Endobiogeny and Cardiology

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Endobiogeny and Cardiology

  1. 1. Introduction toEndobiogeny:An integrative approach toMedicineBy:Jean Claude Lapraz, MDKamyar M. Hedayat, MD
  2. 2. OBJECTIVES• Introduce Endobiogeny and its component elements:• Detailed history• Detailed physical exam• Classical labs and imaging studies• Biology of Functions• Integrative assessment, then…• Therapeutic strategy• Example: application of concepts of Endobiogeny tocardiovascular disease• Discuss opportunities to learn the Endobiogenic method
  3. 3. IntroductionAn introduction to the Endobiogenic conceptA brief review of the history of medicine and itsschools of thought
  4. 4. Endobiogeny• The integrative study of the functional mechanisms ofregulation of the organism in its basic structure duringhomeostasis as well as its functional response tointernal and external stressors:• As a whole system• In its individual units of function• core metabolism• cell, tissue and organ• in and of themselves and in relationship to each other• Endobiogeny evaluates the qualitative and quantitativestate of the human organism and its internal milieu.
  5. 5. Example:Quantitative assessment• Consider a car factory to be like the ovaries. Does thenumber of cars (amount of estrogen) produced tell you howefficiently the factory (ovaries) is functioning or how well thecars produced drive?• A quantitative assessment of productivity tells you how manycars are being produced (serum estrogen levels), but not howwell those cars drive (endocrine and metabolic activity ofestrogen).• For example, if the output of cars meets demand, but thegear shifter is faulty (altered estrogen-receptor binding), eachcar carries fewer people than its normal capacity due todecreased torque. In this case, more cars will be needed tocarry people.• “Normal” factory output for this company (body) is insufficientto meet demand
  6. 6. Example:Qualitative assessment• But what about a qualitative assessment? There may be supplyissues—not enough steel available. The factory cannot producecars without steel (cholesterol as a precursor to estrogenproduction)• Perhaps there are not enough workers on the assembly line(Follicle stimulating hormone) and the workers present are over-worked and will soon decline in productivity (pituitary stress).• Perhaps there are ample supplies and workers, but the manageris inefficient (hypothalamus) in managing the factory, notregulating supply and demand issues.• Perhaps the manager is efficient, but the workers do not alwaysfollow his directives (altered thresholds of responsiveness).• Thus, it is clear that both a quantitative and qualitativeassessment of physiological and endocrine activity is necessaryto properly understand disease and health.
  7. 7. Endocrine management• Thus, Endobiogeny views the endocrine system asthe manager of the body, the controller of anabolismand catabolism—which is what life itself is at everylevel from the cell to the structure of the universe:• destruction and reconstruction• expansion and contraction• growth and apoptosis• birth and death
  8. 8. Philosophy• Endobiogeny integrates the rational and empiricalschools of medicine with philosophy to create asingle coherent system of medicine:• TheEndobiogenic approach begins with theontology (reason for existence) of structures andphysiology• This leads to a logical approach to understandingstructural weaknesses in the organism as well asdetermining the true cause of disease• Endobiogenic approach treats the person, not thedisease; treats global system rather than
  9. 9. Integration of data• Endobiogeny integrates:• History• Physical Exam• Laboratory data and Imaging studies• To reach a conclusion regarding the current, dynamicphysiological state of the individual in order toformulate a treatment strategy which addresses:• the identified imbalances individually• as well as in their relationship to other imbalances
  10. 10. Treatment Options• Endobiogenic treatments consist of various therapeuticelements based on their safety and efficacy with noprejudice to the school of thought from which thetreatment originates:• Phytotherapeutic elements• Homeopathic elements• Pharmaceuticals elements: reasoned usage based onseverity of symptoms, of degree or lack of compensatoryphysiology.• Physical manipulations: craniosacral, myofascial, etc.• Nutrition• Oligoelement supplementation• Stress modification, hydrotherapy, acupuncture, etc.
  11. 11. Individualized medicine• Endobiogeny is individualized medicine based on:• The patient’s symptomization of illness within thecontext of the global functioning of the organism• The physician’s determination of the signs ofphysiological and endocrine dysfunction• The physician’s objective assessment of endocrinerelationships• The particular physical, physiological, psychologicaland emotional realities of the individual.
