but alsogetting an infusion of activated electrons produced on the surface of the earth from solar radiation. Themoment your foot touches the earth your physiology changes. In essence, grounding the body balances theautonomic nervous system by attenuating sympathetic overdrive.I encourage you to take stock of your phone systems. Consider using the speakerphone feature on yourphones in order to protect your head and all its vital contents. Be mindful of the exposure that kids in yourfamily 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 theirnervous 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 thesepotentially upsetting waves are, and how far they extend out from their source. You will be surprised, as Ihave been, at their intensity and range. I was surprised, for instance, when I checked the radiationemanating from a baby monitor. It was really high. Could the frequencies coming out of those monitorsaffect 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 SleepRes 1999;8:77-81.Baris D, Armstrong BG, Deadman J, Theriault G. A case cohort study of suicide in relation to exposure toelectric 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 electromagneticfield 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 realitydisturbance correlate with decreased nocturnal melatonin depressed patients. Acta Psychiatr Scand1987;76:272-275.Coghill RW, Steward J, Philips A. Extra low frequency electric and magnetic fields in the bedplace ofchildren 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 behavioralproblems in children. Epidemiology, 2008;19(4):523-9.Genuis SJ. Fielding a current idea: exploring the public health impact of electromagnetic radiation. PublicHealth. 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 levelsand 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 cordlesstelephones 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 ondiabetes and multiple sclerosis. Electromag Biol Med 2006;25(4):259-68.
  • 84. Havas M, Stetzer D. Dirty electricity and electrical hypersensitivity: five case studies. World Health OrgWorkshop on Elec Hypersensitivity, Oct 2004, Prague, Czech Republic.Mann K, Wagner P, Brunn G, Hassan F, Hiemke C, Roschke J. Effects of pulsed high-frequencyelectromagnetic fields on the neuroendocrine system. Neuroendocrinology 1998a;67:139-144.Milham S, Morgan LL. A new electromagnetic exposure metric: high frequency voltage transientsassociated with increased cancer incidence in teachers in California school. Am J Ind Med. 2008Aug;51(8):579-86.Oschman JL. Energy Medicine in Therapeutics and Human Performance, Can Electrons Act asAntioxidants? A Review and Commentary J Alt Comp Med, 2007;13(9):955-67, 2000 Energy Medicine: Thescientific basis. Harcourt/Churchill Livingston, Edinburgh.Salford LG, Brun AE, Eberhardt JL, Malmgren L, Persson BRR. Nerve cell damage in mammalian brainafter exposure to microwaves from GSM mobile phones. Environ Health Perspect 2003June;111(7):881-883.Savitz DA, Checkoway H, Loomis DP. Magnetic field exposure and neurodegenerative disease mortalityamong electric utility workers. Epidemiology 1998 July;9(4):398-404.Sinatra 1-8, 48 slides 6 per page
  • 85. Objectives & NotesKalpana Patel, M.D. Date of talk: Saturday, June 27, 2009, 2:00 p.m.Allergy and Environmental Health Center - Buffalo Phone: 716/833-221365 Wehrle Dr. Fax: 716/833-2244Buffalo, NY 14225 Email: aehcwny@juno.comTraining: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 ReviewDisclosure Statement: NoneSPEECH TITLE: “Environmental Aspects of Lyme Disease and Autonomic Deregulation”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 86. Dr Patel’s presentation was not available at time of printing of this abstract.
