1. Introduction to
Endobiogeny:
An integrative approach to
Medicine
By:
Jean Claude Lapraz, MD
Kamyar M. Hedayat, MD

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 to
cardiovascular disease
• Discuss opportunities to learn the Endobiogenic method

3. Introduction
An introduction to the Endobiogenic concept
A brief review of the history of medicine and its
schools of thought

4. Endobiogeny
• The integrative study of the functional mechanisms of
regulation of the organism in its basic structure during
homeostasis as well as its functional response to
internal 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 quantitative
state of the human organism and its internal milieu.

5. Example:
Quantitative assessment
• Consider a car factory to be like the ovaries. Does the
number of cars (amount of estrogen) produced tell you how
efficiently the factory (ovaries) is functioning or how well the
cars produced drive?
• A quantitative assessment of productivity tells you how many
cars are being produced (serum estrogen levels), but not how
well those cars drive (endocrine and metabolic activity of
estrogen).
• For example, if the output of cars meets demand, but the
gear shifter is faulty (altered estrogen-receptor binding), each
car carries fewer people than its normal capacity due to
decreased torque. In this case, more cars will be needed to
carry people.
• “Normal” factory output for this company (body) is insufficient
to meet demand

6. Example:
Qualitative assessment
• But what about a qualitative assessment? There may be supply
issues—not enough steel available. The factory cannot produce
cars without steel (cholesterol as a precursor to estrogen
production)
• 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 manager
is inefficient (hypothalamus) in managing the factory, not
regulating supply and demand issues.
• Perhaps the manager is efficient, but the workers do not always
follow his directives (altered thresholds of responsiveness).
• Thus, it is clear that both a quantitative and qualitative
assessment of physiological and endocrine activity is necessary
to properly understand disease and health.

7. Endocrine management
• Thus, Endobiogeny views the endocrine system as
the manager of the body, the controller of anabolism
and catabolism—which is what life itself is at every
level from the cell to the structure of the universe:
• destruction and reconstruction
• expansion and contraction
• growth and apoptosis
• birth and death

8. Philosophy
• Endobiogeny integrates the rational and empirical
schools of medicine with philosophy to create a
single coherent system of medicine:
• TheEndobiogenic approach begins with the
ontology (reason for existence) of structures and
physiology
• This leads to a logical approach to understanding
structural weaknesses in the organism as well as
determining the true cause of disease
• Endobiogenic approach treats the person, not the
disease; treats global system rather than

9. Integration of data
• Endobiogeny integrates:
• History
• Physical Exam
• Laboratory data and Imaging studies
• To reach a conclusion regarding the current, dynamic
physiological state of the individual in order to
formulate a treatment strategy which addresses:
• the identified imbalances individually
• as well as in their relationship to other imbalances

10. Treatment Options
• Endobiogenic treatments consist of various therapeutic
elements based on their safety and efficacy with no
prejudice to the school of thought from which the
treatment originates:
• Phytotherapeutic elements
• Homeopathic elements
• Pharmaceuticals elements: reasoned usage based on
severity of symptoms, of degree or lack of compensatory
physiology.
• Physical manipulations: craniosacral, myofascial, etc.
• Nutrition
• Oligoelement supplementation
• Stress modification, hydrotherapy, acupuncture, etc.

11. Individualized medicine
• Endobiogeny is individualized medicine based on:
• The patient’s symptomization of illness within the
context of the global functioning of the organism
• The physician’s determination of the signs of
physiological and endocrine dysfunction
• The physician’s objective assessment of endocrine
relationships
• The particular physical, physiological, psychological
and emotional realities of the individual.