  12. 12. Conclusion• Endobiogenic treatment is determined by the totality ofthe person:• Static and dynamic aspects of the patient’s constitution• Etiology, ontology, and integration of symptoms• Adaptive and maladaptive aspects of physiology
  13. 13. History of developmentof Endobiogeny
  14. 14. Founders ofEndobiogeny• Endobiogenie is the work of twoFrench medical doctors, ChristianDuraffourd, MD and Jean ClaudeLapraz, MD• Drs. Duraffourd and Lapraz early intheir medical careers called intoquestion the predominant allopathicconcepts of disease as well as thereliance on single-receptor syntheticmedications• Since 1973, their work has focused onthe synthesis of modernphysiology, empirical medicine andclinical phytotherapyDr. DuraffourdDr. Lapraz
  15. 15. Development ofConcepts• The 1970s saw the establishment of the French Society forPhytotherapy and Aromatherapy (SFPA) and the concertedeffort of a group of physicians to go beyond the reductionistconcepts of allopathic medicine• 1980’s: Drs. Duraffourd and Lapraz spent over 7 yearstreating cancer patients in an in-patient oncology ward,which established the importance ofqualitative relationshipof hormones to one another as the basis of health andillness• 1990s: International teachings and publication of majorworks in clinical phytotherapy and their neuro-endocrineimpact on the body
  16. 16. The EndobiogenicMethod
  17. 17. Laboratory studies• Classical lab data is based on binary considerations:• disease vs. no disease• normal vs. abnormal value• However, the human body works across a spectrum offunction.• Pathophysiological disruption with elevated serumenzymes or deranged blood elements is a late finding inthe disease process• Long before this stage, patients experience a functionaldysfunction with sub-optimal activity, but normal labs• Thus, it is self-evident that binary considerations cannotbe applied with any real assurance of its functionalrelevance to a system as complex as the human body.
  18. 18. Laboratory studies• Biological systems are complex, multi-tiered, dynamicinterrelated and integrated systemsYeast Protein Interaction NetworkBader and Hogue (2002) NatureIntegrated, inter-related system
  19. 19. Integrated systems• Objective quantitative data (laboratory values) arerequired to assess the organism• However, one must be able to provide functionaldescriptions of quantitative and qualitative activity bothwithin a particular unit of activity, from one unit toanother, as well as within the system as a whole• Only then can a truly dynamic and individualizedassessment of the patient occur
  20. 20. Laboratory studies• The endocrine system, as the manager of themetabolic activity of the body, is the ideal object ofevaluation.• Serum levels of hormones reflect neither thedegree of stimulation needed nor the metaboliccosts incurred in producing a particular hormone.1-31) Raison CL, Miller AH. When not enough is too much: the role of insufficientglucocorticoid signaling in the pathophysiology of stress-related disorders. Am JPsychiatry. Sep 2003;160(9):1554-15652) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and staticmodification of the epigenome by hormones: A role in the developmental origin ofhormone related cancers. Biochem Biophys Acta. Apr 2009;1795(2):104-109.3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals onhormonal and immunological factors in women with repeated miscarriages. HumReprod Update. May-Jun 1998;4(3):301-309.
  21. 21. Laboratory studies• Serum levels of hormones only reflect quantitative organoutput, not functional activity, which can be affected by:• Hormone receptor binding (affected by over- or under-expression of other hormones)1• Intracellular messenger activity1• Epigenetic changes2• Heavy metal toxicity3, etc.1) Raison CL, Miller AH. When not enough is too much: the role of insufficient glucocorticoidsignaling in the pathophysiology of stress-related disorders. Am J Psychiatry. Sep2003;160(9):1554-15652) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and static modification of theepigenome by hormones: A role in the developmental origin of hormone related cancers.BiochemBiophysActa. Apr 2009;1795(2):104-109.3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on hormonal andimmunological factors in women with repeated miscarriages. Hum Reprod Update. May-Jun1998;4(3):301-309
  22. 22. Laboratory studies• The ideal system of measurement of biological processesthus should examine the metabolic products of hormonalmanagement of cellular activity• Thus, the ideal laboratory system must• Reflect the complex, integrated and dynamic nature ofbiological systems• Describe the functionality of the system in its• Qualitative function• Quantitative function• Individual unit, relative to other units and as a whole• Assess the organism at the metabolic and interstitial level
  23. 23. Biology of functions• The Biology of Functions (BoF) quantifies functionalabilities of the organism, before and after theeffects ofadaptation to stressors. Because functionality isdynamic, a dynamic, integrated and evolutionarymethodology must be used instead of static lab values• BoF is based on a number of specific indices defined bymathematical relations between commonly used bloodanalysis data• The algorithms that permit the calculation of theseindices are based on the physiological relations thatexist between the direct or indirect products ofhormonal activity: cells, hormones or enzymes(eosinophils, TSH and LDH, for example).