  • 87. Objectives & NotesDonald Hillman, Ph.D. Date of talk: Saturday, June 27, 2009, 2:30 p.m.Michigan State University Phone: 517/351-9561750 Berkshire Lane Fax: 517/351-1944East Lansing, MI 48823 Email: donag1@aol.comTraining: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.Disclosure Statement: NoneSPEECH TITLE: “The Electropathic Stress Syndrome--Neuroendocrine Responses to EMF”At the end of this Presentation, the participant should be able to: 1. Recognize signs of Electropathic Stress Syndrome 2. Understand autonomic nervous system responses to EMF 3. Recommend Electropathic Stress therapyThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 88. 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 andanimals via stimulation of peripheral sensors similar to responses to severe environmental temperatures, noise, andatomic radiation. EMF produces a neuroendocrine stress that interferes with normal homeostasis of the autonomicnervous system (ANS). The syndrome is manifested in hypothalamic, pituitary, and pineal gland secretions thatinfluence the performance of other endocrine glands and most organs of the body. Both sympathetic andparasympathetic responses to EMF have been reported to be partially dependent on the body exposure site, the intensityand the frequency of electrical signals. Biological permeability tends to increase as the intensity and frequency ofelectrical 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 inconcentrations of blood proteins, i.e., immunoglobulins, cytokinins, blood viscosity, lymphocytes, erythrocytes, andelectrolytes. Such interference results in proliferation of certain cancers, allergies, cardiovascular disease, impairmentof 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, andproductivity 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 aHigh School Teacher of Vocational Agriculture and County Extension Agent 1951-55. He studied environmentaleffects on dairy cattle performance and investigated effects of electric and magnetic fields on behaviour, health, andproductivity of dairy cattle in some 110 herds assisting farmers, veterinarians, electricians, and engineers in problemcases. He is a member of The American Dairy Science Association-Am..Soc.of Animal.Science, and the AmericanSociety of Agricultural and Biological Engineers. He has investigated EMF effects on humans and other species andserves as a private consultant regarding EMF effects on dairy cattle.Selected Digital References: http://www.powerwatch.org.uk/science/studies.asp http://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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  • 94. Objectives & NotesAruni Bhatnagar, Ph.D. Date of talk: Saturday, June 27, 2009, 3:30 p.m.University of Louisville Phone: 502/852-5724580 S. Preston St.The Baxter II, Room 421Louisville, KY 40202Training: Post-doctoral training in cellular cardiac electrophysiologyCurrent 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: NoneSPEECH TITLE: “Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants"- Part IIAt the end of this Presentation, the participant should be able to:These talks are to discuss the contribution of exposure to environmental pollutants to heart disease. Specific issues thatwill be discussed include evidence implicating that exposure to particulate air pollutants and gaseous co-pollutantsincreases CVD risk. Data relating to an increase in both acute and chronic risk will be examined. The effects of otherpollutants such as metals and aldehydes will also be discussed. 1. Estimate risk due to exposure to particulate air pollution 2. Understand the impact of the environment of cardiovascular disease 3. Understand the pathophysiological mechanisms that impart and mediate the effects of the environment on acute cardiovascular events as well as chronic atherosclerotic diseaseThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 95. Cardiovascular Disease Risk Due to Exposure to Environmental Pollutants Aruni Bhatnagar, Ph.D., FAHA, Division of Cardiology, Department of Medicine, University of Louisville, Louisville, KYHeart 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 stronginfluence of environmental factors, since rates of CVD incidence and mortality could be markedly alteredwithin 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 thatenvironmental factors such as smoking, nutrition, and physical activity are key factors that determine CVDrisk. Nevertheless, it remains unclear how these factors contribute to the incidence and the severity of heartdisease. In addition, the pathologic mechanisms by which environmental factors influence specific featuresof heart disease remain largely unknown. Epidemiological evidence indicates that CVD risk is derived fromseveral 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 developmentof 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 beenreported to either exacerbate CVD or precipitate acute clinical. Multiple studies reporting health effects ofambient particles have been published. These studies provide evidence for a significant associationbetween particulate air pollution levels and short-term mortality as well as increased mortality risk due tolong-term exposure.Over 100 epidemiological studies report a link with daily fluctuations in air pollutants at relatively lowcommonly 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 bystudies using either time series modeling or a case-cross over design. The strength of association appearsto be stronger for PM2.5 than PM10, indicating that PM2.5 may be the more responsible for the observedassociation. The magnitude of the effect (about 1%) is small, variable, and dependent upon severalstatistical considerations including controlling for seasonality and slowly changing covariants. Nevertheless,consistent associations have been reported for risk of death from all causes, but particularly fromcardiopulmonary disease. In some studies significant