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The Theory of Endobiogeny
The Theory of Endobiogeny Volume 4: Bedside Handbook
Kamyar M. Hedayat Jean-Claude Lapraz Ben Schuff
Academic Press is an imprint of Elsevier 125 London Wall, London EC2Y 5AS, United Kingdom 525 B Street, Suite 1650, San Diego, CA 92101, United States 50 Hampshire Street, 5th Floor, Cambridge, MA 02139, United States The Boulevard, Langford Lane, Kidlington, Oxford OX5 1GB, United Kingdom © 2020 Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library ISBN 978-0-12-816965-0 For information on all Academic Press publications visit our website at https://www.elsevier.com/books-and-journals
Publisher: Stacy Masucci Acquisition Editor: Rafael Teixeira Editorial Project Manager: Sandra Harron Production Project Manager: Sreejith Viswanathan Cover Designer: Matthew Limbert Typeset by SPi Global, India
Dedication This book is dedicated to our students, whose questions and enthusiasm has helped us refine our teaching of Endobiogeny. This book is our gift to you to share with all those who come seeking health and healing. This book is also dedicated to all those who seek to be heard, understood and engaged in the affirmation of Life and daily choices for health and healing.
Preface The knowledge of Endobiogeny makes it possible to understand the path traveled, to predict its future, and to anticipate in unaffected individuals the installation of a pathological state, spontaneous or as the consequence of repeated or prolonged use of aggressors. Be it food, habits, drugs or medication, this condition becomes predictable thanks to risk assessment of each individual.1 Christian Duraffourd
Endobiogeny is a theory of terrain first presented by Dr. Christian Duraffourd in 1983. As a theory of terrain, it presents a new approach to medicine based on a complex systems approach to human physiology. What you hold in your hands is a distillation of treatment approaches to common medical conditions seen in clinical practice derived from the genius and originality of Dr. Duraffourd’s theory. The goal of this book is to assist the physician trained in Endobiogeny by recapitulating the essential aspects of the disease, its terrain, assessment, and treatment. While Endobiogeny is a theory of terrain, it is not a theoretical or abstract approach to medicine. To the contrary, it was developed in response to empirical observations and a keen sense of pattern recognition during years of medical practice. Endobiogeny does not supplant the current scientific approach to medicine—far from it. It expands and deepens the scientific approach to medicine. It brings the sensibility of systems theory to human biology and physiology. It integrates the essential elements
of the terrain that regulate material life in its formation, regulation, restauration, and deinstallation. At its core, clinical Endobiogeny is a humanistic approach to medicine. Central to our approach is respect for human life, and the experience of life through health and illness by the patient. More broadly, there is respect for all life, for it is from medicinal plants and other products of the earth that the therapeutic approach of Endobiogeny is based. Never before has the practice of Endobiogeny been so succinctly summarized for the benefit of both physician and patient. This work represents the foundational work of Dr. Duraffourd, the elaborative and clarifying approach of Dr. Jean-Claude Lapraz and his working group in SIMEPI, and the expanding contributions of Dr. Kamyar M. Hedayat to the categorization of disease and utilization of medicinal plants. While Dr. Duraffourd is no longer with us, his ideas live on in his students and in published works such as this one. From a single flame many candles have been lit. May it light the way for you in your practice. Kamyar M. Hedayat Jean Claude Lapraz December 2018
Reference 1. Duraffourd C, Lapraz JC. Traité de Phytothérapie Clinique: Médecine et Endobiogénie. Masson ed. Paris: Masson; 2002.
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Introduction “These things are not explainable in detail. From one thing you learn a thousand things. When you have acquired the Way of Strategy there will not be a thing that you cannot understand. You must study hard.”1
This book was written to be a convenient and quick reference for students and practitioners of Endobiogeny. However, experienced practitioners not trained in Endobiogeny may find it instructive. We hope it inspires you to study Endobiogeny in depth. Very often, in our courses, students would feel like Icarus, only to have their wings melted by the fiery demands of bedside clinical decision making. How can one organize the information contained in three volumes of writing into a concise and accessible reference while seeing patients? It became increasingly clear to us that, what was needed, was a mentor by their side, and a friend in their pocket. This book is that mentor and friend. It is a definitive reference during patient care and a reliable study guide for material presented in The Theory of Endobiogeny, Volumes 1–3. To paraphrase the master Samurai Musashi, you must study hard and frequently to practice Endobiogeny well. You must practice Endobiogeny frequently and seriously to understand the theory well. This book is divided into five sections. They offer a link from the grand theoretical concepts of Endobiogeny to its clinical applications. Section 1: Theory and Foundation of Clinical Practice is a brief review of essential theoretical concepts. Section 2: History, Exam and Biology of
Function reviews key elements of practice: history, physical examination, and Biology of Functions indexes. Section 3: Assessment and Treatment of Clinical Disorders summarizes assessment and treatment of over 30 common clinical disorders, many of which can be read in 5-10 minutes for a quick review. Section 4: Essentials of Therapeutics and Section 5: Essentials of Alimentation offer concise resources to the selection and indication of medicinal plants mentioned in this volume, and key diets and approaches to nutrition. This is a how-to book. It omits the “why” of Endobiogeny fully discussed in our seminars, scientific publications, and The Theory of Endobiogeny, Volumes 1–3. It omits differential diagnosis and best practices in medicine with respect to imaging studies, laboratory work ups, pharmaceutical treatments, etc. We assume that you have this knowledge and are consulting this book to enhance your evaluation of treatment according to the theory of Endobiogeny. The practitioner must determine the severity of illness and capability of recovery when selecting the optimal levels of treatment (c.f. Section A, Chapter 6: Therapeutics in Endobiogeny).
Reference 1. Musashi M, Ashikaga Y. Book of earth. In: Brant R, ed. Book of Five Rings. Astrolog Publishing House; 2003.
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Chapter 1
Theory of Endobiogeny We no longer neglect the biological reality of each individual. We respect his endogenous functioning—his endobiogeny. Christian Duraffourd1
Introduction The theory of Endobiogeny stands at a unique juncture in the history of medicine. It is based on modern notions of physiology. It is rooted firmly within the Western scientific tradition. It is a son who departs from an increasingly stern father. Its departure is not a rejection of its foundation, but growth beyond the limitations of an increasingly reductionist approach to life. Nourishing the scientific foundation of Endobiogeny is systems theory. To be more specific, it is a global systems approach to living systems. While the practitioner is focused on practical clinical applications of Endobiogeny, it is nevertheless important to keep in mind the essential elements of theory. This section offers a brief review of these essential elements to benefit the practitioner in their daily practice.
General theory of complex living systems according to Endobiogeny Complexity theory states that a unit of function is a system unto itself containing smaller subunits and a subunit of a larger system. For example, the liver is a unit unto itself. It contains within itself subunits called hepatocytes. It is a subsystem of the global organism. In turn, a single hepatocyte, subunit of the liver, is a whole unit unto itself containing its own subunits: ribosomes, mitochondria, DNA, etc. Endobiogeny is a global complex systems theory because it evaluates the relationships within a part, between the parts, and of the whole (global) living being (systems). It evaluates the complexity of relationships based on levels and hierarchies, qualities, intensities, duration of interaction. In clinical practice, an individual symptom must be contextualized to an organ, tissue, or system. You focus on the system expressing the symptom, but also the other organs, tissues, or systems that interrelate to it. This is the global systems approach of Endobiogeny. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00001-9 © 2020 Elsevier Inc. All rights reserved.
Example: Wet bronchitis A patient has a productive cough. What produces the mucous in the bronchus that makes the cough wet? It depends on its thickness and color, which implicates certain levels of function of the neuroendocrine system and pancreas. Why did the mucous develop in the first place? Inflamed bronchi. What global neuroendocrine and emunctory factors are most implicated in that? Find your answer and you will find the path to treating the patient who has the disease, and not the disease the patient has, to paraphrase Hippocrates.
Key elements and function of the terrain in practice Definition of terrain The terrain is the sum of all the structural and functional elements of the organism. Structure refers to material elements: mitochondria, organelles, cells, tissues, organs, etc. It is derived from the genetic inheritance and modified by epigenetics to become phenotype. Function refers to dynamic expression of structure: structural, structurofunctional, and functional metabolism. Each terrain is the unique expression of structure and function in space and time.
Clinical pearl: Treating the terrain In Endobiogeny, personalized medicine is treatment of the person according to their phenotype, not genotype. It is a treatment of the dynamic structurofunctional activity at that moment in time and space.
Endocrine system: Regulator of terrain Terrain is everything. It is the ceaseless and dynamic metabolism of material and energy. The system that regulates the terrain is our area of greatest focus. If you regulate the regulator, you regulate the terrain. The regulator of the terrain must have met three criteria: (1) ubiquity of action—for the terrain is all and everywhere, (2) regulations of the elements of metabolism, (3) autoregulation. The endocrine system is the sole system of physiology that meets all three criteria. This is how Endobiogeny places the greatest emphasis on an integrative understanding of the endocrine system. 3
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FIG. 1.1 Integrated neuroendocrine management of metabolism. Alpha sympathetic (αΣ) stimulates and calibrates the intensity and duration of the endocrine management of metabolism. At the cellular level, parasympathetic (πΣ) stimulates the general cellular anabolic tendency through influence on the rate of production of elements, alpha sympathetic calibrates it and beta sympathetic (βΣ) completes it. (© 2015 Systems Biology Research Group.)
From the unitary concept of metabolism arises the duality of catabolism and anabolism. In the sequential regulation of metabolism, there are four lines of endocrine function, alternating in catabolic and anabolic predominance in a sequential manner (Fig. 1.1). Each endocrine axis also relates to a specific type of nutrient mobilization and/or utilization, and, emunctory (cf. below) as well. In this way, the endocrine system is completely integrated into basal metabolism, adaptation syndromes, and recovery from adaptation.
Clinical pearl: Importance of endocrine assessment No matter whether a disorder is acute, chronic, genetic, acquired, somatic, or psychological, the endocrine system will be the heart of assessment and treatment. Evaluate it carefully: its potential at birth, its expression during development, and its current state.
Autonomic nervous system: Calibrator of the regulator The autonomic nervous system (ANS) originates in the brain stem and functions in the peripheral and central body. Its role is to stimulate and calibrate function including that of the endocrine and central nervous systems (cf. below). The ANS is ubiquitous, dynamic, and ceaseless in its actions. It is not self-regulating, which is why it cannot be the regulator of the terrain. Key to ANS function is the notion of autacoids. Assess autacoids in your intake and address them in your treatment of the patient. The autacoid of parasympathetic (para: πΣ) is serotonin. Serotonin prolongs the time of para by delaying the onset of alpha sympathetic (alpha: αΣ). Recall that >90% of all serotonin is in the intestines or peripheral expression of the ANS. Vagotonia and other hyperparasympathetic states are part of the pre- and critical
FIG. 1.2 Normal peripheral autonomic sequencing-activity graph. The sequence starts with parasympathetic (πΣ) and its autacoid serotonin, which delays alpha-sympathetic activity. In effect, serotonin prolongs para activity. With the onset of alpha (αΣ), activity increases, then is sustained thanks to histamine, which prolongs alpha. The activity of beta (βΣ) brings a brief peak of activity, followed by a sudden drop below the baseline level. What follows is the recovery phase back to baseline. (© 2014 Systems Biology Research Group based on the work of the SIMEPI, based on the work of SFEM, based on the concepts of Christian Duraffourd.)
terrain of numerous disorders. The autacoid of alpha is histamine. Histamine prolongs the duration of αΣ. Hyper-alpha states are responsible for initiating or sustaining critical terrains of disorders of adaptation. Beta sympathetic (beta: βΣ) has no autacoid owing to its rapid and brief action. What is key to understand about the ANS are three things: 1. ANS function is timed and sequential (Fig. 1.2) 2. Autacoids calibrate ANS intensity and duration 3. ANS is so indispensable for proper functioning of the endocrine system, the term “neuroendocrine system” is used in Endobiogeny instead of merely “endocrine system” Ultimately, autacoids regulate the ANS regulation of the endocrine system. In Endobiogeny, the notion of the ANS has been extrapolated to the general concept of sequential and timed relationships (Table 1.1) beyond the function of neurons that excrete acetylcholine (para), noradrenaline (alpha), and adrenaline (beta).
Clinical pearl: ANS assessment Remember that para and alpha adapt themselves to each other. The more one rises, the greater the other does in turn. When assessing the level of ANS function, assess both the quantitative and qualitative relationships. An example of a quantitative determination is to conclude that both para and alpha are elevated. An example of a qualitative assessment is that given that both are elevated, alpha is greatly predominant to para. An example of this would be a 52-year-old man who has a wet mouth and is hungry upon waking (elevated para), but, has a gastric ulcer, incomplete urination, enlarged prostate and labial herpes outbreaks when stressed, and cold hands and feet (elevated alpha).
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TABLE 1.1 General concept of parasympathetic, alpha-, and beta sympathetic-like activity throughout the body. Area
Para
Alpha
Beta
General
Initiate
Calibrate
Complete
Metabolism
Basal rate of metabolism
Calibration of duration or intensity of metabolism
Acceleration and completion of metabolism
Endocrine
Basal rate of secretion (production) of a hormone
Calibration of duration or intensity of secretion of a hormone
Excretion of a hormone from its gland
Sensory
Receipt of information
Alertness, contextualization of information
Relatedness of information
Motor
Conceptualization
Planning
Execution
Sensory
Threshold of sensation
Intensity of sensation
Propagation of information
Motor
Basal threshold of contraction
Calibration of timing and intensity of contraction
Contraction
ENS
Basal rate of motricity
Calibration of timing and intensity of motricity
Contraction
Emunctories
Basal rate of flow
Congestion
Decongestion
Basal rate of detoxification
Calibration of rate of detoxification
Excretion of toxins
CNS
PNS
CNS, central nervous system; ENS, enteric nervous system; PNS, peripheral nervous system.
Emunctories Emunctories are the organs of drainage and detoxification. The emunctories are the liver, gallbladder, kidney, intestines, lung, and skin. While not technically an emunctory, exocrine pancreas is included because of its implication with the hepatobiliary unit. The corticotropic axis utilizes the skin, kidneys, bladder, liver, and intestines. The thyrotropic axis utilizes the lungs, liver, and intestines. Consider emunctories in three ways: 1. Catabolic axes: they remove catabolic products 2. General: within each endocrine axis, they support general function 3. Relationship to specific disorders (Table 1.2)
Congestion of emunctories plays an important role in many disorders and diminishes the buffering capacity of the patient. The adaptive role of congestion is to prolong the exposure of blood to an organ. This can be for an emunctory role, i.e., hepatic metabolism of catabolic byproducts, or, nonemunctory, i.e., hepatic glycogenolysis. In either case, congestion compromises tissue functions. Each branch of the ANS can play a role in active or passive congestion.
Clinical pearl: When in doubt, drain Each emunctory plays numerous other roles. Emunctories are related to the precritical and critical terrains of every illness. When in doubt about the critical neuroendocrine terrain, institute therapeutic drainage. Decongesting an
TABLE 1.2 Relationship of hormones and emunctories to various disorders. Endocrine axis
1° Emunctory
2° Emunctory
Disorders
Gonadotropic
Liver-gallbladder
Colon
Skin
Somatotropic
Liver
Pancreas, exocrine
Joints
Thyro-somatotropic
Pancreas, exocrine
Kidney
Lungs
Cortico-thyro-somatotropic
Gallbladder
Pancreas, exocrine
ENT infections
ENT, ear, nose, and throat.
6 SECTION | A Theory and foundation of clinical practice
emunctory can take the patient out of a critical state and relieve symptoms in a short period of time. For example, one type of gastroesophageal (GE) reflux disease involves elevated para tone on the GE sphincter. If the patient does not tolerate fatty foods, suspect gallbladder congestion. In this case, draining the gallbladder will diminish para tone, even if you do not use a parasympatholytic, because improving cholagogy and choleresis will reduce the need for para. This in turn restores normal GE tone, resolving the reflux. A good example of an efficient drainer is Taraxacum officinale (dandelion leaf), which is a hepatobiliary drainer, cholagogue, and choleretic. It can be administered 2 0–30 min before a fatty meal.
Immunity: Recognition, defense, and offense The immune system is not a primary regulator of the terrain. Its creation and function are managed by the neuroendocrine system. The immune system is the third element of adaptation, along with the endocrine system and the ANS. The more dysfunctional the latter two are, the greater the predominance of the immune system must become. This notion is essential when treating all allergic and autoimmune disorders. The immune system is involved in distinguishing self from nonself, and, placing every material element into one of three categories: safe, neutral, and harmful. Inflammation is a key aspect of how elements of the immune system transfer from humoral and lymphatic spaces to tissular spaces. Regulation of the immune system can be an important element of treatment, but it remains a reactive, symptomatic treatment. One must always return to addressing the neuroendocrine elements that have dysregulated immunity: be it the production, mobilization, utilization, or end of immune action.
disorders. It is our opinion that the merit is well placed but the reasoning is in error. The GI tract is the place where all other key elements of the terrain meet. 1. Neuroendocrine: regulation of digestion, distribution of nutrients for metabolism 2. Immunity: largest network of immune cells 3. Emunctory: key role of liver, gallbladder, exocrine pancreas in digestion 4. Buffering capacity: core elements of buffering capacity are within the splanchnic bed (cf. below) 5. Central nervous system: influence of emotions on enteric nervous system effects enteric immunity, digestion, and adaptation capabilities 6. Patient autonomy: alimentation is the aspect of selfcare most easily controlled but least frequently managed by the patient
Buffering capacity The buffering capacity is the ability to immediately respond to adaptation demands without having to institute the production of new elements. Buffering capacity can be achieved through the following ways: 1. Redundancy: Two lungs, two kidneys, two adrenal glands, etc. 2. Flexibility: Alternate and redundant metabolic pathways: glucose vs lipid oxidation for ATP production 3. Excess: >90% of circulating hormones inactive, but ready for use at any time 4. Sequestration: Leukocytes, platelets, immune factors stored and ready to be mobilized near instantaneously 5. Storage: Nutrients stored (glucose as glycogen, amino acids in muscle, calcium in bones) and ready for instantaneous liberation and distribution
Clinical pearl
Clinical pearl: When in doubt, drain and restore
For acute symptomatic relief use antiinflammatories, e.g., topical clay, essential oils of rosemary and lavender, or turmeric. For remission, use polyvalent plants that address two or more of the following: ANS, endocrine, immune, emunctory activity. Three good examples are Viola tricolor (antiinflammatory, contains salicylates, polyvalent drainage), Zea mays (antiinflammatory, contains salicylates; anti-TSH (thyroid-stimulating hormone), hepatorenal drainer), or, Thymus vulgaris (antiinflammatory, broad-spectrum antimicrobial, parasympatholytic, adrenal cortex stimulant).
When a patient easily, rapidly, or frequently succumbs to imbalance or illness, or has a prolonged or insufficient recovery, address the buffering capacity in the follow order: 1st: improve sleep, hydration and stress management, 2nd: drain the liver, 3rd: alkalize the diet then 4th: use oligoelements (trace minerals) such as magnesium, sulfur or boron.
Gastrointestinal tract: Quotidian junction of all other elements of terrain In some approaches to integrative medicine, the gastrointestinal (GI) tract is first among areas of treatment for all
Central nervous system: Information processing The central nervous system (CNS) is not key for human survival. A patient may be brain dead but body-alive. One cannot by body-dead and cogitate. The CNS is a servant leader. It serves at the demands of the periphery. It is an information-processing center that evaluates the internal needs and adapts those needs to internal and external demands. It directs and creates hierarchies of importance.
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FIG. 1.3 The central nervous system (CNS—upper left) is the locus of various perceptions, emotions, memories, and assessments of physiologic state. It creates a milieu or context which alters the threshold or amplitude of neuroendocrine response. For example, alpha sympathetic (αΣ) stimulates TRH, which in turn stimulates (1) the thyrotropic axis (far right, vertical), (2) the limbic area (upper left) affecting memory and emotions, (3) liberation of glucose (bottom panel, right to left). A patient with chronic rumination, activating the limbic area, may have an exaggerated alpha response. (© 2014 Systems Biology Research Group.)
For example, in the summer time, adrenal cortex activity reaches its nadir. However, if one has a summer sinusitis, the priority is to relaunch cortisol to resolve the infection. The CNS plays a role in perception of values, if an event is considered “good” or “bad.” It conveys information to the neuroendocrine unit, indirectly affecting other key elements of terrain (Fig. 1.3).
Clinical pearls: Mindset in practice The mindset of the patient should be assessed in each evaluation. In daily practice, most disorders, no matter how insignificant may appear to be, are precipitated or prolonged by the patient’s emotional reaction to internal or external events, or to the illness itself. An assessment of the cognitive-emotional state can be addressed in indirect or subtle ways in order to avoid giving the impression of performing a psychiatric evaluation, which is not the purpose of this assessment. Observe facial expression and tone of voice. Is the tone flat, animated, or restrained? Observe the rate, regularity, and depth of breathing, related to ANS and emotional states. Is it rapid and shallow or, slow with pauses and sighs? Simple inquiries can reveal important information that contextualizes the patient’s illness to something larger in their life: Have any relationships changed in your life recently? Or, Is this time of year significant for you in any way?
The endocrine system: A brief review For the species, the most important role of the hormones is reproduction, but for the individual it is differentiation and adaptation. It becomes increasingly more obvious, furthermore, that the principal medical application of endocrinology is not the treatment of the primary but secondary diseases of the endocrines. [Primary endocrinopathies] are rare diseases in comparison with the hormonal derangements resulting from maladaptation to stress. Hans Selye2
As the theory of Endobiogeny posits, the endocrine system is the true manager of the terrain. To manage disease, learn to manage the endocrine system. Endobiogeny has developed from its theory a complex, nuanced, and sophisticated approach to applied endocrinology that cannot be fully summarized here (cf. The Theory of Endobiogeny, volume 1). Our purpose here is to recapitulate the most valuable concepts for the clinician.
Overview A hormone is a chemical information unit. It transmits information through signaling. The information transmitted relates to regulation of metabolism by one of two general mechanisms. The first is nongenomic. The action
8 SECTION | A Theory and foundation of clinical practice
occurs within minutes within the cytoplasm. The second is genomic. The action occurs over 12–36 hours based on regulation of DNA transcription. There are five classically described types of hormonal function summarized in Table 1.3, where “Region” refers to the site of action as compared to the site of excretion of a hormone. The theory of Endobiogeny further considers the effects of hormones on metabolism. When evaluating indexes of the Biology of Functions, understand what level of hormonal effect is being described (Table 1.4).
Pineal Overview: Epiendocrine gland with supracontrol function. Through its primary hormone melatonin, it is the, axel around which all axes turn and unfold in chronobiologic functioning. Essence: Protects the organism from exterior aggressions (e.g., ultraviolet light) during the day, repairs the interior during the night (Fig. 1.4). NB: It does not induce sleep, rather, it diminishes diurnal physiology.
TABLE 1.3 Summary of classical hormonal activity based on distance from site of action. Type
Region
Site
Example
Endocrine
Distant cells
Membrane receptors
Cortisol: nongenomic
Intracrine
Within the cell
Cytoplasm, nucleus
Cortisol: nongenomic, genomic
Paracrine
Adjacent cells
Membrane receptors
Fibroblast growth factors
Autocrine
Excreting cell
Membrane receptors
Interleukine-1
Pheromone
Other organisms
Alloreceptors
Androstenedione
TABLE 1.4 Hormone classification based on metabolic action. Activity
Description
Example
Cellular
Cellular metabolism for its own benefit based on cellular demands
Production of mitochondria in a myocyte Myocyte mitochondrial glucose metabolism for intrinsic cellular energy requirements
Tissular
Tissular metabolism for its own benefit based on tissular demands
Healing of muscle fiber injury Muscle metabolism during muscle growth postexercise
Endocrine
Hormonal stimulation of excretion of second hormone
ACTH stimulation of cortisol excretion Negative feedback of cortisol on ACTH
Endocrinometabolic
Hormonal regulation of cellular metabolism for the cell’s benefit based on global demands
FSH upregulation of estrogen receptors within the thyroid Myocyte glucose metabolism alteration due to programmatic onset of puberty
Endocrinotissular
Hormonal regulation of tissular metabolism for the tissue’s benefit based on global demands
Programmatic increase in muscle tissue density and strength during puberty estrogens + androgens
Organometabolic
Hormonal regulation of organ metabolic activity as a whole for the benefit of the global system based on global demands
ACTH stimulation of adrenal cortex to produce (secrete) cortisol by uptake and metabolism of cholesterol Increase in myocyte ATP production during exercise
Organotissular
Hormonal regulation of organ tissular activity for the benefit of the global system based on global demands
FSH and LH regulation of gonad size and activity form fetogenesis through gonadopause Upregulation of muscle fiber contraction and recovery during exercise
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UV protection
Antiinflammatory
FIG. 1.4 Summary of melatonin activity. (© 2014 Systems Biology Research Group.)
Antioxidant
Vasomotricity Diurnal Gastric motility Regulates enteric pacemarkers
Nocturnal
Melatonin Cognitive function
Pancreas Exocrine, endocrine
Neurons
Immunity
Synapsing, repair
Splenohumoral
Regulation ● ●
●
Stimulation: Secretion: αΣ, excretion: πΣ Inhibition: Adrenocorticotropic hormone (ACTH), cortisol Regulation: Oxytocin
Indications for addressing ●
● ●
Seasonal disadaptation: Allergies, migraines, bronchitis, cancer metastasis, etc. Neuropsychiatric: Insomnia, seizures, autism Aging
Treatment options ●
●
Antitumoral
Endocrine: Exogenous: melatonin; Endogenous: to increase melatonin, either reduce cortisol and ACTH, and/ or increase oxytocin activity. Lifestyle: Sleep before midnight, employ rhythmic living.
Hypothalamic-pituitary overview The hypothalamus contains the hormones that regulate pituitary hormones. As we will demonstrate, they have many other central and peripheral activities as well. The pituitary consists of two lobes. The anterior contains the majority
of pituitary hormones (Table 1.5). The posterior produces vasopressin and oxytocin.
Clinical pearl: Peripheral actions of central hormones Pituitary hormones have inter- and intra-axial peripheral activity that complements the activity of its peripheral glands. For example: ACTH stimulates cortisol but also eosinophils and histamine receptors. If you wish to evaluate the terrain of an allergic patient, understand the role of each. A patient may have normal cortisol activity but elevated histamines and eosinophils due to prolonged ACTH activity, in the parlance of Endobiogeny.
Corticotropic Introduction to the corticotropic axis Overview: Ensures survival through adaptation, energy economy, mobilization and distribution of metabolites, electrolytes, and fluids. Metabolism: Catabolism (first loop: cortisol) > anabolism (second loop: aldosterone, adrenal androgens). Metabolite(s) and minerals: Mobilization of: carbohydrates (cortisol), proteins (cortisol, adrenal androgens), lipids (cortisol), calcium (cortisol), sodium and water (aldosterone).
TABLE 1.5 Pituitary volume by cell type. Hypothalamic hormone
Pituitary hormone
Cell type
% of pituitary cell population
CRH (+), vasopressin (+)
ACTH
Corticotroph
15–20
GnRH (+)
LH, FSH
Gonadotroph
10–15
TRH (+), somatostatin (−)
TSH
Thyrotroph
3–5
GHRH (+), somatostatin (−)
GH
Somatotroph
40–50
TRH (+), dopamine (−)
Prolactin
Lactotroph
10–25
(+), Stimulates the pituitary hormone; (−), inhibits the pituitary hormone.
10 SECTION | A Theory and foundation of clinical practice
as a slow-acting thyroid stimulator outside thyrotropinreleasing hormone (TRH), TSH regulation.
POMC
CRH
b-Lipotropin
ACTH
g-Lipotropin
Enkephalins
b-Endorphin
α-MSH
Adaptation syndromes
Pituitary Horizontal stimulation
ACTH efficiency
β-MSH
Short adaptation
Amplifies within adrenal cortex
ACTH receptors Upregulation on adrenal cortex
Adrenal cortex
Stimulation of thyroid
FIG. 1.5 The hypothalamic hormone of the corticotropic axis, corticotropin releasing hormone (CRH) has many roles. Through the stimulation of pro-opiomelanocortin hormone (POMC) we see a myriad of actions, centrally and peripherally. Other direct actions of CRH are discussed in The Theory of Endobiogeny, volume 1. (© 2014 Systems Biology Research Group.)
Hypothalamus CRH: Corticotropin-releasing hormone Essence: Regulates adaptation, energy economy, and pain (Fig. 1.5). Regulation ● ●
Clinical pearl: Evaluating the beta-MSH/ alpha-MSH index The beta-MSH/alpha-MSH index models the relative role of these two derivatives of melanocyte stimulating hormone (MSH) in adaptation. In essence, beta-MSH represents a type of semiautonomous adaptation of cortisol and thyroid hormones outside of central influence. When the index is elevated, use plants with endorphin-like qualities (e.g., Crocus sativa, Eschscholzia californica, Viscum album bud) or cannabinoids. Alpha-MSH reflects an oversolicitation of the long route of adaptation and by extension, insufficient GABA. When the index is low, use GABAergic plants (e.g., Passiflora incarnata, Lavandula angustifolia, etc.).
Stimulation: αΣ, prolactin (PL) Inhibition: Dopamine, ACTH, cortisol
Alpha-MSH Origin: Via ACTH, POMC (Fig. 1.5). Essence: Calibrates adaptation response during “long route” adaptation: the sequential movement across the endocrine axes during the general adaptation syndrome. Mechanisms and actions: Regulates energy homeostasis, augments cortisol release, and complements adaptation syndromes: antipyretic, antiinflammatory, cicatrizing, anorexigenic. Beta-MSH Origin: Via ACTH, POMC (Fig. 1.5). Essence: Immediate, direct optimization of catabolic activity. Mechanisms and actions: Stimulates ACTH and directly stimulates cortisol excretion without ACTH, serves
Pituitary, anterior ACTH: Adrenocorticotropic hormone Essence: Adapts the cortico-immune response, prepares gonadotropic compensation. Mechanism and action: Stimulates the production and excretion of adrenal cortex hormones (cortisol, DHEA, etc.), stimulates eosinophil and basophil excretion from bone marrow, upregulates histamine receptors. Clinical pearl: Role of ACTH in disease ACTH is implicated in a number of disorders from depression to atopy. It can also be implicated in gonadotropic disorders through its radial action on gonadotropin-releasing hormone (GnRH) and horizontal action on both follicle-stimulating hormone (FSH) and luteinizing hormone (LH). ACTH can be sustained with Rhodiola rosea, Quercus pedunculata or Inula helenium, or relaunched with Ocimum basilicum essential oil. Finally, it can be regulated with Ribes nigrum bud. Regulation ●
●
Stimulation: αΣ, CRH, α-MSH, vasopressin, prolactin (PL) Inhibition: Cortisol
Pituitary, posterior Essence: Calibrates central and peripheral effects of the corticotropic axis for internal and external adaptation demands.
Arginine vasopressin, aka Anti-diuretic hormone Essence: Calibrates central and peripheral adaptation responses.
Theory of Endobiogeny Chapter | 1 11
Mechanism and actions: Centrally, stimulates oxytocin and relaunches ACTH, peripherally excretes cortisol and optimizes hemodynamics. Clinical pearl: Regulating vasopressin In patients with chronically imbalanced cortisol activity, consider the role of vasopressin. When cortisol activity is low, relaunch vasopressin. When cortisol activity is elevated and inhibiting alpha is not sufficient, use antivasopressics like Arnica montana. It is most indicated when the following are elevated: alpha-sympathetic, insulin activity and inflammation (e.g., harmful free radicals), and brain fog, fibromyalgia and/or chronic fatigue are prominent symptoms. With disorders rooted in hepatic insufficiency, use or add Taraxacum officinale to Arnica. Regulation ●
●
Stimulation: Osmoreceptors (increased plasma osmolarity), baroreceptors (reduced plasma volume), angiotensin II, melatonin Inhibition: Atrial natriuretic peptide (ANP), oxytocin, cortisol
Oxytocin Essence: Preservation and propagation of the organism. Mechanisms and actions: Additive-competitive actions with serotonin, dopamine, and vasopressin to augment awareness and attention to stimuli, anxiolytic, calibrates general functioning of corticotropic axis, fertility, parturition, lactation, parenting, social integration, mate selection. Regulation ● ●
Stimulation: Vasopressin, estrogen Inhibition: Progesterone (peripheral oxytocin activity)
Oxytocin vs vasopressin Vasopressin integrates internal rhythms of the individual to external milieu. Oxytocin integrates life rhythms of the individual to the species.
Peripheral hormones of the corticotropic axis Overview: The adrenal cortex is the only gland that can be engaged for adaptation and reproduction. It contains multiple hormones across multiple organs: ●
● ●
Adrenal cortex: Cortisol, aldosterone, DHEA, progesterone, estrogens Liver, lungs, kidney and blood: Angiotensin Kidney: Renin
Mechanisms and actions: Adrenal cortex hormones are all derived from cholesterol and produced in three different zones. The peripheral corticotropic hormones are the foundation of structure and manager of function (Table 1.6). Permissive functions of the adrenal cortex include production of anabolic steroids, and cell metabolism. Adaptive functions include production of cortisol, cell nutrition, vigilance and memory.
Clinical pearl: Balancing adrenal cortex activity When selecting medicinal plants to balance the activity of the adrenal cortex, look at the relationship of the cortisol index to the adrenal cortex index. For example, if the cortisol index is absolutely elevated and the adrenal cortex index is low it suggests an insufficiency of adrenal androgens in relationship to cortisol. If appropriate, reduce cortisol activity by inhibiting alpha and/or ACTH. In addition, you may add a plant with adrenal androgenic activity such as Rosa canina. Another approach would be to use a plant that shifts
TABLE 1.6 General actions of adrenal cortex hormones. Action
Cortisol
Structure
Adrenal androgens
Estrogens
Progesterone
✓
Foundation of initial fetal structure
Initiation of regulation of structure
Regulation of structure
Aldosterone
Function of structure
✓
✓
✓
✓
✓
Function
✓
✓
✓
✓
✓
Permissivity
✓
Adaptation
✓
✓
✓
✓
✓
✓
✓
Reproduction
✓ ✓
12 SECTION | A Theory and foundation of clinical practice
adrenal metabolism away from cortisol to adrenal androgens, such as Sequoia gigantea GM.
Regulation ● ●
Cortisol Essence: Ensures adaptability at every moment from every type of aggression, be it internal or external. Mechanisms and actions: Mobilizes material elements of adaptation, augments consciousness and movement. In its permissive function, cortisol potentiates activity of other physiologic processes: endocrine-endocrine regulation across the axes and during the general adaptation syndrome, sensitivity to catecholamines and the rate of glycogenolysis. In its adaptive role, cortisol acts as an agent of adaptation across various adaptation syndromes (Table 1.7). A full discussion can be found in The Theory of Endobiogeny, volume 1. Areas of production: Zona fasciculata, Zona reticularis.
Stimulation: αΣ, CRH, ACTH, α-MSH, β-MSH Inhibition: Endorphins (favor aldosterone), cortisol, estrogens
DHEA (dehydroepiandrosterone) Essence: Foundation and evolution of structure. Mechanisms and actions: Foundation: key role during fetogenesis, sex determination, sexual evolution and devolution: sexual dimorphism during puberty, libido, gonadopause, reservoir of preandrogen and preestrogen material that can be converted within specific tissue by intracrinology (as DHEA-sulfate), Adaptation: Endurance, resilience, creativity, immunity, healthy aging. Area of production: Zona reticulata. Regulation
TABLE 1.7 Actions of cortisol on various systems of the organism. System or tissue
Effects proportional to cortisol activity
ANS
Direct: ↑βΣ receptors → increased adrenaline sensitivity Indirect: ↓Serotonin → ↓para, ↓histamine → ↓alpha
Blood
↑WBC, ↑neutrophils, ↑platelets, ↓lymphocytes, ↓eosinophils, ↓basophils
Bone
↑Osteoclasty → ↑serum Ca, blocks bone Ca reabsorption
Cardiovascular
↑Dromotropy, ↑inotropy, ↑chronotropy, ↓vasodilation
CNS
↑Cognition, emotions, memory, learning (blocks at higher levels)
Electrolytes
↑Renal blood flow, retention: Na, Cl, H2O, loss: K, H, Ca, PO4
Endocrine
Gonadotropic: ↓LH, ↓estrogen sensitivity Thyrotropic: ↑Thyroid hormone production, ↑thyroid hormone activity Somatotropic: ↓Somatostatin, ↓prolactin, ↓insulin resistance/↑insulin
Immunity
↓Inflammation, ↓thymus volume (↓T-cell maturation), ↓wound healing
Metabolites
Liver: ↑Gluconeogenesis, glycogenolysis; muscle: ↑myolysis (amino acids); intestines: ↑uptake of lipids; adipose tissue: ↑adipocytes; general: antianabolic: blocked cellular absorption of all nutrients
CNS, central nervous system; Ca, calcium; Cl, chloride; H, hydrogen; H2O, water; FSH, follicle-stimulating hormone; K, potassium; LH, luteinizing hormone; PO4, phosphate; WBC, white blood cell.
●
●
Stimulation: ACTH (with endorphins favoring it over cortisol) Inhibition: Gonadal androgens, gonadal estrogens
Clinical pearl: Adaptative DHEA vs testosterone During adaptation, overexpression of DHEA can lead to irritability, aggression: verbal or sexual, focusing on results over people, lack of empathy, etc. With irritability, ensure a good cortisol to DHEA ratio by using plants such as Ribes nigrum and if needed, a neurocalmative (Valeriana officinalis, Passiflora incarnata, etc.). Through intracrinologic conversion, DHEA can result in excessive testosterone activity. In this case inhibit LH (Medicago sativa, Alchemilla vulgaris) and/or reduce androgen receptors (Humulus lupulus).
Aldosterone Essence: Hydroelectric integrity Mechanisms and actions: Structure: osmotic pressure, electrolyte balance, tensegrity, Adaptation: perfusion pressure, sodium and water retention with potassium loss, helps end adaptation response with central receptors. Area of production: Zona glomerulosa. Regulation ●
●
Stimulation: ACTH, endorphins, elevated serum potassium (K), elevated serum sodium (Na), angiotensin II, prostaglandin E’s Inhibition: ANP, dopamine, progesterone (antagonizes actions)
Clinical pearl When treating edema or cellulite as a manifestation of hyperaldosteronism, address in one of two ways: (1) use inhibitors of aldosterone (i.e., Borago officinalis), (2) address adrenal cortex imbalance in response to stimulation
Theory of Endobiogeny Chapter | 1 13
(through Biology of Functions). Support veno-lymphatic drainage (Sorbus domestica, Menyanthes trifoliata) and, as indicated, manual lymphatic drainage or exercise. Associated hormones of adaptation There are a host of additional hormones within the corticotropic axis related to adaptation and hydroelectric activity. Refer to The Theory of Endobiogeny volume 1 for details.
Summary of corticotropic activity in adaptation First loop: (Fig. 1.6) 1. ANS: αΣ stimulates excretion of all three levels: a. Hypothalamus: CRH b. Pituitary: ACTH c. Adrenal cortex: Cortisol, DHEA 2. Hypothalamus: a. CRH stimulates pituitary POMC → ACTH b. CRH stimulates pituitary POMC → αMSH 3. Pituitary: a. αMSH i. Stimulates ACTH and general pituitary functioning ii. Increases number of ACTH receptors on adrenal cortex iii. Augments intensity of cortisol release from adrenal cortex b. ACTH stimulates secretion and excretion of cortisol, DHEA
4. Adrenal cortex: a. Cortisol mobilizes glucose, proteins, lipids, electrolytes, and water b. DHEA prepares body to utilize what cortisol has mobilized Second loop: 1. ANS: αΣ continues stimulation 2. Hypothalamus: CRH stimulated by αΣ, PL (not shown, discussed later) 3. Anterior pituitary: ACTH favors the secretion and excretion of aldosterone 4. Posterior pituitary: Vasopressin a. Stimulates ACTH b. Stimulates aldosterone 5. Adrenal cortex: a. Aldosterone: mobilizes electrolytes, water b. Vasopressin: blocks renal water loss, increased vascular tone
Conclusions The corticotropic axis isgreater than the sum of the vertical feed-forward chain of CRH-ACTH-cortisol. It has many diverse hormones in multiple locations. It participates in diverse roles from protection to propagation of the species. In its key roles in adaptation syndromes, it touches all other endocrine axes and numerous emunctories, rate of metabolism, cellular nutrition, as well as cognitive and emotional states. For acute relief of the severity of symptoms, addressing the ANS-corticotropic relationship can offer true relief for the patient. For acute and chronic disorders related to disadaptation, from depression to ulcerative colitis, regulation of the corticotropic axis is essential.
Gonadotropic Introduction to the Gonadotropic axis
FIG. 1.6 Elaborated first- and second-loop corticotropic activity. In the first loop (left), alpha-sympathetic (αΣ) stimulates every level of corticotropic function. In addition, there is the classical vertical feed-forward action from hypothalamus (CRH) to pituitary (ACTH, POMC, αMSH) to adrenal cortex (Cortisol, DHEA). In the second loop (right), αΣ stimulates only the hypothalamus and pituitary. Stimulation of peripheral aldosterone occurs both from the anterior pituitary (ACTH) and posterior pituitary (vasopressin). Central stimulators of vasopressin are not shown here. The first loop mobilizes nutrients for energy (glucose, proteins, lipids). The second loop mobilizes electrolytes and water. Red arrow, stimulates; αΣ, alpha-sympathetic; α-MSH, alpha-melanocyte stimulating hormone; ACTH, adrenocorticotropin hormone; BP, blood pressure; Cl, Chloride; CRH, Corticotropic releasing hormone; Na, Sodium. (© 2015 Systems Biology Research Group.)
Overview: An anabolic axis that maintains the individual and propagates the species. It maintains life by initiating protein metabolism. It propagates the species through its primary role in fertility. The majority of illnesses linked to this axis are related to metabolism of proteins and regulation of the mesoderm. Embryological association: Mesoderm: muscle, renal tubules, erythrocytes, blood vessels, synovial membranes, etc. Metabolism: Anabolism, exclusively. Metabolite(s) and minerals: Proteins (estrogens, androgens), calcium (estrogens: sequester, androgens: utilize).
Clinical pearl: Embryology, endocrinology, organs, and treatment When beginning a practice in Endobiogeny, one may feel unsure which axis is most implicated in disease, which in
14 SECTION | A Theory and foundation of clinical practice
turn would determine the focus of treatment. To focus your treatment in this situation, trace the tissue most affected in the critical state to its embryologic origin. This leads you to the endocrine axis most implicated in the formation and regulation of that embryologic line. When in doubt, this axis and its associated organ or emunctory can be your primary point of regulation. For example, cardiomyopathy is a disorder of muscle, which is a mesodermal tissue. The hormones to treat are gonadotropic, especially estrogens and androgens. The organ to address is the liver, in its anabolic role in protein intake via the portal vein and protein production, as well as its emunctory function filtrating proteins fragments.
Hypothalamus GnRH: Gonadotropin-releasing hormone Essence: Ensures general competency of structural maintenance and reproductive capabilities by stimulating FSH and LH. Mechanisms and actions: Sole hypothalamic gonadotropic hormone that regulates both its pituitary hormones, FSH and LH. GnRH favors LH by default. FSH is favored when endorphins are present in an environment of low estrogens in hypothalamus. Regulation ●
●
●
Stimulation: Declining LH, FSH, or estrogens, or, the presence of any of the following: progesterone, androgens, activin, TRH, leptin Inhibition: ACTH (delays excretion), inhibin, or rising: FSH, estrogens and/or LH Regulation: Endorphins
Clinical implication: Desynchronization of GnRH within the general functioning of the endocrine system can lead to various disorders of: ●
●
Gonadotropic excess: e.g., precocious puberty, polycystic ovarian syndrome Gonadotropic insufficiency: e.g., delayed puberty, amenorrhea, infertility
Clinical pearl: Susceptibility of women to gonadotropic desynchronization Women are more susceptible to desynchronization disorders of gonadotropic origin throughout life. The regular menstrual cycle submits women to significant fluctuations in hormone production and activity. The adaptive demands on other systems (liver, lymphatics, central nervous system, etc.) can lead to adaptative states. Encourage female patients with menstrual cycles to maintain a healthy rhythmicity of living (sleeping before midnight, resting when feeling fatigued, eating seasonal foods, etc.) and ensure adequate endorphin activity through activities such as exercise and orgasm.
Pituitary FSH: Follicle-stimulating hormone Essence: Initiates structure and reproduction. Mechanisms and actions: FSH regulates cholesterol entry and metabolism within the gonads for peripheral gonadotropic hormone production. In women, this occurs in various places within the follicles. In men, it occurs exclusively in Sertoli cells. FSH stimulates conversion of androstenedione to estrogen. Actions are summarized in Table 1.8.
TABLE 1.8 Areas of function of FSH and pathophysiologic implications. Area
Function
Pathophysiology
Gonadotropic
Estrogen receptor upregulation
Excess estrogen receptors: amplifies estrogen activity, uncoupled from serum estrogen levels Insufficiency of receptors: hyper FSH state related to Crohn’s disease, psoriasis, cystitis, etc.
Thyrotropic
TSH calibration to harmonize thyroid to estrogen activity
TSH oversolicitation by FSH can participate in thyroid antibodies and thyroid dysfunction
Mucosa
Mucosal hypertrophy
Mucosal congestion, stasis: related to cystitis, colitis, sinusitis, bronchitis, etc.
Colon
Protein reabsorption: ascending, proximal transverse colon
Skip lesions in this area implicate hyper-FSH activity
Immunity
Formation of immunoglobulins (indirect through regulation of protein metabolism)
Hyperimmune (i.e., atopic disorders) and autoimmune states
Fertility
Timing of estrogen surge: mucosal and endometrial development
FSH pulsatility and estrogen response related to organic infertility
Morphology
Influences development of right half of body
FSH > LH: Right > Left endocrine receptors, hemihypertrophy, disorders of excess on right side of body, curvaceous female bodies, curl of eyelashes
Theory of Endobiogeny Chapter | 1 15
Regulation ●
●
Stimulation: Activin, low-frequency GnRH pulse, declining estrogens, progesterone, androgens, ACTH Inhibition: Inhibin, estrogens, cortisol (blocks release)
Clinical pearl: FSH and laterality The relative size of the eyes, hands, or feet can be a quick way to determine the relative structural influence of FSH in relationship to that of LH. When the right eye, hand or foot is greater than the left, it favors a structural predominance of FSH since fetogenesis. In the history, note a history of disorders on the right side: e.g., fungal toenail growth, right ovarian cysts, right humeral fracture. In such patients, regulating FSH with plants such as Borago officinalis may play a valuable role in treating chronic disorders.
Luteinizing hormone Essence: Manages completion of metabolism and fertility. Mechanism: It stimulates uptake and metabolism of cholesterol for production of progesterone and gonadal androgens. Actions: LH plays key roles in ensuring the regulation and finalization of anabolism. Through its peripheral products, it ensures a sufficient duration of estrogen activity in the first loop (via progesterone) and sufficient androgen activity in the second loop. Regulation ●
●
Stimulation: High-frequency GnRH pulse, declining androgens or progesterone, presence of estrogens, ACTH, or aldosterone Inhibition: Androgens, cortisol (blocks release)
Clinical pearl: LH and laterality The relative size of the eyes, hands, or feet can be a quick way to determine the relative structural influence of LH in relationship to that of FSH. When the left eye, hand, or foot is greater than the right, it favors a structural predominance of LH since fetogenesis. In the history, note a history of disorders on the left sided: e.g., fungal toenail growth, left ovarian cysts, left humeral fracture when falling. In such patients, regulating LH with plants such as Medicago sativa or Prunus africana may play a valuable role in treating chronic disorders.
of these gonadic hormones from cholesterol starts with progesterone → androstenedione. From there, estrogens or androgens can be produced depending on the location and enzymes transcribed within the gonads. Clinical pearl: Treating origin of hyperfunctioning of peripheral gonadotropic hormones The hyperfunctioning of these hormones can be determined by history (e.g., acne, premenstrual breast tenderness, breast cysts, etc.). However, there are many different levels of assessment as to why peripheral gonadotropic function is excessive. These levels can be explored using the Biology of Functions. Based on the terrain, one may downregulate estrogen receptors, e.g., with Vitex agnus castus, downregulate androgen receptors, e.g., with Humulus lupulus or, one may need to reduce rate of production due to central overstimulation by inhibiting FSH, e.g., with Borago officinalis, or LH with Medicago sativa, or both FSH and LH with a plant such as Lithospermum officinale. When the imbalance is due to a combination of factors, use a combination of medicinal plants within the same tincture, tisane, or encapsulated formulation.
Estrogens Essence: initiate cell metabolism and solicit proteins, calibrate thyroid activity, and play a key role in fertility, in that order of importance and frequency of action. Mechanism: Genomic, nongenomic Actions 1. Metabolism of proteins for structure and function 2. Tissue texture: suppleness, elasticity, resilience of internal and external structures 3. Quality of mucosal, serosal, and synovial surfaces 4. Immunoglobulin production 5. Fertility 6. Bone: bone and cartilage growth 7. Muscle: muscle growth and texture 8. Cardiovascular: vasodilatation, electrical discharge 9. Sexual dimorphism 10. CNS: multifactorial decision making, emotive thinking, instinctual knowledge, memory recall, contextualization of events, reflective speaking Regulation
An introduction to peripheral gonadotropic hormones
● ●
The peripheral gonadotropic hormones are six: estradiol, estriol, estrone, progesterone, testosterone, and dihydrotestosterone. ●
Metabolism of hormones vs metabolic action The order of metabolic action of the peripheral gonadotropic hormones is: estrogens (initiate cell metabolism) → progesterone (regulates metabolism) → androgens (complete metabolism). The metabolism, viz. their synthesis,
Stimulation: FSH Reduction of serum levels: Cortisol: indirectly by delaying FSH excretion, directly by stimulating sex hormone binding globulin binding of estrogens Regulation: Progesterone, TRH (sensitizes cells to estrogens), PL (opens up peripheral estrogen receptors)
Particularities of estrogens There are three forms of estrogens. Estradiol, produced from testosterone, is in greatest quantity during fertility.
16 SECTION | A Theory and foundation of clinical practice
After menopause, estriol, derived from androstenedione, typically via DHEA, predominates. This implicates a greater role of peripheral aromatization of nonestrogen steroids into estrogens during gonadopause. A shortcoming of quantitative urinary measurement of estrogens is that it evaluate intrinsic neither intrinsic nor synergistic effects of estrogens with other factors, nor does it distinguish quantitative production from intracrine conversion.
TABLE 1.9 Genomic and nongenomic actions of gonadal androgens.
Clinical pearl: Evaluating estrogen activity In order to properly evaluate estrogen activity, use history, physical examination, and Biology of Functions. Estrogen receptors are distributed in greater or lesser quantity in various tissues according to genetic heritage. A woman can have a history of a hypoestrogenic tissue (i.e., dry skin). The physical exam may confirm that but also show strong estrogens of structure (i.e., voluminous, supple breasts), while the BoF shows hyperestrogenism from aromatization of DHEA (DHEA index elevated). One may conclude that the global rate of estrogen production is elevated due to DHEA conversion, while the envelope (skin) has insufficient estrogen activity. The structural estrogen activity is in its genetically determined homeostasis. In this case, the dry skin is best treated with a topical treatment, i.e., Salvia sclarea and Rosa damascena essential oils in a base of jojoba or other carrier oils, intravaginal estrogen creams, or other methods.
Tissue
Genomic
Nongenomic
Cell
Apoptosis
Proliferation, migration
Muscle
Architecture: mass, density Smooth muscle proliferation
Smooth muscle relaxation
Bone
Epiphyseal lengthening
Cartilage
Closure of cartilage
Cardiovascular
Vasorelaxation
Immunity
Monocyte migration Foam cell production
CNS
Neuronal proliferation Neuronal stability
Gonadal androgens Essence: Completion of metabolism, architecture of structure, and management of function: mental, emotional, and physiologic. Mechanisms and action (Table 1.9): Nongenomic effects are associated with the salutary effects of gonadal androgens. Excessive or insufficient activity of the genomic actions is largely associated with adverse health outcomes. Androgen activity can be evaluated based on the type of androgen and area of activity. There is also a relative strength of receptor affinity that helps explain the relative circulating concentration of the three most commonly used androgens (Table 1.10). In order to properly evaluate androgen activity, use history, physical examination, and Biology of Functions. Determine the type of androgen based on location of action. Also determine situational predominance. For example, with a history of dark, copious hair at birth, it favors the role of DHEA in structural foundation. This could be programmed and genetic (i.e., patients from Mediterranean, African, and Indian subcontinent heritage) or situational due to fetal, placental, or maternal stressors. Determine if adrenarche (adrenal androgen relaunching) occurred early (before 10 years), on time or late (after 12 years) and what the final effectiveness is (i.e., adult muscle mass, color and location of hair or balding pattern, etc.). This may indicate if
Neuroplasticity Neuromuscular signaling Sexual pursuit Problem solving Aggression Reduction in overt expressions of emotions Motivation for reward
the DHEA activity at birth was situational or programmed. Testosterone activity can be assessed from childhood in the comportment of the child as well as neuronal development and certain aspects of immunity (i.e., relative monocytosis). Dihydrotestosterone (DHT) activity is generally commensurate with age. The Biology of Functions assists in the current level of assessment of androgens with respect to rate and location of production (adrenal relative to gonads) as well as their endocrinometabolic vs tissular effects. Regulation ● ● ●
Stimulation: LH, insulin Inhibition: Cortisol Regulation: Progesterone, estrogens (by sex-hormonebinding globulin)
Clinical pearl: Evaluating the role of various androgens The challenge with the physical examination is that all men are inherently androgenic (viz. “virilized”) on the exterior (hair, muscle, etc.) to some degree. Women have a much broader range of relative androgenism of structure
Theory of Endobiogeny Chapter | 1 17
TABLE 1.10 Summary of androgen activity by type of androgen. Effect
DHEA
Testosterone
Dihydrotestosterone
Androgen Receptor affinity
1
10
30
Skin moisture Hair
Increases sebum Low hair line
Receding hair line
Muscle
Skeletal: mass, density, strength Smooth: relaxation, proliferation
Bone
Density, linear growth Epiphyseal closure
Genitals
Epididymis Vas deferens
Thrombosis
Increased clotting
Sexuality
Libido
Comportment Cognition
Erection Capacity to resist and persevere
Neuronal irritability
Neuronal stability Neuroplasticity
and function. Furthermore, cultural norms allow, encourage, or expect women to modify or completely eliminate external androgens (i.e., depilation) and/or modify internal androgens (i.e., raising pitch of voice, appearing less intelligent than men present when making comments in public). In these cases, the Biology of Functions offers a glimpse into the true state of androgenism.