  24. 24. Biology of Functions• These relations allow one to visualize thefunctioning of the organism at every level:maintenance of homeostasis, adaptation, recoveryafter aggression, immunity, etc.• Each function is quantified by an index, specifiedby a level of activity. The index expresses theactual activity of that function, both in and of itselfand in relation to the metabolic and tissue needs ofthe organism.• The whole set of indices gives an evolutionaryassessment of an individual body’s functionality,system by system, organ by organ.
  25. 25. Biology of functions• SUMMARY: Biology of Functions:• Allows one to determine:• Pathogenic tendencies of the organism (i.e. celldysplasia—”pre-cancer”, fatty streaks—earlyatheromatous plaque development, amyloidplaques—degenerative neurological disease),• The stage of development and severity of thatpathology• Can be used as a tool to track• the natural development of pathology• To derive a rational therapeutic treatment• To evaluate the efficacy of the treatment over time
  26. 26. Example:Adaptation Index• According to Dr. Duraffourd, an intra-pituitaryphysiologiclinkage exists in the stimulation of FSH by ACTH• The Adaptation Index evaluates the relative activityofACTH relative to FSH in order to determine the degreeof efficiency of catabolism (cortisol) vs. thedegree ofefficiency of anabolism (estrogen) in response to stress• The Adaptation Index examines thisactivityat themetaboliclevel by examining the products of hormonalactivity (cortisol and estrogen in thisexample) as anassessment of hormonal activity• It iscalculated as the ratio of eosinophils to monocytes
  27. 27. Adaptation Index: Proofs• Eosinophils are inverselyrelated to theefficiency of ACTH activity in its adaptiveresponse to stress1• ACTH stimulates cortisol activity• Cortisol stimulates eosinophil apoptosis• Cortisol resistance occurs during chronicstimulation of the adrenal gland, or duringsevere cases of acute illness31) Giembycz MA, Lindsay MA. Pharmacology of the eosinophil. Pharmacol Rev. Jun1999;51(2):213-340.2) Beishuizen A, Vermes I, Hylkema BS, Haanen C. Relative eosinophilia andfunctional adrenal insufficiency in critically ill patients. Lancet. May 151999;353(9165):1675-1676.)3) Miller GE, Cohen S, Ritchey AK. Chronic psychological stress and the regulationof pro-inflammatory cytokines: a glucocorticoid-resistance model. Health Psychol.Nov 2002;21(6):531-541.
  28. 28. Adaptation Index: Proofs• Cortisol resistance has two effects:• Elevated ACTH activity to stimulate more cortisolproduction• Loss of tonic inhibition of eosinophils, resulting ineosinophilia1• Eosinophilia is correlated with severity of criticalillness21) Giembycz MA, Lindsay MA. Pharmacology of the eosinophil. Pharmacol Rev. Jun1999;51(2):213-340.2) Beishuizen A, Vermes I, Hylkema BS, Haanen C. Relative eosinophilia and functional adrenalinsufficiency in critically ill patients. Lancet. May 15 1999;353(9165):1675-1676.)