associations have also been reported for sulfur oxideconcentrations, while others have found no association with common copollutants (NO 2, SO2, CO, and O3).For obvious reasons, no controlled toxicological studies with mortality as an end point have been conductedto 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 positiveassociation between cardiopulmonary mortality and PM2.5 and sulfate concentrations. No excessive mortalityrisk was associated with exposure to coarse PM or other gaseous pollutants. Similar associations have alsobeen reported by several other long-term exposure studies. Notably, increases in mortality risks were muchlarger (generally more than 10 %) than observed with daily time-series studies. The magnitude of thereported effect is, however, variable.Animals studies with particulate air pollution show that exposure can lead to an increase in cardiovascularinflammation results in an increase in atherogenesis, thrombosis and endothelial dysfunction. Environmental
  • 96. effects on atherogenesis are poorly understood. Data from Watanbe heritable hyperlipidemic rabbits showthat repeated intrapharyngeal instillation of PM10 (twice a week for 4 weeks) stimulates progression ofatherosclerotic 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 thevulnerability of atherosclerotic plaques to rupture. In addition to air pollution and tobacco smoke, there isextensive evidence suggesting that exposure to metals also accelerates atherogenesis.Exposure to arsenic in particular has been linked to an increase in atherosclerotic disease. Studies withhuman populations exposed to arsenic in well water in Taiwan suggest that the incidence of CVD dependsupon the level of exposure to arsenic Epidemiological studies of regions with high arsenic levels in theground water show a marked increase in several forms of CVD including carotid atherosclerosis,hypertension, and ischemic heart disease. Arsenic exposure is also associated with peripheralatherosclerosis, which severely decreases blood flow to extremities and result in gangrene. In Taiwan andBangladesh, 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 cardiovascularmortality in the U.S. Exposure to pollutants could also increase thrombosis. Platelets from smokers demonstrate anincrease in spontaneous as well as agonist (ADP, thrombin) stimulated aggregation. In addition, PM cancontribute to the development and maintenance of a pro-thrombotic state. This is supported by studiesdemonstrating a positive correlation between PM10 exposure, plasma levels of fibrinogen and an increase inblood viscosity. Similarly, ultrafine particles increase platelet number, reduce bleeding times and increaselevels of soluble P-selectin, a marker of platelet activation Aside from PM, component gases of ambient airhave been linked to thrombosis through epidemiological studies demonstrating associations betweenexposure and hospitalizations for ischemic heart disease. Most prominent among these atmospheric gasesinclude ozone (O3), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen oxides (NO2). Ozoneexposure, in particular demonstrates a particularly strong association with enhanced platelet aggregationand 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 cardiovasculardisease. Aldehydes are a significant component of automobile exhaust and smog and have been detectedin high concentrations in cigarette, cotton, wood, and coal smoke. The specific contribution of aldehydes tothe cardiovascular effects of traffic air pollution, however, remains to be fully assessed. In a recent study onthe cardiovascular effects of traffic exposure on highway patrol troopers, aldehydes were strongly correlatedwith an increase in plasma von Willebrand factor and changes in heart rate variability. Cardiovasculartoxicity of environmental aldehydes is also underscored by studies showing increased risk of atheroscleroticdisease 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 theirwork. Nevertheless, it remains unclear whether exposure to ambient levels of aldehydes is associated withan excessive CVD risk and whether long-term repeated exposures to aldehydes has broad impact oncardiovascular 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 healthor could contribute progressively to disease and dysfunction. Although some cardiovascular diseases (suchas familial hypercholesterolemia or the long Q-T syndrome) have clear, well-defined genetic origins, themost common forms of CVD develop in response to environmental injury. This injury might result fromexcessive consumption of saturated fat, lack of exercise or from continuous exposure to environmentalpollutants. In each case, disease appears to develop from failed responses to repair injury and to restorenormal function rather than from common genetic flaws that manifests to greater severity with increasing
  • 97. age. During disease development genetic factors undoubtedly play an important role in modulatingenvironmental influences. As a result, individuals with different genetic makeup display differentsusceptibilities to environmental insults. Nevertheless, given its high prevalence, CVD is unlikely to beentirely or even substantially regulated by genetics. For the same reasons, it is also unlikely that theenvironment plays a secondary role in the etiology of CVD. Migrant population studies and studies withinthe same population with changing environment (lifestyle choice, nutrition, etc) have shown that significantchanges in the environment could substantially alter CVD risk. Both population-based cohort studies andanimal 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 andsignificantly accelerate and exacerbate atherogenesis and thrombosis. This evidence suggests thatenvironments 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 agentsimpair vascular function and promote atherogenesis and to what extent primary interfaces with theenvironment (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.