12. Conclusion
• Endobiogenic treatment is determined by the totality of
the person:
• Static and dynamic aspects of the patient’s constitution
• Etiology, ontology, and integration of symptoms
• Adaptive and maladaptive aspects of physiology

13. History of development
of Endobiogeny

14. Founders of
Endobiogeny
• Endobiogenie is the work of two
French medical doctors, Christian
Duraffourd, MD and Jean Claude
Lapraz, MD
• Drs. Duraffourd and Lapraz early in
their medical careers called into
question the predominant allopathic
concepts of disease as well as the
reliance on single-receptor synthetic
medications
• Since 1973, their work has focused on
the synthesis of modern
physiology, empirical medicine and
clinical phytotherapy
Dr. Duraffourd
Dr. Lapraz

15. Development of
Concepts
• The 1970s saw the establishment of the French Society for
Phytotherapy and Aromatherapy (SFPA) and the concerted
effort of a group of physicians to go beyond the reductionist
concepts of allopathic medicine
• 1980’s: Drs. Duraffourd and Lapraz spent over 7 years
treating cancer patients in an in-patient oncology ward,
which established the importance ofqualitative relationship
of hormones to one another as the basis of health and
illness
• 1990s: International teachings and publication of major
works in clinical phytotherapy and their neuro-endocrine
impact on the body

16. The Endobiogenic
Method

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 of
function.
• Pathophysiological disruption with elevated serum
enzymes or deranged blood elements is a late finding in
the disease process
• Long before this stage, patients experience a functional
dysfunction with sub-optimal activity, but normal labs
• Thus, it is self-evident that binary considerations cannot
be applied with any real assurance of its functional
relevance to a system as complex as the human body.

18. Laboratory studies
• Biological systems are complex, multi-tiered, dynamic
interrelated and integrated systems
Yeast Protein Interaction Network
Bader and Hogue (2002) Nature
Integrated, inter-related system

19. Integrated systems
• Objective quantitative data (laboratory values) are
required to assess the organism
• However, one must be able to provide functional
descriptions of quantitative and qualitative activity both
within a particular unit of activity, from one unit to
another, as well as within the system as a whole
• Only then can a truly dynamic and individualized
assessment of the patient occur

20. Laboratory studies
• The endocrine system, as the manager of the
metabolic activity of the body, is the ideal object of
evaluation.
• Serum levels of hormones reflect neither the
degree of stimulation needed nor the metabolic
costs incurred in producing a particular hormone.1-3
1) Raison CL, Miller AH. When not enough is too much: the role of insufficient
glucocorticoid signaling in the pathophysiology of stress-related disorders. Am J
Psychiatry. Sep 2003;160(9):1554-1565
2) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and static
modification of the epigenome by hormones: A role in the developmental origin of
hormone related cancers. Biochem Biophys Acta. Apr 2009;1795(2):104-109.
3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on
hormonal and immunological factors in women with repeated miscarriages. Hum
Reprod Update. May-Jun 1998;4(3):301-309.

21. Laboratory studies
• Serum levels of hormones only reflect quantitative organ
output, 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 glucocorticoid
signaling in the pathophysiology of stress-related disorders. Am J Psychiatry. Sep
2003;160(9):1554-1565
2) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and static modification of the
epigenome 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 and
immunological factors in women with repeated miscarriages. Hum Reprod Update. May-Jun
1998;4(3):301-309

22. Laboratory studies
• The ideal system of measurement of biological processes
thus should examine the metabolic products of hormonal
management of cellular activity
• Thus, the ideal laboratory system must
• Reflect the complex, integrated and dynamic nature of
biological 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. Biology of functions
• The Biology of Functions (BoF) quantifies functional
abilities of the organism, before and after theeffects of
adaptation to stressors. Because functionality is
dynamic, a dynamic, integrated and evolutionary
methodology must be used instead of static lab values
• BoF is based on a number of specific indices defined by
mathematical relations between commonly used blood
analysis data
• The algorithms that permit the calculation of these
indices are based on the physiological relations that
exist between the direct or indirect products of
hormonal activity: cells, hormones or enzymes
(eosinophils, TSH and LDH, for example).