Progesterone Essence: Regulator of anabolism and reproduction. Mechanisms and actions: General mechanisms are similar to that described for the steroid hormones. Progesterone has membrane receptors with rapid nongenomic effects at the level of the membrane and cytosol, and genomic effects via translocation into the nucleus. The specific actions are summarized in Table 1.11. Progesterone is complementary to androgens and estrogens through dual agonism-antagonism. This is key to the function of the gonadotropic axis in the two loops. When progesterone levels are lower, it is anti-androgenic and proestrogenic. It prevents early expression of androgens and promotes estrogenic activity. As progesterone levels rise, it becomes anti-estrogenic and pro-androgenic. Regulation ●
● ●
Prostate Glans penis
Stimulation: LH, DHEA (indirect: LH, aromatization to estrogens), estrogens (LH relaunching) Inhibition: T4 Regulation: Estrogens (stimulate cortisol-binding globulin binding of progesterone)
TABLE 1.11 Summary of progesterone activity. Tissue
Function
Endocrine
Regulates LH, FSH by sustaining endorphins Inhibits estrogen receptors Inhibits intracellular estrogens Relaunch testosterone
Cellular
Growth factors Increased cell cycling
Bone
Regulates bone mass (cortisol antagonism)
Heart
Antiarrhythmic
Brain
Libido
Uterus/ovaries
Ovulation Implantation of fertilized egg Pregnancy
Mammary gland
Lobular alveolar development Suppresses lactation during pregnancy
Clinical pearl: A nuanced approach to progesterone’s regulatory role Key to progesterone’s regulatory role is the relative environment in which it works. LH produces progesterone in a milieu of elevated estrogens. LH favors androgens when progesterone is elevated and androgens are relative
18 SECTION | A Theory and foundation of clinical practice
or absolutely low. When a woman has a hyperestrogenism with progesterone insufficiency during her late luteal and early menstrual phase (breast tenderness, recurrent clots), one must both inhibit estrogens (i.e., Vitex agnus castus) and augment progesterone without inhibiting LH (i.e., Achillea millefolium NOT Alchemilla vulgaris). If, however, the issue is hyperluteal hyperandrogenism (i.e., polycystic ovaries, acne on the chin), one should inhibit LH while stimulating progesterone (i.e., Alchemilla vulgaris), which favors progesterone production over androgens. Reestablishing adapted progesterone activity will also regulate androgens in turn. Integration of gonadotropic function The gonadotropic axis is a purely anabolic axis with two key roles: maintenance of structure of the individual, and propagation of their genetic material (viz. fertility). The key to both is the notion of initiation and completion of protein metabolism. Rhythmic pulses and chronologic progression between central and peripheral, follicular and luteal activity is key for solicitation and incorporations of amino acids into polypeptides and proteins, ranging from enzymes and neurotransmitters to muscle and the lining of all hollow structures. We can summarize the general actions of this axis as follows (Fig. 1.7): First loop: 1. Hypothalamus: Low-frequency, high-amplitude GnRH → FSH. 2. Pituitary: FSH → Estrogens. 3. Gonad: Estrogens enzymes transcription, growth factors related to use of proteins. Second loop: 1. Hypothalamus: GnRH → LH.
High
frequency,
high-amplitude
FIG. 1.7 Elaborated regulation of the gonadotropic axis. Red arrow: stimulation, blue arrow: inhibition. (© 2015 Systems Biology Research Group.)
2. Pituitary: LH → gonads. a. ↑ Estrogens, ↓ progesterone: LH → progesterone b. ↑ Progesterone, ↓ estrogens: LH → androgens 3. Gonad: a. Progesterone: i. Moderate levels: support estrogens, delay androgens ii. Increased levels: 1. Inhibit intracellular estrogen activity 2. Reduce estrogen receptor activity → Relaunch androgens b. Androgens: complete anabolism (enzymes transcription)
Conclusion The gonadotropic axis is sequentially the first of the two anabolic axes (the other being the somatotropic). The gonadotropic axis initiates metabolism and is key for fertility. The unique quality of having three peripheral hormones from two pituitary regulators creates an agonist-antagonist relationship between estrogens, progesterone, and androgens. Disorders of amplitude, duration, and chronology of gonadotropic hormones play a role in numerous human disorders, including those classically associated with its peripheral hormones (i.e., infertility, osteopenia) and those associated by Endobiogenic theory (e.g., catamenial migraines, acne, prostatic adenoma, seizures, intrinsic asthma, etc.). The endobiogenic approach to terrain offers a particularly nuanced assessment of intrinsic gonadotropic function and its relationship to the other endocrine axes (cf. coupled axes) and emunctories.
Thyrotropic Introduction to the Thyrotropic axis Essence: Management of adaptability and growth. Key: Relative balance of TRH to TSH: imagination vs ideation, potential vs achievement, glucose vs proteins, adenosis vs amylosis, etc (c.f. The theory of Endobiogeny, Vol. 1, chapter 8, Thyrotropic axis). Embryology: Ectoderm: nervous system, pituitary, adrenal medulla (βΣ), immunity, epidermis, etc. The corticotropic and thyrotropic axes are linked (“yoked”) together with regard to disorders of adaptation and adaptability. They are both are relaunched by αΣ, and are linked to conscious, subconscious, and physiologic perceptions of and response to aggression (cf. Adaptation states). Metabolism: Catabolism (TRH, T4, PTH) > Anabolism (TSH, T3, calcitonin). Metabolite(s) and minerals: Carbohydrates (TRH), proteins (TSH), lipids (peripheral thyroid), calcium (Table 1.12).
Theory of Endobiogeny Chapter | 1 19
TABLE 1.12 Mobilization and utilization of metabolites by the thyrotropic hormones. Mobilizes metabolites Metabolite
TRH
Glucose
♦
Amino acids
♦
T4
Utilizes metabolites
PTH/D3
♦
Lipids
♦
Calcium
♦
TSH
T3
♦
♦
♦
♦
♦
♦
♦
Thyrotropin-releasing hormone Essence: Management of potentiality: mental, emotional, physiologic. It is a neuropeptide that happens to also regulate the thyrotropic axis, not vice versa. Mechanisms and actions: TRH has wide-ranging actions in the central and peripheral spheres (Fig. 1.8, Table 1.13). As show, the majority TRH’s activity is not
Pain
Spine Brain stem
Mental
Dreams
♦
slightly elevated and free T4 is slightly low, but the patient is asymptomatic. The Endobiogenic approach is to treat the level of dysfunction be it relative or absolute, central, peripheral, or both.
When evaluating the level of function of the thyrotropic axis, understand two key endobiogenic notions. First, some symptoms attributed to hypo- and hyperthyroidism are due to central thyrotropic dysfunction (viz. TRH, TSH). For example, tremors and insomnia are related to TRH, not T3. Second, most signs, symptoms, and disorders related to the thyrotropic axis are relative and qualitative in nature, not absolute or quantitative. This clarifies the paradoxical results encountered in practice. For example, patients with normal TSH and free T4 feel dysfunctional, or, TSH is
Rate of cognition
Calcitonin
♦
Clinical pearl: Central vs peripheral thyroid dysfunction
Adaptive thinking
D3
Adaptation
Myofunction First loop
TSH
Second loop
T3
Endocrine CNS
Myogenesis
Calcitonin Emotional
TRH
Histamine
Electrophysiologic
Dromotropy
Histamine
Alpha
Endocrinometabolic
Emotive thinking
Beta Amino acids
Glucose Histamine
Endocrino tissular
Exocrine pancreas
Endocrine pancreas
Insulin activity Cell hyperplasia FIG. 1.8 Summary of TRH effects. (© 2015 Systems Biology Research Group.)
Estrogen activity
Myolysis
Location
Physiology
Pathophysiology
Central
Neuromodulation: Central beta: accelerates central metabolism and neuronal transmission for optimal adaptability, creative response to adaptation demands, vivid dreams, creativity
Fugue states, tremors, anxiety, negative imagination, OCD
Chronobiology, pacemakers: modulates SCN activity for diurnal, seasonal adaptation, indirectly augmenting melatonin excretion
Seasonal and circadian disadaptation: insomnia, seasonal depression, spring allergies, seasonal cancer growth, etc.
Rational adaptation: enhances dopamine-induced analytical function for a more rational, equilibrated response to aggressions
Psychiatric disorders of excess: anxiety, panic attacks, schizophrenia
Contextual adaptation: synapses to limbic area to contextualize current aggression to past events and adaptation responses
Consumption of buffering capacity: traumatic rumination, harmful adaptation responses, seasonal depression, winter bronchitis, etc.
Qualification of global adaptation response: in quadratic relationship of αΣ, TRH, DA, limbic system, regulates qualitative, quantitative and chronologic intensity of cognitive, emotional and physiologic response to aggressions
Adaptability: states of adaptability, esp. thyrotropic axis, autoimmunity, seasonal depression, winter bronchitis, etc.
Survival of the most creative: fine tunes threshold of response of reticular activating system, neuroplasticity, introspection, etc.
Overstimulation: diurnal hypervigilance, nocturnal nightmares, night terrors, etc.
Serotonin-dopamine-TRH: enhanced arousal, pain, pleasure, reward, movement, sleep, cardiopulmonary rhythms, gastric secretions
Prolonged adaptative states: migraines, depression, suicide, narcolepsy, pain processing, dysrhythmias, gastric hyperacidity
Muscle tone, posture: colocates with serotonin in spine to allow for more rapid muscle contractions to regulate posture
Peripheral neuromuscular disorders: clonus, tremors, fasciculation, hypertonicity, Parkinson’s disease. Insufficiency of TRH: ataxia
Thyrotropic endocrine: stimulates both loops: TSH, T4 → T3, calcitonin
Thyrotropic disorders: hyperthyroidism, adenosis (tonsils, prostate, breasts), amylosis (Alzheimer’s, diabetes, atherosclerosis), cysts, thyroid cancer, etc.
Thyrosomatotropic endocrine: stimulates PL
Hyperprolactinosis: implosive adaptation, infertility, schizophrenia, menstrual disorders, pancreatic cancer, metastasis of solid tumors, acceleration of aberrant growths
Thyropancreatic: glycemia: stimulates glucagon to adapt serum glucose to needs of central metabolism driven by TRH
Disorders of adaptative TRH with hyperglycemia: depression with traumatic rumination, ADHD, autoimmune flare ups Disorders of hyperplasia: growth of aberrant tissues by cell multiplication
Cell: accelerates DNA transcription
Oncogenesis: DNA fracture, biologic toxin accumulation
Tissue: 1st loop: myolysis: AA mobilization, 2nd loop: T3: tissue reconstruction, adenosis (cell hyperplasia); dromotropy (rate of electro-cardiac impulse transmission)
Adenoidal disorders: tonsils, prostate, breasts (adenofibroids), muscle-wasting disorders, arrythmias
Peripheral
AA, amino acids; ADHD, attention-deficit hyperactivity disorder; OCD, obsessive-compulsive disorder; SCN, suprachiasmatic nucleus.
20 SECTION | A Theory and foundation of clinical practice
TABLE 1.13 Summary of central and peripheral TRH physiology and pathophysiology.
Theory of Endobiogeny Chapter | 1 21
related to stimulating TSH or converting T4 to T3, though these are among its actions.
TABLE 1.14 TSH physiology and pathophysiology.
Regulation
Physiology
Pathophysiology
Apoptosis
High serum TSH: mucosal congestion, i.e. appendicitis
Necrosis
High serum TSH: amyloidosis: Alzheimer’s, Parkinson’s, Huntington’s diseases; diabetes mellitus 2, atherosclerosis, rheumatoid arthritis
Free radical production
High serum TSH: fibrotic disorders
Oxidation
Low serum TSH: chronic inflammation: demyelination, chronic fatigue syndrome, fibromyalgia, brain fog, etc.
Reduction
Low serum TSH: cyst formation
Estrogen sensitivity
High serum TSH: increases estrogen sensitivity; pathophysiology: varied.
Calcium availability
Pathophysiology: varied.
Cellular catabolism
High serum TSH: favors prolonged cell activity; pathophysiology: varied.
Tissue growth, esp. muscle and bone; fibrosis
High serum TSH: favors disorders of overgrowth of bone and muscle. Low serum TSH: disorders of bone and muscle wasting, neuromuscular wasting, sarcopenia, etc.
●
●
Stimulation: Dopamine: Central alpha, αΣ (direct), βΣ (reactionary/compensatory), thyroxin (T4) (low concentrations in pituitary sensitizes pituitary to TRH stimulation of TSH), GnRH, cold Inhibition: TSH, triiodothyronine (T3) (increased concentrations in pituitary reduces pituitary sensitivity to TRH stimulation of TSH), somatostatin, FSH
Clinical pearl: Treating TRH After cortisol, TRH has the most diverse profile of action: adaptation, adaptability, adaptative states, defense, neuroplasticity, and more. The role of TRH is frequently implicated in numerous disorders from insomnia to allergies. Be sure to evaluate TRH activity in your patient, in history (e.g., vivid dreams), examination (e.g., deep tendon reflex, glabellar tap), and Biology of Functions (e.g., TRH/TSH index, thyroid relaunching index). TRH treatment almost exclusively involves downregulation. There are three widely used treatments with varying nuances of indication. Fabiana imbricata is the most diverse and is particularly helpful when addressing how TRH affects the peripheral nervous system (pain, reflexes), thyroid gland disorders, autoimmunity, endocrine pancreatic oversolicitation, and certain cancers (breast, colon, etc.). Vibernum lantana (gemmotherapy only) is helpful when traumatic rumination is predominant in the patient. Leonurus cardiaca is most indicated for insomnia, anxiety with palpitations and cardiac dysrhythmias.
Thyroid-stimulating hormone Essence: Promotion of structuration, achievement of structure (formation of structure, function of structure, adaptation, replication and restoration of structure). The logic of TSH requires its implication not only within the thyroid gland, but across the anabolic axes. Mechanisms and actions: secretion (production) and excretion of T4, T3, estrogen sensibilization and stimulation of growth factors proportional to serum TSH (Table 1.14). Because TSH promotes anabolic activity before the time of glucose entry, TSH solicits intracellular production and use of amyloid proteins. It serves as a “bridging” energy between the rapid effects of glucose and the prolonged effects of lipids. TSH solicits exocrine pancreatic excretion of proteolytic enzymes that break down amyloid proteins. The pathophysiology is rooted in disorders of amyloidosis (high serum TSH) and inflammation/somatotropic desynchronization.
Clinical pearl: Modulating TSH in an endobiogenic treatment Modulating TSH is one of the most fundamental aspects of regulation of the endobiogenic terrain. In a patient with fibromyalgia, chronic fatigue, and brain fog, one will find typically elevated cortisol index and low normal/low serum TSH. With this comes inflammation, harmful free radical activity, and low insulin resistance. Inhibit TSH with plants like Lithospermum officinale, Lycopus europaeus, Zea mays, etc. and lower cortisol. In a patient with intrinsic depression and weight gain, one will likely find a high normal or elevated TSH with low cortisol, catabolism/anabolism, and high insulin resistance. Lower serum TSH with iodine containing substances (e.g., Ascophyllum nodosum, sodium iodide), and use cortico-thyroid stimulant like Salvia sclarea or Zingiber officinale.
Introduction to the peripheral glands of the thyrotropic axis Essence: Cellular energy, and, mobilization, distribution, and utilization of lipids and calcium. The peripheral thyrotropic
22 SECTION | A Theory and foundation of clinical practice
TABLE 1.15 General overview of origin and activity of peripheral thyroid hormones. Gland/organ
1st loop
2nd loop
Thyroid
Thyroxin (T4)
Tri-iodothyronine (T3) Calcitonin
Skin, liver, kidney
Vitamin D3
Vitamin D3
Parathyroid
Parathyroid hormone
General
Thymus
T-lymphocyte maturation
axis is more than the thyroid gland. It includes six glands playing a role in five hormones, and immunity (Table 1.15).
TABLE 1.16 Clinical implications of T4 activity.
Introduction to the thyroid gland
Effect
Excessive
Low
Thermogenesis
Heat intolerance
Cold intolerance
Essence: Furnish structurofunctional energy (ATP) for endocrinometabolic and endocrinotissular activity. The functional energy of movement—that role is played by adrenaline + calcium.
Hair growth
Increased growth of hair Increased density of hair
Thinning of hair (particularly eyebrows) Diminished rate of growth
Clinical pearl: Meaning of thyroid antibodies in Endobiogeny
Vocal cords
Clear voice
Warble
According to the theory of Endobiogeny, antithyroglobulin antibodies represent an attempt by the organism to slow down the production of T4 from oversolicitation by TSH, estrogens, or both. Thyroid peroxidase (TPO) antibodies reflect a response of the peripheral thyroid gland to oversolicitation of T3 production. The presence of antibodies is not a disease. It is an indicator of oversolicitation. Evaluating serum TSH, quantitative T4:T3 ratio, thyroid index, thyroid yield, and TRH/TSH index all together help contextualize the significance of the antibodies and suggest an approach to treatment.
Thyroxin (T4)
Actions and mechanism: Genomic and nongenomic: 1. Carbohydrates a. Upregulates insulin receptors, glucose entry b. Membrane fluidity (thermogenesis), passive diffusion of carbohydrates c. Upregulates enzymes for glucose oxidation d. Upregulates rate of glucose oxidation 2. Oxygen: cellular uptake and consumption 3. Cell respiration: rate of oxidative phosphorylation within mitochondria
Essence: Catabolic hormone that affects structurofunctional (ATP) and functional (adrenaline) energy. Mechanisms and actions: Sensibilizes cells to catecholamines, stimulates lipolysis for ATP production, stimulates osteoclasty for calcium to accelerate enzymatic function and muscle contraction. Clinical implications of T4 are listed in Table 1.16.
Clinical implications:
Regulation
Other peripheral thyrotropic hormones
● ●
Stimulation: Estrogens, TSH Regulation: Progesterone (delays, then favors release)
Triiodothyronine (T3) Essence: Regulates structurofunctional energy of cell: oxidative metabolism for ATP production.
● ●
Excessive: cold sensitivity Insufficiency: hypo-oxidative state, recurrent infections
Regulation ●
Stimulation: Progesterone, TRH: conversion from T4
The other peripheral thyrotropic hormones are briefly summarized by essence (Table 1.17) and actions (Table 1.18).
Thymus Cf. Theory of Endobiogeny, Volumes 1 and 3.
Theory of Endobiogeny Chapter | 1 23
TABLE 1.17 Actions of additional peripheral hormones of the thyrotropic axis. Hormone
Essence
Actions
Clinical pearl
Parathyroid hormone
Prepares for anabolism: serum calcium increase
1st loop: complements T4 in adaptation
PTH activity is inversely related to the efficiency of thyroid metabolic activity and directly related to TSH. Regulate PTH via the latter two
Calcitonin
Regulation of calcium storage and utilization
2nd loop: complements T3 for restoration of bone after adaptation
Not directly evaluated or treated in Endobiogeny. Support thyroid function, measure serum calcitonin when indicated
Vitamin D3
Constitutional regulator of adaptation: complements other thyrotropic hormones
1st, 2nd loops: basal metabolism (gonadothyrotropic): growth, immunity, calcium management
Serum levels not indicative of need for replacement therapy; evaluate endobiogenic terrain across seasons, basal and adaptive metabolism. Can cause growth of certain cancers
TABLE 1.18 Summary of peripheral thyrotropic hormone effects on mineral ecology. Hormone
Ca, serum
Phos, serum
Mg, serum
Resorption, intestines
Resorption, kidney
Vitamin D production
Osteo-clasty
Osteo-blasty
PTH
↑
↓
↑
↑
↑
↑
↑
↓
Calcitonin
↓
↓
↓
↓
↓
↓
↑
D3
↑
↑
↑
↑
–
↑
Integrating the thyrotropic axis
First loop:
Within its own vertical functioning, the thyrotropic axis is catabolic in the first loop and proanabolic in the second loop. The general functioning is summarized as follows and recapitulated in Fig. 1.9.
1. Central a. TRH stimulates TSH b. TSH stimulates the thyroid, parathyroid, and thymus glands 2. Peripheral a. Thyroid: T4 i. Lipolysis: Free fatty acids for ATP production ii. Osteoclasty: Calcium as metabolic catalyst b. Parathyroid i. Increases serum calcium ii. Stimulates vitamin D: Start counteracting osteoclasty of T4, PTH c. Thymus: Maturation of T-lymphocytes Second loop:
FIG. 1.9 Regulation of the thyrotropic axis. See text for details. Red arrow: stimulates, blue arrow: inhibits. (© 2015 Systems Biology Research Group.)
1. Central a. TRH stimulates i. T4 → T3 ii. Calcitonin 2. Peripheral a. T3: Preanabolic: Increases ATP production for metabolic augmentation
24 SECTION | A Theory and foundation of clinical practice
b. Calcitonin: Proanabolic: Restores calcium stores to bone, favors osteoblasty c. Vitamin D i. Metabolic regulator: 1. Restores calcium and phosphorous stores 2. Anti- and proanabolic functions with respect to growth ii. Immunity 1. Supports the immune function initiated in the first loop by TSH and thymus
Conclusion The thyrotropic axis is the axis of internal movements: the energy of cellular function and the movement of ideas and thoughts in the brain. It is an axis closely involved with adaptation and restoration. While it is largely catabolic, it has activity that favors anabolism as well. It is implicated in a range of disorders beyond hyper- and hypothyroidism, from epilepsy to anxiety, from tremors to tachycardia. It plays an important role in disorders arising with the onset of spring (e.g., spring allergies) and autumn (e.g., recurrent bronchitis). When evaluating the axis, remember to evaluate central and peripheral factors: TRH, TSH, T4, T3, vitamin D, and other factors as indicated.
Somatotropic Introduction to the Somatotropic axis Essence: Manages nutrients, cell structure, cell energy, storage of energetic material, and progression of endocrine loops. ●
● ● ●
●
Nutrients: Extraction and processing: exogenous and endogenous sources, availability, distribution, timing of entry of nutrients Architecture: Growth factors Energy: Glucose and lipids for ATP production Storage: Carbohydrates as glycogen, lipids as adipocytes Loops: Starter energy before 1st loop, passage from 1st to 2nd loop, completion of 2nd loop
Embryology: Endoderm: alimentary tract (except mouth, anus), endothelial surface of glands and other hollow structures. Metabolism: Anabolism ≫ Catabolism
Hypothalamic hormones Introduction There are two hypothalamic hormones, unique to the endocrine axes: growth-hormone-releasing hormone (GHRH) and somatostatin (SS).
Essence: They initiate and end somatotropic function, finalize anabolism.
Growth-hormone-releasing hormone Essence: Regulates rhythmic culling and building. Mechanisms and actions: ●
●
●
Growth: Rhythmic building: stimulates growth hormone (GH) Sleep: Rhythmic culling: installs non-REM sleep, assists in installing with REM sleep through GH stimulation Memory: Consolidates long-term memory of facts and knowledge
Regulation ● ●
Stimulation: TRH Inhibition: TSH, SS, growth hormone (GH), prolactin (PL), insulin
Clinical pearl: Supporting restorative sleep GHRH and GH regulate restoration of the physical tissues and restorative non-REM sleep, which promotes a sense of wellbeing. One way to improve the restorative nature of sleep is to stop eating 3 h before sleep. This allows for the digestive nature of somatotropic function to be completed and for its restorative functions to become dominant. A tisane of digestive plants taken around meal time (Agrimonia eupatoria, Juglans regia, Arctium lappa) can help in this regard.
Somatostatin Essence: Inhibitor of anabolic hormones, ultimately proanabolic. Location: Central: hypothalamus, peripheral: digestive organs, endocrine pancreas. Mechanisms and actions: Safeguards organism from self-consumption via dysregulated growth. Centrally, it inhibits TSH, GH, PL. Peripherally, it has local paracrine action that inhibits digestion (stomach, intestines, exocrine pancreas), uptake (intestines), and distribution (endocrine pancreas) of nutrients. Regulation ●
●
Stimulation: PL, GH, insulin, insulin-like growth factor 1 (IGF-1) Inhibition: Cortisol
Pituitary hormones Introduction The true managers of peripheral somatotropic activity are the pituitary hormones: growth hormone (GH) and prolactin (PL). They are directly involved in the growth of cells and the storage of nutrients and stimulate the peripheral
Theory of Endobiogeny Chapter | 1 25
o rgans that further manage these functions. GH and PL have agonist-antagonist function that is competitive and additive in nature. The chronologic relationship of GH and PL is key to the regulation of both somatotropic function and endocrine progression throughout the two loops.
Growth hormone (GH) Essence: A first loop hormone that ensures proper availability, quantity, and timing of nutrients for anabolism. It primarily favors anabolism except for its lipolytic action. Mechanisms and actions: Three key concepts of GH function: pulsatility, duration, growth effects. ●
●
●
Pulsatility: six circadian peaks, greatest postprandial (nutrient distribution), and middle of night (reparation and growth). Duration: 20 min allows for brief calibrations of nutrient distribution and tissue repair, long-term action managed by IGF (insulin-like growth factor) activity. Growth: facilitate construction and growth, does not complete it: analogous to FSH-estrogens. For GH-IGF, PL-insulin-SS ensures completion of fashioning. Its actions are summarized in Table 1.19.
Regulation ●
●
●
Stimulation: αΣ, GHRH, ghrelin, estrogens, testosterone, TSH, hypoglycemia, fasting, intense aerobic exercise Inhibition: Insulin-like growth factor-1 (IGF-1), insulin, SS, serotonin, cortisol, hyperglycemia, free fatty acids Regulation: PL, ACTH (calibrates excretion)
Clinical pearl Somatotropic desynchronization is a concept represented by delayed growth hormone activity proceeded by insulin, with low insulin resistance. It can be seen in a number of autoimmune and inflammatory disorders such as Crohn’s disease, multiple sclerosis, and fibromyalgia. On the Biology of Function, one can see a low GH growth score and insulin resistance, elevated insulin activity and harmful free radicals, and in the labs, low normal or absolutely low serum TSH. In order to resolve the critical state and favor healing, one must reduce alpha and inhibit TSH. In addition, relaunching GH activity with a plant such as Lamium album can help resolve part of the reason why alpha-sympathetic activity was elevated initially.
TABLE 1.19 Summary of GH action by location and endobiogenic mechanism. Location
Mechanism
Action
Comment
Central
Endocrinometabolic
Dreams
GHRH initiates, TRH affects vivacity of dreams
Peripheral
Endocrine (liver)
IGF production
IGF’s responsible for most effects attributed to GH on bone, muscle and cartilage
Endocrinometabolic (nonvital organs)
Insulin resistance
Ensures timing and productivity of GH as a distributor of nutrients by delaying time of glucose entry into cell
Endocrinometabolic (liver)
Glucose: gluconeogenesis, blocks hepatic uptake of glucose
Favors circulating glucose for second loop entry and completion of anabolism
Nutrient distribution
Lipids: lipolysis
Augments free fatty acids for nonglucose ATP production in first loop
Amino acids: uptake into cells
Prepares cells to produce enzymes, DNA when the cell enters a construction phase
Electrolytes: calcium, phosphorous, sodium
Calibrates quantitative entry from effects of catabolic cortico- and thyrotropic activity
Endocrinotissular
General plan of growth and shaping of all organs
Vertical growth of muscle, bone, cartilage, special tropism for liver and endocrine pancreatic integrity
Metabolic
Restoration, reparation of cellular elements
All classes and structures: glycolipids, proteoglycans, cell membrane, DNA integrity, etc.
GHRH, growth-hormone-releasing hormone; IGF, insulin-like growth factors; TRH, thyrotropic-releasing factor.
26 SECTION | A Theory and foundation of clinical practice
Prolactin (PL) Essence: Paces the loops, regulates plenitude of the organism in its self-habituating, self-sustaining and self- perpetuating requirements. Mechanisms and actions: TRH is its primary stimulator, forming a true thyro-somatotropic axis: TRH-PLinsulin. This axis touches both anabolic axes to ensure anabolism and fertility. Overall, though, the majority of PL’s endocrine actions are central. Pacing the endocrine loops ●
●
First loop: PL advances first loop anabolic: reduces FSH and increases estrogen receptors to compensate, turns the loop Second loop: Relaunches CRH and LH, inhibits GnRH to reduce insulin resistance, stimulates insulin PL’s peripheral activity is summarized in Table 1.20.
Clinical pearl: Capital role of PL in disorders Hyperprolactinemia is implicated in a broad array of disorders: hyperplasia, carcinogenesis with metastasis, hirsutism, acne, polycystic ovarian disease, dysmenorrhea, insomnia, disadaptation states, etc. Inhibiting PL with plants such as Poterium sanguisorba, Mercurialis annua and Fragaria vesca is capital. Conversely, insufficient PL can be associated with dysmenorrhea, infertility, failure to thrive, disadaptation states, and intrinsic depression. In these cases, relaunch PL with Sambucus nigra leaf or Lamium album. Neurometabolic: Adaptation, endocrine, and comportmental effects of PL The way in which PL participates in adaptation can have a relationship on behavior. This is because PL relates to alpha sympathetic, dopamine, and TRH in a quadratic relationship (Fig. 1.10). This relationship helps determine if the patient has a successful adaptation response, or one that is
FIG. 1.10 There are two triadic relationships related to adaptability involving prolactin. The first is alpha-sympathetic (αΣ)-Dopamine-Prolactin (upper triangle). This is a true trépied in which alpha stimulates Dopamine (DA) and prolactin (PL). DA stimulates PL but PL inhibits DA. This relationship calibrates both the mental (DA) and corticotropic (via PL relaunching of CRH) aspects of adaptation The second triadic relationship is that of αΣ-TRH-PL (lower triangle). This relationship is exclusively one of stimulation. It is not a trépied. It adapts the emotional and thyrotropic aspects of adaptation. When the two sets of triadic relationships are viewed together by their interrelationship, one has quadratic relationship implicated in myriad disorders. Linking the two triads is the relationship of DA and TRH, and αΣ, which directly stimulates the other three factors. This adds an additional level of dynamism to the final effects of prolactin. Red arrow: stimulates, red broken arrow: makes an appeal, blue arrow: inhibits. (© 2015 Systems Biology Research Group.)
implosive or explosive. Implosive adaptation: fragilized, difficulty handling stressors, traumatic rumination, withdrawal from aggression. Explosive adaptation: dramatic behavior, looped pseudo-logical thinking, expressed anger, fighting, running away. Genetic variations, pancreatic sensitivity, cortisol response, and androgens all color and affect the precise quality of the behavioral response to stress. This quadratic relationship is implicated in disorders as wide ranging spring cancer metastasis, infertility, schizophrenia, bipolar depression, and insomnia.
TABLE 1.20 Actions of PL by location. Location
Action
Comment
Hypothalamus
CRH relaunching
Relaunches ACTH, re-adapts cortisol
Pancreas, endocrine
Insulin excretion
Helps close anabolic loop
General
Width of structure
Suppresses apoptosis, increases proliferation of cells; when activity estrogens + progesterone, favors proliferation of cancer cells in breast, ovaries, uterus
Immunity: autodefender of life
Inflammation, extravasation
Favors pus production
Vasculature: autosustainer of life
Angioneogenesis
Favors metastasis of tumors, especially breast and prostate
Mammary glands: allosustainer of life
Lactation: production and flow
Oxytocin stimulates letdown
Theory of Endobiogeny Chapter | 1 27
In summary, PL is a pituitary hormone that has several unique and indispensable actions. PL helps nourish cells, regulates growth, regulates the pacing and progression of adaptation. It plays a role in psychobiologic phenomenon, and chronobiologic activity in the alterations of day and night, and seasonal changes. Regulation
●
●
●
●
Stimulation: αΣ, estrogens, TSH (secretion), TRH (excretion), suckling (peripartum women only) Inhibition: SS, dopamine, progesterone, T4 (slows down liberation)
●
Regulation
Introduction to peripheral hormones Essence: Adapts organism in its basal, immediate, and chronic demands.
IGF-1: Insulin-like growth factor-1: Liver Essence: Manages growth, adhesion, expansion of cells; barometer of nutritional integrity and somatotropic synchronization. Mechanisms and actions: 1st loop hormone produced in liver by GH, mediates cell growth: sensitization to growth factors, growth regulation, mitogenesis, and cell adhesion. Actions summarized in Table 1.21.
Stimulation: GH, zinc, selenium, magnesium, protein intake Inhibition: IGF binding protein 1 (IGFBP1), protein malnutrition, very low-calorie intake, immune dysregulation Regulation: IGF-2, IGFBP3
Glucagon: Endocrine pancreas Essence: Participates in basal and adaptation states: provides substrates for structural and functional energy (glucose, free fatty acids). Mechanisms and actions: Catabolic hormone in an anabolic axis, produced in Islet cells of the endocrine pancreas. It acts by glycogenolysis and lipolysis. Technically, it is not strictly speaking a first- or second-loop hormone. It constantly functions to regulate glycemia. It has an agonist-antagonist, competitive-additive relationship with insulin, similar to that of GH with PL (Table 1.22). Regulation ●
●
Stimulation: Hypoglycemia, πΣ (acetylcholine), βΣ, TRH, cholecystokinin, amino acids (arginine, alanine) Inhibition: SS, insulin, urea, free fatty acids (FFA)
TABLE 1.21 Actions and effects of insulin-like growth factor. Action
Effect
Comment
Endocrinometabolic
Inhibits apoptosis Promotes oxidation
Oxidation favors increased ATP production, free radical production
Endocrinotissular
Lengthening of tissues and organs
Most targeted: bone, cartilage, muscle
Nutritional integrity
IGF-1 expression commensurate to mineral intake
Most beneficial: zinc, selenium and magnesium
Longevity
Inversely correlated to IGF-1
Reduce caloric intake by 15%
Pathophysiology
Insufficient IGF-1
Failure to thrive in children
Excess IGF-1
Atherosclerosis, uterine fibroids, and tumors
TABLE 1.22 Actions on glucagon by metabolite. Metabolite
Action
Comment
Glucose
Basal glycemia: glycogenolysis, gluconeogenesis a
Lipids a
Constant regulation of glycemia in moderate adjustments
Starter energy to initiate adaptation
Evaluate relative to adrenaline (rapid, large adjustments of glycemia): Children: adrenaline > glucagon, Adults: glucagon > adrenaline
Lipolysis
Beta-oxidation for ATP production
A starter is a noncombustion engine that starts the combustion engine.
28 SECTION | A Theory and foundation of clinical practice
Insulin: Endocrine pancreas Essence: The restorative hormone, counteracting catabolic actions of both loops, growth-promoting hormone par excellence. Mechanisms and actions: Utilization, preservation and storage. Periphery: nutrients, central: structure and function (Table 1.23). Pathophysiology: Hyperinsulinism favors inflammation, inappropriate glycosylation of proteins and receptors, and other deleterious effects associated with hyperglycemic disorders such as diabetes. Like IGF-1, which belongs to the same family of hormones, insulin favors oxidation, free radical species, and mitosis. Regulation ●
●
Stimulation: Hyperglycemia, hyperglycemic hormones: adrenaline, glucagon, T4 (secretion), TRH (excretion), PL Inhibition: Somatostatin
Integrating the somatotropic axis First loop 1. Central a. GHRH stimulates GH b. GH i. Increases circulating free fatty acids ii. Increases uptake of minerals, amino acids iii. Stimulates hepatic IGF-1 excretion iv. Stimulates PL (turn the loop, prepare for insulin) v. Installs insulin resistance (prevent early closing of anabolism by insulin) vi. Inhibits GHRH by classical feedback c. PL: Turns the loop
2. Peripheral: IGF-1 a. Initiates growth b. Prepares cell for insulin c. Inhibits GH by classical feedback Second loop 1. Central a. TRH i. Stimulates PL ii. Stimulates insulin b. PL i. Inhibits GH, releases insulin resistance from insulin receptors ii. Stimulates insulin 2. Peripheral a. Insulin i. Conserves carbohydrates, proteins, and lipids ii. Provides substrates for ATP production iii. Stimulates growth of cell, finalizes all that was prepared preceding it iv. Closes the door of anabolism 3. Central/peripheral a. Somatostatin i. Inhibits all somatotropic hormones and central thyrotropic hormones that relaunch the somatotropic axis: 1. GHRH 2. PL 3. IGF-1 4. Insulin 5. TSH
Conclusion The somatotropic axis is a key axis of energy distribution and growth. In terms of adaptation it is the turnstile that
TABLE 1.23 Conservative effects of insulin. Substance/location
Utilization
Preservation
Storage
Carbohydrates
Glucose entry into cells
Inhibits glycogenolysis
Glycogenesis
Lipids
Free fatty acid entry into cells
Blocks lipolysis
Lipogenesis
Proteins
Blocks proteolysis
Blocks gluconeogenesis (from amino acids)
–
Electrolytes
Potassium entry into cells
Diminishes renal sodium excretion
–
Cell
–
Reduces autophagy of organelles
–
Cardiovascular
Vasodilator: improves microvascular flow for nutrient distribution
–
–
Brain
–
Synaptic plasticity
Memory: formation, consolidation, recall
Theory of Endobiogeny Chapter | 1 29
assures the end of the first loop and beginning of the second loop. It is also the guarantor of the conclusion of the general adaptation syndrome through the conclusion of the second loop. Beyond the activity of insulin and glucose management, this axis is implicated in everything from dreams and memory, to cancer metastasis and lactogenesis. It has the greatest number of hormones owing to its particular role in digestion, and the greatest number of cellular functions that it influences. When evaluating the axis, be sure to consider the role of the endocrine pancreas and its implication in disorders not only of glucose management, but inflammation and adaptation.
Endocrine regulation There are three types of endocrine regulation (Table 1.24). The types of regulation expand the notion of how three key elements are related to each other in basal and adaptive metabolism. These factors are the autonomic nervous system, the endocrine system and emunctories. The relationship of ANS to the endocrine system is discussed under section “Adaptation syndromes and adaptability.” Endocrine coupling is the functional linking of one hormone with another. Coupling is key to understanding how and why particular axes and central-peripheral relationships are linked together in physiology and pathophysiology.
Endocrine-endocrine coupling Essence: Regulatory coupling that calibrates that which follows based on what has already been expressed. Mechanisms and actions: 1. Adjacent axes: The hormone on the same level works in a para fashion: horizontal stimulation of secretion. The hormone downstream works in both alpha (radial delay of excretions) and beta (radial allowance of e xcretion)
fashion. This relationship is true for hypothalamic- pituitary regulation and pituitary-peripheral regulation. Example 1: When CRH stimulates ACTH, FSH must be calibrated to stimulate estrogens proportionally, but at a later time. In calibration of FSH, both CRH and ACTH play a role. CRH plays the “para” role by increasing hypothalamic GnRH secretion (production within the hypothalamus). ACTH plays the “alpha” role by delaying GnRH excretion (release) to the pituitary to stimulate FSH for a time. This is in order for ACTH to have its action on cortisol. As cortisol levels rise and inhibit ACTH, ACTH levels fall. This reduction in ACTH releasing the delaying or alpha action it had on GnRH. This effectively is a beta-like action in that it allows for GnRH to be excreted and start the process of FSH calibration. Example 2: ACTH stimulates cortisol. To calibrate estrogens to match cortisol: ACTH is para (increases FSH secretion), high cortisol is alpha (delays FSH excretion), falling cortisol is beta (allows GnRH to stimulate FSH excretion). 2. Metabolic axes: Axes are linked by net metabolic effect to coordinate efficacy of action. Catabolic-catabolic: Cortico-thyrotropic linkage via Alpha: relaunches CRH and TRH. Downstream, cortisol sensibilizes cells to T4 activity. Anabolic-anabolic: Gonado-somatotropic linkage via Para: estrogens relaunch growth hormone; prolactin relaunches gonadotropic activity to favor androgens and progesterone, while amplifying peripheral actions of estrogens.
Clinical pearl: Managing cortico-thyrotropic disturbance When a patient presents with symptoms or disorders strongly related to inflammation, such as fibromyalgia,
TABLE 1.24 Type of endocrine regulation. Regulation
Example
Logic
Application
ANS-endocrine
Alpha → General adaptation syndrome
Calibrates intensity and duration of endocrine activity
Address ANS in treatment when seeking to modulate insufficient or excessive endocrine activity
Endocrine-endocrine coupling
FSH calibrates TRH production
Vertical FSH activity on gonads helps TRH calibrate quality of thyrotropic catabolic activity in response
In reducing sugar cravings due to elevated TRH in premenstrual syndrome, evaluate FSH-estrogens and peripheral thyroid activity as well
Endocrine-emunctories
Aldosterone → Kidney
Aldosterone regulates tissular and cellular hydroelectric activity, so it modulates the kidney’s role in water and electrolyte
With tissue edema, to improve renal diuretic function, address adrenal cortex production of aldosterone
30 SECTION | A Theory and foundation of clinical practice
chronic fatigue, autoimmune joint disorders, etc., evaluate for signs of excessive activity of the cortico-thyrotropic yoking. On the biology of functions, some typical findings if the patient is in the critical terrain include low serum TSH (>> alpha, quires chronic treatment along with psychological/lifebeta blocked or delayed style interventions. Treatment: reduce para: thyme (Thymus vulgaris) There are two key approaches to use: Example 3: Ulcerative colitis: alpha >>> but all high beta>> para, 1. Iterations of the general functions of each branch: Treatment: reduce global alpha > para: Lavender a. Para-sympathetic: rest and digest (intake and (Lavandula angustifolia) proliferation) 4. Autacoids are key modifiers of the ANS and should be b. Alpha-sympathetic: restraint, refinement, thickening addressed in treatment (Table 7.2) c. Beta-sympathetic: brief bursts of action, contraction, a. Parasympathetic: excretion. Autacoid: serotonin 2. Application of these principles to: Treatment: 1-Improve activity that requires a. Every system: CNS, endocrine, digestion, etc. para activity, and para levels will diminish, e.g., b. Every occasion: adaptation, restoration, basal mefor digestion one can use eupeptics, carminatabolism, etc. tives, enzymatic substitutes, i.e., Yarrow (Achillea millefolium), Agrimony (Agrimonia eupatoria), Papaya leaf (Carica papaya). Quick review b. Alpha-sympathetic: Autacoid: histamine 1. Parasympathetic is the structural and functional Treatment (order of importance depends on foundation of the nervous system. origin of hyper-alpha): (1) reduce alpha (mental, 2. Structure: Acetylcholine (ACh) neurotransmitter for: emotional, or for relaunching adaptation), e.g., a. Parasympathetic (para, or πΣ) pre- and post- Passion flower (Passiflora incarnata), (2) antiganglionic nerves histaminics (if cortisol low or histamines causb. Alpha-sympathetic (alpha, or αΣ) pre-ganglionic ing local symptoms), e.g., Lavender (Lavandula nerves angustifolia), (3) improve beta (in spasmophilia), Clinical significance: Plants can be para- and alphae.g., ginger (Zingiber officinale), and (4) reduce sympatholytics because of pre-ganglionic action, or, para (if initiator of hyper-alpha), e.g., tarragon exclusively parasympatholytic if it only inhibits post(Artemisia dracunculus) ganglionic ACh release. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00007-X © 2020 Elsevier Inc. All rights reserved.
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68 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 7.1 Symptoms related to the autonomic nervous system by system of the body. Category
Finding
Variable
State
General
Vagal crisis: vertigo, nausea, sweats, and vomiting
Para
Hyperfunctioning
CV
Hypertension
Beta
Elevated
Coronary ischemia
Beta
Insufficient
Variceal veins
Para
Elevated
Hot flashes
Beta
Hyperfunctioning
Sweat easily, especially first part of night
Para
Elevated
Psoriasis
Para
Elevated
Eczema
Para
Elevated
Constipation, spasmodic
Alpha
Elevated
Tendency to easily vomit
Alpha
Elevated
Stomach ulcer
Alpha
Elevated
Diarrhea
Beta
Elevated
Vomiting
Beta
Elevated
Aerophagy
Para
Elevated
Abdominal bloating
Para
Elevated
Gastritis
Para
Elevated
Colitis with diarrhea
Para
Elevated
Insufficient digestive secretions
Para
Insufficient
Libido, absent
Beta
Insufficient
Pelvic congestion
Para
Elevated
Streptococcus
Alpha
Elevated
Herpes
Alpha
Elevated
Psoriasis
Alpha
Elevated
Eczema
Alpha
Elevated
Herpes, severe outbreak
Beta
Insufficient, blocked, or delayed
Immune
Allergies
Beta
Insufficient, blocked, or delayed
Metabolic
Diabetes
Beta
Intermittently overreactive
Fatigue, chronic
Beta
Insufficient, blocked, or delayed
Migraines
Alpha
Hyperfunctioning
Hallucinations
Para
Insufficient
Asthma
Alpha
Elevated
Asthma
Beta
Insufficient, blocked, or delayed
Bronchitis
Para
Elevated
Insomnia
Alpha
Elevated
Nightmares
Para
Insufficient
Derm
GI
GU
ID
Neuro
Pulm
Sleep
CV, cardiovascular; Derm, dermatologic; ID, infectious disease; Pulm, pulmonary; Neuro, neurological.
Clinical Essentials of the Autonomic Nervous System Chapter | 7 69
TABLE 7.2 Signs related to the autonomic nervous system noted by observation of temperament. Quality
Finding
Factor
Activity
Internal state
Anxious
Alpha
Elevated
Internal state
Emotionally sensitive
Alpha
Elevated
External state
Impulsive
Beta
Elevated
External state
Fidgety, cannot sit still
Beta
Elevated
Internal state
Mental fatigue that blocks initiative
Beta
Insufficient: blocked or delayed
Internal state
Lacking desires and motivation
Beta
Insufficient: blocked or delayed
Internal state
Smallest effort seems huge
Beta
Insufficient: blocked or delayed
External state
Introverted
Para
Predominant
External state
Avoids speaking in public
Para
Excessive
Internal state
Timid, shy
Para
Excessive
Key historical findings relating to the ANS by system Table 7.1 organizes key ANS findings by system of function. See The Theory of Endobiogeny, volume 2, Chapter 1 for a full discussion. NB: The role of the factor of the a utonomic nervous system presented may not be the sole or exclusive factor.
Key physical examination findings relating to the ANS by system On exam, one can evaluate temperament (Table 7.2) and certain observable qualities (Table 7.3) during the historical intake. On physical examination, dermatologic findings (Table 7.4), head (Table 7.5), chest (Table 7.6), cardiopulmonary (Table 7.7), and nervous system (Table 7.8) signs can also be linked to functioning of the ANS. See The Theory of Endobiogeny, volume 2, Chapter 1 for a full discussion. NB: The role of the factor of the autonomic nervous system presented may not be the sole or exclusive factor.
Biology of Functions indices related to the ANS A few key indexes related to sympathetic function, with definition and relevance to clinical practice are presented in Table 7.9.
Treating the Starter index 5. πΣ-αΣ-βΣ sequence is throughout the body (cf. Table 1.1 in Chapter 1: Theory of Endobiogeny). Select treatments that improve sequencing even if the ANS is not directly involved
Clinical pearl The basic functioning of the ANS is influenced by genetic variations (i.e., receptor distribution and density), lifestyle choices (e.g., diet, sleep habits), and psychological frameworks (e.g., perception and response). It is not uncommon to find discrepant findings of ANS function throughout the body. For example: para predominates in the mouth (increased saliva), with spasmophilia (elevated para and alpha with blocked beta) in musculature (muscle tension with migraine headaches). Plants have tropisms for branches of the ANS and areas of the body. For example, for the mouth, an indirect parasympatholytic such as agrimony (Agrimonia eupatoria) can be used. For migraines, a muscular spasmolytic such as valerian (Valeriana officinalis) can be used, which reduces alpha and parasympathetic tone.
The formula of the Starter index is Leukocyte mobilization/Platelet mobilization. When the Starter index, or the Leukocyte mobilization indexes are elevated, use medicinal plants that are both alpha sympatholytic and splanchnic decongestants. German chamomile (Matricaria recutita) and Roman chamomile (Anthemis nobilis) both meet these criteria. There are numerous medicinal plants that can be used in combination to achieve the same effect. For example, lavender (Lavandula angustifolia) as a sympatholytic, and milk thistle (Carduus marianus) as a liver drainer and portal decongestant. By focusing on the adaptative alpha that delays beta, beta should be reintegrated into the adaptation process. If not, on follow-up evaluation of the Biology of Function, if the Platelet mobilization index is still low, use beta agonist plants. The specific choice depends on the terrain of the patient, in addition to delayed adrenaline activity. For example, if patient complains of fatigue and/or recurring infectious diseases, use cinnamon (Cinnamomum zeylanicum). If the patient has an inflammatory condition, or one affected by hyperandrogenism, such as acne or uterine fibroids, use bogbean (Menyanthes trifoliata).
70 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 7.3 Signs related to the autonomic nervous system noted by observation. Part
Quality
Finding
Factor
Activity
Voice
Volume
Weak, breathy
Beta
Insufficient: blocked or delayed
Body
Movement
Active with fine movements
Alpha
Elevated
Movement
Active with gross movement
Beta
Elevated
Movement
Still
Para
Elevated
Build
Round
Para
Elevated
TABLE 7.4 Signs related to the autonomic nervous system at the level of skin. Quality
Finding
Factor
Activity
Wrinkles
Deep, vertical
Alpha
Elevated
Sensitivity
Sensitive to touch, pain, cold, rubbing
Alpha
Elevated
Temperature and moisture
Cold
Alpha
Elevated
Cold and sweaty
Alpha
Elevated
Hot and without moisture
Beta
Elevated
Moist and often hot
Para
Elevated
Cold and without moisture
Para
Insufficient
Suppurative
Para
Elevated
Eczema
TABLE 7.5 Signs related to the autonomic nervous system at the level of head. Part
Quality
Finding
Factor
Activity
Complexion
Coloration
Rosy and cold
Alpha
Elevated
Alternating pale and rosy
Beta
Elevated
Zygomatic arch
Coloration
Erythema
Alpha
Elevated
Visage
Shape
Round
Para
Elevated
Hair
Fineness
Fine
Para
Predominant
Eye
Pupil size, baseline
Enlarged
Alpha
Elevated
Reduced
Para
Elevated
Vision
Acuity
Far sighted
Para
Elevated
Ears
Color
Rosy
Alpha
Elevated
Cheeks
Complexion
Rosy and warm
Beta
Elevated
Mucosa, oral
Secretions
Increased
Para
Elevated
Palate, hard
Color
Pallor
Alpha
Elevated
Palate, hard
Vascularity
Varicosities
Alpha
Elevated
Submandibular
Lymph nodes
Lymph nodes palpable
Alpha
Elevated
Clinical Essentials of the Autonomic Nervous System Chapter | 7 71
TABLE 7.6 Signs related to the autonomic nervous system at the level of chest. Part
Quality
Finding
Factor
Activity
General
Prominence
Flat
Para
Predominant
Sternum
Concavity
Concave sternum
Para
Predominant
Suprasternal notch
Tenderness
Pain on palpation
Alpha, para
Elevated
Sternum
Orientation
Concave sternum
Para
Predominant
Sternum
Orientation
Concave sternum
Beta
Weak
TABLE 7.7 Signs related to the autonomic nervous system at the level of cardiopulmonary systems. Part
Quality
Finding
Factor
Activity
Heart
Rate
Heart rate regular with diminished blood pressure
Beta
Insufficient: blocked or delayed
Heart
Rate
Heart rate slow
Para
Elevated
Heart
Rhythm
Palpitations
Beta
Elevated
Heart
Rhythm
Extrasystolic beats
Para
Elevated
Pulse
Width
Pulse narrow
Alpha
Elevated
Pulse
Amplitude
Pulse bounding
Beta
Elevated
Pulse
Strength
Pulse weak
Para
Insufficient
Pulse
Width
Pulse full
Para
Elevated
Artery
Blood pressure
Blood pressure weak
Para
Elevated
Vein
Tone
Veins dilated
Alpha
Insufficient
Veins
Varicosity
Veins varicose
Para
Excessive
TABLE 7.8 Signs related to the autonomic nervous system at the level of the other aspects of the nervous system. Part
Quality
Finding
Factor
Activity
Glabellar tap
Upper lid
Eyelid response rapid
Alpha
Elevated
Eye
Pupillary light reflex
Hippus, rapid
Alpha, para central
Elevated
Eye
Pupillary light reflex
Hippus, sustained
Alpha, para central
Elevated, in permanent opposition to each other
Tongue
Fasciculations
Present
Alpha, para
Disequilibrium
Tongue
Tremor
Present
Alpha
Elevated
Hands
Fingers
Tremors, gross
Beta
Elevated
72 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 7.9 Some indexes of the Biology of Functions related to the autonomic nervous system. Index
Definition
Relevance
Thyroid relaunching
Alpha-sympathetic relaunching of TRH and the thyrotropic axis due to exogenous stressors
Use to determine role of organic stressors in adaptation TX: ↓Alpha, ↓TRH
Thyroid relaunching corrected
Alpha-sympathetic relaunching of TRH and the thyrotropic axis due to endogenous stressors
Use to determine role of emotional stress in adaptation TX: ↓Alpha, ↓TRH, address stressors
Leukocyte mobilization
Mobilization capacity of leukocytes for adaptation from the splanchnic bed
Both high and low values indicate chronic stress TX: ↓Alpha, drain liver, drain splanchnic bed
Platelet mobilization
Mobilization capacity of platelets for adaptation from the splanchnic bed
If leukocyte mobilization high or low and platelet mobilization low there is a spasmophilia TX: Spasmolytics
Starter index
Relative predominance of glucagon vs adrenaline for glucose mobilization to start adaptation response
High: Alphaendocrine pancreas (glucagon) implicated; Low: TRH-adrenaline implicated TX: See text
ANS: central
ANS: peripheral
TX, treatment.
Conclusion The ANS is implicated in all aspects of functioning of the terrain and thus in all disorders. It is an efficient aspect to regulate in clinical practice. Acute ANS dysfunction can respond in a short time to Endobiogenic interventions. The ANS can be evaluated by history, physical examination, and Biology of Functions. Through a triangulation of all three methods of evaluation, levels of ANS function can be determined by degree and by branch: parasympathetic, alpha-, and beta-sympathetic. Efficacy of a rational therapy can be tracked objectively over time using the complete Endobiogenic approach of history, exam and Biology of Functions.
Chapter 8
Clinical Essentials of the Corticotropic Axis Introduction
A brief review of key hormones
The Corticotropic axis is the first endocrine responder to aggressions. In this role, it mobilizes glucose, lipids, and proteins and affects the functioning of every other system in the organism. However, its function is much broader than this. In the clinic, the axis can be evaluated at four levels (The Theory of Endobiogeny, volume 1: Chapters 6, 12, and 13, and, volume 2: Chapter 2).
The corticotropic axis ensures survival through adaptation, energy economy, mobilization, and distribution of metabolites, electrolytes, and fluids.
●
●
●
●
Acute change (αΣ + cortisol): adaptive or adaptative activity. Example: acute-onset insomnia for 3 days postnon-fatal motor vehicle accident. Disorders of adaptation (αΣ + ACTH + cortisol): Examples: critical terrains of allergic asthma, ulcerative colitis, and depression. Grand phases of transition (αΣ + adrenal androgens): disorders related to fetogenesis, birth, adolescence, adulthood, gonadopause, and deinstallation of life. Examples: acne, infertility, delayed puberty, menopause, etc. Affective states (αΣ + corticotropic axis): anxiety, fear, nervous asthenia, psychophysiologic insomnia, etc. Example: Insomnia in a 42-year-old divorced, working mother with 2 children: Cortisol 10 in structure (S), 7 in function (F) (normal: 3–7), Global adrenal cortex 1 (S), 2.5 (F) (normal: 2.7–3.3), Cortisol/adrenal cortex 10 (S), 2.8 (F) (normal: 2–3). Treatment approach is to reduce alpha-sympathetic and cortisol, and increase adrenal androgen production: e.g., Passiflora incarnata MT + Eleutherococcus senticosus MT.
While the corticotropic axis may not be implicated in the critical terrain of every disorder, dysfunction of the axis at some level will be implicated in some aspect of common symptoms. Evaluation of corticotropic activity can be performed quickly in even short consultation, offering a foundation for symptomatic and terrain-level treatment. When consultation time is limited, an evaluation and treatment of ANS-corticotropic activity typically offers symptomatic relief, often in a short period of time. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00008-1 © 2020 Elsevier Inc. All rights reserved.