  • 98. Objectives & NotesMohamed B. Abou-Donia, Ph.D. Date of talk: Saturday, June 27, 2009, 4:00 p.m.Duke University Medical Center Phone: 919/684-2221Laboratory of Neurotoxicology Fax: 919/681-8224Dept. of Pharmacology and Cancer Biology, Email: donia@duke.eduBox 3813Durham, NC 27710Training: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 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 ExposureDisclosure Statement: NoneSPEECH TITLE: “Splenda Increases Intestinal P-Glycoprotein and Cytochrome P-450 in Rats”At the end of this Presentation, the participant should be able to: 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 drugsThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 99. Splenda Increases Intestinal P-Glycoprotein (P-gp) & Cytochrome P450 in Male RatsMohamed 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, DukeUniversity Medical Center, Durham, NC 27710 USASplenda is comprised of the high-potency artificial sweetener sucralose (1.1%) and the fillers, maltodextrinand 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 weresacrificed to determine the intestinal expression of the membrane efflux transporter P-glycoprotein (P-gp) andmetabolism enzymes, the cytochrome P450 isozymes, CYP3A4 and CYP2D1 by Western blot. Theremaining animals were allowed to recover for an additional 12-wk period, and further assessments ofexpression of P-gp and CYP isozymes. At the end of the 12-wk treatment period, there was an enhanced theexpression of P-gp up to 2.43-fold, CYP3A4 up to 2.51-fold, and CYP2D1 up to 3.49-fold. Following the12-week recovery period, P-gp and CYP3A4 and CYP2D1 remained elevated. These changes occurred atSplenda dosages that contained sucralose at 1.1 – 11 mg/kg (the US FDA Acceptable Daily Intake forsucralose is 5 mg/kg). Evidence indicates that a 12-wk administration of Splenda caused several adverseeffects, including (1) an enhanced P-gp and (2) CYP3A4 and CYP2D1 expression at levels known to limit thebioavailability 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.
  • 100. SUNDAY, JUNE 28, 2009OBJECTIVES & ABSTRACTS
  • 101. Objectives & NotesAndrea Frustaci, M.D. Date of talk: Sunday, June 28, 2009, 8:30 a.m.La Sapienza University Phone: 39/0630155231Heart and Great Vessels Department Fax: 39/063055535Viale del Policlinico 155 Email: biocard@inmi.itRome, 00161ItalyTraining: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: NoneSPEECH TITLE: “Selenium And Zinc Deficient Cardiomyopathy In Human Intestinal Malabsorption ”At the end of this Presentation, the participant should be able to: 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 contractilityThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 102. SELENIUM AND ZINC DEFICIENT CARDIOMYOPATHY IN HUMAN INTESTINAL MALABSORPTION ANDREA FRUSTACI , MD Department of Cardiovascular and Respiratory Sciences . La Sapienza University, Rome , Italy.ABSTRACTBackground :Patients with intestinal malabsorption may develop cardiac arrhythmias and/or dysfunction which originis often elusive.Methods : Five patients (5F, mean age 23± 7 ys) with Celiac disease and 3 patients with intestinal bypass because ofsevere 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 . Biopsysamples were processed for histology , electron-microscopy , polymerase chain reaction for cardiotropic viruses andinstrumental neutron activation analysis (INAA) of myocardial trace elements Myocardial anti-oxidant reserve and cellautophagy were evaluated by assessment of glutathione peroxidase activity and of LC3-II, respectively . Controls weresurgical samples from patients with mitral stenosis and biopsy samples from patients with idiopathic dilatedcardiomyopathy.Results : Histology and electronmicroscopy showed in malabsorption population hypertrophy/degeneration ofmyocardiocytes with pronounced cell autophagy and increased LC3-II . PCR was negative for viral genomes . INAAshowed 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 monthsby 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 ischaracterized by decline of myocardial anti-oxidant reserve ,oxidative damage of cell membrane and enhanced myocyteautophagy .