24. Biology of Functions
• These relations allow one to visualize the
functioning of the organism at every level:
maintenance of homeostasis, adaptation, recovery
after aggression, immunity, etc.
• Each function is quantified by an index, specified
by a level of activity. The index expresses the
actual activity of that function, both in and of itself
and in relation to the metabolic and tissue needs of
the organism.
• The whole set of indices gives an evolutionary
assessment of an individual body’s functionality,
system by system, organ by organ.

25. Biology of functions
• SUMMARY: Biology of Functions:
• Allows one to determine:
• Pathogenic tendencies of the organism (i.e. cell
dysplasia—”pre-cancer”, fatty streaks—early
atheromatous plaque development, amyloid
plaques—degenerative neurological disease),
• The stage of development and severity of that
pathology
• 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. Example:
Adaptation Index
• According to Dr. Duraffourd, an intra-pituitaryphysiologic
linkage exists in the stimulation of FSH by ACTH
• The Adaptation Index evaluates the relative activityof
ACTH relative to FSH in order to determine the degree
of efficiency of catabolism (cortisol) vs. thedegree of
efficiency of anabolism (estrogen) in response to stress
• The Adaptation Index examines thisactivityat the
metaboliclevel by examining the products of hormonal
activity (cortisol and estrogen in thisexample) as an
assessment of hormonal activity
• It iscalculated as the ratio of eosinophils to monocytes

27. Adaptation Index: Proofs
• Eosinophils are inverselyrelated to the
efficiency of ACTH activity in its adaptive
response to stress1
• ACTH stimulates cortisol activity
• Cortisol stimulates eosinophil apoptosis
• Cortisol resistance occurs during chronic
stimulation of the adrenal gland, or during
severe cases of acute illness3
1) Giembycz MA, Lindsay MA. Pharmacology of the eosinophil. Pharmacol Rev. Jun
1999;51(2):213-340.
2) Beishuizen A, Vermes I, Hylkema BS, Haanen C. Relative eosinophilia and
functional adrenal insufficiency in critically ill patients. Lancet. May 15
1999;353(9165):1675-1676.)
3) Miller GE, Cohen S, Ritchey AK. Chronic psychological stress and the regulation
of pro-inflammatory cytokines: a glucocorticoid-resistance model. Health Psychol.
Nov 2002;21(6):531-541.

28. Adaptation Index: Proofs
• Cortisol resistance has two effects:
• Elevated ACTH activity to stimulate more cortisol
production
• Loss of tonic inhibition of eosinophils, resulting in
eosinophilia1
• Eosinophilia is correlated with severity of critical
illness2
1) Giembycz MA, Lindsay MA. Pharmacology of the eosinophil. Pharmacol Rev. Jun
1999;51(2):213-340.
2) Beishuizen A, Vermes I, Hylkema BS, Haanen C. Relative eosinophilia and functional adrenal
insufficiency in critically ill patients. Lancet. May 15 1999;353(9165):1675-1676.)

29. Adaptation Index: Proofs
• Monocytes are inversely related to the efficiency of
FSH activity during adaptation to stress1
• Mechanism:
• FSH levels are proportional to estrogen
• Estrogen suppresses monocyte production2
• Monocytosis during stress indicates ineffective FSH
activity (even if serum levels are elevated) and is
correlated with increased mortality3, which is
reflected as a LOW Adaptation index
1) Ziegler-Heitbrock L. The CD14+ CD16+ blood monocytes: their role in infection and inflammation. J
Leukoc Biol. Mar 2007;81(3):584-592.
2) Harkonen PL, Vaananen HK. Monocyte-macrophage system as a target for estrogen and selective
estrogen 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 of
CD14+/CD16+ blood monocytes is expanded in sepsis patients. Blood. Nov 15 1993;82(10):3170-
3176.