1. Metabolism: catabolism (cortisol) > anabolism (aldosterone, adrenal androgens) 2. Metabolite(s), minerals, mobilization, utilization: a. Catabolic i. ACTH: eosinophils, basophils, histamine receptors ii. Cortisol: carbohydrates, proteins, lipids, calcium, phosphorous b. Anabolic i. Adrenal androgens, estrogens: proteins (for anabolism) ii. Aldosterone: retention: sodium, water, excretion: potassium, H+ The interaxial relationships of the major corticotropic hormones are summarized in Fig. 8.1.
FIG. 8.1 Simplified first and second loop corticotropic activity. αΣ, alpha-sympathetic; ACTH, Adrenocorticotropic releasing hormone; CRH, Corticotropin-releasing hormone; DHEA, Dehydroepiandrosterone. Red arrow: stimulation. (© 2015 Systems Biology Research Group.)
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74 SECTION | B Essentials of history, physical exam and Biology of Functions
Disorders related to the corticotropic axis are three: ●
●
●
Derm
Psoriasis
ACTH elevated, cortisol insufficient
Endocrine
Delay in puberty
Cortisol insufficient
Energy
Easily fatigued, weak
Cortisol insufficient or excessive
GI
Congestion of gastric crux
ACTH elevated
ID
Mycotic infections
Cortisol elevated
ID
Tendency toward infections
Cortisol insufficient or excessive
ID
Herpes
Cortisol excessive
Metabolic
Hypoglycemia
ACTH insufficient
Metabolic
Thinness
Cortisol excessive
Metabolic
Diabetes
Cortisol excessive
Metabolic
Fatigue, chronic
Cortisol elevated
Psych
Depression
Cortisol insufficient or excessive
TABLE 8.1 Historical findings of the corticotropic axis by system.
Skeletal
Osteoporosis with spinal pain
Cortisol excessive
Category
Finding
Variable
Skeletal
Risk of fracture
Cortisol elevated
Blood
Elevated serum Na Cholesterol, elevated
ACTH increased Cortisol elevated
Sleep
Early wakening
ACTH elevated
Childhood
Dark hair at birth
Adrenal androgens increased Adrenal androgens efficient MSH increased
Adaptation: corticotropic is primary, e.g., ulcerative colitis, allergic asthma, etc. Cortico-gonadotropic coupling: corticotropic affects gonadotropic function, e.g., menorrhagia Somato-corticotropic coupling: Somatotropic axis relaunches corticotropic overactivity, e.g., multiple sclerosis
The corticotropic axis is not associated with an embryologic layer. It allows all the other layers to grow through increase of mass thanks to adrenal androgens (cf. The Theory of Endobiogeny, volume 1: Chapter 6: Corticotropic, section DHEA).
Historical findings by system Historical findings offer insight into historical and current functioning of the axis (Table 8.1). NB: The indication of a single hormone is not indicative of it being the sole determinant of the finding.
Blond hair at birth
Fair complexion that darkens Darker complexion that lightens CV
Cortisol increased
Palpitations Hypotension Hypertension, arterial
ACTH elevated ACTH insufficient Cortisol elevated
Derm
Acne, general tendency
Cortisol insufficient
Derm
Acne, back
ACTH elevated
Derm
Striae, colored
ACTH elevated
Derm
Eczema
ACTH elevated, cortisol insufficient
Evaluation of the Corticotropic axis Examination of the functioning of the corticotropic axis begins with observation of temperament and build (Table 8.2). There are numerous signs to be found on the skin (Table 8.3), head and neck (Table 8.4), cardiothoracic (Table 8.5), abdominal (Table 8.6), adipose distribution (Table 8.7), the back (Table 8.8), and extremities (Table 8.9).
Biology of Functions indices related to the Corticotropic axis βMSH/αMSH index αMSH helps maintain permissive cortisol activity, which favors sleep along with melatonin. During the day, it assists with adaptation. When it is chronically low, it suggests insufficient GABA (γ-aminobutyric acid) to dampen alphasympathetic response in central and peripheral adaptation. This by extension suggests a risk of anxiety, especially when
Clinical Essentials of the Corticotropic Axis Chapter | 8 75
TABLE 8.2 Temperament and build.
TABLE 8.4 Head and neck findings.
Quality
Finding
Factor
Part
Quality
Finding
Factor
External state
Extroverted
ACTH predominant DHEA excessive
Face
Shape
Full moon
Shape
Square and angulated Adiposity
Cortisol excessive Androgens predominant Cortisol, adaptative elevated
Easily irritated and expresses it Easily irritated and cries afterward Internal state
Easily irritated but does not express irritation Difficult with adaptation Depressive tendency, severe Easily overreacts Depressive feeling Anhedonia, lack of reactivity
Build
Corpulent Thin
DHEA excessive
Zygomatic arch
DHEA excessive
ACTH insufficient ACTH elevated or insufficient Cortisol excessive Cortisol disadapted Cortisol insufficient
Hair
Quantity
Hirsutism
Androgens elevated
Hair
Quality
Coarse
Androgens predominant
Hair
Color
Dark
Androgens predominant
Hair
Color
Blond
Adrenals efficient
Eyebrow
Pilosity
Bushy
Length
Touches at midline
ACTH elevated DHEA elevated
Coarseness
Coarse
Color
Darker
Eye
Iris
Melanic spots
MSH elevated
Ears
Antitragus
Hair
ACTH elevated
Lips
Size
Thin
Cortisol elevated
Neck
Posterior adiposity Thickness
Adiposity present Thick
ACTH strong
Length
Short
Cortisol elevated Cortisol excessive or insufficient Eyelashes
TABLE 8.3 Dermatologic findings. Disorder
Finding
Factor
Eczema
Flexor surfaces
ACTH elevated
Lesions
Forehead
ACTH elevated
Lesions
Sides of face
Androgens elevated
Acne
Seborrheic
DHEA elevated
Ecchymosis
Presence
Cortisol elevated
Vascular Nevi
Presence
Cortisol elevated
Vasculature
Thin, fragile with capillary breakage
Cortisol elevated
Pigmentation
Hyper, general Hyper, palmar crease Hyper, striae Hyper, purple
MSH elevated MSH elevated ACTH elevated Cortisol elevated MSH insufficient ACTH insufficient
Hypo Depigmentation
Androgens elevated Androgens elevated
Cortisol strong Androgens strong
the Noxious free radical index is elevated. When the index is low (αMSH > βMSH), use GABAergics: Passiflora incarnata (Passionflower), Artemisia dracunculus (Tarragon), and Melissa officinalis (Table 8.10). βMSH bypasses ACTH to directly stimulate cortisol release. Under TRH stimulation, it directly stimulates the thyroid gland, bypassing TSH. Endorphins inhibit TRH and by extension βMSH. When the index is high (βMSH > αMSH), use endorphin-like products: Eschscholzia californica (California poppy) and Papaver rhoeas (Common poppy).
76 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 8.5 Cardiothoracic findings. Part
Quality
Finding
Factor
Clavicle
Supraclavicular space
Filled out, not hollow
Cortisol increased
Inferior chest
Hair
Hair, inferior chest
DHEA elevated
Breasts
Asymmetry
Right > left
ACTH predominant
Breasts
Coloration
Striae, purple
Cortisol excessive
Areola
Coloration
Hypopigmented
ACTH insufficient
Artery, carotid
Bruit
Bruit, carotid
Cortisol + lipids elevated
TABLE 8.6 Abdominal findings. Part
Quality
Finding
Factor
Colon
Ileocecal junction
Pain on palpation
ACTH elevated
Colon
Rectosigmoid area
Pain on palpation
ACTH elevated
NB: Anterior projection of organs represents the current anatomical congestion and/or state of dysfunction.
TABLE 8.7 Distribution of adipose tissues. Part
Quality
Finding
Factor
General
Adiposity
Increased
Cortisol elevated
Viscera
Omental
Increased
Cortisol elevated
Face
Cheeks
Increased
Cortisol elevated
Arms
General
Increased
Cortisol elevated
Abdominal
Supraumbilical
Increased
Cortisol elevated
Abdominal
Periumbilical
Increased
Cortisol + insulin elevated
TABLE 8.8 Findings on the back. Area
Quality
Finding
Factor
C8-T2
Spine
Buffalo hump
ACTH excessive
T1-T12
Curvature
Scoliosis
Cortisol strong
Scapula, right
Inferiomedial, T10 (scapular tip)
Pain on palpation
ACTH, structure elevated
Scapula, left
Inferiomedial, T10 (scapular tip)
Pain on palpation
ACTH, function elevated
Scapula, left
Level of T4
Pain on palpation
Cortisol excessive or insufficient
NB: Posterior projection of organs represents chronic congestion and/or state of dysfunction; C, cervical; T, thoracic.
Clinical Essentials of the Corticotropic Axis Chapter | 8 77
TABLE 8.9 Findings of the extremities. Part
Quality
Finding
Factor
Activity
Hand, left
Ring-to-index-finger ratio
>1
Androgens
Elevated
Arm
Arm, distal
Hair
DHEA
Predominant
Leg
Leg, distal
Hair
DHEA
Predominant
Leg
Distal, 0.5–1 cm lateral from midline, 2 cm above patella
Pain on palpation
Cortisol
Elevated
TABLE 8.10 Some central and peripheral indexes of the Biology of Functions related to the Corticotropic axis. Index
Definition
Significance
βMSH/αMSH
Relative activity of βMSH in relationship to that of αMSH in adaptation
High: insufficient endorphins Low: insufficient GABA
ACTH
Organometabolic activity of ACTH on adrenal cortex
Use to determine how adapted cortisol is relative to ACTH stimulation
Adaptation
Relative adaptative activity of ACTH to FSH
High: atopic risk, support cortisol activity Low: autoimmune risk, regulate estrogens, cortisol
Adaptogen
Relative role of pineal in noncircular adaptation, relative appeal to central endorphins
Evaluates how busy conscious mind is
Cortisol
Effective tissular activity of cortisol during the syndromes of adaptation
Not related to serum or salivary levels; accounts for genetic and epigenetic modifications of cortisol activity
Adrenal cortex
Global level of adrenal gland activity, cortisol relative to adrenal androgens
Make a ratio of Cortisol to Adrenal gland index, optimal 2–3, if >4, reduce cortisol or increase adrenal androgens; if 10:1 favors hypervigilance Peripheral gonadal response: a. Horizontal overstimulation of TSH, GH, PL: Cystitis, cysts, fibroids, adenosis b. FSH > Estrogens: Crohn’s disease, metrorrhagia c. LH > Gonadal androgens: Acne, prostatic disorders 2. Hyperfunctioning of central and peripheral responses a. Follicular: PMS (estrogen predominance), menorrhagia, breast cancer, uterine cancer b. Luteal: PMS (progesterone predominance), prostatic adenoma, prostate cancer c. Follicular and Luteal: cardiovascular disease 3. Insufficient peripheral gonadal response: a. Estrogens: metrorrhagia b. Progesterone: infertility
c. Gonadal androgens: sarcopenia, impotence d. Global: osteopenia, osteoporosis 4. Chronologic disorders a. Early activation of adult function: precocious puberty b. Late activation of adult function: delayed puberty c. Early deactivation of adult function: premature menopause d. Incomplete deactivation of adult function: climacteric symptoms due to hyperfunctioning of central factors Recognizing and addressing gonadotropic imbalances is aimed toward survival and propagation of the patient, as well as a more equilibrated comportment. Though often overlooked until there is pathology, regulating and treating this axis is not trivial in the grand scheme of health and happiness.
Historical findings by system Some common symptoms related to the gonadotropic axis are listed in Table 9.1. See The Theory of Endobiogeny, volume 3, Chapter 3 for a full discussion.
TABLE 9.1 Common gonadotropic symptoms. Category
History
Endocrine
Dermis
Eczema
FSH excessive
Psoriasis
FSH excessive
Acne
FSH excessive
Hot flashes
Androgens insufficient
Energy
Fatigability
Androgens deficient
Endocrine
Delayed puberty
FSH insufficient
Amenorrhea
FSH insufficient
Absence of secondary sexual characteristics
FSH insufficient
Delay in vertical growth
FSH insufficient
Difficulty with erection
FSH insufficient
Sterility
FSH insufficient
Signs of reduced estrogen
FSH insufficient
Eyes
Eyelashes fall out easily
Estrogen diminished
GI
Crohn’s disease
FSH hyperfunctioning
Disease of right colon
FSH over-soliciting
Libido, weak
FSH insufficient
PMS before ovulation, stops a few days before menstruation
Progesterone prominent, often excessive
PMS: breasts engorged
Progesterone prominent, often excessive
PMS: breasts painful
Estrogen prominent, often excessive
Breasts painful during menstruation
Progesterone excessive
Genitourinary
Clinical Essentials of the Gonadotropic Axis Chapter | 9 81
TABLE 9.1 Common gonadotropic symptoms—cont’d Category
Puberty
History
Endocrine
Heavy menstrual flow
Estrogen excessive
Clotting, day 1 menstruation
Estrogen insufficient
Clotting, day 2,3 of menstruation
Progesterone prominent, often excessive
Prolonged clotting at end of menstruation
Progesterone prominent, often excessive
Post-menstrual herpes outbreak
Progesterone insufficient with hypercompensatory aldosterone relaunching of LH
Menstrual irregularity
Androgens insufficient
Amenorrhea
Estrogen insufficient
Libido, weak
Estrogen insufficient
Libido, strong
Estrogen pronounced
Sexual desire
Progesterone strong
Sexual desire weak
Progesterone diminished
Reduced incidence of morning erection
Androgens insufficient
Weak ejaculation
Androgens deficient
Rapid onset with early end
Androgens prominent and excessive
Evaluation of the Gonadotropic axis There are numerous signs related to the gonadotropic axis. Once can observe temperament (Table 9.2), voice and morphology (Table 9.3). On observation and examination, one can note numerous signs related to the integument (Tables 9.4 and 9.5), head and neck (Table 9.6), and breasts in women (Table 9.7), which are deeply imbedded in evolutionary cues of fertility and evolutionary fitness. In addition, there are signs related to the
TABLE 9.3 Signs of voice and morphology. Quality
Finding
Endocrine
Tonality
Weak
Androgens diminished or blocked
Low pitched
Androgens prominent
High pitched
Estrogen predominant
Curvaceous (woman only)
FSH predominant
Shoulders wider than hips
Androgens predominant
Hips wider than shoulders
Estrogen predominant
Stocky, waist down; in women, minimal curve of hips, congestion of legs
Androgens predominant
Right > left
FSH predominant
Left > right
LH predominant
TABLE 9.2 Signs of temperament. Finding
Endocrine
Socially sensitive, social harmonizer
Estrogen prominent
Strength, confidence, and leadership during crisis
Androgens prominent
Capacity to fight and resist
Androgens strong
Passivity, loss of professional efficacy
Androgens insufficient
Lack of self-esteem, motivation, diminished interest in athletics
Androgens diminished
Emotionally sensitive
FSH reactive
Build
Laterality
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TABLE 9.4 Signs of the skin.
TABLE 9.6 Signs of head and neck.
Quality
Finding
Factor
Part
Quality
Finding
Factor
Quality
Smooth
Estrogen good quality
Eyelashes
Length
Long, fine
FSH predominant
Dry
Estrogen insufficient
Durability
Estrogen diminished
Squamous (scaly)
Estrogen insufficient
Fall out easily
Wrinkles
Present
Estrogen insufficient
Coarseness
Coarse
Adrenal androgens predominant
Sebum
Oily
Estrogen predominant
Color
Darker
Lesions
Nasolabial
FSH oversolicited
Adrenal androgens predominant
Sides of face
Androgens oversolicited
Color
Violaceous
Chin
Androgens oversolicited
FSH increased activity
General tendency
Progesterone insufficient
Slightly violaceous
Estrogen hyperfunctioning
General tendency
Androgens oversolicited
Short
Buttocks, sides
Androgens oversolicited
Androgens predominant
Color
Colored spots on elbows, knees
FSH excessive
Elbow
Melanic spots
FSH excessive
Knee
Melanic spots
FSH excessive
Striae
Horizontal orientation
Estrogen hyperfunctioning
Tissue
Infiltrated with water
Estrogen hyperfunctioning
Palm
Erythema
Estrogen excessive
Acne
Tonsils pillar
Neck
Length
TABLE 9.7 Signs of breasts and areola. Quality
Finding
Factor
Size
Small
FSH predominant
Voluminous, soft and supple
Estrogen prominent
Left > right
LH predominant
Right > left
FSH predominant
Density
Fibrocystic
Gonadal androgens predominant
Tenderness
Tender
Estrogens excessive
Firm and often painful, L > R, SQ > IQ
Progesterone hyperfunctioning
Congestion
Diffuse with tension SQ > IQ, E > I
Progesterone excessive
Areola Hirsutism
Hair growth, areola
Progesterone insufficient
Asymmetry
TABLE 9.5 Gonadotropic signs in hair. Quality
Finding
Factor
General
Purpose
Gonado-corticotropic
Quantity
Hirsutism
Adrenal androgens strong
Receding at temples
Gonadal androgens strong
Location
Quality
Axillary abundance
Gonadal androgens strong
Pubic triangle enlarged
Androgens strong
Abundant
Estrogen good quality
Areola size
Large
Coarseness
Adrenal androgens prominent
Estrogen prominent
Areola coloration
Lightly pigmented
Thinning
Androgens excessive
Estrogen prominent
Dry, breakable
Estrogen insufficient
E, exterior; I, interior; IQ, inferior quadrant; L, left; R, right; SQ, superior quadrant.
Clinical Essentials of the Gonadotropic Axis Chapter | 9 83
TABLE 9.8 Signs of abdomen and genitals. Part
Quality
Finding
Factor
Colon
Ascending, proximal transverse colon
Pain on palpation
FSH oversoliciting
Distal transverse, proximal left colon
Pain on palpation
LH oversoliciting
Size
Small
FSH diminished and insufficient
Penis
TABLE 9.9 Signs of muscles and ligaments. Quality
Finding
Factor
Mass
Wasting
Androgen deficient and/or blocked
Increased
Androgen good quality
Muscle
Texture
Estrogen good quality
Ligament laxity
Lax
Androgens insufficient Estrogen predominant
TABLE 9.10 Signs of adiposity. Location
Factor
Arm, proximal, right
FSH hyperfunctioning
Arm, proximal, left
LH hyperfunctioning
Knee, right
FSH hyperfunctioning
Knee, left
LH hyperfunctioning
Infra-umbilical
Estrogens excessive
abdomen and genitals (Table 9.8), muscles and ligaments (Table 9.9), and adiposity (Table 9.10). See The Theory of Endobiogeny, volume 3, Chapter 3 for a full discussion.
Biology of Function indices related to the Gonadotropic axis FSH and LH indexes evaluate the duration of functions in stimulating their respective gonadal hormones. An elevated index implies delayed feedback from the end-organ hormone. A low index implies shorter duration of action of FSH or LH due to quicker inhibition. These indexes do not strictly implicate efficiency of metabolic or endocrinometabolic activity of estrogens, androgens, or progesterone. One must contextual the FSH and LH indexes (Tables 9.11) to other gonadotropic indexes (cf. Tables 9.12 and 9.13).
Peripheral endocrine evaluation Recall that peripheral gonadotropic activity cannot be precisely determined by serum levels or urinary metabolites (cf. The Theory of Endobiogeny, volume 1, Chapters 7 and 15), owing to genomic vs. nongenomic activity, multiple receptors and genetic determinations of receptor density variations. The Biology of Functions evaluates efficacy of these hormones according to various metabolic effects. Recall that adrenal DHEA can be converted to gonadal androgens or estrogens in peripheral tissues, a process referred to as intracrinology. In addition, gonadal androgens can be converted into estrogens. There are indexes in the Biology of Functions that model these dynamics (Table 9.13).
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TABLE 9.11 Some possible contextualized interpretations of the gonadotropic pituitary indexes. Combinatorial findings
Example
Interpretation
Treatment
↑FSH ↓OTEYi ↓Estrogen corrected
Insufficient organotissular estrogen activity relative to FSH stimulation
Organometabolic yield of FSH is low—not enough estrogen production or activity
Sustain FSH: Inula helenium, Quercus pedunculata (indirect) AND Support Estrogens: Angelica archangelica, Salvia officinalis, Salvia sclarea, etc.
↑LH ↑Genital androgens ↑Comparative genital androgens
LH index elevated despite elevated gonadal androgens activity
Negative feedback faulty or altered
Inhibit LH: Alchemilla vulgaris, Medicago sativa, Prunus africana AND Inhibit androgens: Fragaria vesca, Humulus lupulus, Menyanthes trifoliata
OTEYi, organotissular estrogen yield index.
TABLE 9.12 Some indexes modeling peripheral gonadotropic activity. Index
Definition
Import
Genital ratio
Global tissular activity of androgens relative to estrogens in acute adaptation
Use when evaluating role of androgens and estrogens in function disorders
Genital ratio corrected (GRc)
Global tissular activity of androgens relative to estrogens outside of adaptation
Use when evaluating role of androgens and estrogens in structural disorders
Estrogen index
Endocrinometabolic activity of estrogens
Use as a general evaluation of how TSH acts as a proanabolic factor to complement estrogen activity
Estrogen index corrected
Tissular endocrinometabolic activity of estrogens
Use to evaluate how estrogens regulate tissue integrity, activity, growth, and repair
Organotissular estrogen yield (OTEYi)
Global organotissular activity of estrogens relative to FSH stimulation
Responsiveness of estrogens to FSH stimulation. A higher index implies proliferation of estrogen receptors
Genital androgen
Tissular endocrinometabolic activity of androgens
Complements Estrogen index corrected, should be proportional to each other for well-regulated tissue texture and architecture
TABLE 9.13 Estrogen production site and method. Index
Definition
Import
DHEA
Endocrinometabolic activity of DHEA
High: increased intracrinologic conversion of DHEA to estrogens or androgens • If gonadal estrogen and androgen activity already elevated, reduce stimulation of DHEA • If low, support production of gonadal hormones within the gonads
Aromatization of estrogens
Relative activity of adrenal gland dedicated to producing estrogens
High: if patient is menopausal, may be adaptive; if patient has atopic disease, may play a role in disorder, treat accordingly
Rate of aromatized estrogens
Relative part of compensatory estrogens obtained through aromatization of gonadal androgens
In disorders of hyperestrogenism, use to determine if conversion of gonadal androgens is a source of excess estrogens, and inhibit LH and/or androgens if indicated
Clinical Essentials of the Gonadotropic Axis Chapter | 9 85
Conclusions The Gonadotropic axis is a foundational axis in the life of the organism, going well beyond its role in fertility. The key to its function is regulation of protein metabolism for enzymes, carrier proteins, immunoglobulins, and various tissues. In addition, it influences the exterior, which is influential for mating and social status, as well as b ehavior
and psychology. Numerous disorders of structure and function, from ovarian cysts to atherosclerosis, from colon cancer to Crohn’s disease, are rooted in dysfunction of this axis. The evaluation of this axis by history, examination, and Biology of Function indexes offers a rich tapestry of findings that can be woven into a meaningful assessment of impact of gonadotropic hormones in the regulation of the terrain.
Chapter 10
Clinical Essentials of the Thyrotropic Axis Introduction The Thyrotropic axis is the second of the two catabolic axes, the other being the corticotropic. This axis assists in adaptation, growth, and creation of cell energy (The Theory of Endobiogeny, volume 1, Chapter 8). These actions occur both centrally and peripherally and this observation is key to understanding the types of disorders related to this axis. In general, we can say that this axis is responsible for: 1. Acute change (αΣ + TRH): adaptive or adaptative activity, strongly influenced by perceptions, reactions, and prior experiences. Example: Acute adaptive: situational anxiety with racing mind and tachycardia, acute adaptative: acute on chronic aggravation of Grave’s disease 2. Disorders of adaptation (αΣ + TRH + various hormones): Examples: chronobiologic: spring cancer metastasis, spring allergies, structural adaptation: Crohn’s disease, psoriasis, structural spasmophilia, functional adaptation: Grave’s disease, Hashimoto’s thyroiditis, functional spasmophilia. 3. Disorders of growth (αΣ + TRH vs TSH): quality of growth: hyperplastic vs hypertrophic vs cystic. Examples: tonsil hypertrophy, prostate adenoma, ovarian cyst, cystic acne. 4. Affective states (αΣ + thyrotropic axis): psychophysiologic insomnia, anxiety, fugue psychosis, etc. Example: Insomnia in a 42-year-old divorced, working mother with 2 children: Cortisol 10 in structure (S), 7 in function (F) (normal: 3–7), Global adrenal cortex 1 (S), 2.5 (F) (normal: 2.7–3.3), Cortisol/adrenal cortex ratio 10 (S), 2.8 (F) (normal: 2–3). Treatment approach is to reduce alpha-sympathetic and cortisol, and increase adrenal androgen production: e.g., Passiflora incarnata MT + Eleutherococcus senticosus MT.
A brief review of key hormones Essence: Management of adaptability and growth. Key: relative balance of thyrotropin-releasing hormone (TRH) The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00010-X © 2020 Elsevier Inc. All rights reserved.
to thyroid-stimulating hormone (TSH): imagination vs ideation, potential vs achievement, glucose vs proteins, adenosis vs amylosis, etc. Embryology: Ectoderm: nervous system, pituitary, adrenal medulla (βΣ), immunity, etc. The corticotropic and thyrotropic axes are linked together to disorders of adaptation and adaptability, both are relaunched by αΣ, a process called yoking (cf. The Theory of Endobiogeny, volume 1, Chapter 10, section Yoking). These two axes are particularly linked to conscious, subconscious, and physiologic perceptions of and response to aggression (cf. The Theory of Endobiogeny, volume 1, Chapter 12, Adaptation syndromes). Metabolism: Catabolism (TRH, T4, PTH) > anabolism (TSH, T3, calcitonin). Metabolite(s) and minerals: The catabolic hormones mobilize, the anabolic ones utilize. Its primary metabolite is lipids, used as a source of durable energy. However, all metabolites are mobilized or utilized by the thyrotropic axis (Table 10.1). Its primary mineral is calcium, used to adapt the rate of function of calcium-dependent processes, from clotting to enzymatic function to muscle contraction. This complements the role of the axis in ATP production.
Pathophysiology The four key hormones thyrotropic hormones for which the greatest number of symptoms, signs, and Biology of Function indexes are available are TRH, TSH, thyroxine (T4), and tri-iodothyronine (T3). TRH has wide-ranging effects centrally and peripherally (Table 10.2), as does TSH (Table 10.3) on comportment and metabolism. With respect to peripheral thyroid dysfunction, many of the symptoms attributed to T4 and T3 arise from central dysfunction. The Endobiogenic assessment clarifies this, which allows for a more targeted and rational approach to treatment (Tables 10.4 and 10.5). 87
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TABLE 10.1 Mobilization and utilization of metabolites by the thyrotropic hormones. Mobilization Metabolite
TRH
Glucose
•
Amino acids
•
T4
Utilization PTH/D3
•
Lipids
•
Calcium
•
TSH
T3
•
•
•
•
D3
Calcitonin
•
•
• •
•
D3, Vitamin D3; PTH, parathyroid hormone.
TABLE 10.2 Summary of central and peripheral TRH physiology and pathophysiology. Location
Physiology
Pathophysiology
Central
Neuromodulation
Fugue states, tremors, anxiety, negative imagination, OCD
Chronobiology, pacemakers
Seasonal and circadian disadaptation: insomnia, seasonal depression, spring allergies, seasonal cancer growth, etc.
Rational adaptation: dopamine-induced analytical function
Psychiatric disorders of excess: anxiety, panic attacks, schizophrenia
Contextual adaptation via limbic area
Consumption of buffering capacity: traumatic rumination, harmful adaptation responses, seasonal depression, winter bronchitis, etc.
Qualification of global adaptation response: αΣ, TRH, DA, limbic system
Adaptability: states of adaptability, esp. thyrotropic axis, autoimmunity, seasonal depression, winter bronchitis, etc.
Vigilance, creativity, neuroplasticity
Overstimulation: diurnal hypervigilance, nocturnal nightmares, night terrors, etc.
Serotonin-dopamine-TRH: Intensification of arousal, pain, pleasure, reward, movement, sleep, cardiopulmonary rhythms, gastric secretions
Prolonged adaptative states: migraines, depression, suicide, narcolepsy, pain processing, dysrhythmias, gastric hyperacidity
Muscle tone, posture
Peripheral Neuromuscular disorders: clonus, tremors, fasciculation, hypertonicity, Parkinson’s disease. Insufficiency of TRH: ataxia
Thyrotropic stimulation: TSH, T4 → T3, Calcitonin
Thyrotropic disorders: hyperthyroidism, adenosis (tonsils, prostate, breasts), amylosis (Alzheimer’s, diabetes, atherosclerosis), cysts, thyroid cancer, etc.
Somatotropic stimulation: prolactin
Hyperprolactinosis: implosive adaptation, infertility, schizophrenia, menstrual disorders, pancreatic cancer, metastasis of solid tumors, acceleration of aberrant growths
Thyro-pancreatic stimulation: glucagon, insulin
Disorders of adaptative TRH with hyperglycemia: depression with traumatic rumination, ADHD, autoimmune flare ups; disorders of hyperplasia: growth of aberrant tissues by cell multiplication
Cell: DNA transcription
Oncogenesis: DNA fracture, biologic toxin accumulation
Tissue: myolysis, adenosis (cell hyperplasia), dromotropy
Adenoidal disorders: tonsils, prostate, breasts (adenofibroids), muscle-wasting disorders, arrhythmias
Peripheral
AA, amino acids; ADHD, attention deficit hyperactivity disorder; OCD, obsessive-compulsive disorder; SCN, suprachiasmatic nucleus.
Clinical Essentials of the Thyrotropic Axis Chapter | 10 89
TABLE 10.3 TSH physiology and pathophysiology. Physiology
Pathophysiology
Estrogen sensitivity
High serum TSH: increased estrogen sensitivity, favors hyperestrogenism: adenoidal growth, menorrhagia, atopic disease, etc.
High insulin resistance
High serum TSH: diabetes mellitus type 2
Apoptosis
High serum TSH: mucosal congestion, i.e., appendicitis
Necrosis
Low serum TSH: amyloidosis: Alzheimer’s, Parkinson’s, Huntington’s diseases, atherosclerosis, rheumatoid arthritis
Low insulin resistance
Low serum TSH: chronic fatigue, fibromyalgia, hypoglycemia
Oxidation, harmful free radicals
Low serum TSH: chronic inflammation: demyelination, chronic fatigue syndrome, fibromyalgia, brain fog, etc.
TABLE 10.4 Role of various aspects of the thyrotropic axis in hyperthyroidism. Thyrotropic factor Factor
↑TRH
↓TSH, serum
Endocrine Symptom
Tremors Muscle wasting Insomnia
Exam
↑Deep tendon reflex Eyelid flutter Clonus
Inflammation Hair loss Brain fog
↑T4
↑T3
Overproduced from overstimulation
Overproduction, Overconversion
Heat intolerance (if insufficient conversion to T3)
Cold sensitivity
Skin temperature elevated
↑Osteoclasty
Structural Types of hyperthyroidism Reactive
Hypercatabolic, reactive thyroid state: asthma, Spring arthritis
Fundamental
Low TSH relaunching; peripheral hyperthyroidism: hyper-estrogenic (thus hyper T4), hyper beta, risk of breast cancer; psoriasis Treatment: Lycopus europaeus, Borago officinalis; if DHEA, ACTH implicated in the estrogenism: Fragaria vesca
TABLE 10.5 Role of various aspects of the thyrotropic axis in hypothyroidism. Thyrotropic factor Factor
TRH insufficient
↑TSH, serum
↓T4
↓T3
Endocrine
Insufficient conversion of T4 to T3
Insufficient production of T4
Anabolic predominance
Mitochondrial strain
Symptom
Repetitive dreams
Weight gain
Hair loss Thinning eyebrows Alteration in timber of voice: low, weak, and/or hoarse
Fatigability
Exam
Hyperestrogenism
Types of hypothyroidism Latent
Lymphocytosis; cardiac vegetations; tonsil hypertrophy; appendix hypertrophy
Entrained
Elevated TRH or PL or DA (dopamine); If there is elevated GH → appeal to glucose with diminished effect of GH (from strong insulin response)
Reactive TSH compensation
Fat pad above ankles (like Kurdish pants); cobble stoning of posterior pharynx; Treatment: Avena sativa, Verbascum thapsus
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Clinical pearl Along with the ANS (Chapter 7), regulation of central thyrotropic activity (TRH, TSH) offers the most rapid and effective method of symptomatic relief of psychological and physiological disorders. It involves a three-step process: (1) determine role of αΣ-TRH vs αΣ-TSH vs both, (2) determine level: central, peripheral, or both, (3) select therapies to address all levels of dysfunction simultaneously. 1. Example 1: insomnia with racing thoughts, tachycardia, eye twitching a. Terrain: αΣ, hyper TRH: central and peripheral + Spasmophilia b. Treatment: Lavandula angustifolia (alpha) + Leonurus cardiaca (TRH) + Valeriana officinalis (psychoneuromuscular spasmolytic) 2. Example 2: acute sinusitis with thick, green mucous a. Terrain: αΣ, insufficient TSH and thymus: peripheral + insufficient cortisol: peripheral b. Treatment: Lavandula angustifolia (alpha) + Avena sativa (readapt gonado-TSH-thyroid) + Rhodiola rosea (readapt cortico-thyro-thymic activity) 3. Example 3: Hashimoto’s thyroiditis a. Terrain: αΣ + hyper TRH, TSH: peripheral > central + insufficient thyrotropic: peripheral b. Treatment: Scutellaria lateriflora (alpha), Fabiana imbricata (TRH, TSH), Lithospermum officinale (TSH, Thyroid), Avena sativa (readapt gonado-TSH-thyroid)
TABLE 10.6 Symptoms related to the thyrotropic axis. Category
Finding
Level
Brain
General mental fatigue
Thyroid insufficient or excessive
Dermatologic
Pruritis
Thyroid elevated
Psoriasis
T4 elevated
General physical fatigue
Thyroid insufficient
Chronic fatigue
TSH low serum
Energy, lack of
Thyroid insufficient
Ear, nose, throat
Enlarged tonsils
Thyroid insufficient, serum TSH elevated
Genito-urinary
Reduction in the duration on menstruation
Thyroid excessive
Reduction in the volume of menstrual flow
Thyroid insufficient
PMS with great irritability
Thyroid increased
Menstrual flow heavy
Thyroid insufficient
Heat intolerance
T4 hyperfunctioning
Cold sensitivity
T3 hyperfunctioning
Constantly cold
Thyroid deficient in response
Weight loss despite a good appetite
Thyroid excessive
Weight gain
Thyroid insufficient, especially with elevated TSH serum and relative to global adrenal cortex activity
Insomnia with great agitation
TRH hyperfunctioning
Dreams animated, vivid
TRH predominant
Dreams in black and white
TRH insufficient
Repetitive dreams
TRH insufficient
Energy
Metabolic
In conclusion, when evaluating thyrotropic function, each hormone must be evaluated for signs of hyper- or hypofunctioning: TRH, TSH, T4, and T3, in order to determine the most appropriate type of treatment.
Symptoms related to the Thyrotropic axis There are a number of symptoms related to the thyrotropic axis (Table 10.6). Some are chronic, some acute.
Evaluation of the Thyrotropic axis The signs of the thyrotropic axis can be observed in the temperament and by inviting a discussion of the patient’s inner life (Table 10.7). Neurologic signs are particularly linked to the axis (Table 10.8). There are signs related to the head, ear, eyes, nose, and throat (Table 10.9), thyroid gland and chest (Table 10.10), and miscellaneous findings (Table 10.11).
Sleep
Clinical Essentials of the Thyrotropic Axis Chapter | 10 91
TABLE 10.7 Temperament and internal mental life. Finding
Level
Great vivacity
Thyroid dynamically efficient
Goal oriented
TRH predominant
Process-oriented
TSH predominant
Soft, easily gives in
Thyroid insufficient, especially during adaptation
Fearfulness
Thyroid insufficient
Anxiety and nervousness
TRH hyperfunctioning
Expansive creativity
TRH predominant
Juxtapositional creativity
TSH predominant
Depressive tendency
Thyrotropic dysfunctional
TABLE 10.9 Signs related to head, ears, eye, nose, and throat. Part
Quality
Finding
Level
Body
Build
Sharp features
TSH predominant
Voice
Quality
Weak and hoarse
Thyroid insufficient
Skin
Temperature and moisture
Cold and dry
Thyroid insufficient
Nail
Thickness
Fine and breakable
Thyroid insufficient
Hair
Quality
Thick
Favorably adapted
Curly hair
TRH predominant
Fragile
Thyroid insufficient
Thin
Thyroid not predominant
Falls out easily
Thyroid insufficient
Alopecia
Thyroid insufficient
Arch
Convex
TRH predominant
Pilosity
Fine
Thyroid strong
Thinning from hair loss at the ends
Thyroid diminished
Length
Long
Thyroid wellfunctioning
Curvature
Curled at ends
Thyroid insufficient to demand
Size
Large
TRH, alpha, central strong
Small
Thyroid insufficient
TABLE 10.8 Neurologic signs. Part
Quality
Finding
Level
General
Startle response
Startles easily to the lightest touch or sound
TRH reactive
Eyelids
Flutter
Spontaneous at rest
TRH hyperfunctioning
Eyelids
Flutter
Spontaneous interacting
TRH hyperfunctioning
Glabellar tap
Postglabella tap movement
Eyelid rapid flutter
TRH reactive
Eye
Pupillary light reflex
Exaggerated constriction to light
TRH reactive
Clonus
Foot
Brisk, diffuse
TRH elevated
DTR
Tendons
Brisk, diffuse
TRH elevated
Extremities
Arms, hands, legs
Tremors
TRH excessive
Biology of Function indices related to the Thyrotropic axis A complete assessment of the thyrotropic axis involves (1) serum endocrine evaluation: TSH, free T4, free T3, thyroid antibodies, etc. and (2) Biology of Functions indexes. Quantitative measurement informs you of the output of the pituitary and thyroid, or, amount of circulating hormones
Eyebrow
Eyelashes
Eye
Tonsils
Size
Hypertrophy
Thyroid insufficient responsiveness to TSH
Pharynx
Deformity
Cobble stoning
Thyroid insufficient responsiveness to TSH
from replacement therapy. BoF indexes evaluate notions related to systems thinking according to the theory of Endobiogeny. There are central indexes evaluating the αΣTRH relationship in adaptation (Table 10.12), radial gonadothyrotropic calibration (Table 10.13), the thyroid gland and efficacy of peripheral thyroid hormones (Table 10.14), and parathyroid and bone metabolism activity (Table 10.15).
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TABLE 10.10 Signs related to the thyroid gland and chest. Part
Quality
Finding
Level
Thyroid
Volume
Increased
Thyroid augmented
Consistency
Nodules
Thyroid oversolicited
Consistency
Goiter
Thyroid insufficient
Clavicle, bilateral
Proximal
Pain on palpation
Sternum
Orientation
Convex sternum
PTH elevated
Breasts
Asymmetry
Left > right
TSH predominant
Heart
Rate
Heart rate rapid
Thyroid augmented
TABLE 10.11 Others signs by region. Part
Quality
Finding
Level
Anterior projection of organs represents the current anatomical congestion and/or state of dysfunction Colon
Transverse, distal, left
Pain on palpation
TSH strong
Colon
Transverse, distal, right
Pain on palpation
TRH predominance
Posterior projection of organs represents chronic congestion and/or state of dysfunction T4, left
Para spinal, 2.5 cm lateral
Pain on palpation
TRH oversolicitation of exocrine pancreas
Scapula, right
Inferior-medial, T7–T8
Pain on palpation
FSH, TRH
Scapula, left
Inferior-medial, T7–T8
Pain on palpation
TSH, PL
General
Extremities
Lymphatic congestion
Thyroid latent hypothyroidism
Palm
Central
Erythematous
Thyroid strong
Leg
Medial to ankle, bilateral
Adiposity
TSH elevated
Leg
Proximal tibia, most medial aspect
Pain on palpation
T4 diminished efficiency
Leg
Proximal tibia, most medial aspect
Pain on palpation
TSH strong
Ankle
Superior to ankle
Fat pad
TSH reactive
TABLE 10.12 Central thyrotropic indexes with peripheral impact. Index
Definition
Import
Thyroid relaunching
TRH reactivation by Alpha in response to exogenous adaptation
High: TRH and/or thyrotropic axis relaunched due to a perception of exogenous aggression by alpha. Reduce TRH: Fabiana imbricata, Leonurus cardiaca, Vibernum lantana; Reduce Alpha: higher the index, more sedating the sympatholytic (most to least sedating): Valeriana officinalis, Scutellaria lateriflora, Passiflora incarnata, Lavandula angustifolia
Thyroid relaunching corrected
TRH reactivation by Alpha in response to endogenous adaptation
High: As above, except due to endogenous aggression; emotional perception of threat may also be playing a role. Treatment is the same, but may also require counseling intervention
TRH/TSH
Relative tissular activity of TRH vs TSH
High: TRH > TSH: congestion > hyperplasia, nutrition > metabolic production, neuroendocrine > organo-metabolic adaptation, tangential thinking > concrete thinking Low: Opposite interpretation
Clinical Essentials of the Thyrotropic Axis Chapter | 10 93
TABLE 10.13 Radial gonado-thyrotropic index. Index
Definition
Import
Genito-thyroid
General role of estrogens in relaunching the thyroid vs the responsiveness of TSH in adapting the thyroid
High: Favors inflammation and autoimmunity: TSH responds too quickly to estrogen demand Low: Favors hyperimmunity, atopy: TSH does not respond quickly enough to estrogen demand
TABLE 10.14 Indexes evaluating the thyroid gland and its activity. Index
Definition
Import
Thyroid index
Effective cellular metabolic activity of T4, T3
High: Cellular thyroid metabolic activity elevated, regardless of serum levels of TSH, T4, or T3 Low: Cellular thyroid metabolic activity diminished, regardless of serum levels of TSH, T4, or T3
Thyroid yield
How quickly thyroid is adapted by TSH when its activity declines
High: Thyroid adapted too quickly, risk of mucosal inflammation: sinusitis, urinary cystitis, colitis, etc. Low: Thyroid adaptation delayed, risk of tissular hypertrophy: tonsils, breast mass, prostate adenoma, etc.
TABLE 10.15 Parathyroid and bone indexes. Index
Definition
Import
Parathyroid hormone index (PTH)
PTH endocrinometabolic activity
High: Thyroid inefficient, PTH used to liberate calcium from bone to compensate, risk of mitochondrial strain Treatment: support thyroid activity, e.g., Avena sativa, Zingiber officinale, iodine, selenium, tyrosine, creatine, etc. Low: Opposite; Treatment: diminish thyroid activity if indicated, e.g., Lithospermum officinale, Lycopus europaeus, Cornus sanguinea, etc.
Bone remodeling
Extent of bone turnover to adapt peripheral metabolism through activity of osteocalcin
High: Bone is oversolicited to adapt peripheral metabolism. Treatment: Adapt adrenal cortex: Quercus pedunculata GM, Adapt gonadothyrotropic: Salvia officinalis, Avena sativa
Conclusions The thyrotropic axis is implicated in psychiatric, neurologic, dermatologic, and osseous disorders, as well as in adaptation, gonadotropic, and somatotropic disorders. Thus,
one finds a rich array of signs and symptoms implicated well beyond thyroid disease. The theory of Endobiogeny offers a systematic approach to evaluating central and peripheral thyrotropic function: TRH, TSH as well as peripheral hormones.
Chapter 11
Clinical Essentials of the Somatotropic Axis Introduction The somatotropic axis is the second of two anabolic axes. It is the great fashioner of structure and furnisher of energy. It is the great runner of the endocrine loops. It ends the first loop, and both starts and ends the second loop of adaptation. In sum, this axis sequences catabolism and anabolism. Because of the diverse functions of the axis, it is implicated in disorders of overgrowth (cysts, fibroids, adenosis) and energy (hypoglycemia, diabetes, Alzheimer’s disease), as well as disorders intrinsic to the endoderm: the digestive tract, pancreas, and endothelial surface of hollow organs.
A brief review of key hormones Central ●
●
●
●
Somatostatin (SS): Endocrine: Inhibits anabolic hormones (prolactin, growth hormone, insulin). Growth-hormone-releasing hormone (GHRH): Endocrine: Growth regulation: GH, Neuro: Memory, dreams. Growth hormone (GH): Endocrine, Endocrinometabolic: IGF production, Insulin resistance, gluconeogenesis, lipolysis, amino acid cellular uptake, electrolyte cellular uptake, fashioning of organs, repair of tissues and organs. Prolactin (PL): Endocrine, Endocrinometabolic: stimulates insulin, relaunches CRH/ACTH, upregulates estrogen receptors, angioneogenesis, lactogenesis.
Peripheral ●
●
Insulin-like growth factor 1 (IGF-1): Endocrine, Endocrinometabolic: inhibits apoptosis, tissue/organ lengthening. Insulin: Endocrinometabolic: glycogenesis, lipogenesis, glucose entry, potassium entry, vasodilation, Neuro: synaptic plasticity, memory formation, consolidation, and recall.
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00011-1 © 2020 Elsevier Inc. All rights reserved.
●
●
Glucagon: Endocrinometabolic: Glycogenolysis, gluconeogenesis, starter energy for adaptation, lipolysis. Somatostatin: Endocrine: Inhibits glucagon, insulin.
Pathophysiology Imbalances originating in the somatotropic axis involve disorder of structural integrity, structural adaptation, and functional adaptation (Table 11.1). There are disorders intrinsic to somatotropic function, such as keloids and wound healing. When the gonadotropic axis is implicated, there are two general directions. The first arises from the gonadotropic axis. This can be gonado-thyro-somatotropic (c.f. The Theory of Endobiogeny, Volume 1, Chapter 10), such as in cysts and polyps, or gonado-somatotropic, such as Alzheimer’s disease. The second is somato-gonadotropic. This implicates prolactin’s actions on estrogens, such as in tumor metastasis, or, on LH and luteal hormones, such as pustular acne and uterine fibroids.
Symptoms related to the Somatotropic axis There are a wide variety of symptoms related to this axis (Table 11.2).
Evaluation of the Somatotropic axis Signs related to the axis are numerous: temperament (Table 11.3), skin (Table 11.4), head (Table 11.5), mouth (Table 11.6), chest and breasts (Table 11.7), abdomen (Table 11.8), back, bone, and miscellaneous findings (Table 11.9).
Biology of Function indices related to the Somatotropic axis The most numerous indexes of the BoF are within the somatotropic axis, which has the greatest number of effects on
95
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TABLE 11.1 Pathophysiology related to the Somatotropic axis.
TABLE 11.2 Symptoms related to the somatotropic axis by region—cont’d
Category
Subcategory
Example
Genitourinary
Structural adaptation
Adenosis
Polyps
Cysts
Breast, ovary, kidney, brain, pancreas, ganglion, etc.
Fibroids
Functional adaptation
Menstrual cycle, irregular
Prolactin insufficient
Libido, strong during luteal phase
Prolactin strong
Leiomyoma of uterus
Menstrual cycle blocked
Prolactin excessive or hyperfunctioning
Hyperplasia
Cancer, obesity
Amenorrhea
Hypertrophy
Cancer, obesity, tonsil hypertrophy
Prolactin excessive or hyperfunctioning
Lipomas
Lipomas
General feeling of coldness
Prolactin excessive and predominant
Cicatrization
Keloids, delayed wound healing
General fatigue
Prolactin insufficient
Weight gain
Prolactin insufficient or excessive
Diabetes
Insulin diminished function
Weight gain
Insulin diminished function
Bone
Osteoporosis
Prolactin excessive
Oncology
Angioneogenesis and cancer growth
Prolactin hyperfunctioning
Rheum
Autoimmunity: polyarthritis
Prolactin hyperfunctioning
Cellular metabolism
Diabetes, hypoglycemia
Neurologic metabolism
Multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, sphingolipidosis
Inflammation
General fragilization of terrain
Metabolic
TABLE 11.2 Symptoms related to the somatotropic axis by region Category
Finding
Factor
Dermatologic
Purulent acne
Prolactin hyperfunctioning
Eczema
Pancreas oversolicited
ENT
Recurrent sinus, tonsil infections
Pancreas oversolicited
Breast
Breast milk, abundant postpartum
Prolactin strong
Perimenstrual lactation
Prolactin excessive
Increased appetite
Insulin predominant
Dislike of fruit
Insulin excessive
Hypoglycemia
Insulin hyperfunctioning
Gastrointestinal
Bloating
Pancreas congested
Chronic gastritis
Pancreas congested
Anal fissures
Pancreas congested
Hemorrhoids
Pancreas congested
TABLE 11.3 Signs of temperament related to the somatotropic axis. Quality
Finding
Factor
External
Social tendency
Growth hormone prominent
External
Fear
Prolactin excessive
Internal
Poor adaptation to stress
Prolactin hyperfunctioning
Internal
Maternal feeling
Prolactin prominent
Internal
Lack of maternal feeling
Prolactin ineffectual
Clinical Essentials of the Somatotropic Axis Chapter | 11 97
TABLE 11.4 Dermatologic signs related to the somatotropic axis.
TABLE 11.6 Signs of the mouth related to the somatotropic axis.
Quality
Finding
Factor
Part
Quality
Finding
Factor
Subcutaneous tissue
Infiltrated, dense, woody
Prolactin prominent
Lips
Size
Full, thick
Pancreas congested
Acne
Pus
Prolactin hyperfunctioning
Mucosa, oral
Ulceration
Aphthous ulcer
GH hyperfunctioning
Freckles
Present
Prolactin prominent
Teeth
Spacing
Widely spaced
GH strong
Furuncle
Present
Prolactin excessive
Tongue
Fissures
Fissures
Keratosis
Present
GH hyperfunctioning
GH hyperfunctioning
Scar
Pruritic
GH hyperfunctioning
Tongue
Size
Growth hormone excessive
Skin color
Pale, milky
Prolactin prominent and hyperfunctioning
Large, thick, with dental impression
Uvula
Shape
Bifid
Nail thickness
Thick and strong
GH predominant
Somatotropic excessive
Nail deformity
Pitting
GH overfunctioning
Tonsils
Size
Hypertrophy
Pancreas congested
Tonsils
Color
Erythema
Pancreas congested
Tonsils
Coating
Coating, white
Colon congested
TABLE 11.5 Signs of the head related to the somatotropic axis.
TABLE 11.7 Signs of the chest and breast related to the somatotropic axis.
Quality
Finding
Factor
Part
Quality
Finding
Factor
Hair
Ability to grow long
GH strong
Sternum
Orientation
Convex
GH hyperfunctioning
Brow
Prominent
GH prominent
Breast
General
Underdeveloped
Eyelashes
Thick, overlapping
GH prominent
Prolactin diminished in structure
Thinly spaced
GH not prominent
Size
Voluminous and dense
Prolactin prominent
Polyp
GH hyperfunctioning
Erection
Erect
Prolactin hyperfunctioning
Length of osseous portion
Insulin prominent
Size
Large
Prolactin prominent
Length of cartilaginous portion
GH prominent
Duct
Expression
Prolactin excessive
Bulbous
GH
Nose
Nipple
98 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 11.8 Signs of the abdomen related to the somatotropic axis. Part
Quality
Finding
Factor
General
Proximal
Adiposity, doughy
Insulin excessive and typically reactive and hyperfunctioning
Pancreas
Midpoint between umbilicus and xyphoid
Pain on palpation
Pancreas congestion
Pancreas
Medial-right from umbilicus
Pain on palpation
Pancreas exocrine congestion
Pancreas
Medial-left from umbilicus
Pain on palpation
Pancreas endocrine overtaxed
Colon
Descending, distal
Pain on palpation
GH oversoliciting
TABLE 11.9 Signs of the back, extremities, and bones related to the somatotropic axis. Part
Quality
Finding
Factor
Scapula, right
Inferior-medial, T6–T7
Pain on palpation
Liver congested
Scapula, left
Inferior-medial, T7–T8
Pain on palpation
TSH, PL oversoliciting
T7–T10
Paraspinal
Pain on palpation
Endocrine pancreas congested
Hand
Dorsum
Edematous
Prolactin hyperfunctioning
Knee, right
Thickness
Thick knee
FSH-TSH-GH overfunctioning
Foot
Shape
Hallux valgus (bunion)
GH excessive
Foot
Dorsum
Edematous
Prolactin hyperfunctioning
Foot
Arch
Flat
Prolactin predominant, likely excessive
Bone
Width
Wide
Prolactin prominent
Bone
Length
Long
GH prominent
cellular activity. Bone adapts global metabolism, and, bone metabolism is an indicator of general somatotropic function (The Theory of Endobiogeny, Volume 1, Chapter 15). Thus, when evaluating basic blood work, pay special attention to osteocalcin and alkaline phosphatase bone isoenzymes, which figure prominently in most indexes in this axis. In addition, pay attention to TSH. When it is elevated, it favors more anabolic activity within the somatotropic line of activity, reflected in certain indexes, such as insulin resistance. Conversely, the lower it is, the more it favors oxidative activity, free radicals, and necrosis. The Prolactin index is technically the sole central somatotropic index evaluating its intrinsically central a ctivity
(Table 11.10). GH growth score evaluates timing and distribution of nutrients. Peripheral somatotropic indexes are discussed in Table 11.11. Two of these relate to endocrine pancreatic activity: somatostatin (δ-islet cells), which inhibit insulin, glucagon, and pancreatic enzymes, and, insulin (β-islet cells). Insulin resistance is a subcellular phenomenon, not a hormone, and is evaluated by the Insulin Resistance index. IGF-1 is produced in the liver. Its activity is evaluated by the Growth index corrected. In Table 11.12, indexes reflecting the net effects of somatotropic hormones on metabolism are discussed. Τhe final group of indexes evaluate cellular activity influenced by the somatotropic axis (Table 11.13).
