endobiogeny and cardiology

Introduction to Endobiogeny:

An integrative approach to Medicine

By: Jean Claude Lapraz, MDKamyar M. Hedayat, MD

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

IntroductionAn introduction to the Endobiogenic conceptA brief review of the history of medicine and

its schools of thought

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.

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

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.

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

Philosophy

• Endobiogeny integrates the rational and empirical schools of medicine with philosophy to create a single coherent system of medicine:

• The Endobiogenic 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 symptoms

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

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.

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.

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

History of development of

Endobiogeny

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

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 of qualitative 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

The Endobiogenic Method

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.

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

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

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.

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.



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

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

Biology of functions• The Biology of Functions (BoF) quantifies

functional abilities of the organism, before and after the effects 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).

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.

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

Example: Adaptation Index

• According to Dr. Duraffourd, an intra-pituitary physiologic linkage exists in the stimulation of FSH by ACTH

• The Adaptation Index evaluates the relative activity of ACTH relative to FSH in order to determine the degree of efficiency of catabolism (cortisol) vs. the degree of efficiency of anabolism (estrogen) in response to stress

• The Adaptation Index examines this activity at the metabolic level by examining the products of hormonal activity (cortisol and estrogen in this example) as an assessment of hormonal activity

• It is calculated as the ratio of eosinophils to monocytes

Adaptation Index: Proofs

• Eosinophils are inversely related 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.


• 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




• 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.

Cardiovascular Disease (CVD)

An Endobiogenic Approach

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

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

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 pressure

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

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

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

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

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

http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&itool=AbstractPlus-def&uid=11739466&db=pubmed&url=http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=11739466

http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3051&itool=AbstractPlus-def&uid=11739466&db=pubmed&url=http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=11739466

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.


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.


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. Vascul Pharmacol. Feb-Mar 2008;48(2-3):76-84.


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

Treatment plan based on Thrombogenic index

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.

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.

Conclusions

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

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

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

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

http://www.eimcenter.org/

http://www.fullspectrumhealthmd.com/


http://extranet.endobiogenics.com/en/

PractitionersFor more information contact

Endobiogenic practitioners

United States:

• Kamyar M. Hedayat, MD,• Expertise: Critical care physiology,

neurodegenerative disorders, pediatrics

• Contact: [email protected]

• Web: www.fullspectrumhealthmd.com

mailto:[email protected]


Practitioners

Continental Europe

• Jean Claude Lapraz, MD, co-developer of Endobiogeny

• Expertise: Cancer, all areas


• Patrice Pauly, PhD

• Expertise: Biology of Functions, systems analysis





REFERENCES

SLIDE 22




REFERENCES

SLIDE 23




REFERENCES

SLIDE 291) Giembycz MA, Lindsay MA. Pharmacology of the

eosinophil. Pharmacol Rev. Jun 1999;51(2):213-340.


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.

REFERENCES

SLIDE 30



REFERENCES

SLIDE 31



REFERENCES

Slide 411) 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.

REFERENCES

SLIDE 41 (cont.)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.

REFERENCES

SLIDE 42

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.

REFERENCES

SLIDE 43

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. Vascul Pharmacol. Feb-Mar 2008;48(2-3):76-84

REFERENCES

SLIDE 50

1) Tanimoto A, Sasaguri Y, Ohtsu H. Histamine network in atherosclerosis. Trends Cardiovasc Med. Nov 2006;16(8):280-284

SLIDE 51

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

SLIDE 52

2) Milligan SR, Kalita JC, Pocock V, et al. The endocrine activities of 8-prenylnaringenin and related hop (Humulus lupulus L.) flavonoids. J Clin Endocrinol Metab. Dec 2000;85(12):4912-4915

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SLIDE 53

1) Anderson RA. Chromium and polyphenols from cinnamon improve insulin sensitivity. Proc Nutr Soc. Feb 2008;67(1):48-53.

2) Zhao R, Li Q, Xiao B. Effect of Lycium barbarum polysaccharide on the improvement of insulin resistance in NIDDM rats. Yakugaku Zasshi. Dec 2005;125(12):981-988.

SLIDE 543) Sidani M, Campbell J. Gynecology: select topics. Prim Care. Jun

2002;29(2):297-321

SLIDE 554) Smith R et al. A pilot study to determine the short-term effects of a

low glycemic load diet on hormonal markers of acne: a nonrandomized, parallel, controlled feeding trial. Mol Nutr Food Res. Jun 2008;52(6):718-726.

endobiogeny and cardiology

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