  • 103. Objectives & NotesJean Monro, M.D. Date of talk: Sunday, June 28, 2009, 9:00 a.m.Breakspear Hospital Phone: 011/44-1442-231333Hertfordshire House Fax: 011/44-1442-266388Wood Lane, Paradise Estate Email: jmonro@breakspearmedical.comHemel Hempstead, Herts HP2 4FDEnglandTraining: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: NoneSPEECH TITLE: “Aspects Of Tissue Oxygenation”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 104. Breakspear HospitalTitle: “ASPECTS OF TISSUE OXYGENATION”Author: JEAN A MONRO MB BS MRCS LRCP FAAEM DIBEM MACOEM Medical Director, Breakspear Hospital, Wood Lane Hemel Hempstead, Herts, HP2 4FD, UK ABSTRACT FOR PRESENTATION FOR 27TH ANNUAL MEETING (AEHF) 25 – 28 JUNE 20092,3-bisphosphoglycerate (2,3-BPG), also known as 2,3-diphosphoglycerate (2,3 BPG/DPG) is the carrier ofoxygen from haemoglobin to the tissues.As muscles contract, the presence of hydrogen ions in the muscles allows oxygen to be separated from thehaemoglobin. Equally, as the red blood cells, which are 8 or more microns in diameter, go through capillaries, whichmight be as small as 4 microns in diameter, they have to twist and be wrung out to release the oxygen. The chemicaland physical means of extraction of oxygen from the bloodstream allow its dispersal into the tissues. There, however, itrequires 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 transportWhen glucose is broken down to form pyruvate and lactate, 1,3-bisphosphoglycerate is on the pathway. It can continueto 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 chronicexposure to carbon monoxide. People with chronic anaemia and carbon monoxide poisoning will have an increase in2,3-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 isreleased. 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” toproduce 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. © Breakspear Medical Group Ltd, 2009 /Cont’d… 2 Breakspear Medical Group Ltd. Registered in England 2035350 Registered office: Hertfordshire House, Wood Lane, Hemel Hempstead, Hertfordshire HP2 4FD UK -2-
  • 105. The Krebs Cycle Food Protei Fat Carbohydrates Amino acids Glucose Fatty acids and glycerol e Pyruvate e Acetyl oxalocetate citrate e malate isocitrate Citric acid cycle e Anaerobic = fumarate a-ketoglutarate Aerobic = e e succinate succinylCoA e e e e Energy Water Waste productsTranscutaneous Blood GasesThe 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 thecells, and would contribute to fatigue. Some people have too low levels of carbon dioxide, which can lead to abnormalresponses by the brainstem. Some people have been found to be hypoxic with very low levels of oxygen. The gases areassessed to see if the abnormalities can be corrected by deep breathing, or by other breathing techniques. Breakspear Medical Group Ltd. Registered in England 2035350 Registered office: Hertfordshire House, Wood Lane, Hemel Hempstead, Hertfordshire HP2 4FD UK
  • 106. -3-Transcutaneous Blood Gases (Cont’d):The transcutaneous gases are measured by two different methods and combined together into one sensor. The sensorhas two membranes. One is sensitive to carbon dioxide only and the other membrane is sensitive to oxygen only. Asmall plastic cup is applied to the skin next to the liver, where the skin is warm. The cup is filled with a special fluidthat dissolves both oxygen and carbon dioxide. The sensor with the two membranes is then screwed tightly into thecup. Oxygen and carbon dioxide escape through the skin and dissolve into the special fluid. The dissolved gases arethen detected by the sensor.Carbon dioxide is detected by the change in the pH (hydrogen ion concentration). Meanwhile oxygen is detected by itsmagnetic property which increases with its concentration. In that way, both oxygen and carbon dioxide concentrationscan be measured simultaneously in real-time and these concentrations mirror the concentration in the capillaries. Thisconcentration 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 thecarrier protein for oxygen from the capillaries to the tissues.The correlation between VEGF measurements and transcutaneous gases will be presented.Jean A MonroMedical DirectorGMC No: 0552174
  • 107. Objectives & NotesHartmut Heine, Ph.D. Date of talk: Sunday, June 28, 2009, 9:30 a.m.Billerbeckweg 1-3 Phone: 49 (0) 7234 6246D-75242 Neuhausen, Fax: 49 (0) 7234 949109Germany Email: hartmutheine@aol.comTraining:Current Job Description: Private Scientific Research Institute Professor emeritus of Anatomy Formally full professor and head of the Department of Anatomy and Clinical Morphology of the University of Witten/Herdecke, GermanyOther Information: Heine H, Schaeg G. Kann die Tumorstammzelle morphologisch charakterisiert werden? Deutsche Zeitschrift für klinische Forschung 2008; 12: 42-45Disclosure Statement: NoneSPEECH 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 isnot responsible for the contents of this presentation. AEHF has not altered or modified the contents of theinformation provided by this speaker.