  29. 29. Adaptation Index: Proofs• Monocytes are inversely related to the efficiency ofFSH activity during adaptation to stress1• Mechanism:• FSH levels are proportional to estrogen• Estrogen suppresses monocyte production2• Monocytosis during stress indicates ineffective FSHactivity (even if serum levels are elevated) and iscorrelated with increased mortality3, which isreflected as a LOW Adaptation index1) Ziegler-Heitbrock L. The CD14+ CD16+ blood monocytes: their role in infection and inflammation. JLeukoc Biol. Mar 2007;81(3):584-592.2) Harkonen PL, Vaananen HK. Monocyte-macrophage system as a target for estrogen and selectiveestrogen receptor modulators. Ann N Y Acad Sci. Nov 2006;1089:218-227)3) Fingerle G, Pforte A, Passlick B, Blumenstein M, Strobel M, Ziegler-Heitbrock HW. The novel subset ofCD14+/CD16+ blood monocytes is expanded in sepsis patients. Blood. Nov 15 1993;82(10):3170-3176.
  30. 30. Cardiovascular Disease(CVD)An Endobiogenic Approach
  31. 31. Uniqueness ofVasculature• Vascular system unique system in body:• Ubiquitous throughout the body• Controlled by chemo-, baro-, hormonal, CNS factors• Endocrine and paracrine system itself• Means of transmission of information and nutrition• Subjects global system to local phenomenon• Participates in initiating and responding to localevents• Contains a homunculus of itself: vasovasorum
  32. 32. Vascular Disease:Atheromas• When treating atheromatous lesions one mustdistinguish between:• Ontology: the true reason for the dysadaptation• Etiology: mechanisms of response to the dysadaptation• Primary: Endocrine, Neurovegetative (NV)• Secondary: Paracrine, autocrine, adaptive elements,pathophysiological• Finality: the end result of the dysadaptation
  33. 33. Limitations of Etiology-basedtreatments• Cardiologists classically have focused on the mechanismsof plaque formation rather than the reason for plaqueformation:• Neuro-Vascular: Alpha-, beta-sympathetic activity• Energetic elements: Cholesterol, HDL, LDL, TG, Glucose• Lipids are a necessary but not sufficient factor for atheromatousdisease• Hyperlipidemia ≠ Dyslipidemia• Pathophysiological mediators: Inflammation, Freeradicals, Nitric Oxide, homocysteine, etc.• Thus, we have failed to identify the fundamentalfactors that allows atheromas to form in one patientand not another, all screening factors beingequal, such as age, BMI, cholesterol and blood
  34. 34. Limitations of Etiology-basedtreatments• Treating local phenomena globally with beta-blockersand statins have lead to reduction in CV events, but ata global cost, such as increased risk of stroke andloss of libido, muscle wasting, respectively.• The entire body is subjected to suppression of factorswhich are still adaptive and beneficial for the globalorganism, but not for a particular part of the body• The failure to identify and treat the true causes of CVplaques results in anomalies such as “low risk”patients having fatal MI’s and “high risk” patients livinglong, healthy lives
  35. 35. Endobiogenic approach• True cause of atheromatous plaques is dysadaptiveendocrine response to local needs for increased nutrition:• Internal or external aggressors (viruses, emotionalstressors, tobacco smoke, heavy metals)• Times of restructuring of the body (menopause, andropause)• If the response to anabolic requirements is badly managedby the body, or the demand is prolonged or the body is notable to return to its previous homeostatic thresholds ofendocrine response, a dysmetabolic response ensues• This is the true ontology of disease because endocrinesystem manages all metabolic activity of the body
  36. 36. Etiology of Atheromas• Local tissue or organ demand for anabolic adaptation demandsincreased nutrient delivery:• CATABOLIC: ACTH Cortisol: liberates glucose byglycogenolysis for generation of ATP; TSH Thyroid: liberateslipids for energy and cell wall building• ANABOLIC: ProlactinInsulin: increases nutrient penetrationinto cells; FSH/LH Estrogen and Testosterone: anabolicsteroid for protein incorporation and utilization in the cell• Histamine: capillary leakextravasation of nutrients into extra-cellular matrix• Aldosterone: improve electrolyte presentation to cells, increasecirculating blood volume• HTN: post-capillary increased duration of nutrient presentation