Clinical Essentials of the Somatotropic Axis Chapter | 11 99
TABLE 11.10 Indexes assessing central somatotropic activity. Index
Definition
Import
GH growth score
Timing and distribution of nutrients before the time of prolactin and then somatostatin
High: Increased utilization of nutrients, risk of adenoidal growths. Treatment: Improve TSH and thyroid function Low: Risk of somatotropic desynchronization due to a hyperalpha and/or central hyperthyroid activity. Treatment: Reduce alpha, relaunch growth hormone, Lamium album
Prolactin
Prolactin activity in relaunching second loop corticotropic. Indirectly, may reflect dopamine action on prolactin
High: Prolactin has prolonged action in relaunching cortisol; May indicate insufficient dopamine if brain fog. Treatment: Sambucus nigra leaf Low: Prolactin acts briefly to relaunch cortisol; May indicate inhibition excessive relaunching of and then quick inhibition by dopamine. If insomnia with looped thinking, inhibit prolactin. Treatment: Poterium sanguisorba, Mercurialis annua
TABLE 11.11 Indexes assessing peripheral somatotropic activity. Index
Definition
Import
Somatostatin
Somatostatin active, indirectly its activity on exocrine pancreas
High: Exocrine pancreas oversolicited and somatostatin is not able to sufficiently inhibit it. In conditions of hypertrophy, eczema, etc. Treatment: digestive enzymes, improve cortisol activity Low: Insufficient exocrine pancreas activity, in conditions of wasting or delayed repair. Treatment: digestive enzymes, inhibit cortisol if applicable
Insulin
Insulin sensitivity on cell membrane
High: Hyperinsulinism, risk of somatotropic desynchronization. Treatment: Inhibit insulin activity: Arnica montana, Malva sylvestris Low: Hyperinsulinism due to insufficient membrane sensitivity. Treatment: Insulin sensitizers, e.g., Artemisia dracunculus, Cinnamomum zeylanicum, or, improve insulin production, e.g., Agrimonia eupatoria, Juglans regia
Insulin resistance
Intracellular resistance to insulin during adaptation syndromes
Low: Insufficient insulin resistance, risk of increased free radicals, inflammation, chronic fatigue, fibromyalgia, etc. Treatment: Inhibit insulin activity: Arnica montana, Malva sylvestris, inhibit TSH: Zea mays GM, Lithospermum officinale, etc. High: Excessive or prolonged insulin resistance, risk of mitochondrial insufficiency. Treatment: Insulin sensitizers, e.g., Artemisia dracunculus, Cinnamomum zeylanicum, or, improve cortisol and/or thyroid activity
Growth index corrected
Intracellular activity of growth factors
It evaluates the role of IGF-1 and other growth factors
TABLE 11.12 Indexes assessing general metabolic effects of somatotropic hormones. Index
Definition
Import
Catabolism
Global rate of catabolic activity
Catabolism nourishes anabolism
Anabolism
Global rate of anabolic activity
Anabolism ensures the restoration of the organism
Metabolic yield
Net rate of effective metabolism
High: Hypermetabolic state, if disorders of hypermetabolism (atherosclerosis, eczema, psoriasis, autoimmunity, etc.). Treatment: reduce cortisol and/or thyroid activity or use plants with anabolic adrenal cortex activity, e.g., Sequoia gigantea GM, Rosa canina GM, Salvia officinalis, etc. Low: Net hypometabolic state, may be associated with brain fog or learning difficulties. Treatment: improve cortisol and/or thyroid activity, relaunch prolactin if index high Continued
100 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 11.12 Indexes assessing general metabolic effects of somatotropic hormones—cont’d Index
Definition
Import
Ischemia
Tissular congestion for nutrition and risk of insufficient nutrient entry
High: tissue congestion is impairing nutrient delivery. Treatment: Improve thyroid activity Low: risk of excess nutrition. Treatment: Reduce thyroid activity
Demyelination index corrected
Expressed risk of demyelination of nerves as a marker of quality of GHinsulin relationship
High: Risk of demyelinating disorders: multiple sclerosis, neuropathies, chronic pain, etc. Treatment: Slow down insulin (c.f. Insulin), inhibit cortisol and/or TSH (c.f. Insulin resistance)
Adenosis
Adenosis tendency due to endocrine factors favoring hyperplasia
High: Favorable terrain for all adenoidal growths. Treatment: Reduce TSH by improving thyroid activity Low: Risk of metastasis in known cancer patients. Treatment: Block TSH, reduce thyroid activity if applicable
TABLE 11.13 Indexes assessing cellular metabolic activity as regulated by somatotropic hormones. Index
Definition
Import
Active cell permeability
Nutrient entry via receptors, pumps, etc. against concentration gradient
High: Excessive nutrient entry. Treatment: more protein in diet
Passive cell permeability
Passive flow of small molecules down concentration gradient
High: Excess passive nutrient entry. Treatment: high fiber/whole grain diet
Redox
Global net redox activity of the organism
High: Risk of free radical induced cell injury and inflammation. Treatment: Inhibit TSH, thyroid activity Low: Favors impaired response to microbial infections. Treatment: Improve TSH, thyroid activity
Noxious free radicals
Global rate of circulating harmful free radicals
High: Increased harmful free radicals. Treatment: Inhibit TSH, thyroid activity
Pro-amyloid
General risk of mitochondrial insufficiency for ATP production
HIGH: Favors mitochondrial insufficiency. Treatment: Improve TSH, thyroid activity
Conclusions The somatotropic axis plays a role in the ecology of metabolism, structural fashioning, and energy adaptation. There are many aspects of somatotropic function that can be determined by history, examination, and Biology of
Functions. The axis plays a role in disorders ranging from cancer to chronic fatigue, from diabetes to multiple sclerosis. A proper assessment of somatotropic function allows from a regulation of disorders of structure, adaptation, and metabolism.
Chapter 12
Spasmophilia: A key to many disorders Introduction Spasmophilia represents a dysfunction of two elements of terrain: (1) autonomic sequencing and (2) endocrine calcium management during adaptation. It is in the precritical or critical terrains of numerous disorders and is responsible for countless symptoms and signs: mental (panic attacks, depression), neurologic (migraine), neuromuscular (muscle spasms, asthma), digestive (abdominal colic, gastric reflux), urinary (urgency, voiding difficulties), etc. Recognize and treat spasmophilia to offer symptomatic relief and address root causes of myriad disorders. This also restores a sense of dignity to the patient whose spasmophilic complaints are often dismissed as psychosomatic or idiopathic, and they themselves are labeled as hypochondriac or malingering.
Origins of spasmophilia According to the Endobiogenic approach to disorders, the five levels of analysis of spasmophilia are: 1. Cause (precritical terrain): Latent mismanagement of free calcium with normocalcemia 2. Agent: (aggression): Varied and numerous 3. Response (critical terrain): Neuroendocrine response to adaptation demand that exceeds available calcium or sequesters it 4. Mechanism: Calcium insufficiency relative to demand 5. Effects (disorder): Varied and numerous Note that serum calcium levels are normal. “Mismanagement” refers to insufficient distribution to tissues and cells in two ways: (1) quantity of calcium, (2) quality of timing, both relative to demand. Implicit in this is the calcium-magnesium, which is additive and antagonistic. In order for cycles to complete themselves and resent, there must be sufficient magnesium. This will be key to treatment.
Role of ANS The ANS requires calcium and magnesium for proper sequencing. Even though adrenaline (βΣ) lasts seconds before autolysis, there is residual alpha-sympathetic tone, which The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00012-3 © 2020 Elsevier Inc. All rights reserved.
must be neutralized by magnesium in order for parasympathetic to return to baseline state and maintain a preaggression level of tone. Dysfunctional beta is key. Beta is either delayed or blocked, determined by BoF (Table 12.1). In both cases, it may be from insufficient production of adrenaline or excessive sequestration of elements of adaptation mobilized by adrenaline. In delayed beta, adrenalin excretion is delayed. In blocked beta, there is adaptative alpha+autacoid histamine that prevents beta release, to prolong alpha.
Clinical pearl: Latent spasmophilia and buffering capacity Latent spasmophilia is calcium mismanagement+ANS dysfunction compensated for through buffering capacity consumption. This degrades the buffering capacity over time and is the foundation of most degenerative disorders (Table 12.2). To reduce risk of these disorders, improve buffering capacity (in order of importance by category and subcategory when lettered): 1. Rhythmic living: E.g., seasonal eating, adequate: exercise, sex, meditation, and prayer 2. Diet: Minimize alcohol, alkaline foods (c.f. Section 5: Essentials of alimentation) 3. Neuroendocrine adaptability, as daily tisanes: (a) Adaptogens: Rhodiola rosea, Panax ginseng, (b) Spasmolytics with CNS tropism: Anthemis nobilis, Melissa officinalis, Tilia tomentosa 4. Material elements: (a) Microbiome, (b) Digestive juices and enzymes, (c) Oligoelements: magnesium, calcium, potassium
Role of endocrine system and emunctories Numerous hormones across the four axes and associated emunctories are implicated in calcium absorption, retention, storage, and utilization (Table 12.3). Key to the critical spasmophilic terrain are cortisol and estrogens. Cortisol diminishes available calcium through: (1) increased cellular 101
102 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 12.1 Sympathetic dysfunction in spasmophilia. Spasmophilia
LMI
Histamine
PMI
Delayed beta
↔
↔
↓
Blocked beta
↑ or ↓
↑
↓
Key: ↔: normal, ↑: high, ↓: low.
TABLE 12.2 Physiologic consequences of a spasmophilic terrain. Condition
Excess
Consequence
Insufficiency
Consequence
Perfusion
Hyperperfusion of nutrients
Hypoperfusion
Glucose
Hyperglycemia
Inflammation, hyperanabolism, altered cerebral-mediated consciousness
Hypoanabolism, acidity, ketosis, altered cerebralmediated consciousness
Calcium
Hypercalcemia
Soft-tissue calcification
Hypocalcemia
Muscle tone
Hypertonicity
Hypertension, contractions, reduced range of movement
Hypotonicity
TABLE 12.3 Spasmophilic type by elements of the terrain management. Spasmophilia type Terrain Element
Structurofunctional
ANS
Parasympathetic
Alphasympathetic
Endocrine
Gonadotropic
Corticotropic
Emunctory
Liver Gallbladder Exocrine pancreas
Liver Gallbladder Kidney
Digestive organ
Functional
Intestines
utilization, (2) increased urinary loss, (3) diminished intestinal absorption. Estrogens increase demand for calcium through: (1) stimulation of metabolism, (2) osseous calcium pooling, reducing availability for adaptation.
Types of spasmophilia There are two types of spasmophilia: (1) Structurofunctional, (2) Functional: situational (Table 12.3).
Hypoglycemia
Hypotension, flaccidity, weakness
Evaluating spasmophilia Review of systems 1. Comportment: Asthenia, hyperemotional states, depressive tendency 2. Psychiatric: Anxiety, panic attacks, depression, schizophrenia, etc. 3. Psycho-neurologic: Lipothymia: derealization+1 or more: (a) Dissociation, (b) Imminent loss of consciousness, which never occurs, (c) Disequilibrium, (d) Weakness or emptiness, (e) Hot flushes, (f) Vision: narrowed field, (g) Vision: points of light (seeing stars), (h) Dyspnea with normoxia. Rule out: organic disorders (arrhythmia, carotid blockage, syncope, absence seizures, etc., and postprandial onset 4. Neurologic: Vertigo, paresthesia 5. Musculoskeletal: Myalgia (especially diffuse), muscular spasm 6. Cardiovascular: Palpitations, tachycardia, bradycardia, extrasystolic beats, dysrhythmias, arterial spasm 7. Gastrointestinal: Matinal nausea, aerophagia, biliary dyskinesia, digestive tract spasms 8. Urinary: Cystitis, cystalgia, dysuria (delayed onset), polyuria (with low volume), enuresis 9. Genital: Premenstrual dysphoria, dysmenorrhea, uterine colic, frigidity, erectile dysfunction
Spasmophilia: A key to many disorders Chapter | 12 103
Observation
Case studies in hippus
1. Respiration: Rapid, shallow 2. Posture: Slumped (para>alpha), or, erect and stiff (alpha≫para)
Case 1: Initial response: Rapid, strong pupillary constriction, then rapid, strong dilation; Interpretation: Initial response is serotonin>dopamine: gathering information before making decision; Secondary response: low-amplitude spasm, constriction>dilation; Interpretation: after initial response, patient delays decision, feeling there is never enough information to arrive at final, informed conclusion. Case 2: Initial response: Rapid, strong pupillary dilation then rapid, significant constriction; Interpretation: initial response dopamine>serotonin: jumping to conclusions before sufficient information; Secondary response: rapid, high-amplitude spasm lasting full minute, constriction>dilation during each spasmodic cycle; Interpretation: patient doubts initial conclusion, considers other possibilities, doubts those conclusions and continues in this manner: mental paralysis by analysis.
Examination 1. Chvostek: Latent neuromuscular spasmophilia a. Technique: Strike facial nerve (CN VII) i. 1st point: 0.5–1 cm below lateral zygomatic arch, 2 cm anterior to ear lobe ii. 2nd point: patient supine, mouth passively open and relaxed, strike two-thirds distance from corner of lip to zygomatic arch b. Response: Twitching of facial muscles 2. Trousseau’s sign: Latent vascular spasmophilia a. Technique: Baseline systolic blood pressure (SBP) upper arm, then reinflate manual sphygmanometer, hold at pressure>SPB for 3–4 min b. Response: Primary: Carpopedal spasm of hand with swan-like contortion; Secondary: Paresthesia, Fasciculation, Cramping of ipsilateral fingers 3. Hippus: Latent mental spasmophilia: perception and conclusion a. Technique: Stimulate oculomotor nerve (CN III) i. Shine and hold light directed into eye: place patient supine, diminish or turn off lights ii. Hold bright, focused light to lateral aspect of eye, rapidly move into field of view directing towards pupil, then hold 30–60 s and observe: (1) Rate of initial constriction and dilation, (2) rate and degree of subsequent response, (3) duration of response, (4) laterality of the response (right vs. left pupil) b. Response: cycle of pupillary constriction and dilation c. Interpretation: Varies, c.f. Table 12.4, NB: Pupillary dilation: Serotonin (central para), Pupillary constriction: Dopamine (central alpha) TABLE 12.4 Interpreting hippus. Response
Increased
Diminished
Rate
↑ Qualitative para/alpha
↓ Qualitative para/alpha
Degree
↑ Reactivity of para/alpha
↓ Reactivity of para/alpha Evaluate for depressive terrain
Duration
↑ Severity of spasmophilia
Evaluate for ketosis, iatrogenic sedatives, disorders of dopamine insufficiency (Parkinson’s, Mental retardation—certain types, etc.)
4. Glabella tap: Latent mental spasmophilia: conclusion and reaction a. Technique i. Place patient supine position and have them focus on the ceiling, eyes open ii. Without indicating procedure, briskly strike midline brow b. Response of eyelids i. Closure: Upper: Dopamine (central alpha), Lower: Noradrenaline (alpha) ii. Flutter: TRH (central beta) (Table 12.5) Interpretation of glabella tap and hippus is additive, allowing for the sequencing of serotonin-dopamine-TRH, and, alpha sympathetic on dopamine and TRH (c.f. The Theory of Endobiogeny, Volume 1, Chapter 3, and Volume 2, Chapter 11). 5. Tongue fasciculations: Latent reticular-activating system (RAS) spasmophilia a. Technique: observation of hypoglossal nerve (CN XII), indirect witness of reticular activating system i. Open mouth, observe tongue in neutral state ii. Request patient to fully extend and hold tongue outside mouth a. Response i. Neutral: fasciculations of tongue muscle fibers ii. Extended: tremor of tongue 6. Skeletal muscle fasciculations a. Latent spasmophilia: RAS+TRH+Serotonin action on spinal motor nerves b. Technique: observe musculature c. Response: fasciculation of skeletal muscle bundles
104 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 12.5 Interpreting the glabella tap. Speed of response
Eye lids
Flutter (TRH)
Interpretation
Rapid
Upper>lower
−
Potential for efficient planning
Rapid
Lower>upper
+
Anxious, tangential planning
Normal
Lower≫upper
+
Panic with inefficient planning
+, Present, −, absent.
Diagnostic studies Serum: Within an Endobiogenic context of contextualization and interpretation, certain biomarkers can assist in diagnosing latent or expressed spasmophilia: 1. Alkaline phosphatase bone isoenzyme a. Context: bone turnover due in part to demand for calcium b. Value: quantitative elevation of total value and bone isoenzyme 2. Osteocalcin a. Context: bone matrix protein, restores calcium to bone, increases peripheral metabolic demand for calcium and glucose; blood level inversely proportional to activity in tissue b. Value: elevated: insufficient cellular adaptation, low: increased demand for calcium 3. Phosphorous a. Context: major intracellular ion, complements calcium activity b. Value: elevated: insufficient cellular adaptation with cell death, low: increased cell activity with insufficient phosphorous to complement cell construction rate 4. Magnesium a. Context: major intracellular ion, reverses effects of calcium b. Value: evaluate erythrocyte levels for more accurate interpretation Urine: Calciuria: Evaluate phosphorus and PTH activity. Electrophysiologic: 1. Electromyogram (EMG): repetitive muscular activity that resolves with hyperventilation 2. Quantitative electroencephalogram (QEEG): diminished coherence of CNS activity 3. Electrocardiogram (ECG): U waves, prolonged corrected QT (QTc) interval
Differential diagnosis Rule out organic pathologies—especially life-threatening ones—before diagnosing spasmophilia. The following list is exemplary, not exhaustive.
1. Metabolic: Quantitative deficiencies a. Electrolytes: Calcium, sodium, potassium, phosphorous, magnesium b. Metabolites: Glucose, oxygen 2. Endocrine: Pineal adenoma, hypothalamic adenoma, pituitary adenoma, hypoparathyroidism, hypothyroidism, hyperthyroidism, adrenal insufficiency, hypogonadism, pancreatic disorders 3. Cardiac: Wolf-Parkinson-White, prolonged QT syndrome, syncope 4. Neurologic: Epilepsy, demyelinating disorders, amyloid disorders, spinal cord disorders 5. Muscular: Degenerative muscular disorders 6. Cancer: Primary or metastasis to liver, pancreas, lungs, spine, CNS, etc.
Structuro-functional spasmophilia Introduction There are 10 subtypes of structuro-functional spasmophilia divided into two general groups: constitutional and chronobiologic unfolding (Fig. 12.1) Constitutional spasmophilia involves hyperestrogenism (calcium pooling) or insufficient androgenism (calcium mismanagement). Women are exclusively affected by types 1–3, men by type 4. Chronobiologic unfolding spasmophilia is also related to estrogenism, but occurs in specific ages of life.
Type 1: Pure hyperfolliculinic hysteroid women Terrain: Genetic polymorphism of pituitary FSH sensitivity to estrogen feedback, resulting in hyperfunctioning FSH and estrogens. There is partially compensated LH, progesterone and/or androgens with chronic gonadotropic over-functioning. There is a telling morphology and comportment (Table 12.6). Treatment goals: Reduce FSH, reduce uterine congestion (to reduce excessive estrogen production). 1. FSH inhibition: Lithospermum officinale, Lycopus europaeus, Borago officinalis 2. Pelvic and uterine decongestants: Artemisia dracunculus, Hamamelis virginiana, Achillea millefolium,
Spasmophilia: A key to many disorders Chapter | 12 105
FIG. 12.1 Schematic of spasmophilia nosology. There are 10 types of spasmophilia subphenotypes based on constitutional or time-related genetic changes. (© 2016 Systems Biology Research Group).
TABLE 12.6 Morphologic and comportmental characteristics of pure folliculinic hysteroids. Endocrine
Morphology
Comportment
FSH
Curvy hips Large breasts
Hyperemotive, emotionally labile Hypersexual: favors seduction over stable relationship
Estrogens
Smooth skin complexion Silky hair Small, soft breasts
Open, participatory, communicative Harmonizes personality with that of others Sympathetic suffering of others while forgoing own needs Seeks out archetypal masculine men, but only for a short time favoring seduction
NB: Folliculinic women can have large or small breasts based on the relative predominance of FSH or estrogen receptors in breast tissue. Other hormones also participate in final breast size, volume, and density.
Alchemilla vulgaris, Lavandula angustifolia (Lavender), Cupressus sempervirens (Cypress) Sample treatment: ANS-gonado-pelvic tincture: Lithospermum officinale MT 60 mL, Lycopus europaeus MT 60 mL, Alchemilla vulgaris MT 60 mL, Hamamelis virginiana MT 60 mL+Lavandula angustifolia EO 2 mL, Cupressus sempervirens EO 2 mL: Dose: 3 mL before breakfast and dinner.
Type 2: Hyperfolliculinic hyperthyroid hysteroid women Terrain: Hyperfunctioning FSH and estrogens entrains hyperfunctioning thyroid activity to provide energy for metabolism stimulated by estrogens.
Treatment goals: Reduce central and peripheral gonado-thyrotropic coupling and activity. 1. Inhibition of FSH, LH, TRH, and TSH: Lithospermum officinale, Lycopus europaeus 2. Peripheral estrogen inhibition: Vitex agnus castus (Chaste tree) 3. Progesterone support: Achillea millefolium (Yarrow) 4. Peripheral thyroid inhibition: Lycopus europaeus, Cornus sanguinea GM, Zea mays GM Sample treatment: ANS-gonado-thyrotropic-pelvic tincture: Zea mays GM 60 mL, Lithospermum officinale MT 60 mL, Lycopus europaeus MT 60 mL, Achillea millefolium MT 60 mL+Lavandula angustifolia EO 2 mL: Dose: 3 mL before breakfast and dinner.
Type 3: Androgenic women Terrain: Various factors (Table 12.7) install estrogen dominance in normally androgenic women, inducing a spasmophilia from conflict between estrogens and gonadal androgens. Comportment includes a tendency to guard their independence in relationships due to their inherent androgenism. During times of estrogen predominance, they seek a strong man but are not satisfied with them for long. If they also exhibit inverse relationship of evoked to potential histamine, there is emotional vulnerability and sensitivity. In spasmophilia, these women aggressively resist and attack their male partners, only to feel contrite later. The morphology of these women is shoulders in line or broader than hips, and/or angulated jaw, etc. NB: Children born to mothers treated with estroprogestive therapies during pregnancy can also express a spasmophilic terrain after birth. Treatment goals: Exogenous: Discontinue estroprogestive therapy, Endogenous: Inhibit LH, support progesterone and adrenal cortex (estrogen regulation via sex-hormone-binding globulin [SHBG]).
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TABLE 12.7 Some potential sources of spasmophilia in androgenic women.
TABLE 12.8 Morphologic and comportmental characteristics of children during early toddlerhood.
Origin
Event
Endocrine
Morphology
Comportment
Seasonal
Spring readaptation of T4 by TRH
FSH
Not applicable
Emotional stress
TRH relaunching by locus ceruleus
Menstrual cycle
FSH peaks on menstrual days 7–9, and 12–13a
Hyperemotive, emotionally labile Seduces by helplessness or cuteness to manipulate the behavior of others Unstable relationship with mother: attachment and dependence with periodic running away to play or hide
Estrogens
Smooth skin Silky hair
Open to new experiences and people Participatory and communicative
Estrogen peaks: D10–18, D21–23 TRH peaks: Ovulation, D21–23 Iatrogenic
Estro-progestive therapies Thyroid supplementation with estrogen relaunching
a
Assumes a 28-day menstrual cycle with ovulation on day 12, 13, or 14. See The Theory of Endobiogeny, Volume 3, Chapters 4–5 for a full discussion of the menstrual cycle.
1. Progesteronic: Alchemilla vulgaris (with LH inhibition), Achillea millefolium 2. Adrenal cortex: Ribes nigrum GM, Quercus pedunculata GM Sample treatment: Cortico-LH-progesterone tincture: Alchemilla vulgaris MT 60 mL, Achillea millefolium MT 60 mL, Ribes nigrum GM 60 mL, Quercus pedunculata GM 60 mL: 4 mL twice per day.
Type 4: Constitutional hypoandrogenism: Men Terrain: Genetic tendency of estrogen predominance over androgens in structuro-function, even if with typical virilized male habitus in structure. Treatment goal: Relaunch androgen production. 1. Cortico-Androgenic: Eleuthrococcus senticossus, Zingiber officinale, Rosa canina, Satureja montana 2. Gonadal Androgenic: Zinc, Eleuthrococcus senticossus, Zingiber officinale, Panax ginseng
5a terrain: Physiologic vagotonia of childhood, resolves by 3–4 years. It arises from convergence of mobility, expressive language, will power, and, physiologic vagotonia in the face of strong TRH and estrogens. Conflicts with caregivers or the environment bring out the spasmophilic terrain expressed as emotional lability and tantrums. Treatment goals: Improve pancreas and parent-child relationship. When child is a harm risk to self, others or others’ property, regulate Alpha and TRH. 1. Pancreas: Diet: Low-glycemic, easy to digest foods, Pancreatropes: Agrimonia eupatoria, Juglans regia GM 2. Parent-Child relationship dynamic: Be firm yet flexible, loving and support, but be the adult in the room 3. Alpha-sympatholytics: Tilia tomentosa, Ilex acquafolium GM, Lavandula angustifolia 4. Anti-TRH: Vibernum lantana GM Sample treatment:
Type 5: Vagotonia of childhood: 1.5–6 years
1. Alpha-TRH-pancreas tincture: Tilia tomentosa GM 40 mL, Vibernum lantana GM 40 mL, Juglans regia GM 40 mL: 1–2 mL twice per day before meals 2. Para-alpha topical aromatherapy: Anthemis nobilis EO 5 mL, Lavandula angustifolia EO 5 mL; 5–6 times per day before meals, nap and bath/bedtime, place 1 drop of mixture neat (undiluted) or diluted in carrier oil on pulse points or soles of feet and place socks over feet
General qualities of vagotonia: Sweet personality, good sleeper, good eater, elevated calorie consumption to weight, preference for sweets, enuresis persists after diurnal bladder control. Specific personality in both subtypes is similar to folliculinic hysteroid type (Table 12.8).
5b terrain: Constitutional vagotonia (genetic), persists into school age. Rule out latent hypothyroidism (c.f. Chapter 10, and Theory of Endobiogeny, Volume 1, Chapter 8, and Theory of Endobiogeny, Volume 2, Chapter 10).
Sample treatment: Zinc 15–20 mg at bedtime+Corticogonado androgen-pelvis tincture: Eleuthrococcus senticossus MT 80 mL, Rosa canina GM 80 mL, Hamamelis virginiana MT 80 mL+Satureja montana EO 3 mL, DOSE: 3 mL AM and before bed.
Spasmophilia: A key to many disorders Chapter | 12 107
Treatment goals: As above. In addition: 1. Spasmolysis: a. Oligoelement: Magnesium b. Gemmotherapy: Ilex aquifolium GM (Holly), Tilia tomentosa GM (Linden bud) c. Aromatherapy: Lavandula angustifolia (Lavender), Chamomile (Anthemis nobilis, Matricaria recutita) 2. TRH regulation: Vibernum lantana GM, Lac caninum 3x–6x 3. Self-awareness and self-regulation techniques for the child from 5 years of age
Type 6: Hyperestrogenism, thyrotropic disequilibrium: Emancipation Terrain: Emancipation phase occurs sometime between 28 and 32 and represents maturation of: (1) physical growth, (2) moral growth (individuation from family, friends, societal influence), (3) a committed, serious romantic relationship, (4) established professional career and (5) economic independence from parents (NB: this refers to the ability to be a productive contributor to a household, not simply earning income in exchange for labor. The word economy is derived from the Greek work managing the household—maintaining the integrity and functionality of the family. Thus, a spouse who chooses to manage household affairs or raise children full time is still economically independent if it is in pursuit of their personal goals and they find it a meaningful contribution to their family). It occurs during a re-equilibration of estrogen activity and thus a risk of spasmophilia. Disruption of one or more of these domains of development can install a health crisis. Treatment goals: Work with patient from mid 25–26 to prepare for emancipation through awareness of the areas of development. Reduce TRH and prolactin, regulate estrogens, hepatic drainage if health crisis occurs. Sample treatment: TRH-PL-estro-hepatic tincture: Fabiana imbricata MT, Poterium sanguisorba MT, Vitex agnus castus MT, Carduus marianus MT 4 mL BID.
Type 7: Chronobiologic hypoandrogenism in adolescents Terrain: Fluctuations of gonadotropic hormones during adolescence can lead to periods of estrogen predominance due to insufficient or deficient androgens, with attendant spasmophilia. Treatment goals: Cortico-gonadotropic harmony, regulate estrogens and progesterone, drain pelvis, NB: be careful not to induce closure of epiphyseal growth plates. 1. Cortico-gonadotropic adaptogen: Lepidium meyeneii 2. Cortico-gonado-thyrotropic adaptogen: Panax ginseng
3. Cortico-gonadotropic androgenic harmonizer: Eleuthrococcus senticossus, Sequoia gigantea GM Sample treatment: Cortico-gonadal tincture: Quercus pedunculata GM 60 mL, Rosa canina GM 60 mL, Panax ginseng MT 60 mL, Achillea millefolium MT 60 mL: 4 mL BID.
Type 8: Chronobiologic hypoandrogenism in adults Similar to types 4 and 6, but occurs in post-pubertal times. 8a terrain: Gonadopause, typically abrupt in women, gradual in men. 8b terrain: Genital recycling. 8a, 8b treatment goals: Relaunch androgens, reduce SHBG binding of androgens, inhibit central gonadotropic hyperfunctioning. Sample treatment: Cortico-luteal tincture: Quercus pedunculata GM 60 mL, Rosa canina GM 60 mL, Lycopus europaeus MT 60 mL, Urtica dioica MT 60 mL: 3–4 mL BID.
Functional spasmophilia A number of events can initiate a functional spasmophilia. 1. Exogenous shocks: physical and emotional 2. Lifestyle: nightshift work, sleep after midnight, dysrhythmic living, inappropriate diet 3. Cosmobiologic: seasonal changes, difficulty waking, existential: lead up to birthday 4. Geophysical: solar flares, geomagnetic fluctuation, weather, air travel (multiple time zones, ionizing radiation) There are numerous BoF indexes associated with spasmophilia. ANS indexes were discussed in Table 12.1. Corticotropic and thyrotropic indexes are discussed in Chapters 8 and 10 in this section, as well as in The Theory of Endobiogeny, Volume 2, Chapters 2 and 10, respectively. BoF assessment and treatment 1. ANS: Terrain: In functional spasmophilia, the ANS plays a dual role. One is a precritical terrain of fragilization and degradation of the buffering capacity. To this end, hyperfunctioning of para and alpha play a general role in hypermetabolism. In the critical terrain it is the excessive expression of alpha-sympathetic which is most implicated as the initiator of the adaptation response. a. BoF: See Table 12.1 b. Treatment goals:
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i. Para, Alpha spasmolytics: Passiflora incarnata, Lavandula angustifolia, Anthemis nobilis, Matricaria recutita ii. Beta-acting: Beta-mimetics (Cinnamomum zeylanicum, Satureja montana, Abies balsamea, Thymus vulgaris [indirect through vagolysis]); Beta re-launcher (Menyanthes trifoliata); Beta producer: S-adenosyl menthionine (SAMe) 2. Corticotropic axis: Terrain 1: Low global adrenal cortex function (Chapter 8 and Theory of Endobiogeny, Volume 2, Chapter 2) a. BoF: Adrenal cortex: Low, Cortisol: varies, Cortisol/adrenal cortex ratio4 b. Treatment goals: i. Reduce overstimulation of corticotropic axis: Passiflora incarnata, Lavandula angustifolia, Lithium oligoelement ii. Support metabolic shift from glucocorticoids to adrenal androgens: Sequoia gigantea GM, Rosa canina GM iii. Support adrenal cortex (see prior) iv. Diminish prolactin (Prolactin index low): Mercurialis annua, Poterium sanguisorba Terrain 3: Excessive global adrenal cortex relative to cortisol a. BoF: ACTH: High, Adrenal cortex: high, Cortisol/adrenal cortex ratio 8 h, (3) frequent recurrence.
Magnesium Magnesium is the primary oligoelement used in treatment of critical spasmophilia (Table 12.10). Glycinate and citrate chelates have greater bioavailability than oxide. Use at lower doses. Oral magnesium can cause bowel laxity. Dosing listed per dose, for adults, and can be repeated up to every 3 h with bowel tolerance.
Medical plants Specific medicinal plants are categorized by their area of action in The Theory of Endobiogeny, Volume 2, Chapter 11. Here we discuss acute dosing for up to 24 h based on Galenic preparation. ● ●
●
Encapsulated: 1–2 capsules every 3–4 h Mother tincture: 3–10 mL, every 15 min for 1 h, then up to every 2 h for up to 6 doses, then spaced out, depending on formula Essential oil: Inhalation/Diffusion: continuous, as needed, Oral: 1–3 drops, every 1–4 h, sublingual or in tisane or tincture based or oro-mucous safety, Rectal: 6%–15% concentration, in carrier solution or carrier (e.g., Shea butter)
Regulating exogenous calcium uptake Organic silica improves absorption of calcium. 1. Clay: bioavailable silica with trace amounts of lithium and other minerals 2. Equisetum arvense (Horsetail): NB: avoid in active cancer, edema due to renal or cardiac insufficiency
Calcium and vitamin D 1. Calcium: during latent spasmophilia only: 50–250 mg twice per day 2. Vitamin D: Latent: 400–2000 IU/day in AM, Acute spasmophilia: 4000–10,000 IU for 10–14 days in AM
Other oligoelements In order of therapeutic importance, the following oligoelements can be used: (1) Magnesium (calcium regulation), (2) silica (calcium absorption), (3) potassium (adrenal overstimulation, muscle cramps), (4) phosphorous (cellular
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TABLE 12.9 Selection and dosing of pharmaceutical medications for spasmophilia according to Biology of Functions index. Symptoms
Biology of Functions index
Drug class
Best examples
Anxiety Insomnia Mild to moderate muscular tension
↓ βMSH/αMSH: GABA insufficiency
Benzodiazepines
Alprazolam (short acting) Clonazepam (moderate duration) Diazepam (long acting) • Microdosea: 0.25–0.5 mg • Monotherapy: 2–10 mg
Manic anxiety Severe insomnia Neuromuscular pain or spasms
↑ βMSH/αMSH: Endorphin insufficiency
Endorphins
Opioids Cannabis sativab (Marijuana) CBD oil
Severe muscular spasm and their sequelae
↑/↓ Leukocyte mobilization+↓ Platelet mobilization or by symptoms
Mixed
Orphenadrine (Anticholinergic) • Microdosea: 10 mg • Monotherapy: 100 mg Baclofen (antispasmodic)
Any of the above Emotional or mental reactivity implicated in spasmophilia
↑ Thyroid relaunching corrected: Activated brain stem
Anticonvulsant
Lamotrigine microdose: 5–10 mg: regulates brain stemc,d
Emotional lability/sensitivity that provokes spasmophilia
↑ Evoked histamine+↑ potential histaminee, ratio hepatic
Adaptative alpha Hepatic > splanchnic Vascular hepatic congestion due to solicitation of splanchnic bed for adaptation
PMI
Beta Platelet source
Prominent beta Splanchnic > splenic
Beta blocked Splenic > splanchnic Metabolic hepatic congestion: reliance on de novo platelets in bone marrow by thrombopoietin
LMI, Leukocyte mobilization index; PMI, Platelet mobilization index.
TABLE 13.8 Interpretation of Leukocyte and Platelet mobilization indexes in relationship to one another. LMI
PMI
Interpretation
↑
↑
General sympathetic activity increased on splanchnic bed
↑
↔
Delayed beta, favors spasmophilia
↑
↓
Blocked beta, favors spasmophilia
↓
↓
Adaptative hyper-alpha with blocked beta, favors hepato-splenic congestion
Therapeutics: General considerations The therapeutic approach to hepatic insufficiency involves a rational clinical determination of two questions. The first is: What other organs, systems or processes are also implicated? This will influence the type of plant selected. Example: 4-year-old with recurrent pharyngitis: On history: post-prandial heat when eating sugary foods (liver), on exam: coating on the tongue (cholestasis), dilated opening of canal of Stensen (exocrine pancreas). Conclusion: hepatobiliary-pancreatic unit implicated. Plant: Plantago major: treats the entire block as well as tropism for ear, nose, and throat area, immunomodulation and antimicrobial activity.
The second question is: Is the hepatic dysfunction precritical, critical, or, both, and, what aspect of liver dysfunction is implicated? Example: Crohn’s disease: The liver is primarily implicated in the critical terrain because of its role in adaptation
and processing inflammatory proteins. So, primary drainage of the liver is during the critical state, not the precritical state. In the critical state of a Crohn’s flare up, the liver drainer should be somewhat strong and rapid in action, such as Taraxacum officinale or Cynara scolymus.
Conclusions The liver plays a critical role in health and thus in illness. Long before gross liver histopathology, there is hepatic insufficiency, which brings about an adaptative congestion, which necessitates drainage. The Endobiogenic approach to liver support involves the selection of medicinal plants, oligoelements, and foods that address (1) intrinsic hepatic activity, (2) its functional and anatomical relationship to other organs, (3) its implication in disease with specificity to precritical or critical terrain. History and physical examination are the primary methods of determining evaluating the liver and its role in disbalance. This allows for a rational, clinical selection of the optimal approach to supporting the liver.
Chapter 14
Exocrine pancreas Introduction The exocrine pancreas sits at the crossroads of nutrition and adaptation, making it directly implicated in survival. Its nutritional aspect is direct, related to the production of digestive enzymes. In this sense, it is closely associated with the hepatobiliary unit (Chapter 13). Functionally and anatomically, it is associated with the endocrine pancreas, which manages glucose. Thus, the role of the exocrine pancreas to adaptation and survival is through associations with both the liver and the endocrine pancreas. Exocrine pancreatic dysfunction affects optimal function of both liver and endocrine pancreas. Furthermore, the exocrine pancreas through its nutritive function is directly involved in the quality of nutrition and growth, implicating it in disorders as wide ranging as chronic sinusitis, adenocarcinomas, and ulcerative colitis. As with the liver (Chapter 13), the exocrine pancreas is implicated in numerous precritical and critical terrains. Therefore, evaluation and treatment of the exocrine pancreas is crucial for a well-functioning terrain.
Structure, function, units of function Structure and function The exocrine pancreas is composed of acinar and basophilic cells. Acinar cells produce bicarbonate. Basophilic cells produce digestive enzymes that hydrolyze carbohydrates, lipids, or proteins. Enzymes are released in an inactive form, which is activated in an alkaline environment, hence the importance of the bicarbonate of acinar origin. The endocrine pancreas acts on the exocrine pancreas through a number of hormones, such as somatostatin and pancreatic polypeptide.
Units of function The exocrine pancreas has many functional units of linked function related through proximity and purpose of function. 1. Oro-pancreatic a. Anatomy: Not applicable, functional relationship b. Role: Saliva contains amylase, an enzyme that initiates digestion of carbohydrates in the mouth and stomach. Insufficient mastication or injury to salivary glands increases burden on exocrine pancreas The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00014-7 © 2020 Elsevier Inc. All rights reserved.
c. Effects: Dysbiosis, bloating, flatus, pancreatic congestion, pancreatic insufficiency d. Exemplary plants: Contain amylase activity, e.g., Plantago major, Avena sativa 2. Gastro-duodenal-pancreatic a. Anatomy: Proximal association related to release of chyme b. Role: Timed and proportional excretion of chyme to be neutralized by bicarbonate and hydrolyzed by digestive enzymes c. Effects: Insufficient digestive enzymes or bicarbonate delays release of chyme, increase tendency toward putrefaction in the stomach and gastric reflux d. Exemplary plant: Ficus carica GM: contains substitutive enzymatic activity and stimulates epithelialization of digestive mucosa, indirectly regulates alpha-sympathetic tone 3. Exocrine-endocrine pancreas a. Anatomy: Single fused gland b. Role: Exocrine pancreas calibrates availability of nutrients from diet, impacting endocrine pancreatic hormone activity in calibrating distributing, utilizing, and storing nutrients c. Effects: Various disorders of nutrients storage, utilization, overgrowth, etc. (ovarian cysts, colon cancer, Parkinson’s disease, etc.) d. Exemplary plants: Dual pancreatropes (acts on exocrine and endocrine pancreas), e.g., Agrimonia eupatoria, Juglans regia 4. Hepatobiliary-pancreatic (Chapter 13) a. Anatomy: Exocrine pancreatic ducts merge with the common bile duct in the ampulla of Vater. The sphincter of Oddi allows of bile, bicarbonate, and enzymes into the small intestines. Insufficiency of one can lead to a delay of excretion of the products of both glands b. Role: Timed and proportional excretion of bile and digestive enzymes c. Effects: Oversolicitation of salivary glands, hypertrophied lymphoid tissues, dysbiosis, altered stool composition d. Exemplary plants: Plants with hepatobiliary-pancreatic- immune action, e.g., Agrimonia eupatoria, Plantago major 117
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5. Pancreato-pulmonary a. Anatomy: Not applicable, functional relationship b. Role: Indirect but constant: metabolism of carbohydrates increases carbon dioxide (CO2) production c. Effects: Pulmonary congestion as emunctory for CO2 excretion. (c.f. The Theory of Endobiogeny, Volume 3, Chapter 2, Asthma) d. Exemplary plants: Dual exocrine pancreatic-pulmonary action: Agrimonia eupatoria, Plantago major with or without Corylus avellana as a pulmonary drainer 6. Pancreato-dermato-articular a. Anatomy: Not applicable, functional relationship b. Role: Indirect: general excessive uptake of proteins due to exocrine pancreas, with inability of liver to metabolize these proteins; skin solicited as emunctory, or, deposition or partial proteins in joints if joints inflamed and hypermetabolic c. Effects: Skin disorders (eczema, psoriasis), joint disorders (arthropathies, arthritis) d. Exemplary plants: Dual pancreas-skin action: Arctium lappa, Viola tricolor, Joint action: various in combination with exocrine pancreatic plants, preferably with hepatorenal drainage, e.g., Zea mays GM+Juglans regia 7. Pancreato-immunity a. Anatomy: Not applicable, functional relationship b. Role: General role in protein uptake for immune products; secondary relationship with TSH: proanabolic factor that makes appeal to exocrine pancreas for cell growth c. Effects: Oversolicitation of pancreas participates in congestion of lymphoid tissue: direct from excess nutrients and from TSH, favors recurrent infections d. Exemplary plants: Action on exocrine pancreas, TSH drainage of ear, nose, and throat region, e.g., Avena sativa+Plantago major 8. Neuroendocrine-pancreatic (Table 8.1) a. Anatomy: Not applicable, functional relationship
b. Role: In face of hyperfunctioning of hormones, exocrine pancreas is solicited to accommodate requirement for certain nutrients solicited by particular hormones (e.g., estrogens: proteins, T3: lipids, carbohydrates) c. Effects: Oversolicitation of pancreas participates in adenoidal growth, such as Acne (+LH), Tonsil hypertrophy (+TSH), Eczema (various), skin tags (+GH, insulin) d. Exemplary plants: Action on exocrine pancreas+ endocrine, e.g., LH: Medicago sativa, FSH/ Estrogens: Salvia sclarea, TSH/Thyroid: Avena sativa, GH/Insulin: address TSH and Insulin: e.g., Avena sativa+Juglans regia 9. Pancreato-metabolism: Peripheral TRH, TSH a. Anatomy: Not applicable, functional relationship b. Role: Central thyrotropic hormones make an appeal to the exocrine pancreas: TSH to exocrine, TRH to endocrine pancreas, complementing their actions on the somatotropic axis for growth of cells (The Theory of Endobiogeny, Volume 1, Chapters 8–10) c. Effects: Permanent dialectic of cell growth through multiplication vs. enlargement, related to benign and nonbenign tumors, acne, fibrocystic breast growth, prostate adenoma, etc. d. Exemplary plants: TSH: Ascophyllum nodosum, TRH: Fabiana imbricata+Agrimonia eupatoria 10. Pancreato-central nervous system: Central TSH a. Anatomy: Not applicable, functional relationship b. Role: TSH in its central metabolic activity increases requirements for nutrients, soliciting exocrine pancreas c. Effects: Tendency towards phlegmatic, concrete or rigid thinking, central metabolic disorders such as Alzheimer’s disease d. Exemplary plants: TSH serum low: Zea mays GM+Juglans regia, TSH serum high: Ascophyllum nodosum
TABLE 8.1 Neuroendocrine actions on the exocrine pancreas. Category
Factor
Stimulates
Regulates
ANS
Para
Enzyme production
Sphincter of Oddi tonus
Alpha
Enzyme production
Beta
Enzyme excretion
Gonadotropic
Estrogens
Enzyme production
Thyrotropic
TSH
Enzyme excretion
TRH
Enzyme excretion
Inhibits
Sphincter of Oddi dilation
Corticotropic
Cortisol
Enzyme excretion
Somatotropic
Somatostatin
Enzyme excretion
Glucagon
Enzyme excretion
Exocrine pancreas Chapter | 14 119
General approach to assessment The general approach to evaluating the pancreas is to determine if it is insufficient, oversolicited, congested, or some combination of the three.
Insufficiency Insufficiency refers to a lack of enzymes relative to demand. This can involve any class of enzymes, with specific signs and symptoms related to inadequate digestion of proteins, carbohydrates, or lipids. There is a special relationship of TSH to the exocrine pancreas, related to energy metabolism. In between the time of glucose (acute) and lipid (chronic) oxidation for ATP is a time for the use of amyloid proteins as an intermediate energy. These proteins must be proteolyzed before they are accumulated; otherwise, various disorders may occur (diabetes, atherosclerosis, Alzheimer’s disease, etc.). TSH solicits these proteins and it also stimulates their proteolysis. This last action implicates its relationship to the exocrine pancreas. Insufficiency of proteolytic enzymes can result in an accumulation of amyloid proteins.
Oversolicitation Oversolicitation refers to a state in which the request for one or more classes of exocrine pancreatic enzymes is greater than what is appropriate for the organisms' function, the pancreas’ production capacity, or both. The exocrine pancreas is implicated in disorders of dysregulated metabolism due to excess uptake of proteins, lipids, and/or carbohydrates from the diet, such as adenocarcinomas, eczema, bronchitis, asthma, and ulcerative colitis.
Congestion Congestion refers to a vascular edema of the pancreatic tissue. It arises from oversolicitation or insufficiency states. It reflects an attempt to prolong the perfusion of elements that may assist the pancreas to meet the demands of the organism, be it through hypertrophy, hyperplasia, hyperfunctioning, or some combination thereof.
Historical findings related to exocrine pancreas From the functional units noted, numerous symptoms and signs can be derived. Common signs can be divided into three groups according to clinical disorders: 1. Allergies, infections, immunity a. Chronic, recurrent infections, especially fungal b. Recurrent cough c. Urticaria d. Pruritis: perianal, genital, palmo-plantar
2. Energy and metabolism a. Postprandial fatigue b. Excess generalized sweating: Post-prandial, 5th hour of sleep c. Sugar cravings (related to hyperinsulinism) 3. Maldigestion of fats a. Stools: i. Sticky, messy to wipe after evacuation ii. Poorly formed, pasty, runny like mud iii. Steatorrhea: floating of stool iv. Chronic diarrhea b. Weight loss, unintentional c. Malabsorption of fat-soluble vitamins and B12
Physical exam findings Physical examination findings can be related to nutrient metabolism as well as to the various functional units of relationship with the exocrine pancreas. 1. Carbohydrate metabolism: a. Coating on tongue b. Parotids: i. Sensitive to palpation ii. Hypertrophied iii. Dilated orifice of Stensen’s duct c. Hypersialorrhea d. Flatus, nonodiferous e. Explosive stools, occasionally with pain 2. Protein metabolism: a. Coating on tongue b. Tonsil hypertrophy c. Flatus: odiferous 3. Skin: a. Thickened b. Fatty c. Seborrhea dermatitis: eyebrows, nasolabial folds 4. Anus: a. Pruritis (fungal overgrowth)
Biology of functions: Somatostatin index Centrally, the hypothalamic hormone somatostatin inhibits growth hormone, prolactin, and TSH. Peripherally, produced throughout the digestive tract (including the endocrine pancreas), it inhibits digestive activity (including excretion of digestive enzymes). The index evaluates the level of somatostatin activity, indirectly witnessing the relative level of activity of the exocrine pancreas. Therefore, the index indirectly evaluates the implication of the exocrine pancreas in disease. Implicit in somatostatin’s activity is the balance of growth and antigrowth, of the start of adaptation with cortisol (which inhibits somatostatin), and the end of adaptation with somatostatin. Various therapeutic interventions can be recommended based on these considerations (Table 8.2).
120 SECTION | B Essentials of history, physical exam and Biology of Functions
TABLE 8.2 Somatostatin index: Clinical findings, interpretation, and therapeutic strategies. Therapeutic intervention Value
Clinical
Interpretation
Medicinal plant
Other
High
Lymphoid congestion, recurrent illnesses, atopy, adenomas
1. Prolonged, ineffective somatostatin activity to prevent potential or actual excessive growth 2. Prolonged activity because cortisol is not sufficiently inhibiting it
Adrenal cortex stimulant: Salvia officinalisa Improve thyroid yield: Ascophyllum nodosuma, Avena sativaa
Pancreas sparing diet, Apple-Sardine diet Digestive enzymes
Low
Adenocarcinomas in growth phases, autoimmune flare ups, fibromyalgia, chronic pain, neuropathies, etc.
1. Exocrine pancreatic activity inefficient 2. Cortisol inhibiting somatostatin and excretion of digestive enzymes
Inhibit thyrotropic: Zea mays GM, Lycopus europaeus, Inhibit Alpha+Cortisol: Passiflora incarnata, Lavandula angustifolia, Exocrine pancreatrope: Agrimonia eupatoria, Juglans regia
↓ TSH, ↓ peripheral thyroid ↓ Alpha ↓ Cortisol Zn-Ni-Co Whole ancient grains, root vegetables well cooked
a
Also has direct action on exocrine pancreas.
Therapeutics: General considerations The therapeutic approach to the exocrine pancreas involves a rational clinical determination of two questions. The first is: What other organs, systems or processes are also implicated? This will influence the type of plant selected. Example: 26-year-old with oozing eczema on the face: History: weeping eczema (skin+exocrine pancreas) worse with consumption of sugary foods (exocrine pancreas+hyper parasympathetic), on Exam: dilated opening of canal of Stensen (exocrine pancreas). Conclusion: Parasympathetic+Exocrine pancreatic-dermatologic unit implicated. Plant: Viola tricolor: treats the unit and drains skin+Agrimonia eupatoria, which supports hepatobiliarypancreatic block and indirectly reduces parasympathetic tone by improving digestion.
The second question is: Is the exocrine pancreatic dysfunction pre-critical, critical, or, both, and, what aspect of activity is implicated, e.g., protease vs. amylase, hyperfunctioning or insufficient, etc.? Example: Crohn’s disease (c.f. Chapter 23): The exocrine pancreas is implicated in the precritical terrain. Therapeutic relief using plants with enzymatic-like activity, digestive enzymes, and diet are most effective once the patient is out of the critical terrain of a flare up. In the precritical state, a
persistent and long-term support with a plant that supports the exocrine pancreas, digestive function and which acts as an intestinal astringent and cicatrizant is very valuable, such as Plantago major, Juglans regia, or Agrimonia eupatoria.
In addition to medicinal plants, oligoelements can be used to stimulate production of digestive enzymes, or digestive enzymes can be used as a substitutive therapy. Diet also plays an important role, such as the pancreas-sparing diet (c.f. Chapter 44: Endobiogenic diets and nutrition). In addition, dietary etiquette with respect to chewing and eating in a calm environment should be emphasized for long-term regulation of pancreatic function.
Conclusions The exocrine pancreas plays an important role in the survival of the organism. It is integrated into the functioning of the endocrine pancreas, local intestinal and annexal glands, enteric and central nervous system and with global neuroendocrine regulation of the terrain. Its insufficiency or excess has implications in a host of disorders. The role of the exocrine pancreas can be determined based on history, physical examination and to a limited extent, the Biology of Functions. Address the specific level of dysfunction of the exocrine pancreas in order to reintegrate it into the proper level of structural and functional activity of the organism.
Chapter 15
Acne Summary Essence: An imbalance of androgen regulation with excess protein deposited under the epidermis. Terrain: (1) Luteal insufficiency: Hyper-LH in response to insufficient gonadal androgens and/or progesterone response, or feedback on pituitary with (2) Adrenal androgen compensation, (3) ANS: Para≫alpha with (4) Inflammation: Insulin resistance, ⇓ cortisol, with (5) Congestion: Liver and colon and thus skin as compensatory emunctory resulting in (6) Skin manifestation: due to local hypermetabolism of skin.
Treatment goals Symptomatic: Antimicrobial, anti-inflammatory: topical most effective Terrain: ● ● ●
● ● ●
●
ANS: ⇓ Para, alpha CORTICO: ⇑ Cortisol relative to adrenal androgens GONADO: ⇓ LH, if indicated, ⇓ FSH and regulate progesterone SOMATO: ⇓ GH, PL; regulate insulin THYRO: adapt TSH, ⇓ Thyroid (where indicated) DRAIN: (1) Liver, (2) colon, (3) skin (descending order of importance) DIET: Pancreas sparing
Sample treatment 1. Face mask (c.f. Table 15.5) 2. Cortico-Gonadotropic: Lithospermum officinale MT 60 mL, Alchemilla vulgaris MT 60 mL, Ribes nigrum GM 60 mL, Fragaria vesca MT 60 mL, Lavandula angustifolia EO 3 mL: 3 mL three times per day 3. Drainage: Viola tricolor MT 120 mL, Arctium lappa MT 60 mL, Agrimonia eupatoria MT 60 mL: 3 mL BID
Terrain in detail Precritical terrain 1. Hyperparasympathetic 2. Congested emunctories a. Liver The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00015-9 © 2020 Elsevier Inc. All rights reserved.
b. Colon c. Exocrine pancreas 3. Oversolicitation of skin as metabolic organ and compensatory emunctory
Agent 1. Major endocrine transitions: states of increased androgens: birth, puberty, gonadopause 2. Genital recycling: central-peripheral gonadic recalibration 3. Adaptative states: menstruation, emotional stressors, change of seasons, post-natal 4. Exogenous hormonal therapies (i.e., androgen or progesterone therapy)
Critical terrain 1. Hyper-LH with insufficient gonadal response → ⇑ androgen receptor expression a. Relative insufficiency: progesterone and/or gonadal androgens adequate or excessive, but feedback on LH impaired b. Absolute insufficiency: deficient response to LH demand 2. ⇑ Compensatory adrenal androgen production (not regulated by LH) 3. Insufficient cortisol relative to adrenal androgens 4. Thyro-somatotropic response alters the quality of acne, e.g., pustular, pruritic, cystic, etc. 5. Hyperanabolic state focused on skin→keratin and sebum production excessive
Mechanism and response ⇑ Sebum production+hyperkeratosis→congestion of hair follicle. Overgrowth of commensal skin bacteria (from the lipids in sebum and proteins in keratin) → acne manifestation.
History and BoF findings Evaluate precritical and critical terrains of acne. Some possible correlations between history and Biology of Functions are presented in Table 15.1. The general history includes the presence of diffuse or localized raised erythematous lesions, ± painful papules, pustules, and/or nodules any skin surface; ± fever, scaring. 123
124 SECTION | C Assessment and treatment of common disorders
TABLE 15.1 Historical and Biology of Functions correlations. Subject
Finding
Terrain
BoF
Skin
Acne distribution (c.f. physical exam)
Various
N/A
Pus
⇑ PL
⇑/⇓ Prolactin
Pruritis
Alpha, TRH, or, local factors
⇑ Evoked histamine (if global origin)
Inflammation
⇑ TSH, ⇑GH, ⇑ Insulin
⇑ GH growth score, ⇑ Growth index, ⇑/⇓ Insulin, ⇓ serum TSH
Premenstrual
Progesterone insufficient
⇑ Progesterone, ⇓ LH
Autumn
Insufficient cortisol, relative to ⇑ adrenal androgens (DHEA)
⇓ Cortisol absolute, or, Cortisol/adrenal cortexratio cortisol b. Thyrotropic: i. Hyper TRH: histamine release, inflammation ii. Overadapted thyroid: inflammation, hypermetabolism 3. Exocrine pancreas+emunctory congestion a. Liver b. Large intestines c. Skin
Mechanisms 1. Bronchial hyper-reactivity a. ANS: c.f. Critical terrain b. Local bronchoconstrictors: substance P, neurokinin A, B 2. Local a. Inflammation: mast cells, T-lymphocytes b. Leukocytes: lymphocytes, eosinophils, basophils 3. Airway obstruction a. Mucous b. Substance P, neurokinin A, B
Response: Asthmatic episode 1. Adaptative hyper-reactivity and occlusion of airways→hypoxia 2. Compensatory tachypnea and accessory muscle use 3. Death
History and BoF findings Evaluate precritical and critical terrains during an acute asthma attack. Some possible correlations between history and Biology of Functions are presented in Table 16.2. The presentation in critical terrain is classic: trouble breathing, a feeling of suffocation, anxiety, and discomfort due to dyspnea.
