Transcript of "Urticaria and Vasculitis in Patients with HCV and ..."
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.
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.
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.
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
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
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
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
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.
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
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
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: firstname.lastname@example.orgRome, 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.
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.
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: email@example.comCanadaTraining: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.
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.
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: firstname.lastname@example.orgTraining: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.
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
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: email@example.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:
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: firstname.lastname@example.orgTraining: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.
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: email@example.comTraining: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.
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.
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.
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.
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.
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
• 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.
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: firstname.lastname@example.orgGreenville, 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.
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.
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.
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
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.
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: email@example.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.
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.
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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. 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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: firstname.lastname@example.orgTraining: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.