30. Cardiovascular Disease
(CVD)
An Endobiogenic Approach

31. Uniqueness of
Vasculature
• 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 local
events
• Contains a homunculus of itself: vasovasorum

32. Vascular Disease:
Atheromas
• When treating atheromatous lesions one must
distinguish 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. Limitations of Etiology-based
treatments
• Cardiologists classically have focused on the mechanisms
of plaque formation rather than the reason for plaque
formation:
• Neuro-Vascular: Alpha-, beta-sympathetic activity
• Energetic elements: Cholesterol, HDL, LDL, TG, Glucose
• Lipids are a necessary but not sufficient factor for atheromatous
disease
• Hyperlipidemia ≠ Dyslipidemia
• Pathophysiological mediators: Inflammation, Free
radicals, Nitric Oxide, homocysteine, etc.
• Thus, we have failed to identify the fundamental
factors that allows atheromas to form in one patient
and not another, all screening factors being
equal, such as age, BMI, cholesterol and blood

34. Limitations of Etiology-based
treatments
• Treating local phenomena globally with beta-blockers
and statins have lead to reduction in CV events, but at
a global cost, such as increased risk of stroke and
loss of libido, muscle wasting, respectively.
• The entire body is subjected to suppression of factors
which are still adaptive and beneficial for the global
organism, but not for a particular part of the body
• The failure to identify and treat the true causes of CV
plaques results in anomalies such as “low risk”
patients having fatal MI’s and “high risk” patients living
long, healthy lives

35. Endobiogenic approach
• True cause of atheromatous plaques is dysadaptive
endocrine response to local needs for increased nutrition:
• Internal or external aggressors (viruses, emotional
stressors, tobacco smoke, heavy metals)
• Times of restructuring of the body (menopause, andropause)
• If the response to anabolic requirements is badly managed
by the body, or the demand is prolonged or the body is not
able to return to its previous homeostatic thresholds of
endocrine response, a dysmetabolic response ensues
• This is the true ontology of disease because endocrine
system manages all metabolic activity of the body

36. Etiology of Atheromas
• Local tissue or organ demand for anabolic adaptation demands
increased nutrient delivery:
• CATABOLIC: ACTH Cortisol: liberates glucose by
glycogenolysis for generation of ATP; TSH Thyroid: liberates
lipids for energy and cell wall building
• ANABOLIC: ProlactinInsulin: increases nutrient penetration
into cells; FSH/LH Estrogen and Testosterone: anabolic
steroid for protein incorporation and utilization in the cell
• Histamine: capillary leakextravasation of nutrients into extra-
cellular matrix
• Aldosterone: improve electrolyte presentation to cells, increase
circulating blood volume
• HTN: post-capillary increased duration of nutrient presentation

37. Etiology of Atheromas
 Vasculature as transportation medium for these
factors carries them from local area of need, creating
systemic inflammation
 Vasculature has greatest exposure to these
mediators, thus endothelium becomes damaged by
these mediators
 Now that catabolic and anabolic activities are dysregu-
lated, with increased glucose, lipids and
inflammation, vasculature itself undergoes hyper-
anabolic repair of damaged endothelium and media
smooth muscle proliferation and atheromatous
plaques

38. Endobiogenic approach
• Endocrine factors have been well described since as early as
1950’s, but neither their relationship to each other nor their
ontological significance has been clearly elucidated by classical
medicine
• Two primary indices in the biology of functions describe the
relationship between these elements and assist the clinician in
evaluating the true cause of disease and the optimal treatment
option
• Thrombogenic index: describes the risk of lumenal narrowing from
atheromatous plaques, and by extension, the thrombogenic
potential
• Thrombotic index: describes the actual risk of developing thrombo-
embolic phenomenon from atheromas or due to altered blood
rheology. The thrombotic index contains the thrombotic index