Physical exam and BoF findings Critical terrain 1. ANS a. Alpha-hyperfunctioning in response to allergen: histamines, inflammation, edema, airway obstruction b. Compensatory Para hyperfunctioning: mucous, secretions, airway obstruction c. Installation, or aggravation of spasmophilia: bronchospasm 2. Endocrine a. Corticotropic: i. Hyper ACTH
The following may be observed on physical exam with some possible Biology of Functions correlations (Table 16.3).
Treatment During the critical allergic asthma terrain, in addition to standard of care treatment, support the terrain in the following order of emphasis: symptomatic polyvalent treatments that address mechanisms of disease (Table 16.4), drainage (Table 16.5), and neuroendocrine regulation (Table 16.6).
Asthma, allergic type Chapter | 16 129
TABLE 16.2 Historical and Biology of Functions correlations. Area
Finding
Terrain
BoF
Bronchus
Difficulty breathing, accessory muscle use
c.f. above
c.f. above
Family history
Atopic disease, setting of home (urban, rural, etc.)
N/A
N/A
Past medical history
Atopic disease, maternal antibiotic use, birth history, recurrent URI
N/A
N/A
Environment
Domicile cleanliness, stuffed animals, carpeting, air quality, etc.
N/A
N/A
Para
Shy, introverted, sweats easily, eczema, deep sleeper, does not recall dreams
High para
Alpha
GERD, Gastritis, constipation, recurrent viral/strep infections, migraines, insomnia
High alpha
⇑/⇓ LMI
Cortico
Acne, eczema, psoriasis, recurrent infections, afternoon fatigue
Insufficient cortisol
⇓ Cortisol ⇓ and/or (−): Adaptationpermissivity of adrenal cortex
Thyro
Enlarged tonsils, constipation, weight gain
Latent hypothyroidism with congestion of lymphoid tissue
⇓ Thyroid (precritical) ⇑ Thyroid (critical)
Pancreas
Recurrent sinusitis, tonsillitis, eczema, mucus production with dairy/gluten, bloating, anus fissures
Oversolicited exocrine pancreas
⇑/⇓ Somatostatin
Liver
Poor immune response, loss of appetite, chills
Hepatic congestion
Colon
Constipation, acne on buttocks
Colon congestion
⇓ Pelvic congestion
Key: GERD, gastroesophageal reflux disorder; URI, upper respiratory tract infections.
TABLE 16.3 Examination and Biology of Functions correlations. Area
Finding
Terrain
Observation
Poor posture with compromised respiration Accessory muscle use, nostril flaring Allergic salute
Vagotonia
Airways
Inspiration: cough Expiration: wheeze
Alpha≫para, beta blocked or delayed
⇑/⇓ LMI + ⇓PMI ⇑ Noxious free radicals, Proinflammatory, Inflammation
HEENT
Allergic crease on nose
Allergic rhinitis
Various esp. ⇑ evoked histamine
Injected sclera
Hyper alpha
Enlarged tonsils
(Historical precritical) latent hypothyroidism with lymphoid congestion, exocrine pancreas implication
Enlarged orifice of canals Stensen
Hyper para with exocrine pancreas insufficiency
Enlarged glands of Wharton
Hyper alpha+liver congestion
⇑/⇓ LMI
Glabella tap: rapid eyelid flutter; Brisk DTR, Clonus
⇑ TRH
⇑ Thyroid relaunching, Thyroid relaunching corrected
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓PMI
Neuro
BoF
⇓ Thyroid (precritical)
130 SECTION | C Assessment and treatment of common disorders
TABLE 16.3 Examination and Biology of Functions correlations—cont’d Area
Finding
Terrain
BoF
Liver
Tender, superior-medial
Vascular hepatic congestion
⇑/⇓ LMI
Tender, inferior-lateral
Metabolic hepatic congestion
⇑/⇓ LMI
Tender, above umbilicus
Congestion: general
N/A
Tender, right of umbilicus
Oversolicitation: exocrine
⇑/⇓ Somatostatin
Tender, left of umbilicus
Oversolicitation: endocrine
⇑/⇓ Insulin
Tender, above umbilicus
Congestion: general
⇑/⇓ Somatostatin
Tender, right of umbilicus
Over-solicitation: exocrine
N/A
Tender, left of umbilicus
Oversolicitation: endocrine
⇑/⇓ Somatostatin
Tender: Ileocecal, ascending, hepatic flexure, splenic flexure, sigmoid
Colon congestion related to central overfunctioning: ACTH-S, FSH, TRH/TSH, TSH, ACTH-F, respectively
⇓ ACTH, FSH, ⇑ TRH/TSH indexes
Pancreas
Pancreas
Colon
Key: DTR, deep tendon reflex; HEENT, head, ears, eyes, nose, throat; F, function; LMI, leukocyte mobilization index; PMI, platelet mobilization index; S, structure.
TABLE 16.4 Medicinal plants with polyvalent symptomatic actions. Plant
Antispasm
Agrimonia eupatoria
•
Decongestant
Arctium lappa
• Indirect
Eucalyptus ssp.
•
Lavandula angustifolia
•
Plantago major
•
Thymus vulgaris
•
Anti-inflam.
Antiallergic
Anti-infect.
•
•
•
• Indirect
Expectorant
•
•
• •
• Indirect
Viola tricolor
Mucolytic
•
•
•
•
•
•
•
•
•
•
•
• •
TABLE 16.5 Medicinal plants for drainage. Organ/system
Primary
Alternatives
Pulmonary oxygenator
Passiflora incarnata MT
Crocus sativa MT, Eucalyptus ssp. EO
Pulmonary-pancreatic
Eucalyptus ssp. EO
Lavandula angustifolia EO+Abies balsamea EO+Juniperus communis EO, Glycyrrhiza glabra MT, Agrimonia eupatoria MT
Liver
Arctium lappa MT
Agrimonia eupatoria MT, Plantago major MT, Zea mays GM
Intestines
Agrimonia eupatoria MT
Arctium lappa MT, Plantago major MT
Key: EO, essential oil; GM, gemmomacerate; MT, mother tincture.
Asthma, allergic type Chapter | 16 131
TABLE 16.6 Medicinal plants for neuroendocrine regulation. Axis
Primary
Alternatives
↓ Alpha, para
Lavandula angustifolia EO
Matricaria recutita MT
↑ Beta
Thymus vulgaris EO
Satureja montana EO, Cinnamomum zeylanicum EO
↓ ACTH
Matricaria recutita MT, EO
Quercus pedunculata GM, Ribes nigrum GM, Passiflora incarnata MTa
↑ Adrenal cortex
Rhodiola rosea MT, Ribes nigrum GM, Crocus sativa MT
Eleutherococcus senticosus MT, Rosa canina GM, Quercus pedunculata GM
↓ Central thyrotropic
TRH: Fabiana imbricata MT TSH: Cornus sanguinea GM
TRH: Leonurus cardiaca MT TSH: Zea mays GM
Adapt peripheral thyroid
Melissa officinalis MT, Avena sativa MT
Key: EO, essential oil; GM, gemmomacerate; MT, mother tincture. a
Alpha sympatholytic.
Oligoelements 1. Magnesium: bronchodilation (oral dosing may not work acutely) 2. Selenium: inflammation 3. Sulfur: airway protection and healing 4. Copper-gold-silver: anti-infectious, oxidative support
TABLE 16.7 ANS Corticotropic prescription. Herb
Amount and form
Alternatives
Rhodiola rosea
60 mL MT
Eleuthrococcus senticosus MT
Ribes nigrum
60 mL GM
Quercus pedunculata GM
Environment Critical: avoid allergens Precritical: reduce allergic burden: remove or thoroughly clean carpets, wash bedding and plush toys, avoid dust, tobacco smoke, mold, etc.
Diet Critical: pancreas-sparing Precritical: Mediterranean diet with emphasis on citrus, foods rich in selenium, magnesium, and sulfur; digestive enzymes with meals where indicated
Lifestyle Exercise and postural therapies Education about disease and empowering self-care: action plan, rescue dosing, measuring peak flow, etc.
Exemplary prescriptions Based on an Endobiogenic approach to extrinsic asthma, a number of prescriptions can be derived. The first set is a general approach to an asthma attack in out-patients already receiving standard-of-care therapy. 1. ANS-corticotropic: 4 mL four times per day, 7 days (Table 16.7)
Rhodiola rosea MT 60 mL, Ribes nigrum GM 60 mL, Thymus vulgaris EO 2 mL 2. Bronchial-inflammation-drainage: 4 mL four times per day, 7 days, then twice per day, 7 days (Table 16.8) Plantago major MT 100 mL, Viola tricolor MT 100 mL, Populus nigra GM 40 mL, Eucalyptus ssp. EO 1.5 mL, Thymus vulgaris EO 1.5 mL, Lavandula angustifolia EO 1 mL
TABLE 16.8 Bronchial-inflammation-drainage prescription. Herb
Amount and form
Alternatives
Plantago major
100 mL MT
Agrimonia eupatoria MT
Viola tricolor
100 mL MT
Arctium lappa MT
Populus nigra
40 mL GM
Eucalyptus ssp.
1.5 mL EO
Thymus vulgaris
1.5 mL EO
Lavandula angustifolia
1 mL EO
132 SECTION | C Assessment and treatment of common disorders
3. Selenium oligoelement 1 dropper four times per day×7 days, then 4. Magnesium oligoelement 1 dropper twice per day 5. Topical application (Table 16.9) Prophylaxis: once per day; Mild wheezing (pulmonary function 70%–80%) three per day, acute asthma attack: four times per day
TABLE 16.9 Topical pulmonary prescription. Essential oil
Amount and form
Thymus vulgaris
6 drops
Lavandula angustifolia
3 drops
Eucalyptus globulus leaf
3 drops
Abies balsamea
3 drops
Carrier oil
1.5–2 tsp (7.5–10 mL)
1. Mix essential oils and with carrier oil, such as olive or jojoba, in a glass dish 2. Warm between hands, apply with friction in clockwise circular motion to anterior and posterior chest 3. Apply residual mixture left on hands over cervical lymph nodes and sternal notch. Avoid the eyes. 4. Complete treatment by making a hollow fist and tapping across upper chest (infraclavicular, sternal notch), then over lungs, right and left, anterior and posterior In milder cases of asthma with nocturnal dyspnea only, a simplified treatment can be used. 1. Nocturnal dyspnea: 3 mL at 4 p.m., 3 mL at 8 p.m., or 1 h before bed, whichever comes first for 7 days (Table 16.10) Eleutherococcus senticosus MT 60 mL, Angelica archangelica MT 30 mL, Matricaria recutita MT 30 mL, Eucalyptus ssp. EO 1.25 mL, Lavandula angustifolia EO 1.25 mL
TABLE 16.10 Nocturnal prescription. Herb
Amount and form
Replacements and alternatives
Eleutherococcus senticosus
60 mL MT
Rhodiola rosea MT, Ribes nigrum GM
Angelica archangelica
30 mL MT
Populus nigra GM
Matricaria recutita
30 mL MT
Plantago major MT+Inula helenium MT
Eucalyptus ssp.
1.25 mL EO
Lavandula angustifolia
1.25 mL EO
Chapter 17
Asthma, intrinsic Summary Essence: A spasmophilic disorder of the airways in vagotonics in response to oversolicitation of oxygen for adaptation demands of a nonallergic origin.
Avena sativa MT 120 mL, Agrimonia eupatoria MT 120 mL, Artemisia dracunculus EO 4 mL: 3 mL before breakfast and dinner for 6 months (cf. Table 17.9)
PMS induced asthma with anxiety
Terrain: (1) Spasmophilia: Hyper-Alpha and Para, 1. Para-Gonadotropic: 4 mL twice per day before meals: Lycopus europaeus MT 120 mL, Vitex agnus castus MT Beta: blocked or delayed (2) Hyperanabolic structuro- 60 mL, Alchemilla vulgaris 60 mL MT, Thymus vulgaris EO functional adaptation response: gonado-thyro- 2 mL somatotropic > corticotropic ➔ excessive oxygen demand + insufficient adaptation with (3) Congestion: exocrine 2. Anxiety-Drainage: 4 mL twice per day, menstruation to last 6 days of cycle, then 6 mL twice per day, and, as needed pancreas, lungs, and hepatobiliary unit 6–8 mL for intense conflict or shock: Passiflora incarnata MT 100 mL, Humulus lupulus MT 80 mL, Menyanthes trifoliata MT 60 mL, Lavandula angusTreatment goals tifolia EO 2 mL, Citrus reticulata EO 2 mL Symptomatic: Standard of care + beta-mimetic, antispasmodic, pulmonary decongestant mucolytic, fluidifying, Terrain in detail expectorant Terrain: Cause: Precritical terrain ●
●
●
● ●
●
ANS: ⇓ Alpha, histamines, Para, ⇑ Beta (to resolve spasmophilia) GONADO: ⇓ Hyperestrogenism; if grand phase transitions add luteal support (progesterone, gonadal androgens) THYRO: Support peripheral thyroid commensurate to adaptive gonadotropic demands SOMATO: ⇑ Insulin sensitivity CORTICO: ⇑ Cortisol excretion, general adrenal cortex adaptability DRAIN: 1°-Exocrine pancreas, 2°-Hepato-biliary, 3°-Kidney, 4°-Intestines,
1. ANS: Vagotonia with variable beta response (Table 17.1) 2. Endocrine: anabolic oversolicited, hyperfunctioning with compensated oxygen demand a. Gonadotropic: i. Hyperestrogenism ii. Hypoluteal: insufficient androgens and/or progesterone activity b. Somatotropic: i. Insulin resistance > Insulin sensitivity, congestive tendencies 2. Emunctories: Exocrine pancreas over-solicited and: a. Hepato-biliary congested b. Lungs congested
Sample treatment
Agent
Exercise-induced asthma
1. Structuro-functional demand requiring competent gonadotropic activity a. Childhood b. Grand phases: adolescence, menopause, genital recycling c. Menstrual cycle d. Pregnancy
1. ANS-Corticotropic regulator: 3 mL AM and midafternoon: Rhodiola rosea MT 120 mL, Ribes nigrum GM 60 mL, Quercus pedunculata GM 60 mL, Lavandula angustifolia EO 2 mL, Thymus vulgaris EO ct. linalool 2 mL (c.f. Table 17.8) 2. Thyro-Drainage-Digestion: 3 mL twice per day before meals: The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00017-2 © 2020 Elsevier Inc. All rights reserved.
133
134 SECTION | C Assessment and treatment of common disorders
TABLE 17.1 ANS precritical subtypes. Asthma type
Parasympathetic
Alpha sympathetic
Beta sympathetic
4
++ (Vagotonic)
Normal
Normal
5
++ (Vagotonic)
Normal
Insufficient
Precritical spasmophilia
present
+: Degree of activity.
2. Nonallergic adaptation demand requiring competent corticotropic activity a. Seasonal transition b. Cold c. Exertion d. Functional spasmophilias (Section 2, Chapter 12, and Theory of Endobiogeny, Volume 2, Chapter 11) e. Emotional crisis 3. Miscellaneous: factors diminishing oxygen availability a. Anemia b. Dehydration c. Tissue alkalosis d. Neuromuscular diseases: thoracic cage, diaphragm, accessory muscles
Response: Critical terrain
Result: Extrinsic asthma Airway obstruction (secretory) with bronchospasm: adaptative compensation to prolong alveolar patency and oxygen exchange
History and BoF findings Evaluate precritical and critical terrains during an acute asthma attack. Some possible correlations between history and Biology of Functions are presented in Table 17.2. The presentation in critical terrain is classic: trouble breathing, a feeling of suffocation, anxiety, and discomfort due to dyspnea.
Physical exam and BoF findings
The ANS and emunctory responses are similar, but the endocrine response is based in sequential overactivation of the 4 axes starting with the gonadotropic.
The following may be observed on physical exam with some possible Biology of Functions correlations (Table 17.3).
1. ANS: First response: a. Spasmophilia: Hyper para, hyper alpha, beta: insufficient or delayed 2. Endocrine: Second response (in order): a. Gonadotropic: overfunctioning b. Thyrotropic: overfunctioning (central > peripheral) c. Somatotropic: overfunctioning i. Central: GH, PL per case ii. Peripheral: always implicated d. Corticotropic: insufficient peripheral function 3. Emunctory and digestive organs: a. Exocrine pancreas: oversolicited b. Lungs: congested c. Hepato-biliary: congested d. Chronic: Kidney (chronic ACTH demand) e. Intestines
Treatment
Mechanisms Hypersecretions, mucosal congestion > bronchoconstriction, histamines. (See Extrinsic asthma (Chapter 16) for general mechanism).
The general approach is similar to extrinsic asthma, but emphasizes anabolic response to adaptation: 1. Acute: Symptomatic (Table 17.4) 2. Acute and chronic: Neuroendocrine (Table 17.5) a. Structuro-functional: i. Gonado-thyrotropic regulation (modify basal demand for oxygen, nutrients) especially if structurofunctional spasmophilia co-morbidity (Chapter 12, and Theory of Endobiogeny, Volume 2, Chapter 11) ii. Somatotropic regulation: central and peripheral insulin sensitivity b. Functional: i. Corticotropic: general adaptability 3. Acute and chronic: Drainage (Table 17.6) 4. Chronic: Precritical In cases of emotional shock and exertional onset functional intrinsic asthma, there are additional therapeutic considerations (Table 17.7). For emotional shock, use acutely at high doses (e.g., 3-8 mL up to every hour) if onset of asthma is infrequent but intensity of shock is great, use at lower
Asthma, intrinsic Chapter | 17 135
TABLE 17.2 Historical and Biology of Functions correlations. Area
Finding
Terrain
BoF
Bronchus
Difficulty breathing, accessory muscle use
Spasmophilia
LMI varies + ⇓ PMI
Para
Good sleeper, good eater, seldom cries, shy, introverted, sweats easily, eczema, prolonged expiratory phase
High Para
Alpha
GERD, Gastritis, constipation, insomnia
High Alpha
⇑/⇓ LMI, ⇑ Thyroid relaunching or Thyroid relaunching corrected
Gonado
Hyperestrogenism: Eczema, Psoriasis, Menorrhagia, Premenstrual breast tenderness, large clots during menstruation
Estrogens > Progesterone and/or androgens
Estrogen indices > Androgen indices
Somato
Sugar cravings, diabetes mellitus type 2, midabdominal fat, skin tags
Insulin resistance
Insulin: ⇓ Insulin resistance: ⇑
Pancreas, Exocrine
Recurrent sinusitis, tonsillitis, eczema, mucus production worsened by dairy/gluten, bloating, anal fissures
Oversolicited
⇑/⇓ Somatostatin
Liver
Poor immune response, loss of appetite especially in AM, frequent hypoglycemia
Hepatic congestion
⇑/⇓ LMI
Colon
Constipation, acne on buttocks
Colon congestion
⇓: Pelvic congestion
TABLE 17.3 Examination and Biology of Functions correlations. Area
Finding
Terrain
BoF
Airways
Inspiration: cough Expiration: wheeze Accessory muscle use, altered posture, nostril flaring
Alpha >> Para, Beta delayed
⇑/⇓ LMI + ⇓ PMI ⇑: Noxious free radicals, Proinflammatory, Inflammation index, Evoked histamine
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓PMI
Gonado
Hair: abundant, scalp oily, skin smooth, voluminous, soft breasts, large areola, lower abdominal adiposity, infiltrated subcutaneous fat, ligamentous laxity
Estrogenism
⇓ Genital ratio or corrected, ⇑ Estrogen indexes
Thyro
Cold sensitivity (T3), heat intolerance (T4), weight loss, pruritis
Elevated peripheral thyroid activity
⇑ Thyroid, ⇑/nl Thyroid yield
Liver
Tender, superior-medial
Vascular hepatic congestion
⇑/⇓ LMI
Tender, inferior-lateral
Metabolic hepatic congestion
⇑/⇓ LMI
Tender, above umbilicus
Congestion: general
N/A
Tender, right of umbilicus
Over-solicitation: exocrine
⇑/⇓ Somatostatin
Tender, left of umbilicus
Over-solicitation: endocrine
⇑/⇓ Insulin
Tender various points
Colon congestion related to central over-functioning
⇓: ACTH, FSH, ⇑ GH growth score, ⇑/⇓ PL
Pancreas
Colon
Key: LMI: Leukocyte mobilization index, PMI: Platelet mobilization index.
136 SECTION | C Assessment and treatment of common disorders
TABLE 17.4 Medicinal plants with polyvalent symptomatic actions. Plant
Antispasm
Agrimonia eupatoria
•
Decongestant
• •
Plantago major
•
Thymus vulgaris
•
Mucolytic
Expectorant
•
•
•
Eucalyptus ssp. Lavandula angustifolia
Anti-inflam.
•
• •
• •
Viola tricolor
•
•
•
•
Key: anti-inflam: anti-inflammatory, antispasm: antispasmodic, ssp. species.
TABLE 17.5 Medicinal plants for neuroendocrine regulation. Axis
Primary
Alternatives
⇓ Alpha, Para
Lavandula angustifolia EO
Matricaria recutita MT/EO, Passiflora incarnata
⇑ Beta
Menyanthes trifoliata MT, Thymus vulgaris EO (indirect by vagolysis)
Satureja montana EO, Cinnamomum zeylanicum EO
⇑: Adrenal cortex adaptability
Rhodiola rosea MT, Eleutherococcus senticosus MT,
Ribes nigrum GM, Quercus pedunculata GM
⇓ Estrogens
Borago officinalis MT, Vitex agnus castus MT
Lithospermum officinale MT, Lycopus europaeus MT
Adapt Luteal activity
Achillea millefolium MT Eleutherococcus senticosus MT
Panax ginseng MT Zingiber officinale MT*
Regulate peripheral thyroid
Avena sativa MT
Melissa officinalis MT
Somato: Insulin resistance
Juglans regia GM/MT Artemisia dracunculus EO, BH
Cinnamomum zeylanicum EO
Key: BH: Bulk herb, EO: Essential oil, GM: Gemmomacerate, MT: Mother tincture; * avoid in hyperthyroid states with excess heat.
TABLE 17.6 Medicinal plants for drainage. Organ/system
Primary
Alternatives
Exocrine Pancreatic
Agrimonia eupatoria MT
Plantago major MT, Juglans regia GM
LiverGallbladder
Carduus marianus MT Arctium lappa MT
Agrimonia eupatoria MT, Plantago major MT
Kidney
Betula ssp. GM
Juniperus communis GM, Fagus sylvatica GM, Arctium lappa MT
Intestines
Agrimonia eupatoria MT
Arctium lappa MT, Plantago major MT
Key: Gemmomacerate, MT: Mother tincture.
TABLE 17.7 Miscellaneous medicinal plants. Trigger
Primary
Alternatives
Emotional
Valeriana officinalis EO, MT, Scutellaria latiflora MT
Anthemis nobilis BH, EO, Lavandula angustifolia BH, EO, MT, Tilia tomentosa GM
Exertional
Rhodiola rosea (Rhodiola) BH, DE, MT, Eleutherococcus senticosus BH, DE, MT
Ribes nigrum GM, Panax quinquefolius (American ginseng) BH, DE, MT
Key: BH: Bulk herb, EO: Essential oil, GM: Gemmomacerate, MT: Mother tincture.
Asthma, intrinsic Chapter | 17 137
doses regularly if occurring three or more times per week (e.g., 3 mL 2 to 3 times per day). For exertional asthma, use adaptogens daily at regulating doses.
Exemplary prescriptions Based on an Endobiogenic approach to intrinsic asthma, two sets of exemplary prescriptions are presented. The first set is for functional intrinsic asthma, for treatment of the critical neuroendocrine terrain (Table 17.8) and drainage (Table 17.9). For example, a 39-year-old man who has recently started exercising 5 days per week and experiences dyspnea during exercise. He also has a history of dyspepsia with flatulence. 1. ANS-Corticotropic regulator: 3 mL AM and midafternoon: Rhodiola rosea MT 120 mL, Ribes nigrum GM 60 mL, Quercus pedunculata GM 60 mL, Lavandula angustifolia EO 2 mL Thymus vulgaris EO 2mL
Avena sativa MT 120 mL, Agrimonia eupatoria MT 120 mL, Artemisia dracunculus EO 4 mL The second set is for structuro-functional asthma (Tables 17.10 and 17.11), such as a 24-year-old woman with premenstrual asthma. Her PMS symptoms also include breast tenderness, cystic acne on the chin, and intensification of generalized anxiety, which occurs all month long. 1. Para-Gonadotropic: 4 mL twice per day before meals: Lycopus europaeus MT 120 mL, Vitex agnus castus MT 60 mL, Alchemilla vulgaris 60 mL MT, Thymus vulgaris EO 2 mL 2. Anxiety-Drainage: 4 mL twice per day, menstruation to last 6 days of cycle, then 6 mL twice per day, and, as needed 6–8 mL for intense conflict or shock: Passiflora incarnata MT 100 mL, Humulus lupulus MT 80 mL, Menyanthes trifoliata MT 60 mL, Lavandula angustifolia EO 2 mL, Citrus reticulata EO 2 mL
2. Thyro-Drainage-Digestion: 3 mL twice per day before meals: TABLE 17.10 Para-gonadotropic prescription. TABLE 17.8 ANS corticotropic prescription.
Herb
Amount and form
Replacements and alternatives Lithospermum officinale MT
Amount and form
Replacements and alternatives
Lycopus europaeus
120 mL MT
Herb Rhodiola rosea
120 mL MT
Eleutherococcus senticosus MT, Ribes nigrum GM
Vitex agnus castus
60 mL MT
Alchemilla vulgaris
60 mL MT
Ribes nigrum
60 mL GM
Quercus pedunculata GM
Quercus pedunculata
60 mL GM
Ribes nigrum GM
Achillea millefolium MT 40 mL + Medicago sativa MT 20 mL
2 mL EO
Eucalyptus ssp. EO 2 mL
Lavandula angustifolia
2 mL EO
Matricaria recutita EO
Thymus vulgaris ct linalool
Thymus vulgaris
2 mL EO
Satureja montana EO, Cinnamomum zeylanicum EO
TABLE 17.9 Endocrine-drainage-digestion prescription. Herb
Amount and form
Replacements and alternatives
Avena sativa
120 mL MT
Agrimonia eupatoria MT
Agrimonia eupatoria
120 mL MT
Carduus marianus MT 60 mL + Plantago major MT 60 mL
Artemisia dracunculus
4 mL EO
Mentha piperita EO 2 mL + Carum carvi EO 2 mL
TABLE 17.11 Anxiety-drainage prescription. Herb
Amount & form
Replacements & Alternatives
Passiflora incarnata
100 mL MT
Tilia tomentosa MT
Humulus lupulus
80 mL MT
Salvia sclarea EO
Menyanthes trifoliata
60 mL MT
Satureja montana EO, Cinnamomum zeylanicum EO
Lavandula angustifolia
2 mL EO
Citrus reticulata EO 2 mL
Citrus reticulata
2 mL EO
Artemisia dracunculus EO 2 mL, Lavandula angustifolia
Chapter 18
Acute bronchitis, dry cough Summary Essence: A hyper alpha-sympathetic spasmophilia of fragilized bronchi in response to an aggressor. Terrain: (1) Irritation of the bronchus: environmental or infectious and (2) Spasmophilia: Alpha > Para, low Beta with (3) Inflammation: hyperfunctioning central thyroid + adaptative cortisol with (4) Dry cough: from insufficient mucous to protect irritated bronchus.
Treatment goals Symptomatic: Emollient, antitussive, spasmolytic, antiinfectious (as indicated). Terrain: ●
● ●
●
●
ANS: ⇓ Alpha > Para, relaunch Beta (to resolve spasmophilia) CORTICO: ⇓ Cortisol THYRO: ⇓ TRH and TSH, adapt thyroid according to situation DRAIN: 1-Exocrine Pancreas-Pulmonary axis, 2-Hepato-Splenic, 3-Intestines, 4-Skin (as indicated) DIET: Pancreas sparing
Sample treatment 1. Neuroendocrine-infectious: Passiflora incarnata MT 40 mL, Fabiana imbricata MT 40 mL, Cornus sanguinea GM 40 mL, Lavandula angustifolia EO 1.5 mL, Cinnamomum zeylanicum EO 1 mL: 3 mL three times per day for 10–14 days (Table 18.6). 2. Emollient-drainage-infectious: Agrimonia eupatoria MT 60 mL, Malva sylvestris MT 60 mL, Eucalyptus smithii or globulus EO 2 mL: 3 mL three times per day for 10–14 days (cf. Table 18.8). 3. Topical antispasmodic: Eucalyptus spp. EO 8 drops, Lavandula angustifolia EO 4 drops, Cupressus sempervirens EO 3 drops + 1 tbsp carrier oil.
Terrain in detail Precritical terrain There is, prior to the time of exposure to the inciting agent, a global hyperfunctioning of the terrain that targets and The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00018-4 © 2020 Elsevier Inc. All rights reserved.
fragilizes the bronchi to maintain an increased oxygen requirement: 1. Endocrine, hyperfunctioning a. Pituitary b. Thyroid: TSH, T4 c. Pancreas, Endocrine d. Adrenal cortex (lesser role) 2. ANS: Para, hyperfunctioning 3. Emunctory a. Defense, oversolicited and taxed i. Exocrine pancreas ii. Spleen: Immunity b. Congestion i. Colon ii. Liver iii. Skin
Agent The agent provokes a supraphysiologic oxygen demand that is beyond the adaptation capability of the patient, further diminishing the already-fragilized buffering capacity. This neuroendocrine adaptation response will determine if the bronchitis is wet or dry (cf. Chapter 19: Acute bronchitis, wet). Common aggressors include: 1. Pathogens: viruses most common 2. Particulates: allergens, tobacco smoke, etc. 3. Gastric secretion reflux: microaspiration 4. Cold air
Critical terrain 1. ANS: Hyper Alpha > Para, with spasmophilia: blocked or delayed beta 2. Corticotropic: Adaptive cortisol 3. Thyrotropic: a. Central: Hyperfunctioning TRH, TSH b. Peripheral: Thyroid response varies; greater the activity, greater the inflammation tends to be in the face of elevated cortisol 4. Emunctories: a. Broncho-pulmonary unit: congested due to exocrine pancreatic overactivity 139
140 SECTION | C Assessment and treatment of common disorders
b. Spleen and Liver: oversolicited, overtaxed, and congested c. Intestines: congested d. Skin
Mechanisms Hyperinflammatory response with insufficient mucous to protect the airway, or, high inspissated mucous, which is difficult to expectorate.
History and BoF findings During acute bronchitis, typical symptoms of an irritable, spasmodic cough, with or without fever, of 10 or less days duration will be present. In a patient with known history of recurrent seasonal bronchitis, evaluate the precritical terrain in the preceding season to institute prophylaxis. Some possible correlations between precritical symptoms and Biology of Functions are presented in Table 18.1.
Physical exam and BoF findings During presentation with acute bronchitis, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 18.2)
Result Inspiratory, spasmodic dry cough
TABLE 18.1 Precritical terrain symptoms and Biology of Functions correlations. Area
Finding
Terrain
BoF
Psyche
Acute stress, Exacerbation of chronic stress
Complex, varied
⇑ Serotonin, ⇓ PL, ⇑ Potential histamine, ⇑/⇓ βMSH/αMSH + ⇑ Noxious free radicals ⇑/⇓ LMI, ⇑ Thyroid relaunching, Thyroid relaunching corr.
Insomnia, reduced stress tolerance Alpha
GERD, Gastritis, constipation, insomnia
High Alpha
Para
Good sleeper, good eater, seldom cries, shy, introverted, sweats easily, eczema, prolonged expiratory phase
High Para
Thyro
Vivid dreams, nightmares
TRH
⇑ Thyroid relaunching, Thyroid relaunching corr., HypothalamoMetabolic, TRH/TSH
Hypoglycemic tendencies
TSH + Insulin
TSH serum 3 + ⇓ Genito-thyroid ⇑ fT4
Heat intolerance Pancreas, Exocrine
Recurrent ENT infections, eczema, mucus with dairy/gluten, bloating
Over-solicited, insufficient
⇑/⇓ Somatostatin
Spleen
Unfocused effort, fatigue, impaired adaptability, depressive tendency, recurrent infections
Splenic congestion
⇓ PMI
Liver
Poor immune response, loss of appetite especially in AM, chills
Hepatic congestion
⇑/⇓ LMI
Colon
Constipation, acne on buttocks
Colon congestion
⇓ Pelvic congestion
TABLE 18.2 Critical terrain signs and biology of functions correlations. Area
Finding
Terrain
BoF
Airways
Spasmodic cough: inspiratory, dry
Alpha ≫ Para, Beta delayed
⇑/⇓ LMI + ⇓ PMI + ⇑ Noxious free radicals, Proinflammatory, Inflammation
Alpha
Cold extremities, dry mucous membranes, stringy saliva
Elevated alpha > para
⇑/⇓ LMI + ⇓ PMI
Acute bronchitis, dry cough Chapter | 18 141
TABLE 18.2 Critical terrain signs and biology of functions correlations—Cont’d Area
Finding
Terrain
BoF
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓PMI
Brisk DTR, Clonus, Eyelid flutter on Glabella tap
⇑ TRH
⇑ Thyroid relaunching, Thyroid relaunching corr.,
Adrenals
Tender on palpation, Tender Cortisol point
Adrenal oversolicitation
⇑ Cortisol, Adaptation-permissivity Varies: Adrenal cortex, often: Cortisol/Adrenal cortex ratio > 4
Thyro
Pain of palpation of tibial prominence
Adaptative TSH
⇓ TSH serum
Cold sensitivity (T3), heat intolerance (T4), weight loss, pruritis
Hyperfunctioning peripheral thyroid
⇑ Thyroid index, Thyroid yield
Immuno
Suprasternal notch: Tender on palpation
Thymus congested from oversolicitation
⇑ IL-1
Pancreas
Tender: above umbilicus
Congestion: general
N/A
Tender, right of umbilicus
Oversolicitation: exocrine
⇑/⇓ Somatostatin
Tender, left of umbilicus
Oversolicitation: endocrine
N/A
Tender, right of umbilicus
Vascular hepatic congestion
⇑/⇓ LMI
Tender, right of umbilicus
Metabolic hepatic congestion
⇑/⇓ LMI
Tender: various points
Colon congestion
Depends on points tender
Liver
Colon
Key: DTR: Deep tendon reflex; LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
Treatment Acute bronchitis During acute bronchitis, antibiotics should be avoided unless proven bacterial etiology in a fragilized patient. The general emphasis of treatment is listed in Table 18.3 in columns from left to right. The general approach is three-fold: 1. Symptomatic, localized to bronchi (Tables 18.3 and 18.8) 2. Neuroendocrine, in following order of emphasis (Table 18.4) a. Reduce Alpha
b. Reduce Corticotropic: Cortisol, balance Cortisol:adrenal cortex ratio on BoF c. Reduce Thyrotropic: TRH, TSH, thyroid (as indicated) d. Oligoelements (discussed later) 3. Drainage (Table 18.5), in following order of emphasis a. Pancreas-sparing diet b. Pancreato-Pulmonary axis c. Hepato-Splenic d. Intestines e. Skin (as indicated)
TABLE 18.3 Medicinal plants with polyvalent symptomatic actions. Plant
Antispasm.
Agrimonia eupatoria
•
Arctium lappa
Decon.
Anti-inflam.
Anti-infect.
•
•
•
•
Ceanothus americanus
•
•
Cinnamomum zeylanicum
•
•
Cornus sanguinea
Lavandula angustifolia
•
•
Eucalyptus ssp.
• •
Emol.
•
• •
142 SECTION | C Assessment and treatment of common disorders
TABLE 18.3 Medicinal plants with polyvalent symptomatic actions—Cont’d Plant
Antispasm.
Decon.
Anti-inflam.
Malva sylvestris Plantago major
•
Populus nigra
•
•
Emol.
•
•
• •
Viola tricolor
Anti-infect.
•
•
•
Zea mays
•
•
Key: Anti-infect.: Anti-infectious, Anti-inflam.: Anti-inflammatory, Antispasm.: Antispasmodic, Emol: Emollient.
TABLE 18.4 Medicinal plants for neuroendocrine regulation. Axis
Primary
Other
⇓ Alpha, Para
Passiflora incarnata MT, Lavandula angustifolia EO
Valeriana officinalis MT, Tilia tomentosa GM, Matricaria recutita MT
⇑ Beta
Cinnamomum zeylanicum EO
Satureja montana EO
⇓ ACTH
Matricaria recutita MT
Passiflora incarnata MTa
⇓ Cortisol
Passiflora incarnata MT
Leonurus cardiaca MTb, Sequoia gigantea GM
Support global adrenal
Ribes nigrum GM
Quercus pedunculata GM. Glycyrrhiza glabra MT
⇓ Thyrotropic: Via central inhibition
TRH: Fabiana imbricata MT
TRH: Leonurus cardiaca MT
TSH: Cornus sanguinea GM
TSH: Zea mays GM
Somato: Delay Insulin/⇑ Insulin resistance
Malva sylvestris MT, Arnica montana MT
Indirectly: ⇓ Cortisol, block TSH
Key: EO: Essential oil, GM: Gemmomacerate, MT: mother tincture. a
Indirect via Alpha-sympatholysis.
b
Reduces cortisol fixation.
TABLE 18.5 Polyvalent medicinal plants with drainage and pulmonary tropism. Plant
Pancr.-pulm
Agrimonia eupatoria Plantago major
Liver
Intestines
•
•
•
•
•
•
•
•
Ceanothus americanus
Hepato-splenic
Skin
•
Viola tricolor
•
Key: Pancr.-Pulm: Pancreatic-Pulmonary axis.
Exemplary prescriptions Based on an Endobiogenic approach to acute dry bronchitis, a number of prescriptions can be derived. 1. Neuroendocrine-infectious: 3 mL three times per day for 10–14 days (Table 18.6) Passiflora incarnata MT 40 mL, Fabiana imbricata MT 40 mL, Cornus sanguinea GM 40 mL, Lavandula
angustifolia EO 1.5 mL, Cinnamomum zeylanicum EO 1 mL; An alternate formula is presented in Table 18.7. 2. Emollient-drainage-infectious: 3 mL three times per day for 10–14 days (Table 18.8) Agrimonia eupatoria MT 60 mL, Malva sylvestris MT 60 mL, Eucalyptus ssp. EO 2 mL. 3. Topical antispasmodic: Apply up to every hour for relief of cough
Acute bronchitis, dry cough Chapter | 18 143
Eucalyptus spp. EO 8 drops, Lavandula angustifolia EO 4 drops, Cupressus sempervirens EO 3 drops + 1 TBSP carrier oil; Instructions: (a) Mix carrier oil and EOs in glass bowl, (b) Apply with friction rub in circular and up/down motions for 3–4 min, (c) Cover chest with a shirt or blanket, then heated pad or towel; Alternative: Diffuse undiluted essential oils within 2 feet (0.6 m). 4. Oligoelements: (a) Spasmodic cough: Magnesium oligo: 1–2 droppers every 4 h for first three days; (b) Inflammation: Selenium: 1–2 droppers every 4 h for first three days. 5. Diet Pancreas sparing, favor root vegetables: turnip, black radish, yams, and, juices of carrot, quince, chervil, cabbage, lettuce, mulberry, apple, and turnip.
TABLE 18.6 Neuroendocrine-infectious prescription. Amount and form
Replacements and alternatives
Passiflora incarnata
40 mL MT
Matricaria recuctita EO
Fabiana imbricata MT
40 mL MT
Leonurus cardiaca MT, Fabiana imbricata MT
Cornus sanguinea
40 mL GM
Zea mays GM, Lycopus europaeus MT
Lavandula angustifolia
1.5 mL EO
Eucalyptus ssp. EO 1.5 mL
Cinnamomum zeylanicum
1 mL EO
Thymus vulgaris EO 0.5 mL + Satureja montana EO 0.5 mL
Herb
TABLE 18.7 Neuroendocrine-infectious prescription alternate. Herb
Amount and form
Replacements and alternatives
Ribes nigrum
60 mL GM
Quercus pedunculata GM
Populus nigra
60 mL GM
Ceanothus americanus MT
Satureja montana
0.5 mL EO
Cinnamomum zeylanicum, Menyanthes trifoliata MT
Cinnamomum zeylanicum
0.5 mL EO
Satureja montana, Rosa canina GM
TABLE 18.8 Emollient-drainage-infectious prescription. Amount and form
Replacements and alternatives
Agrimonia eupatoria
60 mL MT
Plantago major MT
Malva sylvestris
60 mL MT
Arnica montana MT 40 mL + Glycyrrhiza glabra MT 20 mL
Eucalyptus smithii
2 mL EO
Eucalyptus globulus (unrectified) EO 2 mL
Herb
Chapter 19
Acute bronchitis, wet cough Summary
Terrain in detail
Essence: A hyperparasympathetic spasmophilia of fragilized bronchi in response to an aggressor. Terrain: (1) Spasmophilia: Para > Alpha > Beta with (2) ENDO: Adrenal cortex insufficiency and central hyperthyroidism and hyperhistaminemia ➔ inflamed bronchi and (3)-Exocrine pancreatic and pituitary over-activity ➔ mucous (various qualities) resulting in (4) Spasmodic, wet cough.
Precritical terrain
Treatment goals Symptomatic: Anti-infectious, antiallergic, antispasmodic, antitussive, expectorant, mucolytic Terrain: ● ANS: ⇓ Para > Alpha, ⇑ Beta (resolve spasmophilia) ● CORTICO: ⇑: Adrenal cortex ● THYRO: ⇓ TRH (mast cell degranulation) ● Reduce excess production of secretions: ⇓ Exocrine pancreas solicitation ● Break up mucous: mucolytics ● DRAIN: 1-Pulmonary-Pancreatic axis, 2-Intestines, 3-Liver, 4-Skin (as indicated) ● DIET: Pancreas sparing
Sample treatment 1. Neuroendocrine-Infectious: 3 mL three times per day for 10–14 days (cf. Table 19.6): Inula helenium MT 30 mL, Fabiana imbricata MT 30 mL, Ribes nigrum GM 60 mL, Lavandula angustifolia EO 1.5 mL, Satureja montana EO 1 mL 2. Drainage: 3 mL three times per day for 10 days (cf. Table 19.7): Agrimonia eupatoria MT 60 mL, Plantago major MT 30 mL, Arctium lappa MT 30 mL, Eucalyptus smithii EO 2 mL 3. Antispasmodic cough topical essential oil blend: Eucalyptus spp. EO 8 drops, Lavandula angustifolia EO 4 drops, Cupressus sempervirens EO 3 drops + 1 TBSP carrier oil
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00019-6 © 2020 Elsevier Inc. All rights reserved.
There is, prior to the time of exposure to the inciting agent, a global hyperfunctioning of the terrain that targets and fragilizes the bronchi to maintain an increased oxygen requirement. The net effect is a local congestion and fragilization of the bronchi. 1. Endocrine: Hyperfunctioning a. Pituitary b. Thyroid: TSH, T4 c. Pancreas, Endocrine d. Adrenal cortex (lesser role) 2. ANS: Para, hyperfunctioning 3. Emunctory: a. Defense, oversolicited and taxed i. Exocrine pancreas ii. Spleen: Immunity b. Congestion i. Colon ii. Liver iii. Skin
Agent The agent in wet bronchitis is typically an allergen or virus, which provokes a supraphysiologic oxygen demand that is beyond the adaptation capability of the patient, further diminishing the already-fragilized buffering capacity. This neuroendocrine adaptation response will determine if the bronchitis is wet or dry (cf. Chapter 18: Acute Bronchitis, Dry).
Critical terrain 1. ANS: Hyper Para > Alpha, with spasmophilia: blocked or delayed beta 2. Pituitary: Oversolicited and inefficient in relaunching peripheral glands 3. Corticotropic: ACTH ≫ Cortisol, absolute cortisol typically insufficient to help resolve infection
145
146 SECTION | C Assessment and treatment of common disorders
TABLE 19.1 Precritical and critical terrain symptoms and Biology of Functions correlations. Area
Finding
Terrain
BoF
Bronchus
Spasmodic cough: expiratory, wet
Para ≫ Alpha, spasmophilia
↑/↓ LMI + ↓ PMI
Para
Good sleeper, good eater, seldom cries, shy, introverted, sweats easily, eczema, prolonged expiratory phase
↑Para
N/A
Alpha
GERD, Gastritis, constipation, insomnia
↑Alpha
↑/↓ LMI
Thyro
Vivid dreams, nightmares
↑TRH
↑: Thyroid relaunching, Thyroid relaunching corr., HypothalamoMetabolic, TRH/TSH
Cortico
General fatigue, lassitude
Adrenal insufficiency
↓Cortisol, ↓Adrenal cortex, Cortisol:Adrenal cortex ratio < 2 regardless of absolute value
Pancreas, exocrine
Recurrent sinusitis, tonsillitis, eczema, mucus production with dairy/gluten, bloating, anus fissures
Over-solicited
↑/↓ Somatostatin
Spleen
Unfocused effort, fatigue, impaired adaptability, depressive tendency, recurrent infections
Splenic congestion
⇓ PMI
Liver
Poor immune response, loss of appetite especially in AM, chills
Hepatic congestion
⇑/⇓ LMI
Colon
Constipation, acne on buttocks
Colon congestion
⇓ Pelvic congestion
4. Thyrotropic: insufficient TSH-T4 response: abundant, thick mucous 5. Immune: Hyperimmunity 6. Emunctories: a. Exocrine pancreas i. Insufficient: abundant, thick, inspissated mucous ii. Hyperfunctioning: abundant, fluid mucous easy to expectorate b. Spleen and Liver: oversolicited, overtaxed, and congested c. Intestines: congested
Mechanisms Hypersecretory response with mucous that is excessive, inspissated, or both.
Result Expiratory, spasmodic wet cough.
History and BoF findings During acute bronchitis, typical symptoms of an irritable, spasmodic cough, with or without fever, of 10 or less days’ duration will be present. In a patient with known history of recurrent seasonal bronchitis, evaluate the precritical terrain in the preceding season to institute prophylaxis. Some
possible correlations between precritical symptoms and Biology of Functions are presented in Table 19.1.
Physical exam and BoF findings During presentation with acute wet bronchitis, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 19.2).
Treatment During acute bronchitis, antibiotics should be avoided unless proven bacterial etiology in a fragilized patient. The general emphasis of treatment is listed in Table 19.3 in columns from left to right. The general approach is three-fold: 1. Symptomatic, localized to bronchi (Tables 19.3 and 19.7) 2. Neuroendocrine, in following order of emphasis (Table 19.4): a. Reduce Para and Alpha and reinstall beta sequencing b. Support global adrenal function, especially cortisol c. Regulate thyrotropic activity d. Oligoelements (discussed later) 3. Drainage (Table 19.5), in following order of emphasis: a. Pancreas-sparing diet b. Pancreato-Pulmonary axis c. Hepato-Splenic d. Intestines e. Skin (as indicated)
Acute bronchitis, wet cough Chapter | 19 147
TABLE 19.2 Critical terrain signs and Biology of Functions correlations. Area
Finding
Terrain
BoF
Bronchus
Spasmodic cough: expiratory, wet
Para ≫ Alpha
↑/↓ LMI
Beta delayed
↓ PMI
Chvostek
Spasmophilia
↑/↓ LMI + ↓ PMI
Brisk DTR, Clonus, Eyelid flutter on Glabella tap
⇑ TRH
⇑: Thyroid relaunching, Thyroid relaunching corr., HypothalamoMetabolic, TRH/TSH
Para
Moist, warm skin; constricted baseline pupil; iris rosette, abdominal bloating, sweating, increase salivation, lacrimation
Hyper Para
Thyro
Cold sensitivity (T3), heat intolerance (T4), weight loss, pruritis
Elevated peripheral thyroid activity
⇑ Thyroid, ⇑/nl Thyroid yield
Immune
Suprasternal notch: Tender on palpation
Thymus congested
⇑/Normal: IL-1, ↓ Genito-thyroid, ↑Evoked histamine
Pancreas
Tender, above umbilicus
Congestion: general
N/A
Tender, right of umbilicus
Over-solicitation: exocrine
⇑/⇓ Somatostatin
Tender, left of umbilicus
Over-solicitation: exocrine
N/A
Tender, superior-medial
Vascular hepatic congestion
⇑/⇓ LMI
Tender, inferior-lateral
Metabolic hepatic congestion
⇑/⇓ LMI
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
⇓: Pelvic congestion
Neuro
Liver
Colon
Key: DTR: Deep tendon reflex; LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
TABLE 19.3 Medicinal plants with polyvalent symptomatic actions. Plant
Antispasm
Agrimonia eupatoria
•
Decongestant/ pulm. drainer
Anti-inflam.
Anti-Allergic
Anti-infect.
•
•
•
•c
Arctium lappa Cupressus sempervirensa
•
Eucalyptus ssp.a
•
•
•
•
•
•
•
•
•
• •
•
Matricaria recuctita Inula helenium Plantago major Malva sylvestris Viola tricolor a
•
•
•
•
•
•
•
•
•
•
•
•
•
c
•
c
•
b
•c
•
Can be diffused or nebulized as an essential oil. Parasympathomimetic: use at regulating doses in wet, hyper-para bronchitis. Indirect decongestant.
b
Emollients
•
Glycyrrhiza glabra Lavandula angustifoliaa
Mucolytic/ expectorant
•
•
148 SECTION | C Assessment and treatment of common disorders
TABLE 19.4 Medicinal plants for neuroendocrine regulation. Axis
Primary
Other
⇓: Para > Alpha
Thymus vulgaris EO, Lavandula angustifolia EO
Matricaria recuctita MT
⇑: Beta
Satureja montana EO
Cinnamomum zeylanicum EO
Relaunch Pituitary
Inula helenicum MT
Rhodiola rosea MT, Quercus pedunculata GM
⇓: TRH
Fabiana imbricata MT
Leonurus cardiaca MT
⇑: Adrenal cortex
Ribes nigrum GM, Quercus pedunculata GM
Satureja montana EO, Eleutherococcus senticosus MT
Key: EO: Essential oil, GM: Gemmomacerate, MT: mother tincture.
TABLE 19.5 Medicinal plants for drainage. Plant
Pancr.-Pulm
Agrimonia eupatoria Plantago major
Liver
Intestines
•
•
•
•
•
•
•
•
Ceanothus americanus
Hepato-Splenic
Skin
•
Viola tricolor
•
Key: Pancr.-Pulm: Pancreatic-Pulmonary axis.
Exemplary prescriptions Based on an Endobiogenic approach to wet bronchitis, a number of prescriptions can be derived. 1. Neuroendocrine: 3–4 mL three times per day 10– 14 days (Table 19.6): Inula helenium MT 30 mL, Fabiana imbricata MT 30 mL, Ribes nigrum GM 60 mL, Lavandula angustifolia EO 1.5 mL, Satureja montana EO 1 mL 2. Drainage: 3 mL three times per day for 10 days (Table 19.7): Agrimonia eupatoria MT 60 mL, Plantago major MT 30 mL, Arctium lappa MT 30 mL, Eucalyptus smithii EO 2 mL 3. Topical antispasmodic: Apply up to every hour for relief of cough:
Eucalyptus spp. EO 8 drops, Lavandula angustifolia EO 4 drops, Cupressus sempervirens EO 3 drops + 1 TBSP carrier oil; Instructions: (a) Mix carrier oil and EOs in glass bowl, (b) Apply with friction rub in circular and up/down motions for 3–4 min, (c) Cover chest with a shirt or blanket, then heated pad or towel; Alternative: Diffuse undiluted essential oils within 2 feet (0.6 m). 4. Oligoelements: (a) Spasmodic Cough: Magnesium oligo: 1–2 droppers every 4 h for first three days; (b) Inflammation: Selenium: 1–2 droppers every 4 h for first three days 5. Diet: Pancreas sparing, favor root vegetables: turnip, black radish, yams, and, juices of carrot, quince, chervil, cabbage, lettuce, mulberry, apple, and turnip.
TABLE 19.6 Neuroendocrine-infection prescription. Herb
Amount and form
Replacements and alternatives
Inula helenium
30 mL MT
Rhodiola rosea MT 15 mL + Quercus pedunculata GM 15 mL
Fabiana imbricata
30 mL MT
Leonurus cardiaca MT, Lycopus europaeus MT
Ribes nigrum
60 mL GM
Quercus pedunculata GM, Glycyrrhiza glabra MT
Lavandula angustifolia
1.5 mL EO
Eucalyptus ssp. EO 1.5 mL
Satureja montana
1 mL EO
Thymus vulgaris EO 0.5 mL + Cinnamomum zeylanicum EO 0.5 mL
Acute bronchitis, wet cough Chapter | 19 149
TABLE 19.7 Drainage prescription. Herb
Amount and form
Replacements and Alternatives
Agrimonia eupatoria
60 mL MT
Arctium lappa MT 30 mL + Plantago major MT 30 mL
Plantago major
30 mL MT
Agrimonia eupatoria MT 30 mL
Arctium lappa
30 mL MT
Viola tricolor MT 15 mL, Agrimonia eupatoria MT 15 mL
Eucalyptus smithii
2 mL EO
Eucalyptus globulus (unrectified) EO 2 mL
Chapter 20
Burping (eructation), borborygmus, flatus Summary Essence: Excessive intake or production, or, delayed evaluation of gasses related to food consumption, related to hyper parasympathetic gastrointestinal activity.
Treatment goals Varies by cause.
Sample treatment Cf. Treatment and Tables 20.1 and 20.2.
Terrain in detail Precritical terrain 1. ANS: Vagotonia or hyper parasympathetic state (primary or reactionary) 2. Gastrointestinal a. Insufficient digestive juices b. Dysbiosis c. Delayed transit d. Constipation
Agent Eating food is the provoking event, especially with the following qualities 1. Psychological: inattentiveness during eating 2. Mastication: insufficient before swallowing 3. Food a. Rapid consumption b. Difficult to digest: unfermented dairy, gluten, fried, fatty, etc.
Critical terrain, mechanisms, results The nature of the origin and evaluation of the gas determines the terrain: Eructation: Burping: air evacuated from stomach through the mouth. It is typically due to excess consumption of air during the swallowing process The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00020-2 © 2020 Elsevier Inc. All rights reserved.