  37. 37. Etiology of Atheromas Vasculature as transportation medium for thesefactors carries them from local area of need, creatingsystemic inflammation Vasculature has greatest exposure to thesemediators, thus endothelium becomes damaged bythese mediators Now that catabolic and anabolic activities are dysregu-lated, with increased glucose, lipids andinflammation, vasculature itself undergoes hyper-anabolic repair of damaged endothelium and mediasmooth muscle proliferation and atheromatousplaques
  38. 38. Endobiogenic approach• Endocrine factors have been well described since as early as1950’s, but neither their relationship to each other nor theirontological significance has been clearly elucidated by classicalmedicine• Two primary indices in the biology of functions describe therelationship between these elements and assist the clinician inevaluating the true cause of disease and the optimal treatmentoption• Thrombogenic index: describes the risk of lumenal narrowing fromatheromatous plaques, and by extension, the thrombogenicpotential• Thrombotic index: describes the actual risk of developing thrombo-embolic phenomenon from atheromas or due to altered bloodrheology. The thrombotic index contains the thrombotic index
  39. 39. Biology of functions (BoF):Thrombogenic IndexProportional to [labs] (related BoF index) :• Acute stress [LDH] (Thyroid index)1• Elevated ACTH (Adaptation index)2,3• Relative Eosinophilia [eosinophil %] (Adaptation index)4-6• Cortisol [salivary cortisol] (Anabolism index)71) Karacalioglu O et al. Baseline serum levels of cardiac biomarkers in patients with stable coronary arterydisease. Biomarkers. Sep-Oct 2007;12(5):533-540.2) Bloom B, Pierce FT, Jr. Relationship of ACTH and cortisone to serum lipoproteins and atherosclerosis inhumans. Metabolism. Mar 1952;1(2):155-162.3) Letizia C, Barilla F, Cerci S, et al. beta-Endorphin and propiomelanocortin-correlates peptides response insuspected and confirmed ischemic heart disease during exercise. Acta Cardiol. 1996;51(1):27-36.4) Siddiqui S et al. Factors predicting outcome in a cohort of patients with atherosclerotic renal artery diseasediagnosed by magnetic resonance angiography. Am J Kidney Dis. Dec 2005;46(6):1065-1073.5) Emanuele E et al. Association of plasma eotaxin levels with the presence and extent of angiographiccoronary artery disease. Atherosclerosis. May 2006;186(1):140-145.6) Atkinson JB et al. Association of eosinophils with cardiac rupture. Hum Pathol. Jun 1985;16(6):562-568.7) Dekker MJ et al. Salivary cortisol is related to atherosclerosis of carotid arteries. J Clin Endocrinol Metab.Oct 2008;93(10):3741-3747.
  40. 40. Biology of functions (BoF):Thrombogenic IndexProportional to [labs] (related BoF index) :• Gonadal Androgens [free Testosterone] (Androgenic)1• Insulin (Anabolism index)9• Sub-clinical hypothyroidism [TSH] (Bone remodelingindex)10-131) Dogramaci AC, Balci DD, Balci A, et al. Is androgenetic alopecia a risk for atherosclerosis? J Eur AcadDermatol Venereol. Feb 23 2009.2) de Rooij S, Dekker J, Kozakova M, et al. Fasting insulin has a stronger association with an adverse cardio-metabolic risk profile than insulin resistance: The RISC study. Eur J Endocrinol. May 13 20093) Stamatelopoulos KS, Kyrkou K, Chrysochoou E, et al. Arterial Stiffness but Not Intima-Media Thickness IsIncreased in Euthyroid Patients with Hashimotos Thyroiditis: The Effect of Menopausal Status. Thyroid. Apr 62009.4) Sidorenko BA, Begliarov MI, Titov VN, Masenko VP, Parkhimovich RM. [Blood thyroid hormones in ischemicheart disease (a comparison with coronary angiographic data, severity of stenocardia and blood lipid level)].Kardiologiia. Dec 1981;21(12):96-101.