39. Biology of functions (BoF):
Thrombogenic Index
Proportional 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)7
1) Karacalioglu O et al. Baseline serum levels of cardiac biomarkers 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 cortisone to serum lipoproteins and atherosclerosis in
humans. Metabolism. Mar 1952;1(2):155-162.
3) Letizia C, Barilla F, Cerci S, et al. beta-Endorphin and propiomelanocortin-correlates peptides response in
suspected 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 disease
diagnosed 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 angiographic
coronary 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. Biology of functions (BoF):
Thrombogenic Index
Proportional to [labs] (related BoF index) :
• Gonadal Androgens [free Testosterone] (Androgenic)1
• Insulin (Anabolism index)9
• Sub-clinical hypothyroidism [TSH] (Bone remodeling
index)10-13
1) Dogramaci AC, Balci DD, Balci A, et al. Is androgenetic alopecia a risk for atherosclerosis? J Eur Acad
Dermatol 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 2009
3) Stamatelopoulos KS, Kyrkou K, Chrysochoou E, et al. Arterial Stiffness but Not Intima-Media Thickness Is
Increased in Euthyroid Patients with Hashimoto's Thyroiditis: The Effect of Menopausal Status. Thyroid. Apr 6
2009.
4) Sidorenko BA, Begliarov MI, Titov VN, Masenko VP, Parkhimovich RM. [Blood thyroid hormones in ischemic
heart disease (a comparison with coronary angiographic data, severity of stenocardia and blood lipid level)].
Kardiologiia. Dec 1981;21(12):96-101.

41. Biology of functions (BoF):
Thrombogenic Index
Inversely proportional to [labs] (related BoF index) :
• Estrogen [Estradiol, free] (Estrogen index; Bone
Remodeling index)1
• Adrenal Androgens [DHEAS] (Androgenic index)2-4
1) Gopalakrishnan P, Ragland MM, Tak T. Gender differences in coronary artery
disease: 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 dehydroepiandrosterone
sulfate inhibits vascular remodeling following arterial injury. Atherosclerosis. Feb
27 2009.
3) Savastano S, Valentino R, Belfiore A, et al. Early carotid atherosclerosis in
normotensive severe obese premenopausal women with low DHEA(S). J
Endocrinol Invest. Mar 2003;26(3):236-243.
4) Altman R, Motton DD, Kota RS, Rutledge JC. Inhibition of vascular inflammation
by dehydroepiandrosterone sulfate in human aortic endothelial cells: roles of
PPARalpha and NF-kappaB. VasculPharmacol. Feb-Mar 2008;48(2-3):76-84.

42. Biology of functions (BoF):
Thrombogenic Index
 The biology of function allows you to evaluate the risk
of lumenal narrowing from atheromas both from the
gestalt of risk factors
 Allows the physician to indentify the risk factors
particular to the patient.
 Allows the physician to assess risk on physiological
data rather than generalized risk factors based on
epidemiological data

43. Treatment plan based on Thrombogenic index

44. Other Indices: Physiological
 Thrombogenic index: Examines the risk of thrombo-
embolic phenomenon. Factors in all the risk factors
associated with atherogenesis as well as the role of
histamine1
 Tx: Reduce histamine with Plantain, Vitamin C, or Lavender
 Ischemia index: relates degree of tissue congestion relative
to rate of metabolism
 Tx: Correct sick euthyroid: iodine, wolfberry, stone steed
 Pro-amyloid: examines the degree of cellular nutritional
and oxygen deficiency, indirectly examining the degree of
mitochondrial 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. Other Indices:
Psychological
 betaMSH/alpha MSH: characterizes the degree of
intrapsychic activity originating from Dopamine vs.
Norepinephrine
 Adaptogenic: characterizes the degree of internal dialogue
 Thyroid relaunching, corrected: characterizes the degree of
endocrine dysfunction originating from emotional issues
 Interleukin-1: characterizes the impact of emotional and
endocrine factors on immune activity, immune regulation
and cellular proliferation (intimal thickening is a carcinoid
type of dedifferentiation of the smooth muscle)1
1) Argaman M, Gidron Y, Ariad S. Interleukin-1 may link helplessness-hopelessness with cancer
progression: a proposed model. Int J Behav Med. 2005;12(3):161-170.