1. ANS: Hyperparasympathetic GI tone resulting in excessive swallowing of air (>500 mL of air per meal) Borborygmus: Intestinal gurgling due to presence of air (or fluids) 1. ANS: Hyper-parasympathetic GI tone due to insufficient digestive juices Flatus: Gas produced during digestion, evacuated from rectum 1. ANS: Reactive hyper alpha state to precritical hyperpara GI tone resulting in prolonged exposure of due to insufficient digestive juices 2. Enteric flora: dysbiosis with overconsumption of nutrients a. Nonodiferous: carbohydrate-consuming commensal flora b. Odiferous (sulfurous): protein-consuming commensal flora
Treatment The approach to treating these disorders depends on the symptoms and its origins. The general approach is as follows: 1. Symptomatic (Table 20.1) a. Upper GI: oral and inhaled essential oils work most quickly b. Lower GI: inhaled and topical essential oils work most quickly 2. Chronic a. Regulate parasympathetic tone b. Lifestyle modification i. Mindful eating: focus on mastication in a calm environment ii. No television iii. Nonsyncopated, instrumental music or no music c. Dietary modification i. Easy to digest foods ii. Soak grains, meats, etc. iii. Start meal with sour or bitter foods to stimulate digestive juices 151
152 SECTION | C Assessment and treatment of common disorders
TABLE 20.1 Treatment of eructation, borborygmus, and flatus. Location of air
Clinical
Medicinal plants
Best galenic form
Route
Stomach
Eructation
Achillea millefolium
Tisane, oral
Tisanea
Rosmarinus officinalis
EO, inhalation
EO inhalationb > topical
Mentha piperita
EO, tisane
Tisanea, EO inhalationb > topical
Mentha piperita
EO, tisane
Tisanea, EO Topicalc > inhalationb
Lavandula angustifolia
EO
Origanum vulgare
EO, tisane
Thymus vulgaris
EO, tisane
Achillea millefolium
Tisane
Carum carvi
EO
Mentha piperita
EO, tisane
Rosmarinus officinalis
EO
Intestines
Rectum
Borborygmus
Flatus
Tisanea: Oral, Rectald EO inhalationb or topicalc, Rectald
a
Tisane: 3–5 min steep, ½ tsp per 200 mL water, use less if feeling distended; avoid Mentha piperita with known gastric reflux. EO inhalation: 2–3 min. EO topical: should be diluted; works within 5–10 min with friction rub or heat. d Rectal: Dilute; NB: DO NOT USE Mentha piperita in rectal application > 1% dilution. b c
TABLE 20.2 Dysbiosis prescription for flatus. Plant
Amount
Alternatives
Juglans regia GM, MT
60 mL
Plantago major MT
Agrimonia eupatoria MT
30 mL
Plantago major MT, Juglans regia GM, MT
Achillea millefolium MT
30 mL
Avena sativa MT 15 mL + Carduus marianus MT 15 mL
Origanum vulgaris EO
3 mL
Thymus vulgaris EO 2 mL + Cinnamomum zeylanicum EO 1 mL
Exemplary prescriptions Based on an Endobiogenic approach, a number of prescriptions can be derived for these disorders.
Eructation 1. Medicinal plants a. Acute: Inhale peppermint essential oil for 3–5 min b. Chronic: Tisane: 1 tsp of mixture of Achillea millefolium, Mentha piperita steeped 6–8 min in 150 mL water, consumes 15 min before start of meal 2. Lifestyle: a. Take smaller bites b. Eat in a calm environment, avoid talking or watching TV
Borborygmus 1. Medicinal plants a. Acute: Inhale peppermint essential oil for 3–5 min b. Chronic: Tisane: 1 tsp of mixture of Origanum vulgare and Thymus vulgaris steeped 4–8 min in 200 mL
water, consume slowly allowing taste to register in mouth before swallowing during and/or after meal 2. Diet: avoid hard-to-digest foods (cf. earlier)
Flatus 1. Medicinal plants a. Acute: Topical application of Mentha piperita 3 drops, Carum carvi 2 drop in 1 tsp carrier oil, mix, apply with friction to affected area of small intestines (peri-umbilical) and intestines b. Chronic: Tisane or tincture of Juglans regia GM or MT 60 mL, Agrimonia eupatoria MT 30 mL, Achillea millefolium MT 30 mL + Origanum vulgare EO 3 mL, DOSE: 4 mL before dinner and 4 mL at bedtime (Table 20.2) 2. Diet a. Nonodiferous: avoid simple carbohydrates, soak grains before cooking or avoid all together b. Odiferous: avoid legumes, avoid red meat, or, soak for 12–24 h in acidic medium before consuming
Chapter 21
Constipation, normal transit Summary Essence: Painful defecation ≥ 3 times per week due to insufficient moisture of the stool often with biliary stasis. Terrain: Unfavorable stool composition due to one or more: (a) Diet: Insufficient fiber and/or water intake, (b) Dysbiosis, (c) Biliary stasis (sphincter of Oddi spasmophilia): Para insufficiency, excess alpha, beta blocked or delayed.
Treatment goals Symptomatic: Soluble fiber, lubricant, osmotic/stimulant laxatives Terrain: ●
● ●
ANS: ⇓ Alpha, support Para, ⇑ Beta--resolve spasmophilia on gallbladder DRAIN: 1°Hepato-biliary-Exocrine Pancreatic unit GI: Correct dysbiosis as indicated
Sample treatment 1. Diet: Hydration, soluble fiber, fruit, fermented foods, probiotics, oils 2. ANS-Emunctory-dysbiosis: Carduus marianus MT 160 mL, Cynara scolymus MT 160 mL, Raphanus niger MT 160 mL, Artemisia dracunculus EO 6 mL, Satureja montana EO 4 mL: 3 mL three times per day before meals × 3–4 months 3. Lifestyle: Exercise, sleep optimization (before midnight, 6.5–8 h total, excluding night waking and time in bed)
Terrain in detail
iii. Beta: blocked or insufficient for excretion of bile b. Gonadotropic: i. Estrogen excess: diminishes biliary secretion ii. Progesterone excess: favors biliary stasis 2. Intestinal: Dysbiosis (cf. Theory of Endobiogeny, Volume 2, Chapter 6: Disorders of dysbiosis) 3. Emunctory: Hepatobiliary-Exocrine pancreas dysregulation delaying biliary excretion due to exocrine pancreatic insufficiency
Agent The quality of food or iatrogenic causes challenges the competency of the gallbladder: ● ●
●
●
Insufficient intake of sufficient soluble fiber Insufficient water intake for Endobiogenic equilibrium (neuroendocrine fluid management) Overconsumption of fatty, fried food diet (oversolicits congested gallbladder) Contraceptive medication (estro-progestive impairs biliary function)
Critical terrain Parasympathetic tone is solicited to compensate for the dietary or iatrogenic aggression on the gallbladder. The reactive nature of alpha exceeds that of para, and expressed specifically at the level of the gallbladder. 1. ANS hyperfunctioning: Spasmophilia of sphincter of Oddi ● Hyper-Alpha > Para, Beta blocked, or delayed on gallbladder
Precritical terrain
Mechanisms
Bile increases intestinal motricity and has antimicrobial effects. In the precritical terrain, there is an underlying dysfunction of biliary dynamics:
Insufficient movement of stool from insufficient bile + insufficient roughage to stimulate optimal moisture content of stool
1. Gallbladder: insufficient excretion: a. ANS: dysfunctional relationships impair choleresis i. Para insufficiency: diminished rate of bile production ii. Alpha excess: tonic closure of sphincter of Oddi
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00021-4 © 2020 Elsevier Inc. All rights reserved.
Result Normal transit constipation: pain defecation, stool dry or hardened, normal defecation frequency per week
153
154 SECTION | C Assessment and treatment of common disorders
History and BoF findings
●
The precritical terrain can be evaluated in order to apply a prophylactic treatment, especially with intermittent normal transit constipation. Some possible correlations between precritical and/or critical symptoms and Biology of Functions are presented in Table 21.1.
●
●
●
Stool not palpable in distal colon Evaluate ANS loco-regional (digestive) and global dysfunction Evaluate gallbladder points: palpable on abdomen, right leg and feet Evaluate hepato-pancreatic blockage
Treatment
Physical exam and BoF findings During presentation with constipation, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 21.2).
In the treatment of normal transit constipation, there are numerous symptomatic treatments, focused primarily on evacuating the stool already formed and difficult to pass. They can be stratification based on severity of symptoms (Table 21.3).
TABLE 21.1 Precritical and critical terrain symptoms and biology of functions correlations. Area
Finding
Terrain
BoF
Stool frequency
3 or more per week
cf. above
Defecation quality
Difficult to pass, painful to pass, straining
Insufficient bile production, excretion, and timing ANS imbalance, ⇑ Alpha > Para, blocked Beta
Intestines
Post-prandial bloating, headache, joint pain, etc.; flatulence
Dysbiosis
ANS
Post-prandial fatigue
Hyperparasympathetic digestive
Spasmophilia
Spasmophilia
↑/↓ LMI + ↓ PMI
Gonadotropic
PMS: Estro-progestive excess: breast swelling, breast tenderness, Menstruation: multiple days with clotting
Estro-progestive excess
↑ Estrogen indexes ↓ Progesterone
Medications
Oral estro-progestin-type contraceptive pills
Iatrogenic estro-progestive excess
↑ Estrogen indexes ↓ Progesterone
Key: LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
TABLE 21.2 Critical terrain signs and Biology of Functions correlations. Area
Finding
Terrain
BoF
Colon
Stool is nonpalpable in distal colon
Neuro
Chvostek
Spasmophilia
⇑ LMI, ⇓ PMI
Brisk DTR, Clonus, Eyelid flutter on Glabella tap
⇑ TRH
⇑: Thyroid relaunching, Thyroid relaunching corrected, Hypothalamo-Metabolic, TRH/TSH
Gallbladder
Tender on deep palpation: gallbladder sphincter of Oddi
Sphincter dysfunction
N/A
Liver
Tender, superior-medial
Vascular hepatic congestion
⇑/⇓ LMI
Tender, inferior-lateral
Metabolic hepatic congestion
⇑/⇓ LMI
Tender, above umbilicus
Congestion: general
N/A
Tender, right of umbilicus
Over-solicitation: exocrine
⇑/⇓ Somatostatin
Tender, left of umbilicus
Over-solicitation: exocrine
N/A
Tender: Ascending, Transverse colon
FSH, LH over-solicitation
⇓: FSH, LH
Pancreas
Colon
Key: DTR: Deep tendon reflex; LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
Constipation, normal transit Chapter | 21 155
TABLE 21.3 Overview of symptomatic treatment based on severity of symptoms. Priority
Symptoms
Treatment
Rational
Urgent
Feeling of toxicity, aggravation of other conditions
Laxative
Stimulate contraction of colon
Hyperosmotic
Hydrate stool
Complications, e.g., anal fissure
Cicatrizant
Heals wound
Timely
Chronic, discomforting but tolerable
Monodiet, Hydration
Acutely increase fiber and fluid intake
Chronic
Intermittent or frequent
Diet Lifestyle Medicinal plants
Regulate the Endobiogenic terrain
Based on an Endobiogenic reflection, an elaboration of this approach to treatment is as follows: 1) Urgent a. Stimulant laxatives i. Short-term relief from constipation, can cause bloating, gas, spasmophilia. b. Glycerin suppository i. Hyperosmotic lubricant, for occasional use in all ages, up to 3 times per week c. Treatment of anal fissures: i. Ingredients: 1 tsp peanut oil, diatomaceous earth to make paste 1. Burning pain: add 1 pinch Sodium bicarbonate 2. Infection: add 1 drop Lavandula angustifolia EO ii. Instructions: Anus: clean, pat dry, apply 2–3 times per day after defecation 2) Timely a. Hydration and hyperosmotics: i. Water: Alkaline, Artesian well water: 1–2 L per day ii. Fruit juices, 4–12 oz (120–350 mL) per day in divided doses: 1. Spring: white grape, celery 2. Summer: watermelon 3. Autumn: prune, pear, apple (unfiltered) 4. Winter: grapefruit iii. Honey: hyperosmotic, demulcent: 1 tbsp AM and before bed followed by glass of water with lemon b. Lubricants: Oils i. Options: Olive: Lubricating, choleretic; Sesame: Lubricating, use in anxious or hyperactive patients; Borage: Lubricating: use in obese or anxious patients
ii. Dosing: 0–11 months: ¼ tsp, 12–23 months: ½ tsp, 2–4 years: 1 tsp, 5–7 years: ½ tbsp, 8 years and older: 1 tbsp iii. Frequency: AM before breakfast and before bed, followed by 250 mL of spring water if it does not interfere with sleep and urinary habits. c. Monodiets (cf. Chapter 44: Endobiogenic diets and nutrition) i. Grape cure ii. Apple-sardine iii. Fruit-Vegetable-Brown rice diet 3) Chronic a. Diet i. High-fiber foods (Table 21.4) ii. Fermented foods (for dysbiosis) b. Lifestyle: regulates autonomic tone and colon motricity i. Movement: exercise, yoga, meditative movement ii. Sleep: Restorative, before midnight, 6.5–8 h per night c. Long-term regulation of stool quality (Table 21.5) d. Drainage (Table 21.6) e. Regulation of dysbiosis (Table 21.7)
Exemplary prescriptions Based on an Endobiogenic approach to normal transit constipation, a number of prescriptions can be derived. 1. Neuro-drainage-dysbiosis, Adults: 4 mL three times per day before meals Agrimonia eupatoria MT 120 mL, Plantago major MT 120 mL, Mentha piperita EO 2 mL, Artemisia dracunculus EO 2 mL, Origanum vulgare EO 1 mL 2. Neuro-drainage-dysbiosis, Children: 1–3 mL three times per day before meals Rosmarinus officinalis GM 60 mL, Juglans regia GM 60 mL, Mentha piperita EO 0.5 mL (Optional) In patients with chronic issues of constipation with poor eating habits and a sedentary lifestyle, the following transformational approach to wellness can be offered: Week 1: Symptomatic relief and starting a new lifestyle 1) Fruit-Vegetable-Brown rice diet×6 days 2) Olive oil and 6 glasses of water per day 3) AM: 1 tbsp olive oil+1 glass water 15 min before meal 4) 2 glasses water between breakfast and dinner Week 2: High-fiber foods: 10 g per day Week 3: Increasing fiber: 20–30 g per day ● ● ● ●
1 cup Puréed sweet potatoes 2–3 per week (6g fiber) 1 cup hummus 2–3 times per week (6g fiber) Buckwheat, 1 cup once 2–3 times week (4g fiber) High-fiber flax bread (10 g fiber per square)
TABLE 21.4 High-fiber foods by category. Category
Food
Serving
Fiber (g)
Grains
Bran Cereal
1 cup
20
Barley
1 cup
14
Bulgur
1 cup
8
Freekeh
1 cup
7
Flax seeds*
3 tsp
7
Quinoa*
1 cup
6.5
Whole wheat spaghetti
1 cup
6
Buckwheat*
1 cup
4.5
Groats (Kasha)*
1 cup
4.5
Ezekiel bread
2 slices
4
Oats, raw*
1 cup
4
Corn*
1 cup
4
Brown rice*
1 cup
3.5
Lentils*
1 cup
15
Black beans*
1 cup
15
Pinto beans*
1 cup
15
Kidney beans*
1 cup
13
Lima beans*
1 cup
13
Navy beans*
1 cup
11
Chick peas*
1 cup
6
Split peas*
1 cup
16
Green peas*
1 cup
9
Kale*
1 cup
7
Yam*
1 cup
6
Broccoli*
1 cup
4
Spinach, cooked*
1 cup
4
Pistachios*
4 oz
12
Hazelnuts*
4 oz
9
Pumpkin*
4 oz
4
Almonds*
4 oz
2.5
Grapefruit*
1
14
Avocado*
1, med
12
Raspberries*
1 cup
8
Pear*
1
5
Apple*
1
5
Banana*
1
4
Blueberry*
1
4
Orange*
1
4
Figs, dry*
2
4
Dates*
4
3
Legumes
Vegetables
Nuts
Fruits
Key: *=gluten-free, Bold=high in protein.
Constipation, normal transit Chapter | 21 157
TABLE 21.5 Medicinal plants with polyvalent symptomatic actions. Plant
Demulcents
Althea officinalis
•
Laxatives
Bulking
Balance microbiota
Artemisia dracunculus
•
Glycyrrhiza glabra
•
Eugenia caryophyllata
•
Trigonella foenum
•
•
Mentha piperita
•
Plantago ovata (Psyillium)
•
•
•
Satureja montana
•
Taraxacum officinale
•
TABLE 21.6 Medicinal plants for ANS regulation and drainage. Plant
HBExP
Agrimonia eupatoria
•
Plantago major
•
Arctium lappa
•
HB
ExP
ANS
Other properties a
Vagolytic
Immunomodulation
Mentha piperita
•
•
Sympatholytic
Antiflatulent, regulates dysbiosis
Fumaria officinalis
•
•
Digestive spasmolytic
Acts on sphincter of Oddi,
Juglans regia
•
•
Rosmarinus officinalis
•
Raphanus niger
•
Regulates dysbiosis, digestive astringent, cicatrizing Digestive spasmolytic
Eupeptic, hepatoprotector, intestinal antispasmodic Regulates dysbiosis, cicatrizing
Key: ANS: Autonomic nervous system, ExP: Exocrine pancreas; HB: Hepatobiliary; HBExP: Hepatobioliary-Exocrine Pancreatic unit. a
Indirect by improving digestive function.
TABLE 21.7 Polyvalent medicinal plants for dysbiosis. Plant
GI
ANS
Mentha piperita
Antiflatulent, digestive, eupeptic, cholagogue, choleretic, exocrine pancreatic stimulant (lipase, amylase), antinausea,
Mild: sympatholytic, parasympathomimetic
Origanum vulgare
Digestive antispasmodic
Sympatholytic, parasympathomimetic
Artemisia dracunculus
Digestive antispasmodic, aperitif, carminative, antinausea, drainage: splanchnic bed, pancreas, pelvis
Vagolytic
Syzygium aromaticum
Eupeptic, digestive, carminative, choleretic
158 SECTION | C Assessment and treatment of common disorders
●
Smoothie for breakfast (17 g fiber): a. Protein powder, 1 scoop b. ½ Avocado (6 g fiber) c. ½ cup frozen raspberries (4 g fiber) d. 1 cup kale (7 g fiber) e. Dilute with unsweetened vanilla almond milk to taste
Week 4: Expanding diet 1) 1 serving of fermented food four times per week Week 5: Movement 1) Standing up every 55 min and walking around for 5 min 2) 20 min of brisk walking 4 times per week with a friend
Chapter 22
Constipation, slow transit Summary Essence: A hyper alpha-sympathetic state impairing intestinal motricity. Terrain (1) ANS overactivity with Alpha ≫ Para at the level of intestinal motor complex resulting in (2) slowed intestinal peristalsis, thus reduce frequency of defecation resulting in (3) Constipation
Treatment goals Symptomatic: Enemas, Insoluble fiber Terrain: ●
● ● ●
ANS: ⇓ Alpha, adapt Para to re-establish a proper Para-Alpha relationship, ⇑ Beta (to resolve spasmophilia as indicated) ID: Correct dysbiosis as indicated GI: Supper proper choleresis DRAIN: Hepato-biliary-exocrine pancreatic complex
Sample treatment Adult with yearly prespring constipation with adrenal fatigue pattern (cf. end of chapter for pediatric treatment) 1. Neuroendocrine: 4 mL AM, 4 mL at 4 pm January 18 to March 18 (Table 22.7) Passiflora incarnata MT 80 mL, Ribes nigrum GM 80 mL, Quercus pedunculata GM 80 mL + Satureja montana EO 3 mL 2. Drainage: 3 mL before lunch, 4 mL before dinner (Table 22.8) Raphanus niger MT 60 mL, Carduus marianus MT 80 mL, Agrimonia eupatoria MT 80 mL + Mentha piperita 2.5 mL, Rosmarinus officinalis EO 1 mL 3. Oligoelements: Magnesium chelate 250 mg AM, 250 mL before bed 4. Diet: 4 cups leafy green vegetables per day, cooked or in smoothie, 1 serving of root vegetable per day, fruit or fruit smoothie as desired 5. Lifestyle: If chronic, especially since childhood: Behavioral counseling, biofeedback The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00022-6 © 2020 Elsevier Inc. All rights reserved.
Terrain in detail Precritical terrain The primary level of dysfunction is ANS hyperfunctioning at the level of the gastrointestinal tract. This impairs production and excretion of digestive juices, sequencing of actions, and adaptability of motricity. There are numerous permutations of dysfunction. The most impactful are: 1. ANS: overfunctioning alpha and para, with normal or compensated beta at the level of the intestinal tract 2. Emunctory stress: individually or in some combination a. Liver metabolic b. Gallbladder choleresis > cholagogy c. Exocrine pancreas 3. Fragilized regulation of intestinal microbiotic, viz. intermittent a. Flatulence b. Bloating c. Post-prandial fatigue 4. Endocrine: may be overfunctioning
Agent The aggressors are numerous but typically include one or more of the following: 1. Adaptative stressors: major and/or persistent a. Physical trauma b. Grand phase transitions: post-natal, growth spurt, adolescence, gonadopause, etc. c. Seasonal and circannual adaptation 2. Adaptive or adaptative stress: Emotional and/or mental 3. Adaptive or adaptative requirement for nutrients a. Small intestines: Hydrolysis b. Large intestines: Absorption (cf. Appendix 1: Essential physical exam images and The Theory of Endobiogeny, Volume 3, Chapter 10) 4. Insufficient intake of insoluble fiber
Critical terrain 1. ANS: Hyperfunctioning Alpha ≫ Para; Beta: blocked or delayed (spasmophilia)
159
160 SECTION | C Assessment and treatment of common disorders
Mechanisms 1. Delayed motricity of intestines at the level of motor complexes and musculature 2. Impaired excretion of digestive juices, further delaying motricity to allow time for digestion
Result Constipation: prolonged transit time with excess absorption of moisture from stool: strained defecation < 3 per week
History and BoF findings During acute constipation, the patient will have had 2 or less stools in 1 week, with no sense of urgency. There will be increased strain during defecation, with complaint of lower abdominal fullness, and sometimes, a feeling of “toxicity.” Some possible correlations between precritical symptoms and Biology of Functions are presented in Table 22.1.
Physical exam and BoF findings During presentation with slow transit constipation, there are four levels of evaluation to be performed in the following order (Table 22.2): 1. ANS hyperfunctioning: local, regional, or global.
TABLE 22.1 Precritical terrain symptoms and Biology of Functions correlations. Area
Finding
Terrain
Stool Frequency
Less than 3 bowel movements per week
cf. above
Defecation quality
Difficult to pass with straining
cf. above
Abdomen
Abdominal fullness, colo-rectal fullness
Large or hardened stool distending colon
ANS
Alpha: anxious, emotionally sensitive; History: GERD, gastritis, constipation, insomnia Para: Introverted, shy, timid, increased salivation, lacrimation, sweating
⇑ Alpha
BoF
↑/↓ LMI, ↓ PMI
⇑ Para
Key: LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
2. Emunctory digestive gland dysfunction (cf. Appendix 1: Essential physical exam images) 3. Colon tenderness: indicative of central endocrine dysfunction (cf. Appendix 1: Essential physical exam images) 4. Endocrine dysfunction: a. Adaptative or adaptability: cortico-thyrotropic response to alpha-sympathetic b. Dysfunctional response by individual or coupled axes (The Theory of Endobiogeny, Volume 1, Chapter 10) according to the adaptive needs of specific types of tissues and the associated endocrine axis For evaluations 1–3, exam finding with some possible Biology of Functions correlations (Table 22.2) is presented. For the fourth level, refer to Section 2: Essentials of history, exam and Biology of Functions and The Theory of Endobiogeny, Volume 2, chapters 1,2, 10, and, Volume 3, chapters 3 and 6).
Treatment In the treatment of normal transit constipation, there are numerous symptomatic treatments, focused primarily on evacuating the stool already formed and difficult to pass. They can be stratification based on severity of symptoms (Table 22.3). Based on an Endobiogenic reflection, an elaboration of this approach to treatment is as follows: 1) Urgent a. Stimulant laxatives i. Short-term relief from constipation, can cause bloating, gas, spasmophilia. b. Glycerin suppository i. Hyperosmotic lubricant, for occasional use in all ages, up to 3 times per week c. Treatment of anal fissures: i. Ingredients: 1 tsp peanut oil, diatomaceous earth to make paste 1. Burning pain: add 1 pinch Sodium bicarbonate 2. Infection: add 1 drop Lavandula angustifolia EO ii. Instructions: Anus: clean, pat dry, apply 2–3 times per day after defecation 2) Timely a. Hydration: i. Lemon juice treatment (see The Theory of Endobiogeny Volume 3, Chapter 10) ii. Insoluble fiber: fruit and vegetable smoothies (with skin pulp): 8–16 oz (240–480 mL) per day in divided doses: b. Monodiets (cf. Chapter 44: Endobiogenic diets and nutrition) i. Grape cure ii. Apple-sardine iii. Fruit-Vegetable-Brown rice diet
Constipation, slow transit Chapter | 22 161
TABLE 22.2 Critical terrain signs and Biology of Functions correlations. Area
Finding
Terrain
BoF
ANS local
Mouth: Saliva stringy ± dilated opening of canal of Stensen; Colon: Palpable stool in distal colon; abdominal distension
Alpha ≫ Para
⇑/⇓ LMI
ANS regional
Pelvic congestion: Feet cooler than hands
Alpha ≫ Para
⇑/⇓ LMI, ↓Pelvic congestion
ANS global
Skin: Pale, cool, moist; Eyes: spiculated rosette; Lips: dry; Palate: pale; Hands or feet: cool ± moist
Alpha ≫ Para
↑ Thyroid relaunching, ↑ Thyroid relaunching corrected
Liver
Tender, superior-medial Tender, inferior-lateral
Vascular hepatic congestion Metabolic hepatic congestion
⇑/⇓ LMI ⇑/⇓ LMI
Gallbladder
Tender: Murphy’s point, left superior tibia
Congested
Pancreas
Tender, above umbilicus Tender, right of umbilicus Tender, left of umbilicus
Congestion: general Over-solicitation: exocrine Over-solicitation: exocrine
N/A ⇑/⇓ Somatostatin N/A
Colon
Tender: reflection points
Colon over-solicited
Varies
Key: LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
TABLE 22.3 Overview of symptomatic treatment based on severity of symptoms. Priority
Symptoms
Treatment
Rational
Urgent
Feeling of toxicity, aggravation of other conditions Complications, e.g., anal fissure
Laxative Hyperosmotic Cicatrizant
Stimulate contraction of colon Hydrate stool Heals wound
Timely
Chronic, discomforting but tolerable
Monodiet, Hydration
Acutely increase fiber and fluid intake
Chronic
Intermittent or frequent
Diet Lifestyle Medicinal plants
Regulate the Endobiogenic terrain
3) Chronic a. Regulate ANS (Table 22.4) b. Regulate Endocrine terrain (varies) c. Diet i. High-insoluble fiber foods 1. Fruits: with skin and pulp, raw or as compote 2. Vegetables: root (sweet potatoes, yams, carrots, parsnips, etc.), leafy green raw or lightly steamed ii. Fermented foods (for dysbiosis) d. Long-term regulation of stool quality (cf. Chapter 21, Table 21.5) e. Drainage (cf. Chapter 21, Table 21.6) f. Regulation of dysbiosis (cf. Chapter 21, Table 21.7) g. Lifestyle: regulate autonomic tone and colon motricity
i. Movement: biofeedback, exercise, yoga, meditative movement ii. Sleep: Restorative, before midnight, 6.5–8 h per night
Exemplary prescriptions Based on an Endobiogenic approach to slow transit constipation, a number of prescriptions can be derived. Two sets of exemplary prescription are presented, one each for child and adult. 5-year-old girl: Constipation, anger issues, insomnia 1. ANS: 2 mL, 3 times per day: AM, after school, before bed (Table 22.5) Tilia tomentosa GM 50 mL, Rosmarinus officinalis GM 10 mL
162 SECTION | C Assessment and treatment of common disorders
TABLE 22.4 Medicinal plants for ANS regulation. Plant
Alpha-lytic
Antihistamine GI
Matricaria recutita MT, EO
•
•
Rosmarinus officinalis EO
•
•
Citrus aurantium (Neroli) EO
•
Melissa officinalis MT
•
Origanum majorana (Marjoram) EO
•
Anthemis nobilis EO
•
Agrimonia eupatoria MT
•
Plantago major (Plantain)
•
Fumaria officinalis (Fumitory) EO
•
Para-mimetic
Beta-mimetic
•
Syzygium aromaticum (Clove) EO
•
Mentha piperita EO
•
Satureja montana (Savory)
•
Cinnamomum zeylanicum
•
Key: EO: Essential oil, GM: Gemmomacerate, MT: mother tincture.
TABLE 22.5 ANS prescription for children. Plant Tilia tomentosa GM 50 mL
Replacements and alternatives Ilex aquifolium GM, Crataegus oxyacantha GM
Rosmarinus officinalis GM 10 mL
TABLE 22.6 ANS-drainage prescription for children. Plant
Replacements and alternatives
Agrimonia eupatoria 40 g BH
Plantago major
Matricaria recutita 40 g BH
Rosmarinus officinalis
Mentha piperita 40 g BH
Fumaria officinalis, Matricaria recutita
2. ANS-Drainage: ½ tsp of mixture steeped 4–6 minutes in 120 mL water, drink three times per day in divided doses before meals (Table 22.6) Agrimonia eupatoria 40g BH, Avena sativa 40g BH, Mentha piperita 40g BH 3. Topical Essential oils: Apply to abdomen twice daily: AM and before bed in a centripetal motion from umbilicus, then in a “U” shape following the anatomical
progression of the colon from ileocecal valve to sigmoid colon. Perform each sequence three times before starting the next Origanum majorana EO 2 drops, Lavandula angustifolia EO 1 drop, Rosmarinus officinalis EO 1 drop in 2 tsp carrier oil. 4. Diet: Inulin fiber added to food or drink, Fruit compote for desert 5. Lifestyle: (a) If power struggle with parent over stooling: dyadic behavioral counseling; (b) General: Bodysensing and awareness skills to avoid with holding Adult with yearly prespring constipation with adrenal fatigue pattern 1. Neuroendocrine: 4 mL AM, 4 mL at 4 pm January 18 to March 18 (Table 22.7) Passiflora incarnata MT 80 mL, Ribes nigrum GM 80 mL, Quercus pedunculata GM 80 mL + Satureja montana EO 3 mL 2. Drainage: 3 mL before lunch, 4 mL before dinner Raphanus niger MT 60 mL, Carduus marianus MT 80 mL, Agrimonia eupatoria MT 80 mL + Mentha piperita 2.5 mL, Rosmarinus officinalis EO 1 mL 3. Oligoelements: Magnesium chelate 250 mg AM, 250 mL before bed 4. Diet: 4 cups leafy green vegetables per day, cooked or in smoothie, 1 serving of root vegetable per day, fruit or fruit smoothie as desired 5. Lifestyle: If chronic, especially since childhood: Behavioral counseling, biofeedback.
Constipation, slow transit Chapter | 22 163
TABLE 22.7 Neuroendocrine prescription for adults. Plant
Replacements and alternatives
TABLE 22.8 Drainage prescription for adults. Plant
Replacements and alternatives
Passiflora incarnata MT 80 mL
Matricaria recutita MT, Scutellaria latiflora MT
Raphanus niger MT 80 mL
Cynara scolymus MT 40 mL + Secale cereale GM 40 mL
Ribes nigrum GM 80 mL
Eleutherococcus senticosus MT
Carduus marianus GM 80 mL
Taraxacum officinale MT
Ribes nigrum GM + Rosa canina GM
Agrimonia eupatoria GM 80 mL
Plantago major MT
Quercus pedunculata GM 80 mL
Mentha piperita 2.5 mL EO
Carum carvi EO
Satureja montana 3 mL EO
Cinnamomum zeylanicum EO
Rosmarinus officinalis 1 mL EO
Chapter 23
Colitis, Crohn’s Illite clay 1 tbsp + 100 mL water + 5 mL of tincture: Lamium album MT 30 mL, Poterium sanguisorba MT Essence: Chronic inflammatory bowel disease of 30 mL, Malva sylvestris MT 30 mL, Hamamelis virginiana hypersympathetico-corticotropic response to aggression MT 30 mL + Lavandula angustifolia EO 2.5 mL and insufficient restorative gonadotropic capabilities, 2. ANS-cortico-gonado-thyrotropic: 6 mL three times resulting in ulceration of the gastrointestinal mucosa. per day until hemorrhagic stools have abated, then 4 mL Terrain: (1) Structural factor of initiation: (a) FSH three times per day until follow up (cf. Table 23.13): >> estrogens, and androgens > estrogens, (b) exocrine Salvia sclarea MT 80 mL, Lithospermum officinale MT pancreatic insufficiency with (c) compensatory hy- 80 mL, Fabiana imbricata MT 80 mL + Citrus reticulata per para state in vagotonic patient but (d) sympathetic EO 2 mL, Eucalyptus ssp. EO 2 mL, Syzygium aromaticum > parasympathetic with (e) exhausted parathyroid EO 0.5 mL (insufficient calcium for adaptation) resulting in (f) 3. Drainage: 6 mL three times per day until hemorrhagic fragilized intestinal mucosa, which in the face of agstools have abated, then 4 mL three times per day ungression one finds (2) Strong reactive Alpha with til follow up (Table 23.14): Agrimonia eupatoria MT (3) hypercortico-thyrotropic response ≫ gonado- 240 mL somatotropic expressed at the level of (5) Structuro- 4. Vitamin D: 10,000 IU in AM for 10 days functional disadaptation of intestines induces 5. Diet: High purine protein, pescatarian, low fat, low fiber (6) Crohn’s disease (Crohn’s colitis).
Summary
Treatment goals Symptomatic: Dual sympatholytic/parasympatholytics, anti-hemorrhagics, corticosteroids, biologic agents, antibiotics Terrain: ● ●
●
●
●
● ● ●
ANS: ⇓ Alpha, Para, ⇑ Beta (to resolve spasmophilia) CORTICO: Central: ⇓ ACTH, Peripheral: Support adrenal activity, GONADO: Central: ⇓ FSH, LH; Peripheral: Support tissular estrogens THYRO: Central: ⇓ TRH, TSH; Peripheral: Support parathyroid SOMATO: Central: Inhibit PL, relaunch GH; Peripheral: delay insulin DRAIN: 1°-Liver, 2°-Exocrine pancreas, 3°-Intestines DIET: high purine protein, low fat, low fiber LIFESTYLE: Calming activities
Terrain in detail Types of terrain In inflammatory bowel disease (IBD), we can speak of four types of terrain: (1) precritical, (2) critical, (3) suppressed critical and (4) remission. In IBD, precritical terrain refers to the terrain before the disorder expresses itself for the first time. The critical terrain is terrain of hemorrhagic colitis. Suppressed critical terrain is that in which hemorrhagic colitis is resolved because of suppressive or symptomatic therapy, but for which aspects of the critical terrain have not been fully resolved. The patient remains fragilized and at higher risk for relapse. Remission is the not critical terrain that the patient reverts to when they are asymptomatic and for which the majority of their elements of the critical terrain have resolved. The reason we do not refer to it as the precritical terrain is that it is in a sense a quiescent but permanently fragilized state due to the unresolved structural factor of initiation.
Sample treatment
Precritical terrain
1. Symptomatic: every 2–3 h until hemorrhagic stools have resolved (Table 23.12):
The precritical terrain of Crohn’s disease is particularly complex as it has two aspects. The first is the structural
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factor of initiation (SFI), a genetic predisposition to have a disadapted maintenance of a structural activity (cf. The Theory of Endobiogeny, Volume 1, Chapter 13). The second is the precritical terrain that arises to compensate for the SFI before the expression of disease. Structural factor of initiation: High demand for proteins at the level of the intestines with gonadotropic mismanagement of response 1. FSH ≫ Estrogens, both absolutely elevated 2. Androgens > Estrogens Precritical terrain: Compensation for protein demand 1. ANS: Vagotonic patient with spasmophilia a. Para: hyperfunctioning to relaunch exocrine pancreas for proteolytic enzymes to re-adapt protein absorption from diet b. Alpha: reactive to para to relaunch parathyroid and calcium availability; Alpha > Para favoring catabolism > anabolic para 2. Endocrine: a. Parasympathetic: exhausted, insufficient mobilization of calcium for adaptation of tissular metabolism for structural maintenance 3. Emunctory: a. Exocrine pancreatic insufficiency
Agent The aggressor in Crohn’s disease can be internal external, chronobiologic or unique in nature (cf. The Theory of Endobiogeny, volume 3, Chapter 11: Inflammatory bowel diseases): 1. Physical 2. Mental or emotional 3. Physiological 4. Metabolic 5. Change of season 6. Infection
Critical terrain The critical terrain is a sequential neuroendocrine general adaptation response, which is mismanaged centrally vs. peripherally as well as catabolic vs. anabolic axes 1. ANS: Sympathetic ≫ Parasympathetic, both absolutely elevated 2. Endocrine: a. Corticotropic hyperfunctioning: ACTH > Cortisol > Adrenal cortex b. Gonadotropic: FSH ≫ Estrogens > Androgens c. Thyrotropic: Hyperfunctioning: TRH, TSH, T4, T3 d. Somatotropic
i. PL ≫ GH ii. Hyperinsulinism 3. Emunctories: a. Exocrine pancreas: congested, insufficient b. Liver: oversolicited and congested c. Intestines: congested
Mechanisms The mechanisms relate to hyperfunctioning of the immune system (by cortico-thyrotropic factors) and inability to install wound healing (gonado-somatotropic factors): ● ●
● ●
T-helper1 hyperfunctioning Interleukin-2, tissues necrosis factor alpha, arachidonic acid, proteases, platelet-activating factor Free radicals Neutrophilia within crypts and mucosa.
Result 1. Chronic intestinal inflammation with mucosal ulceration forming crypts in the mucosal endothelium, muscularis layers and affecting the mesentery and lymph nodes. 2. Depth of lesions: all layers 3. Location of lesions: anywhere from mouth to anus; location in colon witnesses relative predominance of central endocrine factors: ● Ileocecum, Distal Sigmoid: ACTH ● Ascending and proximal transverse colon: FSH ● Mid- and distal transverse colon: LH ● Splenic portion of colon: TSH ● Hepatic portion of colon: TRH ● Mid-descending colon: PL ● Distal descending colon: GH 4. Hemorrhagic stools 5. Intestinal pain 6. Fever 7. Fistulas 8. Abscesses
History and BoF findings Symptoms related to the precritical terrain of Crohn’s disease are presented in Table 23.1. This includes symptoms before initial diagnosis as well as symptoms related to remission post-flare up.
Physical exam and BoF findings During presentation with acute Crohn’s colitis, the salient examination findings relate to tenderness of the affected areas of the gastrointestinal tract, as well as congestion of the liver, gallbladder, pancreas (exocrine and endocrine).
Colitis, Crohn’s Chapter | 23 167
TABLE 23.1 Precritical terrain symptoms in Crohn’s disease. Area
Finding
Terrain
Demographic
Pediatric: Boys > Girls Adult: Women > Men Industrialized countries, cooler climates
Strong structural FSH in androgenic patients
Morphology
Pale skin, darker hair
Prolactigenic (skin), Androgens (hair)
Feminine face with masculine build
Prominent gonadotropic hormones with androgens>estrogens
Systemic
Anorexia, weight loss, growth delay in children
Catabolism > anabolism, insufficient vitamin D and calcium
Bowel habits
Diarrhea, intermittent, typically NOT bloody or mucopurulent unless rectosigmoid Urgency to defecate Foul stool (especially with rectal abscess)
Fragilized bowel mucosa
Abdominal pain
RLQ or periumbilical, often relieved with defecation LLQ with greater involvement of rectosigmoid
Fragilization of transition zones of colon with small intestinal dysbiosis
Fistula presentation
Recurrent UTIs, vaginal discharge Soiling of skin, retroperitoneal abscess
Chronicity of colonic inflammation with fistulas, abscesses, etc.
ROS
Keen on sports
Need to discharge sympathetic excess and prominent structural androgenic
Vivid dreams
⇑ TRH
Diet: rich in animal proteins, refined carbs, animal fats
Strain on exocrine pancreas
Alpha: anxious, emotionally sensitive
⇑ Alpha
Para: Introverted, shy, timid, increased salivation, lacrimation, sweating, etc.
Vagotonia with hyperparasympathetic state
ANS
RLQ: right lower quadrant; LLQ: left lower quadrant; UTI: urinary tract infectious.
Examine these areas carefully in order to select more precisely the combination of medicinal plants related to endocrine response to the aggressor. The BoF pattern is quite particular in Crohn’s disease, which allows us to create a series of criteria to objectively
determine in which terrain they are in (Table 23.2). The specific derangements by endocrine axis, sympathetic nervous system, and psychological profile are presented in Tables 23.3–23.7. Refer to The Theory of Endobiogeny, Volume 3, Chapter 11 for additional discussion and context.
TABLE 23.2 Criteria of indexes deranged per stage of terrain of Crohn’s disease. Axis
Critical
Suppressed critical
Pre-critical
Neuro-corticotropic
>5/11
3–5/11
3/7
2–4/7
6/9
4–7/9
6/9
4–7/9
3/5
2–3/5
1–2/5
Total indexes deranged
28–41
15–28
adrenal response b. Thyrotropic: weak peripheral thyroid activity 3. Emunctory a. Exocrine pancreatic insufficiency b. Rectosigmoid colon congestion → fragilization
Medicinal plant
Alternatives
Carduus marianus MT 60 mL
Plantago major MT, Arctium lappa MT
Taraxacum officinale MT 60 mL
Cynara scolymus MT
Agrimonia eupatoria MT 120 mL
Carduus marianus MT + Arctium lappa MT
Agent For discussion of agents of induction of the critical terrain for Ulcerative colitis, refer to The Theory of Endobiogeny, volume 3, Chapter 11. 1. Stressors: physical, mental, emotional 2. Changes of season 3. Infections
Critical terrain The critical terrain can be understood in three parts: (1) autonomic, (2) endocrine central ≫ endocrine peripheral, key being ACTH, which localized disease to the distal colon, and (3) disruption of alpha-prolactin-growth hormone trépied, key being blocked GH, which results in ulceration of the distal colon. 1. ANS: hyperfunctioning sympathetic (αΣ + βΣ) a. Alpha → beta → favors hyperglycemia → inflammation 2. Endocrine: stimulated by intense alpha in the following order: a. Corticotropic i. Central: ACTH hyperfunctioning: 1. ACTH ≫ cortisol, adaptive, and thus blocking anabolism 2. ACTH on rectosigmoid colon: hypermetabolism for augmentation of water and electrolyte absorption for functional adaptation ii. Peripheral: insufficient adrenal cortex 1. Cortisol > global adrenal cortex (relative): blocked anabolism 2. Net effect: mucosal proliferation > nutrient entry → ulceration → hemorrhage b. Thyrotropic i. Central: 1. TRH hyperfunctioning: relaunches a. TSH b. Prolactin (PL) 2. TSH hyperfunctioning: a. Expansion of cell membranes beyond anabolic capacity due to cortisol’s blockage of anabolism
Colitis, ulcerative Chapter | 24 175
b. Favors insulin > insulin resistance, favors somatotropic desynchronization ii. Peripheral: 1. Peripheral thyroid insufficiency: absolute or relative to central functioning → insufficient lipid incorporation into growing and repairing cells → hemorrhage, blocked wound healing c. Somatotropic i. Central: 1. PL hyperfunctioning: a. Hyperinsulinism → inflammation of mucosa b. ACTH relaunching → prolonged hypermetabolism with blocked anabolism of distal colon c. Abscess formation favored d. GH delay → impaired wound healing 2. GH delay: insufficient insulin resistance → desynchronized nutrient entry in relationship to insulin → impaired cicatrization → ulceration, hemorrhage ii. Peripheral
1. Hyperinsulinism proceeding GH with low insulin resistance→ a. Elevated free radicals → inflammation → necrosis b. Delayed wound healing c. Fistula formation 3. Emunctories: rectosigmoid colon oversolicited and congested
Mechanisms 1. TNF-α, proinflammatory cytokines 2. Distal colon mucosa proliferates with blocked anabolism, inflammation, desynchronized growth factors → ulceration affecting only superficial layer
Result Ulcerative colitis.
History and BoF findings There are a number of key findings related to the precritical, partial remission, and critical terrains (Table 24.5). A
TABLE 24.5 Historical and terrain findings in ulcerative colitis. Area
Finding
Terrain
Demographic, past history
Family history- higher risk History of: autoimmunity, dysbiosis Diet: rich in dairy products
Precritical
Systemic
Anorexia, weight loss, growth delay in children Fever
Precritical, suppressed critical, critical, and remission terrains
Bowel habits
Diarrhea, intermittent, bloody, or mucopurulent Urgency to defecate Foul stool (esp. with rectal abscess)
Partial remission, critical terrains
Stool severity
Mild colitis: 6 blood stools per day with fever, anemia, tachycardia, elevated inflammatory markers
Partial remission, critical terrains
Abdominal pain
RLQ or periumbilical, often relieved with defecation LLQ with greater involvement of rectosigmoid
Precritical, suppressed critical, critical and remission terrains
Fistula presentation
Recurrent UTIs, vaginal discharge Soiling of skin, retroperitoneal abscess
Partial remission, critical terrains: chronicity of ulcerative tissue
ROS
Keen on sports
Precritical and remission terrain: helps discharge alpha and readapt beta and cortisol ⇑ TRH adaptative in precritical, suppressed critical, critical, and remission terrains Precritical, suppressed critical, critical, and remission terrains
Vivid dreams Diet: rich in animal proteins, refined carbs, animal fats ANS
Alpha: anxious, emotionally sensitive Para: introverted, shy, timid, increased salivation, lacrimation, sweating, etc.
Key: LLQ, left lower quadrant; RLQ, right lower quadrant.
Precritical, suppressed critical, critical, and remission terrains Precritical, suppressed critical, critical, and remission terrains
176 SECTION | C Assessment and treatment of common disorders
detailed discussion of BoF findings follows since they are highly specific for UC.
Physical exam and BoF findings During presentation with acute ulcerative colitis flare, the following may be observed on physical exam (Table 24.6). The BoF pattern is quite particular in ulcerative colitis with response to each endocrine axis, sympathetic nervous system, and psychological profile (Tables 24.7–24.11). Refer to The Theory of Endobiogeny, volume 3, Chapter 11 for additional discussion and context.
Treatment The conventional approach to ulcerative colitis depends on severity but generally consists of mono- or poly- pharmaceutical therapy. Refer to The Theory of
Endobiogeny, volume 3, Chapter 11 for more detailed discussion. In addition to standard therapy, from an Endobiogenic perspective, the general emphasis of treatment of the terrain is as follows: 1. Symptomatic: a. Polyvalent treatments emphasizing reduction in alpha and antihemorrhage (Table 24.12). NB: many elements of symptomatic treatment also address elements of the critical terrain related to mucosal ulceration and hemorrhage b. Clay (see Colitis, Crohn’s) 2. Treatment of critical terrain a. Autonomic reduction: alpha, beta, and parasympathetic b. Central endocrine inhibition, emphasizing inhibition of ACTH and relaunching of GH c. Adaptation of peripheral endocrine activity (Table 24.13)
TABLE 24.6 Examination and Biology of Functions relationships in ulcerative colitis. Area
Finding
Terrain
Colon
Pain on palpation along distal colon from splenic flexure to recto-sigmoid region
Above
Morphology
Pale skin, darker hair Feminine face with masculine
High para, androgens > estrogens
HEENT
Dilated veins on eyelids, nasal bridge, forehead; dilated sublingual veins Dark eyebrows, possibly bushy Enlarged salivary glands
Strong ACTH Oversolicited exocrine pancreas
Abdominal
Tender points associated with organs and hormonal solicitation Hepatic/portal congestion Pancreas/dysbiosis tender
Oversolicitation of pancreas, liver, gallbladder, central hormones based on terrain
Colon
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
TABLE 24.7 Neurocorticotropic terrains of ulcerative colitis. Axis
Index
Critical terrain
Suppressed critical
Remission
ANS
Starter
↑↑ or ↓↓
↑ or ↓
Normal
Neurocorticotropic
Immediate adaptation Adaptation entrainment score adj.
↑↑ ↑↑
↑ ↑
Normal Normal
Corticotropic
Oxytocin Vasopressin corrected CRH ACTH Cortisol Adaptation permissivity Aldosterone comparative Adrenal yield
↓↓ ↑↑ ↑↑ ↑↑ ↑↑ ↑↑, may be negative ↑↑, may be negative ↑↑
↓ ↑ or ↓ ↑ ↑ or ↓ ↑ ↑ ↑, may be negative ↑
Normal Varies Varies Varies Normal or ↓ Normal Normal or slightly elevated Normal
Colitis, ulcerative Chapter | 24 177
TABLE 24.8 Thyrotropic terrains of ulcerative colitis. Index
Critical terrain
Suppressed critical
Remission
TSH serum
↓↓
↓
Normal
Thyroid relaunching
↑↑
↑
Normal to slightly elevated
Thyroid relaunching corrected
↑↑↑
↑↑
Normal to slightly elevated
Thyroid
↑↑↑
↑↑ or ↓↓
Normal to slightly low
Vitamin D adaptation index
↓, negative or both
Varies
Varies
TABLE 24.9 Somatotropic terrains of ulcerative colitis. Axis
Index
Critical terrain
Suppressed critical
Remission
Somatotropic
Prolactin
↓↓↓
↓↓
Normal
GH growth score
↓↓↓
↓↓
Normal
Somatostatin
↓↓
↓
Normal
Insulin
↑↑↑
Varies
Normal
Insulin resistance
↓↓
Varies, often low
Normal
Expansivity #2
↑↑
Varies
Normal
Redox
↑↑ to ↑↑↑
↑ to ↑↑
Normal
Necrosis corrected
↑↑↑
↑↑
Normal
Autophagy 2
↑↑↑
↑↑
Normal
TABLE 24.10 Psychological indexes related to ulcerative colitis. Index
Critical terrain
Suppressed critical
Remission
Closed off from receiving
↑↑
↑
Normal
Permeability adjusted
↑↑↑
↑↑
Normal to ↑
Traumatic memory
↑↑
↑
Normal
Acceptance-contentment
↓↓
↓
slightly ↓, Normal, or ↑
Frustration score 2
↑↑
↑
Slightly ↑ to normal
TABLE 24.11 Gonadotropic terrains of ulcerative colitis. Axis
Index
Critical terrain
Suppressed critical
Remission
Gonadotropic
LH FSH Organotissular estrogen yield Estrogens Estrogen corrected Genital androgens
↓↓ ↓↓ ↑↑
↓ ↓ ↑
Normal Normal Normal
↑↑ ↑↑ ↑↑
↑ ↑ ↑
Normal Normal Normal
Genito-thyroid
↑↑
↑
Normal
Gonado-thyrotropic
178 SECTION | C Assessment and treatment of common disorders
TABLE 24.12 Symptomatic treatment of ulcerative colitis. Medicinal plant
Alpha-lytic
Antiinflammatory
Astringent
Antihemorrhagic
Endocrine
Intestinal tropism
•
Aldosterone antagonist
Antispasmodic, antimicrobial
Alchemilla vulgaris
•
Angelica archangelica
•
Estrogenic, (−) FSH
Antispasmodic, antimicrobial
• Indirecta
Delays insulin activitya
Hemostatic
Artemisia dracunculus
•
Estrogenic (mild)
Antispasmodic, antimicrobial
Fragaria vesca
•
•
(−) ACTH, (−) conversion of androgens to estrogens
Antimicrobial
•
Relaunches GH
Arnica montana
•
•
Lamium album
• Indirectb
•
Lavandula angustifolia
•
•
(−) Adrenal cortex
Hepatobiliary drainer Cicatrizing antimicrobial
Matricaria recutita
•
•
(−) ACTH
Antispasmodic, antimicrobial Cicatrizant Decongestant: hepatic, splanchnic, pelvic
Plantago major
Poterium sanguisorba
•
Antispasmodic, antimicrobial, antiulcerative Hepatopancreatic drainer
•
•
(−) PL and by extension hyperinsulinism and inflammation, and corticotropic relaunching
Antiseptic
a
By delaying the actions of insulin in the cell membrane.
b
By relaunching GH and re-establishing the alpha-PL-GH trépied, Arnica montana diminishes inflammation rooted in somatotropic desynchronization.
TABLE 24.13 Summary of treatment of the global critical terrain. Category
Goal
Medicinal plant
Autonomic
↓ Para-alpha
Passiflora incarnata (Passionflower) MT Melissa officinalis (Melissa) EO, BH, MT Ilex aquifolium (Holly Tree) GM
↑ Beta
Cinnamomum zeylanicum (Cinnamon) EO, BH, HL Citrus paradisii (Grapefruit) EO Crataegus oxyacantha (Hawthorne): MT, GM, DE
Colitis, ulcerative Chapter | 24 179
TABLE 24.13 Summary of treatment of the global critical terrain—Cont’d Category
Goal
Medicinal plant
Corticotropic
↑ Adrenal ↓ ACTH
Ribes nigrum (Cassis) leaf > bud Fragaria vesca (Strawberry leaf) MT, BH Salvia sclarea (Sage) MT, EO, DE, BH Quercus pedunculata (Oak) GM (hepato-splanchnic drainage)
Thyrotropic
↓ Central
Lithospermum officinale (Stoneseed) MT, DE, BH Lycopus europaeus (Gipsywort) MT Leonurus cardiaca (Motherwort) MT Avena sativa (Oat) MT Selenium oligo (reduces inflammation, supports hepatic detox)
↑ Peripheral Somatotropic
Regulate GH-PL Delay Insulin on cell membrane Inhibit PL
GH low, cortisol low: Lamium album (White deadnettle) MT, BH Arnica montana (Arnica) MT Malva sylvestris (Mallow) MT Fragaria vesca (Strawberry leaf) MT, BH Poterium sanguisorba (Salad Burnet) MT, FE, BH
Drainage
Hepatobiliary
Arctium lappa (Burdock): MT, BH Agrimonia eupatoria (Agrimony): MT, BH Plantago major (Plantain) MT, BH, DE Alchemilla vulgaris (Lady’s Mantle): MT, BH, FE, DE Avena sativa (Oat) MT Plantago major (Plantain) MT, BH Digestive enzymes Fragaria vesca (Strawberry leaf) MT, BH Lamium album (White deadnettle) MT, BH Agrimonia eupatoria (Agrimony): MT, BH Poterium sanguisorba (Salad Burnet) MT, BH, FE Green illite clay
Exocrine pancreas
Intestinal
Exemplary prescriptions Based on an Endobiogenic approach to ulcerative colitis, a number of prescriptions can be derived. 1. Clay: 1 tbsp four times per day (Table 24.1). 2. Antihemorrhagic, cicatrizant: 3 mL four timed per day until bleeding has resolved, then 4 mL twice per day until in remission as a regulator of the somatotropic axis and intestinal drainage (Table 24.2). Lamium album MT 60 mL, Poterium sanguisorba MT 60 mL, Malva sylvestris MT 60 mL, Hamamelis virginiana MT 60 mL. 3. ANS-cortico-thyrotropic: 3 mL four times per day until hemorrhaging has stopped, then 4 mL twice per day until in remission. Passiflora incarnata MT 40 mL, Matricaria recutita MT 40 mL, Sequoia gigantea GM 40 mL, Rosa canina GM 40 mL, Fabiana imbricata MT 20 mL, Cornus sanguinea GM 60 mL, Eucalyptus ssp. EO 4 mL, Syzygium aromaticum EO 0.5 mL.
4. Hepatobiliary-pancreatic-intestinal drainage: 3 mL four times per day until hemorrhaging has stopped, then 4 mL twice per day until in remission. Carduus marianus MT 60 mL, Taraxacum officinale MT 60 mL, Agrimonia eupatoria MT 120 mL. 5. Oligoelements: a. Vitamin D i. Critical, suppressed critical: 5000–10,000 IU in AM ii. Remission: 3000–4000 IU in AM if consistent with Endobiogenic terrain b. Vitamin A: i. Critical, suppressed critical: 2000–4000 IU per day ii. Remission: 1000–4000 IU per day (Table 24.14) c. Vitamin E: (Table 24.15) i. Critical, suppressed critical: 300–400 mg per day 6. Diet: avoid dairy, red meat, favor vegetarian wholegrain diet. 7. Lifestyle: critical: calming activities, remission: aerobic exercise.