  • 108. Objectives & NotesKaye H. Kilburn, M.D. Date of talk: Sunday, June 28, 2009, 10:15 a.m.P.O. Box 5374 Phone: 626/798-4299Pasadena, CA 91107 Fax: 626/798-3859 Email: khkilburn@sbcglobal.netTraining: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 2004Disclosure Statement: NoneSPEECH TITLE: “Heart Disease and Rotten Egg Gas”At the end of this Presentation, the participant should be able to: 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).The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker. Heart Disease and Rotten Egg Gas
  • 109. By Professor Kaye H. Kilburn, M.D. USC Keck School of Medicine (ret.) Neuro-Test Inc., Pasadena, CA 91107Dennis thought his job smelled to high heaven, but he liked the pay. He worked at thewastewater treatment plant in Las Vegas for Nevada Power Company from 1983 to 1994. Beginning in 1990, he wastreating wastewater at what was described as “all comes and nothing leaves” sewage plant, but he knew that rotten egggas and water passed into the air. Prior to 1983, Dennis experienced no health problems while working 18 yearsmaking gypsum board, which is composed of calcium sulfate.Four of the 13 workers at the wastewater plant developed palpitations, rapid, irregular heart activity and showeddisorders 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 coronaryangiograms showed normal vessels and blood pressure was not elevated so his heart disease was diagnosed ascardiomyopathy. A biopsy confirmed a heart muscle fault. He was not an alcoholic or a cocaine user and had none ofthe 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 ofage and another age 32 years had a heart transplant. Shifting concerns to his brain, Dennis’ testing showed he could notdiscriminate between the pale colors in a spectrum. He had impaired problem solving, but other mind-brain functionswere normal. A year later and without further exposure, color discrimination and potential of H2S problem solvingwere normal and other functions remained intact, but he remained crippled by his heart’s low output of blood, itpumped badly.Tragic exposure is exemplified by eight sewer workers (aged 23 to 42 years), four killed at the scene and four admittedto the intensive care unit in Athens Greece. One died of pulmonary edema and circulatory failure, three recovered fromthe acute poisoning and were discharged, one needed a cardiac pacemaker. The others died later of myocardialinfarctions. 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 Mexicocommunity and others in Ohio and Hawaii have furnished additional examples of cardiopulmonary disorders fromrotten egg gas.The impression that damage to the brain and lung from H2S always went away when they awakened from coma, waiteduntil 1990 to be disproved. But in 1951, shale oil workers were reported having headaches, lethargy, dizziness, poormemory, fatigue, irritability, insomnia and depression from long term low dose H2S exposures. In the Alberta provinceof Canada from 1969 to 1973, 221 workers were exposed to H2S and 14 died. One of every 400 oil and gas workerswas poisoned in that period. Lungs of those who died from high doses of H2S were heavy and wet from pulmonaryedema and red froth poured from cut surfaces. Based on deaths and symptoms of distress of the brain, 10 states have setambient 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 therelated compound carbon disulfide (CS2) in the rayon (synthetic cloth) industry in the 1930’s. A pound of CS2 wasneeded to produce 3 pounds of rayon. Serious brain disability – dementia in workers was observed in Italy, Britain, andin Pennsylvania, where it triggered two public health investigations. The survey of 120 workers found psychiatricsymptoms, peripheral neuropathy, losses of cranial nerve functions, and a Parkinson’s disease disorder. Of the 120, 30workers had peripheral vascular disease, hypertension, and elevated cholesterol. Also, 43 Italian rayon workers hadvertigo, painful muscles, (myopathy) and inflamed blood vessels. Those groups are a form fuste of the coronary arterydisease epidemics later in the century. Use of carbon disulfide to fumigate grain elevators and corn bins exposedworkers in the American Midwest who showed hypertension, peripheral vascular insufficiency, and coronary ischemia.