46. Conclusions

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 of
human life
• In order to create a rational, individualized treatment
plan

48. Conclusions
• It combines in an integrative understanding:
• a philosophical consideration of the ontology of structures and
functions of the body,
• a rational approach to understanding physiology
• an empirical assessment of history and symptoms
• utilization of a dynamic, integrative and integrated metabolic
assessment of endocrine management of the organism called
the “Biology of Functions”
• an integrated assessment of all clinical data to obtain a precise
understanding of maladaptive physiology

49. Conclusions
• The Biology of Functions is an algorithmic assessment of the
qualitative and quantitative relationships of hormones in terms of
metabolic activity from nuclear, cellular, tissue, organ and
system-wide perspectives
• The Biology of Functions allows for an objective, longitudinal
assessment of the effects of therapy over time
• Endobiogeny relies on phytotherapy, oligotherapy, and diet as
well as lifestyle modification as its preferred methods of
ameliorating physiological imbalances
• It reserves the use of synthetic drugs for urgent cases, or when
the body is not able to establish an equilibrium by the effects of
functional regulation

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. Practitioners
For more information contact Endobiogenic
practitioners
United States:
• Kamyar M. Hedayat, MD,
• Expertise: Critical care
physiology, neurodegenerative
disorders, pediatrics
• Contact: kmhedayat@aromamd.net
• Web: www.fullspectrumhealthmd.com

52. Practitioners
Continental Europe
• Jean Claude Lapraz, MD, co-developer of
Endobiogeny
• Expertise: Cancer, all areas
• Contact: jc.lapraz@orange.fr
• Patrice Pauly, PhD
• Expertise: Biology of Functions, systems analysis
• Contact: patricepauly@yahoo.fr

53. REFERENCES
SLIDE 22
1) Raison CL, Miller AH. When not enough is too much: the role of
insufficient glucocorticoid signaling in the pathophysiology of stress-
related disorders. Am J Psychiatry. Sep 2003;160(9):1554-1565
2) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The dynamic and static
modification of the epigenome by hormones: A role in the developmental
origin of hormone related cancers. Biochem Biophys Acta. Apr
2009;1795(2):104-109.
3) Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on
hormonal and immunological factors in women with repeated
miscarriages. Hum Reprod Update. May-Jun 1998;4(3):301-309

54. REFERENCES
SLIDE 23
1) Raison CL, Miller AH. When not enough is too much: the
role of insufficient glucocorticoid signaling in the
pathophysiology of stress-related disorders. Am J
Psychiatry. Sep 2003;160(9):1554-1565
2) Chiam K, Tilley WD, Butler LM, Bianco-Miotto T. The
dynamic and static modification of the epigenome 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 and immunological factors in
women with repeated miscarriages. Hum Reprod Update.
May-Jun 1998;4(3):301-309

55. REFERENCES
SLIDE 29
1) Giembycz MA, Lindsay MA. Pharmacology of the
eosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.
2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.
Relative eosinophilia and functional adrenal
insufficiency in critically ill patients. Lancet. May 15
1999;353(9165):1675-1676.)
3) Miller GE, Cohen S, Ritchey AK. Chronic
psychological stress and the regulation of pro-
inflammatory cytokines: a glucocorticoid-resistance
model. Health Psychol. Nov 2002;21(6):531-541.

56. REFERENCES
SLIDE 30
1) Giembycz MA, Lindsay MA. Pharmacology of the
eosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.
2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.
Relative eosinophilia and functional adrenal
insufficiency in critically ill patients. Lancet. May 15
1999;353(9165):1675-1676.)

57. REFERENCES
SLIDE 31
1) Giembycz MA, Lindsay MA. Pharmacology of the
eosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.
2) Beishuizen A, Vermes I, Hylkema BS, Haanen C.
Relative eosinophilia and functional adrenal
insufficiency in critically ill patients. Lancet. May 15
1999;353(9165):1675-1676.)

58. REFERENCES
Slide 41
1) Karacalioglu O et al. Baseline serum levels of cardiac
biomarkers in patients with stable coronary artery disease.
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