180 SECTION | C Assessment and treatment of common disorders
TABLE 24.14 Sources of Vitamin A.
TABLE 24.15 Sources and servings of vitamin E.
Food
Vitamin A per 1 cup
Source
Per 100 g serving
Sweet potato
1900
Wheat germ oil
150 mg
Carrots
1000
Almond oil
95 mg
Spinach
940
Canola oil
44 mg
Kale
885
Sunflower oil
41 mg
Mustard greens
865
Hazelnuts
20 mg
Collard greens
770
Almonds
15 mg
Squash
535
Olive oil
14 mg
Cantaloupe
270
Papaya
100
Apricots
33
Chapter 25
Diarrhea, malabsorptive Summary Essence: A disorder of impaired uptake of nutrients relative to intake resulting in excessive water content of stool. Summary: (1) Nutrient intake is greater than rate of hydrolysis and absorption: water is drawn into intestines to dilute the hyperosmotic content, resulting in watery stools inducing (2) Diarrheal episodes.
Treatment goals Symptomatic: Reduce osmotic intake, adsorption of stool water content Terrain: Treat according to particular origin of disorder
Sample treatment 1. Illite clay: 1 tsp. 3 times per day before meals (chronic), 1 tbps 3–4 times per day (acute): Add to water, or, prepare a tisane of Juglans regia leaf or Agrimonia eupatoria leaf and flower 1 tsp. steeped 10 min in 1 cup water, strain and add clay. 2. Neuroendocrine-Antiinfectious-Astringent-Emunctory: 3 mL TID before meals added to clay (Table 25.9): Fragaria vesca MT 60 mL, Hamamelis virginiana MT 30 mL, Plantago major MT 30 mL + Artemisia dracunculus EO 1 mL, Carum carvi EO 0.5 mL, Mentha piperita EO 0.5 mL.
Terrain in detail Precritical terrain, critical terrain, and agent Malabsorption diarrhea is an osmotic diarrhea. It can occur for three general reasons: (1) excess nutrient intake relative to the Endobiogenic terrain of the patient, (2) insufficient digestive capability, (3) insufficient absorptive capability, (4) a combination of the prior three causes. Thus, the precritical terrain is particular to origin of the disorder. The agent can be congenital, in which case compensatory or substitutive treatments must be offered. Or, it may be chronic, in which case, a treatment of the critical and then precritical terrains The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00025-1 © 2020 Elsevier Inc. All rights reserved.
must be offered (c.f. The Theory of Endobiogeny, Volume 3, Chapter 10). In other cases, symptomatic and restorative treatments will be sufficient (Table 25.1).
Mechanisms 1. Loss of enteric microvilli 2. Increased bowel motricity 3. Osmotic gradient
Result Malabsorptive diarrhea ≥3 stools per day of watery consistency.
History findings During acute malabsorptive diarrhea, the symptoms presented in Table 25.2 can be observed correlated to various nutrients.
Physical exam findings During presentation with acute malabsorptive diarrhea in the critical phase, the following may be observed on physical exam with some possible terrain correlations (Table 25.3).
Treatment It is important to rule out consumptions of hyperosmotic foods in diet, either quantitatively or qualitatively excessive for the individuals Endobiogenic terrain, such as high volumes of grape or pear juice or carrot juice. When the origin is malabsorption of specific nutrients (Table 25.2), avoidance of those foods, or, consumption of foods with a low concentration of those nutrients is recommended (Tables 25.4 and 25.5). When the origin relates to insufficient digestive capability or congestion of specific organs related to the digestive tract, polyvalent plants with drainage (Table 25.6) and/or substitutive digestive qualities can be utilized (Table 25.7). Other plants have broader actions on local intestinal flora, epithelial regeneration, and global neuroendocrine function (Tables 25.8). 181
182 SECTION | C Assessment and treatment of common disorders
TABLE 25.1 Agent of malabsorption diarrhea, elements of terrain, and symptomatic approaches to treatment. Agent
Precritical
Critical
Symptomatic/substitutive
Infectious, acute
Antiinfectious
Infectious, chronic
Disadaptation of immunity terrain
Food allergies
Antiinfectious Digestive enzymes Astringent/cicatrizing, food avoidance
Acquired malabsorption
Intestinal restoration
Digestive enzymes, Food avoidance
Congenital
Pancreatic drainage
Intestinal restoration
Digestive enzymes
Vitamin or Mineral excess or deficiency
Varies
Varies
Varies
TABLE 25.2 Correlation of GI symptoms with nutrient intolerance. Stool
Nutrient intolerance
Watery
Carb
•
Abdominal Bloody
Lipids
Steatorrhea
Distention
Pain
•
±
•
••
•
•
Nausea
Vomiting
Perianal excoriation •
•
Proteins
•
Giardia
•
• •
TABLE 25.3 Examination findings of digestive secretion insufficiency in the critical terrain of malabsorptive diarrhea. Area
Finding
Terrain
Oral
Enlarged parotids glands, dilated opening of duct
⇑ Para: insufficient pancreatic amylase for carbohydrate digestion Hepatic congestion Dysbiosis Biliary congestion
Sublingual veins congested White coating on tongue Green coating on tongue Abdomen
Congestion, tenderness at splanchnic congestion point on abdomen Rumbling, gurgling on auscultation Tenderness at liver, exocrine pancreas, duodenum, and hepato-splanchnic points
⇑ Alpha, impairing circulation and turnover of intestinal epithelium, local microbiota Hyper-Para ⇑ Alpha
Perianal
Excoriation of skin, anal irritation
Exocrine pancreatic insufficiency
Diarrhea, malabsorptive Chapter | 25 183
TABLE 25.4 A list of low-fructose foods. Fruits
Vegetables
Others
Pineapples
Asparagus
Eggs
Berries
Leafy green vegetables
Chicken, Duck, Turkey
Lemon and lime
Celery
Sardines, herring, anchovies
Rhubarb
Mushrooms
Bison: pasture raised, grass fed
Potatoes Root vegetables: parsnips, turnips, beets
TABLE 25.5 Short- and medium-chain fatty acids appropriate for malnutrition. Fatty acid
Example
Source
Absorption
Short chain
Acetic acid Butyric acid Proprionic acid
Pectin: Blackberries, carrots Fructo-oligosaccharides, Inulin: Jerusalem artichoke, onions, leeks, asparagus Kombucha Parmigiano Reggiano cheese, aged 24 months or longer
Large intestine (production and absorption)
Coconut oil Olive oil
Small intestines
Butyric acid
Medium chain
Small intestines
TABLE 25.6 Polyvalent medicinal plants with emunctory and other properties. Plant
Hepato-biliary
Exocrine pancreatic
Intestines
Other
Arctium lappa
Choleretic Hepato-protectant
Dual pancreatrope
Reduces inflammation by immuno-modulation
Cutaneous drainer
Alchemilla vulgaris
Choleretic
Astringent
Antiinflammatory Cicatrizing Hemostatic
Agrimonia eupatoria
Stimulates hepatobiliary secretions
Dual pancreatrope
Astringent
Portal decongestant Cicatrizing
Fumaria officinalis
Choleretic Hepatic drainer
Drainer
Drainer
Spasmolytic: Sphincter of Oddi
Juglans regia
Stimulates hepatic macrophages
Dual pancreatrope
Astringent
Antiseptic Cicatrizing
Plantago major
Induces hepatic enzymes
Carbohydrates
Astringent Antiinflammatory
Antiinfectious Hepato-renal drainer
Salvia sclarea
Choleretic
Stimulates flow of secretions
Astringent
Para-Alpha sympatholytic Muscular antispasmodic Cicatrizing
184 SECTION | C Assessment and treatment of common disorders
TABLE 25.7 Substitutive pancreatic actions of medicinal plants. Plant
Amylase
Disaccharidases
Plantain (Plantago major)
•
•
Milky oat (Avena sativa)
•
•
Rye bud (Secale cereale)
•
•
Fig bud (Ficus carica)
•
•
•
Papaya leaf (Carica papaya)
•
•
•
Pineapple (Ananassa sativa)
•
•
•
•
•
Alfalfa (Medicago sativa)
Proteases
•
Lipase
TABLE 25.8 Summary of medicinal plants that reduce global autonomic activity, intestinal spasms, balance GI flora, splanchnic congestion, epithelial regeneration, remineralization.
Plant
Sympatholytic
Portal/ splanchnic decongestant
Matricaria recuctita EO
•
•
Artemisia dracunculus EO
•
•
Melissa officinalis MT
•
•
Ficus carica GM
•
•
Digestive spasmolytic •
Microflora balance
Epithelial regeneration
Remineralization
•
•
Illite clay
•
Urtica dioca root MT
•
Diet: Carbohydrates
Diet: Fats
Avoid
Focus on short-chain fatty acids (SCFA) and mediumchain triglycerides (MCT). SCFA aid in colon and systemic health. MCT is directly absorbed into the blood stream without aid of bile as an emulsifier (Table 25.5).
●
● ●
●
High glycemic carbohydrates (semolina pasta, white bread, sweets) High-fructose fruits and honey (if necessary) Nonfermented dairy (it may be necessary to avoid fermented dairy, i.e., yoghurt as well) Cheeses: Exception: >23 month-aged Parmigiano Reggiano cheese
Eat 1. A diet rich in low fiber, complex carbohydrates a. White rice b. Potatoes (not yams) 2. A diet rich in low fructose foods (Table 25.4). Berries are well tolerated, will not induce diarrhea in moderate amounts, and have antioxidant properties.
Diet: Proteins Ensure sufficient acid for the digestion of proteins in the stomach ● ●
●
Eat ½ lemon with pith and skin before a meal 1 tbsp apple cider vinegar in warm water 15 min before a meal Betaine hydrochloride Easy-to-digest proteins:
1. Baked, boiled, broiled, or grilled a. Legumes: Lentils, Black beans
Diarrhea, malabsorptive Chapter | 25 185
b. High purine fish: Sardine, Herring, Tuna, Salmon c. Fowl: Turkey > Chicken > Duck d. Red meat: Lamb > Goat > Beef 2. Raw: Sprouts: Alfalfa, broccoli, radish
TABLE 25.9 Diarrhea tincture. Medicinal plant Fragaria vesca MT 60 mL
Ribes nigrum leaf MT 30 mL + Ribes nigrum GM 30 mL
Hamamelis virginianus MT 30 mL
Agrimonia eupatoria MT, Plantago major MT
Plantago major MT 30 mL
Agrimonia eupatoria MT, Hamamelis virginiana MT
Artemisia dracunculus EO 1 mL
Anthemis nobilis EO 1 mL
Carum carvi EO 0.5 mL
Artemisia dracunculus EO 0.5 mL
Mentha piperita EO 0.5 mL
Carum carvi EO 0.5 mL
Exemplary prescriptions Based on an Endobiogenic approach to malabsorptive diarrhea, a number of prescriptions can be derived. The specific prescription should be based on the particular cause. If the cause is multifactorial or unclear, focus on medicinal plants with the following qualities: astringent, cicatrizing, substitutive digestive, and eupeptic qualities. Add antimicrobial and ANS-regulating plants as indicated. 1. Illite clay: 1 tsp. 3 times per day before meals (chronic), 1 tbps 3–4 times per day (acute). Add to water, or, prepare a tisane of Juglans regia leaf or Agrimonia eupatoria leaf and flower 1 tsp. steeped 10 min in 1 cup water, strain, and add clay. 2. Neuroendocrine-Antiinfectious-Astringent-Emunctory: 3 mL TID before meals added to clay (Table 25.9).
Replacements and alternatives
Key: EO, essential oil; GM, gemmomacerate; MT, mother tincture.
Fragaria vesca MT 60 mL, Hamamelis virginiana MT 30 mL, Plantago major MT 30 mL + Artemisia dracunculus EO 1 mL, Carum carvi EO 0.5 mL, Mentha piperita EO 0.5 mL.
Chapter 26
Diarrhea, rapid transit Summary Essence: A functional disorder of excessive motricity of the enteric system for the Endobiogenic terrain Terrain: (1) Vagotonic individuals in which in the face of a (2) Stressor experience (3) A hyperfunctioning parasympathetic tone ≫ hypersympathetic activity with rapid ANS cycling leading to (4) Rapid motricity of the entire enteric system inducing (5) Diarrheal episodes
Treatment goals Symptomatic: Hydration with low-osmotic fluids, intestinal spasmolytics Terrain: ● ●
●
●
ANS: ⇓ global ANS tone CORTICO: regulate axis to prevent compensatory ANS relaunching THYRO: regulate axis to prevent compensatory ANS relaunching Medications: reduce or eliminate inducers such as magnesium products, laxatives, opiate withdrawal, antacids
Sample treatment 1. Amino acid therapy: 1 capsule 2–3 times per day: GABA (γ-aminobutyric acid) 100–250 mg 2. Oligoelement: 1 tablet AM and evenings starting 3 days before events that provoke anticipatory anxiety: Lithium 5 mg 3. Neuroendocrine-anxiolytic: 1–2 mL up to every 1 h PRN (as needed) until diarrhea resolves, or, 3–4 mL three to four times per day starting 3 days before events that provoke anticipatory anxiety (Table 26.1): Melissa officinalis MT 80 mL, Ilex aquifolium GM 20 mL, Leonurus cardiaca MT 20 mL + Artemisia dracunculus EO 1 mL
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4. Neuroendocrine-anxiolytic essential oil blend: inhale as needed and/or apply to templar arteries or to pulse points or under nose: Cananga odorata 1 mL, Salvia sclarea EO 1 mL, Lavandula angustifolia EO 3 mL
Terrain in detail Precritical terrain The precritical terrain varies. It can be a localized sensitivity to autonomic tone, especially parasympathetic, at the level of the motor complex. More often, it is a central or global parasympathetic and alpha sympathetic tone in vagotonic individuals with anxiety, most often anticipatory in nature. Thus, many are spasmophilic in the precritical terrain. There may be insufficient GABA (γ-aminobutyric acid) or dysregulated central-peripheral serotonin activity that fragilizes the patient, making them more susceptible to anticipatory anxiety.
Agent The most common type of aggression is an anticipatory anxiety related to performance or iatrogenic causes (cf. The Theory of Endobiogeny, volume 3, Chapter 10).
Critical terrain It involves overstimulation of the enteric motor complexes typically by the regional ANS enervation. This, in turn, is typically overstimulated by global ANS activity and involves a hyperfunctioning central or global ANS response to a perceived aggressor that also focalizes at the level of the motor complexes of the enteric motor complex. External or internal aggressors relaunch alpha, with a sufficiently strong beta response that the cycle of para-alpha-beta remains entrained until there is a sufficient reduction of alpha-sympathetic tone. 1. ANS: hyper para ≫ hyper alpha with strong beta: hypercycle of ANS
187
188 SECTION | C Assessment and treatment of common disorders
TABLE 26.1 Historical findings, terrain and BoF correlations. Symptom
Terrain
BoF
Anxiety
↑ αΣ + TRH + central inflammation + insufficient GABA
↑ Thyroid relaunching corrected + ↑ noxious free radicals + ↓ βMSH/αMSH
Spasmophilia
↑ Leukocyte mobilization ↓ Platelet mobilization
Hypervigiliance Spasmophilic symptoms (cf. Spasmophilia)
2. Endocrine: a. Corticotropic Peripheral: insufficient response or output of global adrenal cortex hormones may entrain or sustain a hyperfunctioning alpha-sympathetic tone, αMSH and/or βMSH. b. Thyrotropic i. Central: a hyperfunctioning TRH may also play a role in sustaining an adapted peripheral beta-sympathetic activity and prolonging the anxiety state ii. Peripheral: insufficient response or output of peripheral thyroid hormones may entrain a hyperfunctioning alpha-sympathetic or βMSH activity to compensate.
Mechanisms The rate of intestinal motricity (viz. peristalsis) does not allow for sufficient regulation of the water content of stool for the Endobiogenic terrain.
Result Rapid transit diarrhea: ≥ 3 stools per day of watery consistency.
History and BoF findings During acute rapid transit diarrhea, patient will present with ≥3 stools per day of watery consistency usually in association with anticipatory anxiety. Other aspects of the history and Biology of Functions correlations are presented in Table 26.1.
Treatment The general emphasis of treatment is to regulate autonomic tone globally and at the level of the intestines using medicinal plants and lifestyle stress management strategies.
Medicinal plants 1. ANS: reduce global ANS, favor plants that are spasmolytic and/or with an intestinal tropism and/or anxiolytics: a. Artemisia dracunculus EO b. Matricaria recutita MT/EO c. Angelica archangelica EO
d. Artemisia dracunculus EO e. Origanum majorana EO 2. Alpha-sympatholytics with digestive tropism and endocrine activity: a. Melissa officinalis MT: thyrotropic adaptogen b. Salvia sclarea MT: neuroendocrine adaptogen, supports adrenal cortex and peripheral thyroid gland 3. General anxiolytics: a. Inhalation of essential oils during stress: Cananga odorata EO, Citrus aurantium amara EO b. Oral: Ilex aquifolium GM, Leonurus cardiaca MT, FE, BH BH, bulk herb; EO, essential oil; FE, fluid extract; GM, gemmomacerate; MT, mother tincture.
Lifestyle Encourage active ways of managing anxiety: breathe work, meditation, mindfulness, visualization, dyadic therapy.
Exemplary prescriptions Based on an Endobiogenic approach to rapid transit diarrhea, a number of prescriptions can be derived. One or more can be used based on the preference of the patient and efficacy. 1. Amino acid therapy: 1 capsule 2–3 times per day: GABA (γ-aminobutyric acid) 100–250 mg 2. Oligoelement: 1 tablet AM and evenings starting 3 days before events that provoke anticipatory anxiety: Lithium 5 mg 3. Neuroendocrine-anxiolytic: 1–2 mL up to every 1 h PRN until diarrhea resolves, or, 3–4 mL three to four times per day starting 3 days before events that provoke anticipatory anxiety: Melissa officinalis MT 80 mL, Ilex aquifolium GM 20 mL, Leonurus cardiaca MT 20 mL + Artemisia dracunculus EO 1 mL 4. Neuroendocrine-anxiolytic essential oil blend: inhale as needed and/or apply to templar arteries or to pulse points or under nose: Cananga odorata 1 mL, Salvia sclarea EO 1 mL, Lavandula angustifolia EO 3 mL
Chapter 27
Diarrhea, Secretory Summary Essence: A hypersecretory diarrhea initiated by infection of the intestinal mucosa. Terrain: (1) Fragilized intestinal and immune terrain allows for (2) Microbial invasion of endothelium of intestines with (3) Local enterotoxins release leading to (4) Altered ion-channel fluid flow ≫ Absorption: ⇑ water and ion movement into lumen results in (5) Diarrheal episodes.
Treatment goals Symptomatic: Hydration, clay, medicinal plants with antiinfectious, antiinflammatory, astringent actions, and intestinal tropism. Terrain: ●
●
●
●
● ●
Neuroendocrine: In chronicity, adapt local and global elements of immunity and cicatrization ANS: ↓ alpha and histamine if installing adaptative congestion, ↓ hypervagal tone if congesting, increase local parasympathetic tonus for intestinal endothelial reconstruction SOMATO: Address somatotropic desynchronization if present (delay insulin, increase insulin resistance, block TSH if low, regulate cortisol if activity increased) IMMUNITY: Adapt immune function in cases of persistent infection DRAIN: 1°-Splanchnic bed, 2°-Liver, 3°-Pancreas DIET: Easily digestible solid foods, avoid raw foods, hyperosmotic liquids
Sample treatment 1. Medicinal clay: 1 tbsp prepared with 250 mL of Neuroendocrine-Immunity-Drainage tisane (Table 27.6): Allow mixture to sit 15 min or longer, stir and consume 2. Neuroendocrine-Immunity-Drainage: 1 tsp. steeped 8–10 min in 300 mL water, drink 3–4 times per day (Table 27.7):
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Matricaria recutita BH 100 g, Plantago major BH 100 g, Fragaria vesca leaf BH 100 g 3. Oligoelement: acute infection: Cu-Ag-Au, chronic: Selenium + Sulfur 4. Topical abdominal rub: Apply 3–4 times per day with consumption of clay-tisane mixture: Lavandula angustifolia EO 3 drops, Matricaria recutita EO 2 drops in 1 tsp. carrier oil, apply to abdomen and then apply gentle heat 5. Diet: Easily digestible solid foods. Avoid raw foods and hyperosmotic beverages
Terrain in detail Precritical terrain The specific elements of the precritical terrain vary. Fragilization of the local terrain may be relative in nature in relationship to the quantity or virulence of the infecting agent. Otherwise, there is often some combination of local congestion and disadapted local and global immunity, which may be related to local or global neuroendocrine imbalances.
Agent Infectious agents induce this type of diarrhea. Location may be suggestive of typical types of organisms (Table 27.1).
Critical terrain Varies based on the Endobiogenic terrain of the patient. What is presented are the elements of adaptative congestion that either impair the immune response, restoration of the enteric mucosa, or, both. Some possible findings are presented in Table 27.2. 1. Emunctory and vasculature congestion: a. Splanchnic bed b. Liver, hepatobiliary, hepato-splenic c. Pancreas d. Spleen
189
190 SECTION | C Assessment and treatment of common disorders
TABLE 27.1 Summary of secretory diarrhea characteristics by history and stool testing. Stool characteristics
Small bowel
Large bowel
Appearance
Watery
Mucoid and/or bloody
Volume
Large
Small
Frequency
Increased
Highly increased
Blood
Possibly positive but never gross blood
Commonly grossly bloody
pH
Possibly 5.5
Anion gap
Normal ( 4:1
Corticotropic
ACTH Cortisol Adrenal cortex Leukocyte mobilization Platelet mobilization Adaptation permissivity of the adrenal cortex Inflammation
↑ ↓ Varies, often ↓ Varies, often ↓ Varies, often ↓ Varies, often ↓
Gonadotropic
Estrogen index corrected
↓
Thyrotropic
Genito-thyroid Thyroid Thyroid relaunching corrected
↓ Nl/↓ Varies
Somatotropic
Insulin Somatostatin (exocrine pancreas) Redox Free radicals
Nl/↓ Nl/↑
Interleukin (IL-1) index
↓
Gonadotropic Thyrotropic
Somatotropic
Carcinogenesis
Adaptation permissivity of the adrenal cortex Inflammation Estrogen index corrected
↓ ↑ Varies, ↑ is more deleterious ↑, may also be negative ↑ ↑
Genito-thyroid Thyroid Thyroid relaunching corrected
↑ Varies, often ↑ ↑
Insulin Somatostatin (exocrine pancreas) Redox Noxious free radicals
↑ ↓
Interleukin (IL-1) index
↑
↑ ↑
regulation (flora, digestive juices, transit time), then, dietary changes, drainage and finally global neuroendocrine regulation as indicated. Considering the polyvalent nature of medicinal plants, many treatments that are symptomatic, also play other roles. For example, Mentha piperita has actions that address all categories (except diet): antiflatulent, digestive, eupeptic, balances enteric flora, cholagogue, choleretic, and stimulant of exocrine pancreatic activity (lipase, amylase).
Carcinogenesis
Varies, often ↓
↓ ↓
1. Symptomatic: a. Polyvalent plants with carminative, eupeptic properties (Table 28.5) b. Address acute food poisoning as indicated 2. Intestinal regulation: a. Equilibrate of intestinal flora i. Medicinal plants (Tables 28.5) ii. Medicinal clay b. Eupeptics to stimulate digestive juices (Table 28.5)
198 SECTION | C Assessment and treatment of common disorders
TABLE 28.4 Examination, terrain, and Biology of Functions relationships for dysbiosis. Area
Finding
Terrain
Tongue
White coating Green coating Raised red papules
Microbial overgrowth Biliary congestion Duodenal inflammation
Salivary glands
Dilated or hypertrophied opening of canal of Stensen Dilated or hypertrophied opening of opening of Wharton’s gland
Exocrine pancreatic insufficiency of amylase Exocrine hepatic insufficiency
Small intestine
Left peri-umbilical region tender to palpation
Dysbiosis
Splanchnic
Tenderness to moderate palpation 1/3 of distance from xyphoid tip to umbilicus
Splanchnic congestion resulting in hepatopancreatic congestion
Liver
Enlarged liver Tender, superior-medial Tender, inferior-lateral
Vascular hepatic congestion Metabolic hepatic congestion
BoF
⇓ Splanchnic index ⇓ Leucocyte mobilization and Platelet mobilization ⇑/⇓: LMI ⇑/⇓ LMI ⇑/⇓ LMI
Gallbladder
Murphy’s point tender to palpation (midpoint between umbilicus and midright costal margin)
Gallbladder congestion
Pancreas
Right, superior-lateral in relationship to umbilicus tender to palpation Tender: head or general point
Exocrine pancreatic congestion
⇑/⇓ Somatostatin
Exocrine Congestion
⇑/⇓ Somatostatin
Tender on deep palpation
Colon congestion with oversolicitation by central factors (correlate to area tender)
⇓: ACTH, FSH, LH indexes; ⇓ serum TSH; ⇑: TRH/TSH, Thyroid relaunching, Thyroid relaunching corrected
Colon
c. Regulate transit time; address constipation if indicated i. Medicinal plants (spasmolytics: Tables 28.7) ii. Medicinal clay 3. Dietary changes: (c.f. The Theory of Endobiogeny, Volume 2, Chapter 6 for detailed discussion) a. General: i. Food hygiene: chew well, eat in a serene environment, avoid overeating, etc. ii. Fermented foods iii. Prebiotic-rich foods iv. Address constipation if present (c.f. Chapters 21 and 22) b. Grape Cure (seasonal), c.f. Chapter 44: Endobiogenic diets and nutrition c. Intermittent fasting: 14–16 h (end of last meal of prior day to first meal of current day) 4. Drainage: Emunctories and circulatory bed with other actions targeting the intestines and dysbiosis (Table 28.6) 5. Neuroendocrine regulation: a. General: Polyvalent medicinal plants with both neuroendocrine and digestive tract tropism are the most
efficient in regulating dysbiosis, its symptoms and its terrain (Table 28.7) b. ANS i. GI Spasmolytics and regional/global reducers of parasympathetic and/or alpha-sympathetic tone: relieves congestion of digestive organs, emunctories ii. Beta-sympathomimetics to improve excretion of digestive juices, bile, pancreatic enzymes c. Endocrine: address the particular aspects of terrain that have either dysregulated the alimentary tract ecology of function, or, which have been affected by dysbiosis
Exemplary prescriptions Based on an Endobiogenic approach to dysbiosis and number of basic prescriptions can be utilized for rapid, acute treatment as well as chronically. Many involve medicinal clay, which can be used alone or in conjunction with medicinal plants in various Galenical forms (tisane, tincture, essential oil).
Dysbiosis Chapter | 28 199
TABLE 28.5 Polyvalent medicinal plants for dysbiosis. Plant
Antispasmodic
Eupeptic
Carminative
Microbial balance
Agrimonia eupatoria
•
Artemisia dracunculus
•
•
•
•
Melissa officinalis
•
•
Mentha piperita
•
•
•
•
Ficus carica
•
•
Achillea millefolium
•
•
•
Satureja montana
•
•
Cichorium intybus
•
•
• •
Juglans regia
•
Cinnamomum zeylanicum
•
•
•
TABLE 28.6 Emunctory drainers with additional properties. Plant
Portal
Splanchnic
Hepatobiliary
Achillea millefolium
Vagolytic, hepatic drainer, digestive antispasmodic, eupeptic
Agrimonia eupatoria
•
Artemisia dracunculus Carduus marianus
• •
•
•
Choleretic, cholagogue, antiviral Hepato-splenic drainer, eupeptic
•
•
Plantago major Raphanus niger
Antimicrobial, dual pancreatrope Antibacterial, regulates dysbiosis, aperitif
Ceanothus americanus Matricaria recutita
Other
Antimicrobial, choleretic, aperitif, eupeptic, antiinflammatory Antimicrobial, immunostimulant, hepato-renal drainer, dual pancreatrope, digestive antispasmodic
•
1. Acute food poisoning: every 2–4 h until resolution of illness: 30–200 mL water, 1–2 tbsp. clay, Mentha piperita EO 1 drop, Thymus vulgaris EO 1 drop (avoid in children para, delayed or blocked beta. In the face of a potential allergen, (4) Hyperimmune response with insufficient regulation: Alpha-sympathetic, central cortico-thyrotropic (ACTH, TRH) > peripheral thyroid ≫ cortisol with (5) Emunctory congestion: liver (as emunctory) soliciting (6) Skin as Emunctory: resulting in production and expression of excessive proteinaceous material on the epidermis: Eczema.
Avena sativa MT 60 mL, Rosa canina GM 60 mL, Ribes nigrum GM 60 mL 2b. Neuroendocrine, Adult: 3 mL three times per day (Table 29.11): Rhodiola rosea MT 60 mL, Inula helenium MT 60 mL, Ribes nigrum GM 60 mL, Quercus pedunculata GM 60 mL, Lavandula angustifolia EO 4 mL 3. Hepato-pancreatic-dermal drainage: 3 mL three times per day before meals, or before breakfast and dinner, and, before bed (Table 29.12): Arctium lappa MT 120 mL, Agrimonia eupatoria MT 120 mL 4. Oligoelements: Mn-Cu-Co: 1 ampule evenings before bed 5. Diet: High-fiber, gluten and dairy-free diet
Terrain in detail Precritical terrain
Symptomatic: antiallergic, antihistaminic, antipruritic, antiedematous, steroidals Terrain:
The precritical terrain of Eczema consists of an hyperimmune state related to overproduction of immune elements with a latent incompetency of response to immune challenges. The less competent neuroendocrine adaptation is, the greater the overreliance on immune function will be.
ANS: ⇓ Alpha > Para, ⇑ Beta (to resolve spasmophilia) CORTICO: ⇑ Cortisol and adaptation response of adrenal cortex, ⇓ aromatization of adrenal products to additional estrogens THYRO: ⇓ Central (TRH and TSH) ± thyroid GONADO: ⇓ Estrogen, FSH SOMATO: Adapt according to state of somatotropic synchronization and corticotropic competency DRAIN: 1°-Hepatobiliary, 2°-Intestines, 3°-Skin, preferably simultaneously
1. Immune incompetency a. Spasmophilia b. Permissive adrenal cortex > adaptive cortisol i. Often favors increased production of adrenal estrogens (c.f. overproduction) 2. Overproduction of proteinaceous immune elements a. Endocrine: Hyperestrogenism: initiates production b. Exocrine pancreas: increased uptake of proteins c. Liver as metabolic organ: increased production of immune elements
Treatment goals
● ●
● ● ●
●
Sample treatments 1. Symptomatic: Topical antipruritic, use as needed: 1 tbsp baking soda, 2 drops Lavandula angustifolia essential oil, 2–4 tsp. tisane of Matricaria recutita 2a. Neuroendocrine, Pediatric: (Table 29.10) 1.5 mL twice per day: The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00029-9 © 2020 Elsevier Inc. All rights reserved.
Agent The agent that provokes an eczematous outbreak is a protein-based moiety that contacts the organism topically, through diet, or less frequently via the lungs. For a detailed discussion refer to The Theory of Endobiogeny, Volume 3, Chapter 1.
203
204 SECTION | C Assessment and treatment of common disorders
cient regulation of this response. Peripheral thyroid is often overadapted, which favors inflammation and increased metabolic activity of immune cells. The global neuroendocrine response determined the quality and location of eczematous lesions (Table 29.2). The increased turnover of inflammatory material congests the liver as an emunctory (it is oversolicited in the precritical terrain as a metabolic organ). This makes an appeal to the skin as an emunctory. Thus, the increase in protein metabolism established in the precritical terrain localizes on the skin as eczematous lesions.
Critical terrain The critical terrain is one in which the neuroendocrine response is now hyperfunctioning. However, since the central endocrine response exceeds the peripheral response, it actually creates the terrain of hypermobilization and activation of immune elements that will result in eczema, especially histamine (Table 29.1). The demand for histamines, the number of receptors, and rate of release are all augmented due to central factors: alpha-sympathetic (αΣ), ACTH, and TRH. Due to the incompetency of cortisol, there is insuffi-
TABLE 29.1 ANS-endocrine mediators of histamine activity. Origin
Factor
↑Demand
↑Receptors
↑Release
↓Activity
Brain Stem: ANS
αΣ
•
Pituitary: Corticotropic
ACTH
Hypothalamus: Thyrotropic
TRH
Peripheral: Corticotropic
Cortisol
•
Variable: Corticotropic
Endorphins
•
• •
TABLE 29.2 Topology of allergic disorders. Anatomy
Neuroendocrine Alpha + ↑Para
Alpha + ↓Betaa
ACTH
Forehead
•
Retro-Auricular
•
Visage
•
Cheek bones
•
Cheeks
•
Sinuses
•
Upper thorax
•
Upper Arms
FSH: ACTH >1
FSH: E2 > 1
Pit. + Thyroid
GH > ACTH
•
•
Buttocks
•
•
Back
•
•
Flexural folds
•
Flexor surfaces Extensor surfaces Trunk Peri-articular Distal extrem. a
Beta: beta insufficiency without prejudice to quantitative value.
Key: Extrem., extremities; Pit., pituitary; E2, estyens.
• • • • •
Eczema Chapter | 29 205
Mechanisms
History findings
In response to the localization of the global hypermetabolic hyperimmune activity on the skin, there is a response to antibody–antigen complexes deposited on the epithelium:
During acute eczema, the most fruitful evaluation is that of the eczematous lesions. Inquire about its location: flexor or extensor surfaces, face, body, hands, etc. Inquire about its quality: dry, wet, oozing, pruritic, etc. This information offers precise information about the global neuroendocrine response to the allergen (Table 29.2). If the patient had a prior history of eczema during childhood (or earlier in childhood if still a child), inquire about the same qualities, which indicates the prior adaptation terrain (Table 29.3). If addition information is required, the significance of certain historical findings with respect to the eczematous terrain are presented in Table 29.4.
1. T-helper 2 (Th2)-dominated immune response: secreting cytokines IL-4, IL-5, and IL-13 2. Increased IgE antibodies
Result Eczematous plaques. The logic of the localization of lesions, especially in children, is related to the evolution of the neuroendocrine activity related to various phases of growth (Table 29.3, and, c.f. The Theory of Endobiogeny, Volume 3, Chapter 1).
TABLE 29.3 Logic of the topological evolution of eczema. Age
Mobility
Location
Endocrine adaptative role
2–6 months
Stationary Sitting
Face and scalp
Alpha > Beta ↑ACTH for adrenal cortex relaunching
6–12 months
Crawling
Extensor surfaces Trunk
FSH > ACTH by vertical stimulation as ACTH continues to attempt to relaunch the adrenal cortex FSH > Estrogens
Flexor folds: antecubital, popliteal
Alpha + Para: to relaunch metabolism, relaunch catabolic activity for movement
Flexor surfaces
ACTH: cortico-thyrotropic harmonization for gross motor activity with ambulation
≥1 year
Ambulatory
TABLE 29.4 Historical and terrain findings for eczema. Area
Finding
Terrain
Alpha
GERD, Gastritis, constipation, insomnia
High Alpha
Cortico
Fatigue, recurrent infections Irritability, body odor, hirsutism, acne
Insufficient Cortisol ⇑ DHEA
Gonado
Menorrhagia, Premenstrual breast tenderness, large clots during menstruation
Estrogens > Progesterone and/or androgens
Thyro
Vivid dreams
TRH
Somato
Intense fatigue, myalgia, pain, intense sugar cravings
Somatotropic desynchronization: Insulin > Insulin resistance
Pancreas, Exocrine
Past history of eczema, recurrent ear, nose, or throat infections or congestion, increased mucus production with dairy or gluten, bloating, anal itching
Oversolicited
Liver
Poor immune response, loss of appetite, chills
Hepatic congestion
ANS
Anxious, sensitive, fine (intentional) motor movements
Hyper Alpha-spasmophilia
Key: ANS, autonomic nervous system; Cortico, corticotropic; Gonado, gonadotropic; Somato, somatotropic; Thyro, thyrotropic; GERD, gastroesophageal reflux.
206 SECTION | C Assessment and treatment of common disorders
Physical exam and BoF findings According to the theory of Endobiogeny, because of the role of the endocrine system in morphology and tissue development, the relative predominance of various ANS and endocrine responses to the allergen will localize the allergic response with respect to the exterior of the organism. Topical allergic disorders, such as eczema and hives, offer a direct ability to determine the neuroendocrine influence on the specific localization of lesions (Table 29.2 and 29.3). In addition, specific aspects related to the Endobiogenic terrain can be evaluated, which will vary as evidenced by the location and quality of the eczematous lesions. Some possible findings are presented in Table 29.5, along with related BoF index findings.
Treatment Treatment begins with symptomatic relief of itching and/ or oozing of the lesion. Topical treatments are preferred to
oral therapies for ultra-rapid relief. Essential to this therapy is medicinal clay or sodium bicarbonate. Oral therapies can be pharmaceutical, especially sedating antihistamines when sleep is impaired by intense pruritis (c.f. The Theory of Endobiogeny, Volume 3, Chapter 1). Second priority is neuroendocrine regulation of the critical terrain; third is drainage. Typically, they are started simultaneously. As neuroendocrine regulation can be challenging to address due to the strong genetic nature of eczema, efficient drainage becomes an expedient method of regulating the eczema terrain. Once returned to the precritical terrain, relief of hepato-pancreatic oversolicitation can prevent further flare ups, even in the face of exposure to known allergens. Particular plants address multiple areas of the terrain simultaneously. Thus, the treatment is often quite simple but addresses multiple areas at the same time. For example, Agrimonia eupatoria is a symptomatic dual antiallergic and antihistaminic for the critical terrain, but also hepato-pancreatic
TABLE 29.5 BoF values of the general atopic terrain. Axis
Examination
Terrain
Index
Cortico
Tender rolling of skin, subxyphoid region
Prolonged ACTH
↑ACTH ↑Adaptation
Tender, distal lateral surface of tibia (2/3rd distance from origin)
Oversolicited cortisol demand
↓/normal Cortisol ↑ / normal Adrenal cortex Cortisol /Adrenal Cortex ratioa < 2 ↑Aromatization ↑Permissivity ↓ or negative Adaptationpermissivity of adrenal cortex
Prolonged erythema of skin after vertical rolling over back
Elevated dermal histamines
↑Evoked Histamine
Gonado
↑FSH
Thyro
↓Genito-thyroid Glabellar tap: lower eyelid faster than upper, and flutter of eyelids
Elevated Alpha relaunching TRH
↑/normal Interleukin-1
Immunity
Hyperimmunity
Pancreas
Tender to palpation, superior and right of umbilicus
Oversolicited exocrine pancreas
Liver
Tender to palpation, superior or inferior borders
General oversolicitation of pancreas
Intestines
Tender inferior to gastrum in midline
Duodenal inflammation
Intestines
Tender to palpation left of umbilicus
Dysbiosis
a
Not an index; the individual indexes are divided to obtain the value.
↑/normal Thyroid relaunching corrected
↑/normal Somatostatin
Eczema Chapter | 29 207
support for the precritical terrain. Ribes nigrum buds improve cortisol production and inhibit ACTH, but is also antiallergic, relevant to the critical and precritical terrains. 1. Symptomatic a. Antihistaminic (Table 29.6) b. Antiallergic (Table 29.7) c. Dual antihistaminic and antiallergic (Table 29.8) 2. Neuroendocrine regulators (Table 29.9) 3. Drainage (Table 29.9) 4. Diet and lifestyle 5. Oligoelements (to improve the buffering capacity): a. Manganese: healing dermis, clearing toxic material i. Manganese-Copper (Mn-Cu): When superinfections persists due to poor oxidation
ii. Manganese-Copper-Cobalt (Mn-Cu-Co): 1. Chronic, degenerative eczema 2. Strong emotional disturbance or stress related to aggravation of disease b. Sulfur (S): poor quality of skin repair. c. Zinc (Zn): recurrent skin superinfections
Exemplary prescriptions Based on an Endobiogenic approach to eczema, a number of prescriptions can be derived. 1. Symptomatic: Topical antipruritic, use as needed: 1 tbsp medicinal clay or 1 tbsp baking soda constituted with carrier fluid
TABLE 29.6 Antihistaminic medicinal plants. Medicinal plant
Galenical
Indication/comment
Arnica montana
BH, MT
Alpha > Para and/or low insulin resistance
Artemisia dracunculus
EO, BH
Mental spasmophilia: anxiety, depression, etc.
Hamamelis virginiana
BH, DE, MT
Constipation, pelvic congestion
Eucalyptus globulus
EO
Asthma comorbidity
Matricaria recutita
BH, EO, DE, MT
Anger exacerbates eczema, strong inflammatory component Safe on open wounds
TABLE 29.7 Antiallergic medicinal plants. Medicinal plant
Galenical
Indication/comment
Arctium lappa
BH, MT
Polyvalent pancreatic-skin drainer, advanced inflammatory state
Borago officinalis
BH, MT
Regulation of edema and estrogenism
Cichorium intybus
BH, HL
Dysbiosis prominent in immune dysregulation
Citrus limon
EO
Congestion around wound
Cnicus benedictus
BH, MT
Difficulty initiating liver drainage, secondary fungal infection
Glycyrrhiza glabra
BH, MT
Asthma comorbidity Food allergy comorbidity Intestinal permeability
Ribes nigrum
GM
Adrenal insufficiency, tissue drainage required
Rosmarinus officinalis
BH, DE, EO, GM
Adrenal insufficiency, delayed wound healing
Rubus idaeus
GM
Asthma comorbidity and menstrual cycle dysregulation
Sambucus nigra
MT, leaf
Brain fog, viral implication
Taraxacum officinale
BH, DE, MT
Autotoxicity, low insulin resistance, elevated CRH, Strong hepatic implication
Urtica dioica
BH, DE, MT, Leaf
Skin drainage where hyperglycemia and elevated insulin resistance play an important role
208 SECTION | C Assessment and treatment of common disorders
TABLE 29.8 Dual antihistaminic, antiallergic plants. Medicinal plant
Galenic
Indication/comment
Agrimonia eupatoria*
BH, MT
Indirect antiallergic through drainage of pancreas
Fagus sylvatica
GM
Hypogammaglobulinemia
Fumaria officinalis
BH, HL
Strong implication of biliary congestion
Inula helenium
BH, MT
Asthma comorbidity Recurrent ENT infections Peripheral cortico-gonadotropic insufficiency
Lavandula angustifolia*
BH, DE, EO, MT
Prominent spasmophilia, anxiety
Plantago major
BH, MT
Hepato-pancreatic implication Asthma comorbidity
Syzygium aromaticum
EO
Recidivistic infections; Avoid in open wounds
Viola tricolor*
BH, MT
Indirect antiallergic through drainage of pancreas Hyperhistaminemia and multiemunctory congestion
Key: *, most efficient plants; BH, bulk herb; GM, gemmomacerate; HL, hydrolat; DE, dry extract; EO, essential oil; MT, mother tincture.
TABLE 29.9 Summary of treatment of global terrain of eczema. Category
Goal
Medicinal plant
Autonomic
↓ Para-Alpha
Lavandula angustifolia EO, BH, HL, MT Anthemis nobilis EO, BH, HL, MT Matricaria recutita EO, MS, BH, MT Cinnamomum zeylanicum EO, BH, Citrus paradisii EO Crataegus oxyacantha: MT, GM, DE
↑ Beta
Corticotropic
↑ Cortisol
↓ Aromatization Somatotropic
Regulate GH-PL ↓ Insulin resistance
Drainage
Hepatobiliary Intestinal
a. Fluid 1–3 tsp., for a thin, paste-like consistency i. Water ii. Hydrolat: rose (all), peppermint (3 and older) iii. Tisane (antiallergic, antihistaminic, skin drainer): Arctium lappa, Agrimonia eupatoria, Matricaria
Ribes nigrum GM, Abies pectinata GM Quercus pedunculata GM Thymus vulgaris EO, BH Satureja ssp. EO, BH Achillea millefolium EO, BH, MT GH Low, Cortisol low: Lamium album MT, BH GH elevated, Cortisol low: Fragaria vesca (leaf) MT, BH Arctium lappa: MT, BH Agrimonia eupatoria: MT, BH Juglans regia: MT, GM Arctium lappa: MT, BH Agrimonia eupatoria: MT, BH Viola tricolor: MT, BH Agrimonia eupatoria: MT, BH Lamium album MT, BH
recutita, Anthemis nobilis, ¼ tsp. in 4 tbsp hot water for 8–15 min b. Optional: 1–2 drops essential oil (antiallergic, antihistaminic): Lavandula angustifolia, Matricaria recutita, Anthemis nobilis
Eczema Chapter | 29 209
If using essential oils, add to dry ingredient, mix well, then add carrier fluid once cooled. Apply to affected area. If skin sensitive, add paste to cheesecloth and lightly apply to affected area. 2a. Neuroendocrine, Pediatric (Table 29.10) 1.5 mL twice per day: Avena sativa MT 60 mL, Rosa canina GM 60 mL, Ribes nigrum GM 60 mL 2b. Neuroendocrine, Adult (Table 29.11) 3 mL three times per day: Rhodiola rosea MT 60 mL, Inula helenium MT 60 mL, Ribes nigrum GM 60 mL, Quercus pedunculata GM 60 mL, Lavandula angustifolia EO 4 mL
3. Hepato-pancreatic-dermal drainage: 3 mL three times per day before meals, or before breakfast and dinner, and, before bed (Table 29.12): Arctium lappa MT 120 mL, Agrimonia eupatoria MT 120 mL 4. Oligoelement: Mn-Cu-Co: 1 ampule evenings before bed 5. Diet: High-fiber, gluten and dairy-free diet (except fermented dairy if tolerated). Often soy needs to be avoided. Encourage cruciferous vegetables and foods rich in magnesium (c.f. The Theory of Endobiogeny, Volume 2, Chapter 11) and those that support the liver (i.e., beets).
TABLE 29.10 Neuroendocrine prescription; DOSE: 1.5 mL twice per day with meals. Herb
Replacements and alternatives
Avena sativa MT 60 mL
Rhodiola rosea MT
Rosa canina GM 60 mL
Ribes nigrum GM 30 mL + Crataegus oxyacantha GM 30 mL
Ribes nigrum GM 60 mL
Quercus pedunculata GM
Key: DE, dry extract; EO, essential oil; GM, gemmomacerate; MT, mother tincture.
TABLE 29.12 Drainage prescription; DOSE: 3 mL three times per day. Herb
Replacements and alternatives
Arctium lappa MT 120 mL
Viola tricolor MT
Agrimonia eupatoria MT 120 mL
Plantago major MT 60 mL + Juglans regia GM, MT 60 mL
Key: EO, essential oil; MT, mother tincture; GM, gemmomacerate.
TABLE 29.11 Neuroendocrine prescription; DOSE: 3 mL two times per day with meals. Herb
Replacements and alternatives
Rhodiola rosea MT 60 mL
Eleutherococcus senticosus MT 20 mL + Inula helenium MT 40 mL
Inula helenium MT 60 mL
Rhodiola rosea MT 40 mL + Eleutherococcus senticosus MT 20 mL
Ribes nigrum GM 60 mL
Quercus pedunculata GM, Lavandula angustifolia EO, MT
Quercus pedunculata GM 60 mL
Ribes nigrum GM
Lavandula angustifolia EO 4 mL
Matricaria recutita EO 2 mL, Citrus aurantium EO 2 mL
Key: EO, essential oil; GM, gemmomacerate; MT, mother tincture.
Chapter 30
Esophageal varices Summary Essence: Compensatory esophageal drainage for portal hypertension results in dilation and weakening of esophageal veins. Terrain: (1) Portal vein hypertension or obstruction resulting in compensatory (2) Splanchnic venous return in part via (3) Esophageal drainage toward superior vena cava; (4) Prolonged esophageal flow results in (5) esophageal varices.
Treatment goals Symptomatic: Reduce sympathetic tone, drain portalsplanchnic system, Beta-blockade, surgery. Terrain: ●
●
●
ANS: ⇓ Alpha tone regionally (splanchnic system in toto) and globally if indicated DRAIN: 1°-Splanchnic bed, 2°-Portal circulation, 3°-Liver VASCULAR: vasorelaxation, improve vascular elasticity and tensegrity
Sample treatment 1. Neuroendocrine: ANS-Drainage-Vascular: 4 mL before lunch and dinner and 8 mL before bed during acute phase of recovery, then 2.5 mL before lunch and dinner, and 5 mL before bed: ● Hypertensive patient with partially controlled diabetes mellitus: Matricaria recutita MT 80 mL, Carduus marianus MT 80 mL, Vaccinium myrtillus GM 80 mL, Citrus limon EO 4 mL, Mentha viridis EO 1 mL ● Alcoholic steatosis with anxiety: Carduus marianus MT 120 mL, Matricaria recutita MT 40 mL, Corylus avellana GM 80 mL, Lavandula angustifolia EO 4 mL 2. Oligoelement: Sulfur 2 ampules AM, 1 ampule before bed Diet: Glutathione 500 mg AM, 250 mg before bed 3. Diet: Bone broth, vegetable juices (high potassium), white fish, whole grains, avoid meat, animal fat, fruits, sweets The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00030-5 © 2020 Elsevier Inc. All rights reserved.
Terrain in detail Precritical terrain The precritical terrain in essence involves chronic hepatic oversolicitation for any reason that results in congestion and delayed flow (c.f. Chapter 13: Hepatic insufficiency). It could be metabolic, exocrine, endocrine, immune, storage, etc.
Agent The agent can be of three types: (1) further oversolicitation, (2) gross hepatic injury or damage, (3) clotting of the portal vein. A number of causes, such as alcoholic steatosis fall under the first and second categories. A nonexhaustive list of common instigators is: 1. Hepatic steatosis, alcoholic or nonalcoholic 2. Drug abuse 3. Hepatitis 4. Cirrhosis 5. Chronic inflammatory disorders 6. Iatrogenic dysendocrinism, e.g., oral contraceptives, glucocorticoids 7. Diabetes mellitus 8. Diminished portal blood flow
Critical terrain The critical terrain involves two types of response. The first is a compensatory sympathetic adaptation to absolute hepatic insufficiency. This results in portal hypertension, which is compensated for by shunting splanchnic drainage partially through esophageal veins to the superior vena cava. The second is a terrain that results in thrombosis, partially occluding the portal vein. This chapter discusses the first response. 1. ANS a. Alpha: Adaptive to further congest the liver to allow more time for hepatic processing of blood b. Beta: compensatory to increase splanchnic inflow
Mechanisms 1. Hydrostatic pressure on portal vein 211
212 SECTION | C Assessment and treatment of common disorders
2. Shunting of splanchnic venous return to esophageal veins 3. Hydrostatic pressure on esophageal veins leading to dilation and loss of vascular tensegrity
4. Diet: avoid foods that tax the liver and gallbladder (fried foods, animal products), avoid high purine foods; consume bone broths, collagen protein powders, vegetable juices, white fish, and whole grains
Result
Exemplary prescriptions
Esophageal varices.
Based on an Endobiogenic approach to esophageal varices, a number of prescriptions can be derived. We present two based on patients with other particular comorbidities.
Treatment Symptomatic: Antihypertensives (sympathetic blockade), anticoagulants. Terrain: The approach to the terrain involves addressing the sympathetic and vascular imbalances of the critical terrain, and strongly supporting hepatic function. The two most efficient plants for portal and splanchnic drainage are Carduus marianus and Matricaria recutita. Use them in conjunction with a vasculotonic plant (e.g., Corylus avellana) and/or a vasculoprotective plants (e.g., Vaccinium myrtillus). 1. ANS (Table 30.1) a. Sympatholytics b. Parasympathomimetics for venous relaxation 2. Vasculature (Table 30.1) a. Portal drainers b. Splanchnic drainers c. Vasculotonic plants d. Vasculoprotective plants 3. Heme: regulate thrombus formation
1. Neuroendocrine: ANS-Drainage-Vascular: 4 mL before lunch and dinner and 8 mL before bed during acute phase of recovery, then 2.5 mL before lunch and dinner, and 5 mL before bed: a. Hypertensive patient with partially controlled diabetes mellitus Matricaria recutita MT 80 mL, Carduus marianus MT 80 mL, Vaccinium myrtillus GM 80 mL, Citrus limon EO 4 mL, Mentha viridis EO 1 mL b. Alcoholic steatosis with anxiety Carduus marianus MT 120 mL, Matricaria recutita MT 40 mL, Corylus avellana GM 80 mL, Lavandula angustifolia EO 4 mL 2. Oligoelement: Sulfur 2 ampules AM, 1 ampule before bed Diet: Glutathione 500 mg AM, 250 mg before bed 3. Diet: Bone broth, vegetable juices (high potassium), white fish, whole grains, avoid meat, animal fat, fruits, sweets
TABLE 30.1 Polyvalent medicinal plants for esophageal varices. Plant
Drainage
Vascular
Autonomic
Other actions
Carduus marianus
Portal, splanchnic, Hepatobiliary
Circulatory tonic
Alpha-sympathomimetic (mild, on microcirculation)
Hemostatic
Matricaria recutita
Hepatic, splanchnic
Hypotensive
Sympatholytic, Vagolytic
Eupeptic, antiulcerative (gastric), platelet antiaggregant
Cichorium intybus
Portal
Vasculoprotective, hypotensive
Parasympathomimetic
Eupeptic, exocrine pancreatic stimulant
Vaccinium myrtillus
Intestines, pancreas
Vasculoprotective, capillary tonic
Corylus avellana
Lungs, heart, neurologic
Vasculotonic
Italic: hematologic effects.
Hypoglycemant, antigastritic, diuretic Alpha-sympatholytic (indirect by action on locus ceruleus)
Eupeptic, antiulcerative (gastric), hepatic anticirrhotic, erythropoietic, antianemic
Chapter 31
Gastroesophageal reflux disease (GERD) Summary Type 1: Lower esophageal sphincter Essence: Hypervagal tone on the lower esophageal sphincter results in reflux of gastric content with normal gastric pressure Summary: (1) Hyperparasympathetic tone leads to (2) relaxed lower esophageal sphincter tone and (3) reflux of gastric content
Type 2: Pyloric sphincter Essence: Hyper-alpha-sympathetic spasmophilia of pyloric sphincter with increased gastric pressure resulting in retrograde flow of gastric content Summary: (1) Spasmophilia of pyloric sphincter, leads to (2) increased intragastric pressure to overcome resistance to dilation resulting in (3) reflux of gastric content into esophagus
Treatment goals Symptomatic: antacids, proton pump inhibitors Terrain: Type 1: Lower esophageal sphincter: ● ANS: reduce parasympathetic tone ● GI: improve efficient of production of digestive juices and motricity Terrain: Type 2: Pyloric sphincter: ● ANS: spasmolysis ● GI: biliary-pancreatic competency
Sample treatment Type 1: Lower esophageal sphincter 1. Neuro-GI-fatigue: 1 cup 15–30 min before meals (Table 31.1): Carum carvi seeds ¼–½ tsp, Thymus vulgaris ¼ tsp steep 6–8 min in 150 mL water 2. Diet: eat lightly cooked (steamed, baked, broiled, lightly sautéed) foods, boiled eggs, fish, fowl; if red meat, grass
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00031-7 © 2020 Elsevier Inc. All rights reserved.
fed and marinated and tenderized before cooking. Eat in a calm environment, focusing on chewing until liquefaction, placing utensils down on table while chewing. Avoid acidic, fatty or fried foods, poor-quality red meat, acidic food and beverage, rapid or high-volume consumption of food
Type 2: Pyloric sphincter 1. Neuro-digestive-anxiety/anger: 3–4 mL with meals (Table 31.5): Matricaria recutita MT 60 mL, Plantago major MT 60 mL, Cinnamomum zeylanicum EO 2 mL 2. Diet: see GERD type 1
Terrain in detail: Type 1 GERD: Lower esophageal sphincter Precritical terrain The precritical terrain is one in which the demand for vagal activity at the level of the digestive tract is adapted to local requirements. It can be in response to regional or global autonomic activity, to the quality or quantity of food, or, to calibrate or adapt the quality or quantity of digestive juices: 1. ANS a. Vagotonic patients b. Systemic hyper parasympatheticism with secondary elevation of local vagal tone c. Reactionary elevation of vagal tone to regional or global elevation of alpha-sympathetic tone 2. Alimentation a. Chronic consumption of foods that strain the digestive capacity of the organism 3. Digestion a. Oversolicitation of digestive juices: salivary, gastric, exocrine pancreatic b. Loss of absorptive capacity: denudation of intestinal villi
213
214 SECTION | C Assessment and treatment of common disorders
Agent
History and BoF findings
Solicitation of sufficiently elevated parasympathetic tone that expresses itself on the lower esophageal sphincter:
During acute GERD type 1, the patient will complain about the symptoms noted under “Results.” Inquire about diet and dietary hygiene, and the presence of the various aggressors noted earlier.