  41. 41. Biology of functions (BoF):Thrombogenic IndexInversely proportional to [labs] (related BoF index) :• Estrogen [Estradiol, free] (Estrogen index; BoneRemodeling index)1• Adrenal Androgens [DHEAS] (Androgenic index)2-41) Gopalakrishnan P, Ragland MM, Tak T. Gender differences in coronary arterydisease: review of diagnostic challenges and current treatment. Postgrad Med.Mar 2009;121(2):60-68.2) Ii M, Hoshiga M, Negoro N, et al. Adrenal androgen dehydroepiandrosteronesulfate inhibits vascular remodeling following arterial injury. Atherosclerosis. Feb27 2009.3) Savastano S, Valentino R, Belfiore A, et al. Early carotid atherosclerosis innormotensive severe obese premenopausal women with low DHEA(S). JEndocrinol Invest. Mar 2003;26(3):236-243.4) Altman R, Motton DD, Kota RS, Rutledge JC. Inhibition of vascular inflammationby dehydroepiandrosterone sulfate in human aortic endothelial cells: roles ofPPARalpha and NF-kappaB. VasculPharmacol. Feb-Mar 2008;48(2-3):76-84.
  42. 42. Biology of functions (BoF):Thrombogenic Index The biology of function allows you to evaluate the riskof lumenal narrowing from atheromas both from thegestalt of risk factors Allows the physician to indentify the risk factorsparticular to the patient. Allows the physician to assess risk on physiologicaldata rather than generalized risk factors based onepidemiological data
  43. 43. Treatment plan based on Thrombogenic index
  44. 44. Other Indices: Physiological Thrombogenic index: Examines the risk of thrombo-embolic phenomenon. Factors in all the risk factorsassociated with atherogenesis as well as the role ofhistamine1 Tx: Reduce histamine with Plantain, Vitamin C, or Lavender Ischemia index: relates degree of tissue congestion relativeto rate of metabolism Tx: Correct sick euthyroid: iodine, wolfberry, stone steed Pro-amyloid: examines the degree of cellular nutritionaland oxygen deficiency, indirectly examining the degree ofmitochondrial strain and oxidative phosphorylation Tx: CoQ10, L-Carnitine (if  triglycerides), Creatine (if  CPK)1) Tanimoto A, Sasaguri Y, Ohtsu H. Histamine network in atherosclerosis. Trends Cardiovasc Med.Nov 2006;16(8):280-284.
  45. 45. Other Indices:Psychological betaMSH/alpha MSH: characterizes the degree ofintrapsychic activity originating from Dopamine vs.Norepinephrine Adaptogenic: characterizes the degree of internal dialogue Thyroid relaunching, corrected: characterizes the degree ofendocrine dysfunction originating from emotional issues Interleukin-1: characterizes the impact of emotional andendocrine factors on immune activity, immune regulationand cellular proliferation (intimal thickening is a carcinoidtype of dedifferentiation of the smooth muscle)11) Argaman M, Gidron Y, Ariad S. Interleukin-1 may link helplessness-hopelessness with cancerprogression: a proposed model. Int J Behav Med. 2005;12(3):161-170.
  46. 46. Conclusions
  47. 47. Conclusions• Endobiogeny is the study of the internal milieu of the organism• Within itself• In its relationship with its environment, stressors, etc.• From the standpoint of the endocrine system as the manager ofhuman life• In order to create a rational, individualized treatmentplan
  48. 48. Conclusions• It combines in an integrative understanding:• a philosophical consideration of the ontology of structures andfunctions of the body,• a rational approach to understanding physiology• an empirical assessment of history and symptoms• utilization of a dynamic, integrative and integrated metabolicassessment of endocrine management of the organism calledthe “Biology of Functions”• an integrated assessment of all clinical data to obtain a preciseunderstanding of maladaptive physiology
  49. 49. Conclusions• The Biology of Functions is an algorithmic assessment of thequalitative and quantitative relationships of hormones in terms ofmetabolic activity from nuclear, cellular, tissue, organ andsystem-wide perspectives• The Biology of Functions allows for an objective, longitudinalassessment of the effects of therapy over time• Endobiogeny relies on phytotherapy, oligotherapy, and diet aswell as lifestyle modification as its preferred methods ofameliorating physiological imbalances• It reserves the use of synthetic drugs for urgent cases, or whenthe body is not able to establish an equilibrium by the effects offunctional regulation