  • 110. Humane and scientific interventions (experiments) are required . After measuring neurobehavioral, pulmonary andcardiovascular functions of H2S exposed people, they must reduce their exposure to the, presumed to be safe levels, thatare monitored and have functions be re-measured. When people become their own “controls,” matched comparisonsprovide 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, CRCCritical Reviews in Toxicology, 13: 25-97Bhambhani Y, Burnham R, Snydmiller G, MacLean L, Effects of 10-ppm Hydrogen Sulfide Inhalation in ExercisingMen 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.
  • 111. 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 withchronic exposure to hydrogen sulfide gas Environ Res 2004, 95: 53-61Lewey FH, Neurological, Medical and Biochemical Signs and Symptoms Indicating Chronic Industrial CarbonDisulphide Absorption, Ann. Intern. Med., 1941, 15: 869-883.Lowicha, E Beltowski J, Hydrogen sulfide(H2S)—the third gas of interest for pharmacologists PharmacologicalReports 2007,59:4-24.Nurminen M, Survival Experience of a Cohort of Carbon Disulphide Exposed Workers from an Eight-Year ProspectiveFollow-up Period, Intern J Epi; 1976; 179-185.Peters HA, Levine RL, Matthews CG, et al. Carbon Disulfide-Induced Neuropsychiatric Changes in Grain StorageWorkers, Am J. Industr. Med. 1982; 3: 373-391.Snyder JW, Safir EF, Summerville GP, et al. Occupational Fatality and Persistent Neurological Sequelae After MassExposure 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 workersexposed 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 ofmitogen-activated protein kinases and caspase-3, The FASEB J 2004; 18: 1782-1784.
  • 112. Objectives & NotesRussel J. Reiter, Ph.D. Date of talk: Sunday, June 28, 2009, 10:45 a.m.University of Texas Health Science Center Phone: 210/567-38597703 Floyd Curl Drive Fax: 210/567-6948San Antonio, TX 78229-3900 Email: reiter@uthscsa.eduTraining: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 ResearchDisclosure Statement: NoneSPEECH TITLE: “Melatonin Protects Heart From Free Radical Damage”At the end of this Presentation, the participant should be able to: 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.The American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.
  • 113. Objectives & NotesRichard G. Jaeckle, M.D. Date of talk: Sunday, June 28, 2009, 11:45 a.m.8220 Walnut HIll Lane, Ste. 404 Phone: 214/696-0964Dallas, TX 75231 Fax: 214/696-1094 Email: rgjmd@airmail.netTraining:Current Job Description: Private Practice of Psychiatry & Environmental MedicineCurrent Faculty Appointments:Medical School/ University AttendedInternship:Residency:Board Certifications:Other Information:Disclosure Statement: NoneSPEECH TITLE: “The Crosstalk Between the Central and Autonomic Nervous System”At the end of this Presentation, the participant should be able to: 1. Understand the dual branches of the Sypathic Nervous System 2. The two branches function separately or together. 3. Medications/precursors affect the two branchesThe American Environmental Health Foundation and the University of North Texas Health Science Center is notresponsible for the contents of this presentation. AEHF has not altered or modified the contents of the informationprovided by this speaker.