  50. 50. Resources• To learn more about Endobiogeny:• Web:• General information:• www.eimcenter.org• www.fullspectrumhealthmd.com• Biology of Functions demonstration:• http://extranet.endobiogenics.com/en/• Seminars:• Call: 858-455-9726
  51. 51. PractitionersFor more information contact EndobiogenicpractitionersUnited States:• Kamyar M. Hedayat, MD,• Expertise: Critical carephysiology, neurodegenerativedisorders, pediatrics• Contact: kmhedayat@aromamd.net• Web: www.fullspectrumhealthmd.com
  52. 52. PractitionersContinental Europe• Jean Claude Lapraz, MD, co-developer ofEndobiogeny• Expertise: Cancer, all areas• Contact: jc.lapraz@orange.fr• Patrice Pauly, PhD• Expertise: Biology of Functions, systems analysis• Contact: patricepauly@yahoo.fr
  53. 53. REFERENCESSLIDE 221) Raison CL, Miller AH. When not enough is too much: the role ofinsufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. Am J Psychiatry. Sep 2003;160(9):1554-15652) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and staticmodification of the epigenome by hormones: A role in the developmentalorigin of hormone related cancers. Biochem Biophys Acta. Apr2009;1795(2):104-109.3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals onhormonal and immunological factors in women with repeatedmiscarriages. Hum Reprod Update. May-Jun 1998;4(3):301-309
  54. 54. REFERENCESSLIDE 231) Raison CL, Miller AH. When not enough is too much: therole of insufficient glucocorticoid signaling in thepathophysiology of stress-related disorders. Am JPsychiatry. Sep 2003;160(9):1554-15652) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. Thedynamic and static modification of the epigenome byhormones: A role in the developmental origin of hormonerelated cancers. BiochemBiophysActa. Apr2009;1795(2):104-109.3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact ofheavy metals on hormonal and immunological factors inwomen with repeated miscarriages. Hum Reprod Update.May-Jun 1998;4(3):301-309
  55. 55. REFERENCESSLIDE 291) Giembycz MA, Lindsay MA. Pharmacology of theeosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.Relative eosinophilia and functional adrenalinsufficiency in critically ill patients. Lancet. May 151999;353(9165):1675-1676.)3) Miller GE, Cohen S, Ritchey AK. Chronicpsychological stress and the regulation of pro-inflammatory cytokines: a glucocorticoid-resistancemodel. Health Psychol. Nov 2002;21(6):531-541.
  56. 56. REFERENCESSLIDE 301) Giembycz MA, Lindsay MA. Pharmacology of theeosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.Relative eosinophilia and functional adrenalinsufficiency in critically ill patients. Lancet. May 151999;353(9165):1675-1676.)
  57. 57. REFERENCESSLIDE 311) Giembycz MA, Lindsay MA. Pharmacology of theeosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.Relative eosinophilia and functional adrenalinsufficiency in critically ill patients. Lancet. May 151999;353(9165):1675-1676.)
  58. 58. REFERENCESSlide 411) Karacalioglu O et al. Baseline serum levels of cardiacbiomarkers in patients with stable coronary artery disease.Biomarkers. Sep-Oct 2007;12(5):533-540.2) Bloom B, Pierce FT, Jr. Relationship of ACTH and cortisoneto serum lipoproteins and atherosclerosis in humans.Metabolism. Mar 1952;1(2):155-162.3) Letizia C, Barilla F, Cerci S, et al. beta-Endorphin andpropiomelanocortin-correlates peptides response insuspected and confirmed ischemic heart disease duringexercise. Acta Cardiol. 1996;51(1):27-36.4) Siddiqui S et al. Factors predicting outcome in a cohort ofpatients with atherosclerotic renal artery disease diagnosedby magnetic resonance angiography. Am J Kidney Dis. Dec2005;46(6):1065-1073.
  59. 59. REFERENCESSLIDE 41 (cont.)5) Emanuele E et al. Association of plasma eotaxin levelswith the presence and extent of angiographic coronaryartery disease. Atherosclerosis. May 2006;186(1):140-145.6) Atkinson JB et al. Association of eosinophils withcardiac rupture. Hum Pathol. Jun 1985;16(6):562-568.7) Dekker MJ et al. Salivary cortisol is related toatherosclerosis of carotid arteries. J Clin EndocrinolMetab. Oct 2008;93(10):3741-3747.
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