1. Quality of meal: animal protein, fatty or fried foods, acidic foods or drinks, caffeinated beverages 2. Quantity of meal: large portions 3. Rate of consumption: rapid 4. Decrease in production or expression of digestive juices a. Elevated cortisol: suppresses excretion b. Elevated somatostatin activity: ends production 5. Elevation of sympathetic tone (with reactionary rise in parasympathetic tone) 6. Chronobiologic demand for increased parasympathetic tone (e.g., physiologic vagotonia of childhood) 7. Restorative adaptation states requiring increased parasympathetic tone (e.g., recovery from injury)
Critical terrain ANS: hypervagal tone on the lower esophageal sphincter (LES).
Mechanisms Diminished resting (closed) tone of the LES.
Result During contraction of the stomach, with normal intragastric pressure, there is retrograde movement of chyme and acid into the lower esophagus causing a feeling of (one or more of the following): 1. Retrosternal burning, pain or discomfort 2. Recurrent asthma, especially cough-variant 3. Aspiration pneumonia (especially in the elderly) 4. Arching of the back with wincing and/or crying (in infants)
Physical exam and BoF findings During presentation with acute GERD Type 1, a number of physical exam findings may be present, with some possible Biology of Functions correlations (Table 31.2) In the Biology of Functions, the Parasympathetic index may be elevated or low as an indicator of the general parasympathetic tone of digestion and nutrition.
Treatment 1. Alimentation a. Specific: avoid known offending foods, e.g., nightshades (e.g., potatoes, tomatoes), pizza, etc. b. General: avoid acidic, fatty, or fried foods, poorquality red meat, acidic food and beverage, rapid or high-volume consumption of food 2. Terrain a. ANS/GI: parasympatholytics with digestive, eupeptic activity (Table 31.1) b. General endocrine terrain, address according to comorbidities related to onset of GERD type 1
Exemplary prescriptions Based on an Endobiogenic approach to type 1 GERD, a number of prescriptions can be derived. One example is presented here: 1. Neuro-GI-fatigue: 1 cup 15–30 min before meals: Carum carvi seeds ¼–½ tsp, Thymus vulgaris ¼ tsp steep 6–8 min in 150 mL water
TABLE 31.1 Polyvalent medicinal plants for type 1 GERD. Parasympatholytics
Other properties
Comorbidities
Thymus vulgaris: EO, BH
Adrenal cortex stimulant Emmenagogue
Depression, fatigue, insomnia, amenorrhea, infertility
Ocimum basilicum: EO, BH
Adrenal cortex stimulant FSH/LH stimulant, Estrogenic
Carum carvi: EO, BH
Reduces adrenal androgens
Key: BH, bulk herb; EO, essential oil; MT, mother tincture.
Irritability, acne on jawline
Gastroesophageal reflux disease (GERD) Chapter | 31 215
2. Diet: a. Eat: lightly cooked (steamed, baked, broiled, lightly sautéed) foods, boiled eggs, fish, fowl; if red meat, grass fed (not grass finished), and, marinated before cooking b. Hygiene: eat in a calm environment, focusing on chewing until liquefaction, placing utensils down on table while chewing c. Avoid: acidic, fatty, or fried foods, poor-quality red meat, acidic food and beverage, rapid or high- volume consumption of food
Terrain in detail: Type 2 GERD: Pyloric sphincter Precritical terrain Timing of release of chyme from the stomach is related to the rate and quality of release of bile and digestive enzymes and bicarbonate from the gallbladder and exocrine pancreas, respectively. In the precritical terrain, there is a chronic oversolicitation of these digestive glands due to the consumption of fatty, fried, and acidic foods (c.f. Type 1 GERD for details) with a compensated vagal tone for production and excretion of digestive juices. 1. Biliary-pancreatic strain: oversolicited due to diet 2. ANS: adapted (often elevated) parasympathetic (vagal) tone
Agent The inciting agent may be (1) level of dietary consumption that exceeds the threshold of digestive competency, (2) sympathetic tone that installs a spasmophilia, or (3) some combination. 1. Biliary-pancreatic: insufficiency or deficiency of timing or quantity of digestive juices 2. ANS: hyper alpha-sympathetic a. Emotional stress b. Physiologic stressors c. Overadapted to chronically elevated vagal tone d. Chronobiologic adaptation (transition to spring, autumn, etc.: (c.f. Chapter 12 and The Theory of Endobiogeny, volume 2, Chapter 11: Spasmophilia)
Critical terrain 1. ANS: spasmophilia (hyper alpha>hyper para, beta blocked or delayed) on pylorus
Mechanisms Insufficiency of bile and/or pancreatic juices makes an appeal to the stomach to delay passage of chyme, resulting in an elevated tone on the pyloric sphincter (spasmophilia). The stomach must develop supraphysiologic pressure to overcome pyloric tone.
Result During contraction of the stomach, with supraphysiologic intragastric pressure, there is retrograde movement of chyme and acid into the lower esophagus causing a feeling of (one or more of the following): 1. Retrosternal burning, pain or discomfort 2. Recurrent asthma, especially cough-variant 3. Aspiration pneumonia (especially in the elderly) 4. Arching of the back with wincing and/or crying (in infants)
History and BoF findings During acute GERD type 2, evaluate for the presence of the symptoms noted earlier, as well as the possible aggressors, and address them as indicated. A general evaluation of spasmophilia symptoms can also be explored, such as anxiety, depression, muscle cramps, etc. Symptoms related to dyspepsia rooted in biliary-pancreatic insufficiency can include: 1. Gallbladder a. Intolerance of fried or fatty foods: prolonged feeling of gastric fullness, burping, and “tasting” the foods for hours b. Subhepatic pain with or without movement toward the back related to consumption of fried or fatty foods c. Clay-colored stool 2. Exocrine pancreas a. Bloating within 20 min of eating b. Floating stools (steatorrhea) c. Intolerance of specific types of foods (legumes, red meat, fat, carbohydrates)
Physical exam and BoF findings During presentation with acute GERD type 2, a number of signs can be noted with correlation with certain BoF indexes. Some are specific to biliary-pancreatic oversolicitation or insufficiency, others may be related to spasmophilia (Table 31.2).
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TABLE 31.2 Critical terrain signs and Biology of Functions correlations. Area
Finding
Terrain
BoF
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓PMI
Mouth
Dilated opening of canal of Stensen
Insufficient pancreatic amylase
↑/↓ Somatostatin
Mouth
Saliva stringy
Alpha>para
↑/↓ Leukocyte mobilization
Pancreas
Tender, above umbilicus Tender, right of umbilicus Tender, left of umbilicus
Congestion: general Oversolicitation: exocrine Oversolicitation: endocrine
N/A ⇑/⇓ Somatostatin ⇑/⇓ Insulin
Gallbladder
Murphy’s point tender (midpoint umbilicus to right costal margin)
Gallbladder congested
Treatment GERD type 2 is a spasmophilia; thus, there is hyperfunctioning alpha greater than hyperfunctioning vagal tone. The goal of treatment is three-fold: 1. ANS (Table 31.3) a. Spasmolysis
b. Relaunch or restore the proper sequencing of beta 2. Digestive (Table 31.4) a. Assure choleresis and cholagogy where required b. Assure adequate production of digestive enzymes where required 3. Diet: see Type 1 GERD
TABLE 31.3 Polyvalent medicinal plants with autonomic properties. Plant
ANS
Other properties
Comorbidities
Matricaria recutita
Parasympatholytic Alphasympatholytic
Anti-inflammatory, eupeptic, hepatosplanchnic drainer, neurotropic antispasmodic
Anxiety, anger, inflammatory conditions, dyspepsia
Salvia sclarea
Parasympatholytic Alphasympatholytic
Supports adrenal cortex and thyroid, estrogenic, eupeptic, pancreatic drainer
Nervous asthenia, fatigue, amenorrhea, hypothyroidism, etc.
Lavandula angustifolia
Parasympatholytic Alphasympatholytic
Reduces adrenal cortex activity, hepatobiliary drainer, antiallergic, antispasmodic
Insomnia, chronic fatigue, allergies, migraines, etc.
Cinnamomum zeylanicum
Beta-mimetic
Eupeptic, regulates intestinal flora, antimicrobial with tropism for digestive tract
Intestinal candidiasis or intestinal parasites, dysbiosis with bloating and gas, asthma
Menyanthes trifoliata
Beta-mimetic
Anti-inflammatory, antiandrogenic, estrogenic, beta-sympathomimetic
Inflammation, acne, prostatic hypertrophy, uterine leiomyoma, etc.
TABLE 31.4 Polyvalent medicinal plants with biliary-pancreatic tropism. Medicinal plant
Exocrine pancreas
Gallbladder
Other
Agrimonia eupatoria
General stimulation of enzyme production
•
Dual pancreatrope and drainer, digestive astringent
Arctium lappa
General stimulation of enzyme production
•
Dual pancreatrope, immunomodulator
Plantago major
Amylase, disaccharidase
•
Digestive antispasmodic, hepatobiliary drainer
Gastroesophageal reflux disease (GERD) Chapter | 31 217
Exemplary prescriptions Based on an Endobiogenic approach to type 2 GERD, a number of prescriptions can be derived. One example is presented: 1. Neuro-digestive-anxiety/anger: 3–4 mL with meals (Table 31.5) Matricaria recutita MT 60 mL, Plantago major MT 60 mL, Cinnamomum zeylanicum EO 2 mL 2. Diet: see GERD type 1
TABLE 31.5 Treatment of GERD, type 2, DOSE: 2 mL three times per day before meals. Plant
Replacements and alternatives
Matricaria recutita MT 60 mL
Salvia sclarea MT
Plantago major MT 60 mL
Agrimonia eupatoria MT
Cinnamomum zeylanicum EO 2 mL
Lavandula angustifolia EO
Key: MT, mother tincture; EO, essential oil.
Chapter 32
Menstruation, normal cycle Summary Essence: The human menstrual cycle matures ova for fertility and continuation of the human species. Terrain:: The cycle has two phases. The follicular half is predominated by follicle-stimulating hormone (FSH) and estrogens. Its purpose is to mature follicles and the endometrium, respectively. It determines length of cycle and duration of menstruation. The follicular half begins with menstruation and ends with ovulation. The luteal half is predominated by luteinizing hormone (LH) and progesterone, with the goal of sustaining implantation of a fertilized ovum. The relationship of progesterone to estrogens, both relative and absolute, will determine if and what type of premenstrual symptoms present in the late luteal phase. The phase ends when there is no implantation. The “ideal” cycle lasts 28 days, with a normal range of 25–30 days. In a 28-day cycle, each of the two phases, follicular and luteal, is 14 days long. Central and peripheral hormones across all four axes play a role in calibrating the activity of the gonadotropic hormones throughout the cycle. Disruption in the timing, duration, sequencing, quantity, or quality of the suite of hormones results in abnormalities in the menstrual cycle, be it duration, quantity, or timing of bleeding, frequency of cycles, and/or fertility.
Follicular phase The follicular phase has three main actions of maturation: (1) ova, (2) endometrium, (3) cervical fluids, with one purpose: optimizing implantation of a fertilized ova for continuation of the species (Fig. 32.1).
D5–10: Midfollicular: Estrogens, prolactin 1. Ovaries: selection of dominant follicle→Estrogen relaunching via androstenedione conversion a. With declining FSH, TRH relaunches prolactin (PL) to augment estrogen receptors 2. Endometrium: proliferation 3. Cervix: copious, clear, elastic, para>alpha
D11–13: Late follicular: GnRH, FSH second relaunching 1. Ovaries: TRH relaunching to optimize estrogen activity: (1) GnRH relaunching, (2) FSH relaunching, (3) estrogen receptor sensitivity augmented, (4) prolactin relaunching: estrogen receptor proliferation a. FSH peak days 12–14: increases man’s desire for and female’s attractiveness: optimum time for coitus b. LH double peaks, days 12–13: TRH→PL alters GnRH to favor LH 2. Endometrium: proliferation 3. Cervix: copious, clear, elastic, para>alpha
Day 14: Ovulation: LH+progesterone+T4+prost aglandins ●
●
●
D1–4: Early follicular: GnRH, FSH 1. Ovaries: GnRH relaunches FSH for recruitment of follicles developed in prior cycles 2. Endometrium: necrosis, sloughing if no fertilization in prior cycle: 4–5 days a. Range: 3–8 days, based on estro-thyrotropic relationship in luteal phase+early follicular phase 3. Cervix: mucous thin, scanty, para>alpha
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00032-9 © 2020 Elsevier Inc. All rights reserved.
Ovaries: peak LH; prostaglandins allow for rupture of Graafian follicle for ovulation; progesterone begins rise; pique of T4 causes rise in basal body temperature Endometrium: peak proliferation, will determine duration of menstruation, thus duration of next cycle Cervix: copious, clear, elastic, ferning seen under microscope
Summary of follicular phase The follicular phase of the menstrual cycle has three stages: (1) Early: FSH, follicle recruitment, (2) Mid: FSHestrogen: follicle selection, uterine proliferation, (3) Late: LH-Estrogen+TRH+PL, culminating in ovulation.
219
220 SECTION | C Assessment and treatment of common disorders
FIG. 32.1 Summary of hormonal activity during the menstrual cycle. E2: estrogens; P2: progesterone.
Luteal phase
D21–24: Mid-luteal
The primary purpose is to serve the fertilized ova. A new, temporary organ is created, the corpus luteum, under the influence of LH, which is an estro-progestive endocrine unit. We can divide the luteal phase into three stages: early, mid-, and late. The early and mid-stages are spent in anticipation of implantation. If this does not occur, the later stage proceeded with a dramatic reduction in the activity of all hormones related to the menstrual cycle.
1. Ovaries a. D21–24: peak progesterone: implantation of fertilized ovum must take place within 10 days from ovulation. Estrogens reach their final peak thanks to TRH and PL, then decline b. D21: ACTH rises to limit PL, preventing excessive estrogen sensitivity 2. Endometrium: secretory phase 3. Cervix: copious, thick, opaque, alpha>para
D15–20: Early luteal 1. Ovaries: corpus luteum a. D15–20: Rising progesterone: competitive antagonism again estrogens, diminishing action on GnRH, FSH, LH, to be counteracted on days 18, 19 b. D18: Alpha+CRH relaunch GnRH: global gonadotropic recalibration c. D19: TRH, PL recalibrate estrogen activity in compensation for rising progesterone 2. Endometrium: secretory phase 3. Cervix: copious, thick, opaque, alpha>para
D25-Menstruation: Late luteal ●
●
●
Ovaries: Corpus luteum degenerates into corpus albican absent human choriogonadotropin hormone (hCG) → precipitous drop in progesterone. Inhibin A (not depicted in Fig. 32.1) peaks, preventing FSH, estrogen relaunching Endometrium: ischemic necrosis, sloughing, expulsion with rise in prostaglandins Cervix: production and quality diminishes
Menstruation, normal cycle Chapter | 32 221
Summary of luteal-phase endocrinology A temporary endocrine organ, the corpus luteum, manages the significant and sustained activity of progesterone and estrogens. There are three stages to the luteal phase: (1) Early: progesterone predominance to assist with implantation and pregnancy, (2) Mid: sustained progesterone, estrogen relaunching, (3) Late: in absence of implantation, precipitous decline of estro-progestive activity and atrophy of corpus luteum (corpus albican). Key points about the relationship of progesterone to estrogens: ● ●
●
Most determinant of implantation and pregnancy Quantitative and qualitative relationship determine the presence and primary premenstrual symptoms Attempts by TRH, PL, Alpha, ACTH shape the quality and secondary symptoms related to premenstrual symptoms, such as vivid dreams, sugar cravings, etc.
Conclusions The human female menstrual cycle constitutes a repetitive longitudinal variation in neuroendocrine activity in which there are significant variations in the quantitative production
and qualitative activity of hormones. This fluctuation implicates emunctory activity and a dynamic function is part of a strategy of preparing the female of childbearing age on a monthly basis for the possibility of fertility with a mate. This activity, as metabolically demanding as it is, is a necessary requirement for propagation of the species. Its proper functioning not only ensures survival of the species, but diminishes the risk of disorders of menstruation and congestion of emunctories. The theory of Endobiogeny posits that given the significant variations of quantitative output of hormones during the menstrual cycle, this is not a valid way to determine what the model of optimal function is. Instead, the construct of optimal menstrual function must consider multiple nongonadotropic hormones and their functional and effective synergistic interaction with the key gonadotropic hormones. The menstrual cycle can be divided into two pages: follicular and luteal. The follicular is the time of absolute estrogen predominance and preparation of the endometrium for possible implantation of a fertilized follicle. The luteal phase is the time of absolute progesterone predominance to nurture any possible implantation. The sequencing of these two phases is key for optimal fertility and a symptom-free menstrual cycle.
Chapter 33
Menstruation disorders: Metrorrhagia Summary Essence: Untimely uterine bleeding due to diminished tissular estrogen activity outside the time of menstruation. Terrain: (1) Expression of various central and/or peripheral factors that (2) Diminish tissular estrogen activity at the level of the endometrium impairing (3) Continued development of endometrium resulting in (4) Areas of focal endometrial necrosis expressed as (5) Intermittent and light uterine bleeding outside the time of total menstrual sloughing.
Treatment goals Terrain: ● Regulate tissular estrogen competency through central/ peripheral management ● Drainage and emunctories: pelvis, liver
Sample treatment: Follicular metrorrhagia types Type 1: Diminishment of estrogens by cortisol Type 1A: Sympatholytic-corticotropic: 4 mL AM and before bed on menstrual days 10–14, and 3 mL twice per day the remainder of the cycle (Table 33.1): Passiflora incarnata MT 60 mL, Leonurus cardiaca MT 60 mL+Lavandula angustifolia EO 2 mL Type 1B: Cortisol regulator/anabolic adrenal cortex support: 4 mL AM and afternoons on days 1–16 of the menstrual cycle (Table 33.2): Passiflora incarnata MT 60 mL, Ribes nigrum GM 160 mL, Fragaria vesca MT 40 mL+Lavandula angustifolia EO 3 mL Type 1C: Global corticotropic regulator: 3 mL AM, 3 mL PM and before bed on days 4–14 of the menstrual cycle; increase up to 5 mL per dose commensurate to levels of stress or lack of sleep the night before (Table 33.3): Passiflora incarnata MT 60 mL, Rhodiola rosea MT 40 mL, Sequoia gigantea GM 80 mL, Quercus pedunculata GM 60 mL+Lavandula angustifolia EO 3 mL The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00033-0 © 2020 Elsevier Inc. All rights reserved.
Type 2: Interruption of production of estrogens Type 2A: 1. Sympathetico-cortico-gonadotropic adaptation: 3 mL before breakfast and dinner on days 1–15 of the menstrual cycle (Table 33.4): Passiflora incarnata MT 60 mL, Ribes nigrum GM 80 mL, Salvia officinalis MT 100 mL+Lavandula angustifolia EO 3 mL 2. Gonado-hepato-pelvic drainage: 3 mL before breakfast and dinner on days 1–15 of the menstrual cycle (Table 33.5): Avena sativa MT 60 mL, Agrimonia eupatoria MT 120 mL, Hamamelis virginiana MT 60 mL+Angelica archangelica root EO 1 mL, Artemisia dracunculus EO 2 mL Type 2B: 1. FSH relaunching-cortico-gonado: 6 mL twice daily on days 1–18, then 4 mL twice daily until onset of menstruation. Re-evaluate after 3–4 cycles, if regular, reduce dose to 4 mL twice daily all month long and then reevaluate 4 months later (Table 33.6): Inula helenium MT 60 mL, Salvia sclarea MT 120 mL, Avena sativa MT 60 mL 2. Drainage: 3 mL BID all month long (Table 33.7): Viola tricolor MT 120 mL, Hamamelis virginiana MT 80 mL, Achillea millefolium MT 40 mL 3. Zinc-copper oligoelements daily in the evenings with second dose of tinctures Type 2C: 1. GnRH switching-thyro-somatotropic: 4 mL BID from day 10 to onset of menstruation (Table 33.8): Fabiana imbricata MT 60 mL, Poterium sanguisorba MT 60 mL, Medicago sativa MT 60 mL, Melissa officinalis MT 60 mL+Lavandula angustifolia EO 3–4 mL 2. Cortico-drainage: 4 mL BID before meals all month long (Table 33.9): Ribes nigrum GM 60 mL, Arctium lappa MT 60 mL, Carduus marianus MT 60 mL, Hamamelis virginiana MT 60 mL 223
224 SECTION | C Assessment and treatment of common disorders
TABLE 33.1 Metrorrhagia Type 1A prescription.
TABLE 33.5 Metrorrhagia Type 2A drainage prescription.
Medicinal plant
Replacements and alternatives
Medicinal plant
Replacements and alternatives
Passiflora incarnata MT 60 mL
Melissa officinalis MT
Avena sativa 60 mL MT
Zea mays GM
Leonurus cardiaca MT 60 mL
Fabiana imbricata MT
Agrimonia eupatoria 120 mL MT
Juglans regia MT
Lavandula angustifolia EO 2 mL
Matricaria recutita EO
Hamamelis virginiana 60 mL MT
Alchemilla vulgaris MT, Aesculus hippocastanum MT
Angelica archangelica 1 mL EO
Salvia officinalis EO
Artemisia dracunculus 2 mL EO
Citrus aurantium amara EO
Key: MT, mother tincture; EO, essential oil.
TABLE 33.2 Metrorrhagia Type 1B prescription. Medicinal plant
Replacements and alternatives
Passiflora incarnata MT 60 mL
Matricaria recutita MT
Ribes nigrum GM 160 mL
Quercus pedunculata GM
Fragaria vesca MT 60 mL
Poterium sanguisorba MT
Lavandula angustifolia EO 3 mL
Citrus aurantium amara EO
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
TABLE 33.6 Metrorrhagia Type 2B neuroendocrine prescription. Medicinal plant
Replacements and alternatives
Inula helenium 60 mL MT Salvia sclarea 120 mL MT
Salvia officinalis MT
Avena sativa 60 mL MT
Melissa officinalis MT
Key: MT, mother tincture
TABLE 33.3 Metrorrhagia Type 1C prescription. Replacements and alternatives
TABLE 33.7 Metrorrhagia Type 2B drainage prescription.
Medicinal plant Passiflora incarnata 60 mL MT
Matricaria recutita MT
Medicinal plant
Replacements and alternatives
Rhodiola rosea 40 mL MT
Eleutherococcus senticosus MT
Viola tricolor 120 mL MT
Arctium lappa MT
Hamamelis virginiana 80 mL MT
Alchemilla vulgaris MT
Sequoia gigantea 80 mL GM
Magnolia officinalis bark
Achillea millefolium 40 mL MT
Alchemilla vulgaris MT
Quercus pedunculata 60 mL GM
Ribes nigrum GM
Lavandula angustifolia 3 mL EO
Citrus aurantium amara EO
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Key: MT, mother tincture.
TABLE 33.8 Metrorrhagia Type 2C neuroendocrine prescription. Medicinal plant
Replacements and alternatives
Fabiana imbricata 60 mL GM
Leonurus cardiaca MT
Medicinal plant
Replacements and alternatives
Poterium sanguisorba 60 mL MT
Mercurialis annua MT>Fragaria vesca MT
Passiflora incarnata 60 mL MT
Matricaria recutita MT
Medicago sativa 60 mL MT
Lithospermum officinale MT, Alchemilla vulgaris MT
Ribes nigrum 80 mL GM
Quercus pedunculata GM
Melissa officinalis 60 mL MT
Salvia officinalis 100 mL MT
Salvia sclarea MT
Passiflora incarnata MT 30 mL+Avena sativa MT 30 mL
Lavandula angustifolia 3 mL EO
Citrus aurantium amara EO
Lavandula angustifolia 4 mL EO
Citrus aurantium amara EO
TABLE 33.4 Metrorrhagia Type 2A neuroendocrine prescription.
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Menstruation disorders: Metrorrhagia Chapter | 33 225
TABLE 33.9 Metrorrhagia Type 2C endocrine-drainage prescription.
TABLE 33.11 Metrorrhagia Type 4 central endocrinedrainage prescription.
Medicinal plant
Replacements and alternatives
Medicinal plant
Replacements and alternatives
Ribes nigrum 60 mL GM
Quercus pedunculata GM
Medicago sativa 120 mL MT
Alchemilla vulgaris MT
Arctium lappa 60 mL MT
Agrimonia eupatoria MT
Leonurus cardiaca 60 mL MT
Fabiana imbricate GM
Carduus marianus 60 mL MT
Cynara scolymus MT
Poterium sanguisorba 60 mL MT
Hamamelis virginiana 60 mL MT
Piper methisticum MT
Mercurialis annua MT, Fragaria vesca MT
Hamamelis virginiana 60 mL MT
Rubus idaeus GM
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Type 3: Dopamine inhibition of pituitary activity 1. Alpha-TRH-Pituitary: 4 mL AM, 3 mL evenings (Table 33.10): Matricaria recutita MT 60 mL, Tilia tomentosa GM 20 mL, Inula helenium MT 60 mL, Fabiana imbricata MT 60 mL, Poterium sanguisorba MT 60 mL, Lavandula angustifolia EO 3 mL
TABLE 33.12 Metrorrhagia Type 4 peripheral endocrine prescription. Medicinal plant
Replacements and alternatives
Angelica archangelica 120 mL MT
Salvia officinalis MT 60 mL+Rubus idaeus GM 60 mL
Sample treatment: Luteal metrorrhagia type
Hamamelis virginiana 60 mL MT
Matricaria recutita MT
Type 4: Progesterone predominance with absolute hypoestrogenism
Rosmarinus officinalis 3 mL EO
Lavandula angustifolia EO, Cupressus sempervirens EO
Salvia officinalis 1 mL EO
Salvia sclarea EO, Cupressus sempervirens EO
1. Central luteal regulation: 3 mL AM, 6 mL 1 h before bed, days 14–25 (Table 33.11): Medicago sativa MT 120 mL, Leonurus cardiaca MT 60 mL, Poterium sanguisorba MT 60 mL+Lavender EO 4 mL 2. Peripheral estrogen-progesterone regulation: 3 mL before meals, days 14–25 (Table 33.12): Angelica archangelica MT 120 mL, Hamamelis virginiana MT 120 mL, Rosmarinus officinalis EO 3 mL, Salvia officinalis EO 1 mL 3. Zinc-copper oligoelements: In evenings in follicular phase, twice daily in luteal phase TABLE 33.10 Metrorrhagia Type 3 neuroendocrine prescription. Medicinal plant
Replacements and alternatives
Matricaria recutita MT 40 mL
Tilia tomentosa GM
Tilia tomentosa GM 20 mL
Passiflora incarnata MT, Corylus avellana GM
Inula helenium MT 60 mL
Rhodiola rosea MT
Fabiana imbricata MT 60 mL
Leonurus cardiaca MT
Poterium sanguisorba MT 60 mL
Mercurialis annua MT>Fragaria vesca MT
Lavandula angustifolia EO 3 mL
Citrus aurantium amara EO
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Key: MT, mother tincture; EO, essential oil; GM, gemmomacerate.
Terrain in detail Refer to The Theory of Endobiogeny, Volume 3, Chapter 5: Menstruation Disorders, for detailed discussion of the terrain, historical, physical examination findings, and possible Biology of Function correlations associated with each type and subtype of metrorrhagia. For a review of the normal menstrual disorder, c.f. The Theory of Endobiogeny, Volume 3, Chapter 4: Regulation of the Menstrual Cycle, or, this volume, Chapter 32: Normal menstruation.
Precritical terrain The precritical terrain has to do with insufficient buffering capacity relating to the production, mobilization or utilization of estrogens for their tissular effects. This can be from three origins. The first is genetic/epigenetic. A family history of similar timing of metrorrhagia favors this conclusion. The second is dysadaptability rooted in the autopathogenic axis (c.f. The Theory of Endobiogeny, Volume 1, Chapter 13: Art of the History). For example, if a woman has a history of cystic acne and ovarian cysts, her autopathogenic axis is gonadotropic, and it specifically involves a predominance of luteal hormones. She may be
226 SECTION | C Assessment and treatment of common disorders
more susceptible to metrorrhagia Type 4, which is luteal in timing and due to absolute hypoestrogenism from progesteronic predominance. The third type is mixed, where the inherited nature was latent and become liminal due to autopathogenicity.
Agent The agent is the demand to regulate repeated fluctuations in estrogen production, receptor proliferation, and sensitivity against countervailing forces, such as cortisol, progesterone, etc. (c.f. The Theory of Endobiogeny, Volume 3, Chapter 4: Regulation of the Menstrual Cycle, or, this volume, Chapter 32).
Critical terrain The critical terrain is particular to each phenotypic sub-type.
Follicular phase Type 1: Estrogen availability is impaired by elevated cortisol Cortisol increases sex hormone binding globulin’s (SHGB) binding of estrogen in the serum. 1. Type 1A: Hyper Alpha-sympathetic over-stimulates the corticotropic axis in toto 2. Type 1B: Intrinsic overstimulation of cortisol from CRH and/or ACTH with insufficient anabolic adrenal steroids 3. Type 1C: Intrinsic overstimulation of cortisol from CRH and/or ACTH with adapted response by anabolic adrenal steroids Type 2: Estrogen production is interrupted 1. Type 2A: Inhibition of FSH: cortisol has an alphalike effect on FSH that impairs its excretion from the pituitary 2. Type 2B: Insufficient stimulation of FSH: ACTH is inhibited too quickly by cortisol before it can have a paralike effect on the production of FSH within the pituitary
3. Type 2C: Early switching away from FSH: Thyrosomatotropic stimulation (TRH→Prolactin) alters pulsatile release of GnRH to favor LH rather than FSH too early in the follicular phase Type 3: Central inhibition of the pituitary: Dopamine relaunching (e.g., alpha-sympathetic, prolactin) slows down pituitary function, in this case, most prominently affecting FSH activity.
Luteal phase Type 4: Luteal predominance inhibits estrogens: Progesterone predominance results in absolute hypoestrogenism.
Mechanisms Impairment in the tissular actions of estrogens on sustaining the development of the endometrium in preparation of a possible pregnancy.
Result Focal areas of necrosis with “spotting,” or, light bleeding with a general continuation of the menstrual cycle.
Treatment Exemplary prescriptions Based on an Endobiogenic approach to all types of metrorrhagia, a number of prescriptions can be derived. Refer to The Theory of Endobiogeny, Volume 3, Chapter 5 for detailed discussion of possible Biology of Functions relationships and medicinal plant indications for each metrorrhagia type and subtype. Formulas are listed at the beginning of the chapter under “Sample treatments”. Substitutions for medicinal plants are listed in Tables 33.1–33.10.
Chapter 34
Menstruation disorders: Oligomenorrhea Summary Essence: Menstrual cycle longer than 35 days due follicular phase incompetence to develop the endometrial lining. Terrain: (1) Catabolic predominance, absolute or relative, resulting in (2) Insufficient proliferation of the uterine lining which requires a (3) Prolonged follicular phase to develop the endometrium before ovulation is initiated resulting in (4) Infrequent episodes of menstrual bleeding.
3. Oligoelement: Inositol 400–500 mg twice per day 4. Vaginal dysbiosis douche: Matricaria recutita BH 1 tsp, Hamamelis virginiana BH 1 tsp, 1 tsp Illite clay: steep 15 min in 200 mg water. Cool, shake well, aliquot into a douche bottle, and apply in the evenings before bed for 3–4 weeks 5. Alkaline diet favoring fermented foods, and tisane of Anthemis nobilis 4 cups per day
Terrain in detail
Treatment goals
Precritical terrain
Symptomatic: Emmenagogues, pelvic decongestants, ovarian anti-inflammatories Terrain:
The precritical terrain varies.
●
● ●
● ●
Regulate neuroendocrine terrain favoring catabolism>anabolism Emmenagogues Drainage: (1) Utero-pelvic unit (included decongestion), (2) liver, (3) gallbladder, (4) intestines (may be secondary of dysbiosis) Alkalization of tissues Correct dysbiosis if indicated
Sample treatment 1. Neuroendocrine: 4 mL twice a day for 3–6 months (Table 34.4): Passiflora incarnata MT 60 mL, Lithospermum officinale MT 60 mL, Leonurus cardiaca MT 60 mL, Poterium sanguisorba MT 60 mL, Artemisia dracunculus EO 4 mL 2. TSH-drainage: 4 mL twice a day for 3–6 months (Table 34.5): Zea mays GM 80 mL, Malva sylvestris MT 80 mL, Carduus marianus MT 80 mL, Cupressus sempervirens EO 4 mL
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1. Global a. CNS, hyperfunctioning, resulting in disruption of: b. Neuroendocrine regulation of metabolic efficiency 2. Regional: Congestion: emunctory, vascular: impairs quality of nutritional efficiency. In order of importance: a. Hepatobiliary i. Exocrine: impaired anabolism of proteins ii. Metabolic: impaired excretion of (catabolically derived) inflammatory proteins b. Pelvic: impairs adaptability of endometrial nutrition c. Uterine congestion and/or tissular acidity (implicates veno-lymphatic stasis) d. Intestines: inflammation, permeability
Agent Augmented CNS-ANS functioning with adaptative focus on thyrotropic axis during follicular phase of menstrual cycle: 1. Emotional stress 2. Stressors: seasonal changes, chronobiologic evolution, intense exercise, etc. 3. Iatrogenic and lifestyle choices
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228 SECTION | C Assessment and treatment of common disorders
Critical terrain
Mechanisms
The terrain blocks, delays, or inhibits anabolism, favors catabolism or both.
1. Catabolic predominance: insufficient (anabolic) proliferation of uterine lining 2. Follicular phase prolonged until sufficient endometrial growth prior achieved prior to ovulation
1. Reduced anabolism: impaired phasic pulsatility of central trophins in the follicular phase a. Dopamine: hyperfunctioning: inhibits FSH>LH b. Prolactin: hyperfunctioning: GnRH switching favors LH>FSH 2. Increased catabolism a. CNS: insufficient neurocalmative factors i. Insufficient GABA, endorphins, enkephalins ii. Insufficient nocturnal serotonin: cortisol relaunching→absolute catabolic predominance b. CNS: excessive stimulating factors i. Excess diurnal serotonin: augmented information intake, hyperfunctioning CNS-sympathetic activity→cortico-thyrotropic relaunching: favors catabolism ii. Dopamine, elevated: TRH→thyrotropic relaunching→catabolic predominance c. Excessive alpha, cortico-thyrotropic yoking i. Corticotropic: cortisol>adrenal cortex: anabolism blocked or delayed ii. Thyrotropic 1. TRH: thyrotropic relaunching: absolutely hypercatabolic 2. TSH (low serum): somatotropic desynchronization: inflammation, hyperinsulinism, and/ or low insulin resistance iii. Cortico-thyrotropic yoking (mixed effects) 3. Regional congestion a. Uterine b. Pelvic c. Lymphatic d. Endometrial tissular acidity, toxin accumulation (c.f. Biology of Functions) e. Dysbiosis
Result Oligomenorrhea: menstrual cycle >35 days.
History, Physical exam and BoF findings The history of oligomenorrhea is infrequent menstruation occurring less frequently than 35 days. Associated symptoms depend on the origin of the disruption in follicular anabolism. Historical and examination findings related to CNS-ANS activity may be significant. It will be more constant and during the follicular phase, compared to what which occurs in polymenorrhea (Tables 34.1 and 34.2). In order for the Biology of Functions to be significative, it should be drawn after menstruation but before ovulation. If the menstrual cycles have some regularity to them, this should be easy to calculate. For example, assume the cycle lasts 36 days. The luteal phase is approximately 14 days in duration. This leaves 36−14=22 days for the follicular
TABLE 34.1 Historical findings. Finding with irregular variability Mind: diminished concentration, attention, focus Mood: irritability, tearfulness, anger, anxiety, melancholy, etc. Cravings, especially for salty, sweet and/or crunchy foods Altered body temperature: chest, extremities Sleep: increased latency, diminished quality, pronounced vivacity of dreams, etc.
TABLE 34.2 Examination findings. Technique
Result
Interpretation
Glabellar tap (c.f. Theory of Endobiogeny Vol 2, Chapter 11: Spasmophilia)
Rapid response of either or both eyelids
Strong dopamine and/or alpha relaunching dopamine Strong TRH when provoked
Flutter Hippus
Rapid, prolonged response favoring dilation>contraction
Strong and reactive dopamine>serotonin
Chvostek
Twitching
Spasmophilia
Deep tendon reflex
Brisk
Strong TRH in the periphery
Menstruation disorders: Oligomenorrhea Chapter | 34 229
phase (versus the “optimal” 14 days). If there are 4 days of menstrual bleeding, there are 22−4=18 follicular days of development of the endometrium. To err on the side of caution, wait at least 5 additional days to ensure that the neuroendocrine terrain of endometrial growth is well established. Thus, blood samples can be drawn during days 10 to 22. The essential indexes and relationships to evaluate are: (1) Catabolism/anabolism index, (2) a ratio of the Catabolism index (function value) divided by the Anabolism index (structure value), and (3) Metabolic yield in structure versus function (Table 34.3). The remainder of the indexes listed may show the abnormalities noted depending on the terrain and contingent on the value of serum TSH.
Treatment The general emphasis of treatment is to restore the proper metabolic relationship, and address the precritical and critical elements of congestion: 1. Polyvalent symptomatic treatments with utero-pelvic tropism (Table 34.4) 2. Neuroendocrine (Table 34.5) a. Catabolic: diminish neuro-cortico-thyrotropic elements that favor catabolism b. Anabolic: ensure proper folliculo-estrogenic competency if low
TABLE 34.3 Biology of Functions indexes. Index
Value
Catabolism/anabolism
F>S, absolute or relative
Catabolism (F)-to-anabolism (S) ratio
↑ (>2.4)
Metabolic yield
S>F, absolute or relative
Values of following indexes contingent on conditional value of TSH
↓ TSH, serum
↑ TSH, serum
Insulin
↑
↓
Insulin resistance
↓
↑
GH growth score
↓
↑
Ischemia
↑
↓
Nucleocytopathogenicity
↑
↓
Redox
↑
↓
Noxious free radicals
↑
↓
Autophagy (any of the indexes)
↑
↓
Thyroid relaunching
↑
↓
Thyroid relaunching corrected
↑
↓
Key: F, function value; S, structure value.
TABLE 34.4 Polyvalent plants with symptomatic and critical terrain actions. Indication
Medicinal plant
General pelvic actions
Hamamelis virginiana
Crocus sativa
Emmenagogue
• (Indirect)
Utero-pelvic Pelvic drainer, decongestant, anti-inflammatory, antiinfectious Favors ovarian-uterine function as an integrated block
Neuroendocrine
Estrogen regulator, oxytocic, adaptogenic, improves MSH, serotonin, endorphins, GABA activity Continued
230 SECTION | C Assessment and treatment of common disorders
TABLE 34.4 Polyvalent plants with symptomatic and critical terrain actions—cont’d Indication
Medicinal plant
Emmenagogue
For catabolic excess or predominance
Rhodiola rosea
•
Leonurus cardiaca
•
Malva sylvestris Matricaria recutita Anthemis nobilis For anabolic insufficiency
Thymus vulgaris Artemisia dracunculus Foeniculum vulgare Salvia sclarea Achillea millefolium
• • • •
Angelica archangelica Cupressus sempervirens Melaleuca leucadendron
Utero-pelvic
Central nervous system sedative Pelvic decongestant, antiinflammatory Anti-inflammatory, pelvic decongestant
Neuroendocrine Adaptogen, serotonergic, dopaminergic, cholinergic, Estrogenic (mild), (−) TRH, reduces cortisol fixation Blocks insulin Sympatholytic, parasympatholytic
Uterine anti-inflammatory, antimicrobial, renal drainer
Sympatholytic, parasympatholytic
Spasmolytic Utero-pelvic drainer Uterine antispasmodic Pelvic drainer Anti-inflammatory, pelvic decongestant Uterolytic, uterine antiinflammatory Pelvic drainer, uterine antispasmodic, lymphatic decongestant, anti-infectious Uterotonic antispasmodic, pelvic decongestant
Improves estrogen binding Estrogenic Estrogenic, oxytocic Estrogenic, (−) PL Progesteronic Estrogenic, CNS sedative Estrogenic
Estrogenic, oxytocic, sympatholytic, parasympatholytic
Key: (−), inhibits; CNS, central nervous system; GABA, γ-aminobutyric acid; MSH, melanocyte-stimulating hormone; PL, prolactin; TRH, thyrotropin-releasing hormone.
TABLE 34.5 Medicinal plants addressing endocrine aspects of the critical terrain of oligomenorrhea. Endocrine
Medicinal plant
Comments
Corticotropic
Passiflora incarnata
All cases of absolutely elevated Cortisol due to adrenal overstimulation
Sequoia gigantea GM
When Cortisol elevated and Cortisol/adrenal cortex ratio>4
Lithospermum officinale Medicago sativa
Use when hyperfunctioning of FSH, LH and TSH implicated Inhibits LH, estrogenic, antiandrogenic; use if history of acne on jawline or chin, or, aggressive irritability Inhibits LH but progesteronic; use when LH inhibition is required while supporting progesteronic activity for ovulation and the luteal phase activity.
LH
Alchemilla vulgaris (−) TRH
Leonurus cardiaca Fabiana imbricata
Can indirectly reduce PL activity if it is primarily dependent on TRH vs. dopamine
(−) TSH, serum
Zea mays GM Lithospermum officinale Lycopus europaeus
Hepatorenal drainer Use when hyperfunctioning LH also implicated Use with absolute hyperthyroidism
Thyroid
Melissa officinalis
Thyrotropic adaptogen, Alpha-sympatholytic and spasmolytic Use with variable thyroid symptoms (hyper- and hypofunctioning) Harmonizes the estro-thyrotropic relationship Supports exocrine pancreatic function by substitutive properties Use in patients at risk of Hashimoto’s thyroiditis, or, weaning thyroid replacement therapy
Avena sativa
GH
Lamium album
Relaunches growth hormone to re-establish somatotropic synchronization and quality of anabolism (use when GH growth score index is low)
Menstruation disorders: Oligomenorrhea Chapter | 34 231
TABLE 34.5 Medicinal plants addressing endocrine aspects of the critical terrain of oligomenorrhea—cont’d Endocrine
Medicinal plant
Comments
PL
Poterium sanguisorba
Reduces dopamine relaunching. Use favored in women with insomnia described as “tired but wired” when trying to initiate sleep Broader inhibition of pituitary than Poterium sanguisorba; supports adrenal cortex function; use in woman with a history of ovarian cysts, fibrocystic breast disease, polyps, and other disorders of hypertrophy or hyperplasia
Fragaria vesca
Key: GH, growth hormone; PL, prolactin; TRH, thyrotropin-releasing hormone.
Exemplary prescriptions Based on an Endobiogenic approach to oligomenorrhea, a number of prescriptions can be derived. For example, in the case of oligomenorrhea rooted in central hyperfunctioning with high cortisol and somatotropic desynchronization, one may use the following: 1. Neuroendocrine: 4 mL twice a day for 3–6 months (Table 34.6): Passiflora incarnata MT 60 mL, Lithospermum officinale MT 60 mL, Leonurus cardiaca MT 60 mL, Poterium sanguisorba MT 60 mL, Artemisia dracunculus EO 4 mL 2. TSH-drainage: 4 mL twice a day for 3–6 months (Table 34.7): Zea mays GM 80 mL, Malva sylvestris MT 80 mL, Carduus marianus MT 80 mL, Cupressus sempervirens EO 4 mL 3. Oligoelement: Inositol 400–500 mg twice per day
TABLE 34.6 Neuroendocrine prescription. Medicinal plant
Replacements and alternatives
Passiflora incarnata 60 mL MT
Matricaria recuctita MT
Lithospermum officinale 60 mL MT
Lycopus europaeus MT
Leonurus cardiaca 60 mL MT
Fabiana imbricata MT
Poterium sanguisorba 60 mL MT
Mercurialis annua MT, Fragaria vesca MT
Lavandula angustifolia 4 mL EO
Matricaria recutita EO
Key: MT, mother tincture; GM, gemmomacerate; EO, essential oil.
TABLE 34.7 Drainage-decongestion-endocrine prescription. Medicinal plant
Replacements and alternatives
Zea mays 80 mL GM
Cornus sanguinea GM
Malva sylvestris 80 mL MT
Arnica montana MT
Carduus marianus 80 mL MT
Cynara scolymus MT
Cupressus sempervirens 4 mL EO
Artemisia dracunculus EO
Key: MT, mother tincture; GM, gemmomacerate; EO, essential oil.
4. Vaginal dysbiosis douche: Matricaria recutita BH 1 tsp, Hamamelis virginiana BH 1 tsp, 1 tsp Illite clay: steep 15 min in 200 mg water. Cool, shake well, aliquot into a douche bottle, and apply in the evenings before bed for 3–4 weeks 5. Alkaline diet favoring fermented foods, and tisane of Anthemis nobilis 4 cups per day
Chapter 35
Menstruation disorders: Polymenorrhea Summary Essence: Shortened menstrual cycle due to inability to maintain endometrium during the luteal phase. Terrain: (1) Interruption in peripheral thyroid tissular metabolism (various causes) in the luteal phase leads to (2) Impaired maintenance of the endometrium, resulting in (3) Shedding of the endometrium early in the luteal phase hence (4) Polymenorrhea.
Treatment goals Terrain: ● THYRO: Support peripheral thyroid activity ● PITUITARY: Adapt gonado-thyrotropic competency ● DRAIN: (1) Uterus, (2) pelvis, (3) liver
Sample treatment 1. Neuroendocrine: 3 mL twice per day in days 1–10, 4 mL three times per day days 11 to menstruation (Table 35.6): Quercus pedunculata GM 80 mL, Inula helenium MT 40 mL, Melissa officinalis MT 60 mL, Salvia sclarea MT 60 mL, Lavandula angustifolia EO 4 mL 2. Utero-tissular: 3 mL twice per day in days 1–10, 4 mL three times per day days 11 to menstruation (Table 35.7): Crocus sativa MT 80 mL, Prunus amygdalus root GM 80 mL, Achillea millefolium MT 40 mL, Hamamelis virginiana MT 60 mL, Melaleuca leucadendron EO 3 mL, Cupressus sempervirens EO 1 mL 3. Oligoelement: Zn-Cu oligo daily in AM for 3–4 months 4. Nutrition: Pumpkin seed oil: 15 mL in evening from day 10 to menstruation
Terrain in detail
1. CNS oversolicitation with hyperfunctioning: irregularly irregular in intensity (in oligomenorrhea, it is constant— see Chapter 34) 2. Cortico-thyrotropic surges of activity followed by periodic reductions in activity that are brief (milliseconds to minutes)
Agent The instigator of polymenorrhea is a critical level of CNSANS activity that is sufficiently intense and/or prolonged in activity resulting in dysfunctional thyrotropic activity lasting 24 h or longer.
Critical terrain Prolongation of intensity or duration of precritical terrain in the luteal phase such that peripheral thyroid tissular activity lasts 24 h or longer. One possible scenario is: hyperfunctioning TRH appeal to prolactin to adapt estrogen activity in luteal phase (c.f. Chapter 32: Menstruation, Normal Cycle, and, The Theory of Endobiogeny, Volume 3, Chapter 4: Regulation of Menstrual Cycle) → inadvertent peripheral thyroid stimulation (by rise in TRH) → drop in thyroid activity during “recovery phase.”
Mechanisms Relates to insufficient oxidative metabolism to produce ATP for endometrial metabolism. ● ●
Insufficient tissular thyroid activity Insufficient perfusion and distribution of nutrition to endometrium
Result Polymenorrhea: Menstrual bleeding that occurs less than every 21 days.
Precritical terrain
History and Physical exam findings
The precritical terrain varies based on cause of peripheral thyroid insufficiency. One typical scenario is:
The history of polymenorrhea is offered by the patient. Various signs or symptoms may be present based on the
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234 SECTION | C Assessment and treatment of common disorders
o rigin of the precritical and critical terrain. The most common would be irregular irregularity of CNS-ANS functioning. This may vary within the hour, or the day, or day to day. On history, one may ask about such variability (Table 35.1). During presentation, examination findings will depend both on the cause, as well as the menstrual phase that the
TABLE 35.1 Historical findings.
patient is in during the evaluation. Optimally, one will perform various neurologic and autonomic assessments in both follicular phases (days 1–14) and luteal (14-next phase of menstruation) to observe the irregular irregularity of CNSANS functioning (Table 35.2). However, this irregularity may occur within the same day, or even the same hour. In this case, the findings may not be substantially different throughout the cycle at the precise moment of evaluation. This is why a careful history is valuable to support the evaluation of the terrain.
Finding with irregular variability Mind: diminished concentration, attention, focus Mood: irritability, tearfulness, anger, anxiety, melancholy, etc. Cravings, especially for salty, sweet and/or crunchy foods Altered body temperature: chest, extremities Sleep: increased latency, diminished quality, pronounced vivacity of dreams, etc.
Biology of Functions If the patient’s polymenorrhea has a regular pattern, e.g., every 18 days, labs for the Biology of Functions must be drawn 24–48 h before menstruation. There are three groups of indexes to be evaluated: (1) thyrotropic, (2) gonadotropic, and (3) metabolic (Table 35.3). Focus on structure (S) values.
TABLE 35.2 Examination findings. Technique
Result
Interpretation
Glabella tap (c.f. Theory of Endobiogeny, Volume 2, Chapter 11: Spasmophilia)
Rapid response of either or both eyelids
Strong dopamine and/or alpha relaunching dopamine Strong TRH when provoked
Flutter Hippus
Rapid, prolonged response favoring dilation>contraction
Strong and reactive dopamine>serotonin
Chvostek
Twitching
Spasmophilia
Deep tendon reflex
Brisk
Strong TRH in the periphery
TABLE 35.3 Biology of Function indexes related to the polymenorrhea terrain. Axis
Index
Value
Interpretation
Gonadotropic
Somatotropic estrogen yield (S) (2.1–206)
↓, low normal (2.1
The thyroid is not sufficiently efficient in responding to demand for and distributing the material required for tissular maintenance or growth
Somatotropic
Catabolism (S)
↓
Anabolism (S) Metabolic yield (S)
↓ ↓
There is an absolute catabolic insufficiency to nourish anabolism and sustain metabolic activity There is an absolute anabolic insufficiency There is an absolute hypometabolic state
a
This is a ratio of two existing indexes. For both indexes, there are only function values.
Menstruation disorders: Polymenorrhea Chapter | 35 235
Treatment The general emphasis of treatment is to adapt thyroid functioning and use uterine tonics and decongestants that allow for sufficient nutritive activity.
1. Symptomatic: Polyvalent plants with utero-pelvic and neuroendocrine actions (Table 35.4) 2. Terrain: Thyrotropic adaptation, by extension, CNS, ANS, and corticotropic as indicated (Table 35.5)
TABLE 35.4 Polyvalent utero-pelvic plants with neuroendocrine activity for treatment of polymenorrhea. Medicinal plant
Utero-pelvic
Neuroendocrine
Hamamelis virginiana
Pelvic drainer, decongestant, anti-inflammatory, anti-infectious
Crocus sativa
Favors ovarian-uterine function as an integrated block
Estrogen regulator, oxytocic, adaptogenic, improves MSH, serotonin, endorphins, GABA activity
Malva sylvestris
Pelvic decongestant, anti-inflammatory
Blocks insulin
Matricaria recutita
Anti-inflammatory, pelvic decongestant
Sympatholytic, parasympatholytic
Anthemis nobilis
Uterine anti-inflammatory, antimicrobial, renal drainer
Sympatholytic, parasympatholytic
Artemisia dracunculus
Utero-pelvic drainer
Estrogenic
Foeniculum vulgare
Uterine antispasmodic
Estrogenic, oxytocic
Salvia sclarea
Pelvic drainer
Estrogenic, (−) PL
Achillea millefolium
Anti-inflammatory, pelvic decongestant
Progesteronic
Angelica archangelica
Uterolytic, uterine anti-inflammatory
Estrogenic, CNS sedative
Cupressus sempervirens
Pelvic drainer, uterine antispasmodic, lymphatic decongestant, anti-infectious
Estrogenic
Melaleuca leucadendron
Uterotonic antispasmodic, pelvic decongestant
Estrogenic, oxytocic, sympatholytic, parasympatholytic
Key: (−), inhibits; CNS, central nervous system; GABA, γ-aminobutyric acid; MSH, melanocyte-stimulating hormone; PL, prolactin; TRH, thyrotropin-releasing hormone.
TABLE 35.5 Polyvalent neuroendocrine regulators. Medicinal plant
CNS
Rhodiola rosea
•
Inula helenium
ANS
Pituitary
Thyrotropic
Adaptogen •
Quercus pedunculata bud GM
Other Adaptogen
Supports ACTH, FSH, LH Endocrine redistributor
Leonurus cardiaca
•
(−) TRH
Reduces cortisol fixation to receptors
Melissa officinalis
•
•
Thyrotropic adaptogen
Salvia sclarea
•
•
Thyroid stimulant
Improves estrogen activity, pelvic drainer
Thyroid stimulant
Improves microvilli structure for absorption of nutrients; improves quality of tissular nutrition
Prunus amygdalus root GM
236 SECTION | C Assessment and treatment of common disorders
3. Oligoelement: a. Pituitary and ovarian competency: Zinc-copper b. Thyroid efficiency: Selenium, manganese-copper 4. Nutrition: Pumpkin seed oil, later follicular phase
Exemplary prescriptions Based on an Endobiogenic approach to polymenorrhea, a number of prescriptions can be derived. For example: 1. Neuroendocrine: 3 mL twice per day in days 1–10, 4 mL three times per day days 11 to menstruation (Table 35.6): Quercus pedunculata GM 80 mL, Inula helenium MT 40 mL, Melissa officinalis MT 60 mL, Salvia sclarea MT 60 mL, Lavandula angustifolia EO 4 mL
TABLE 35.6 Neuroendocrine prescription. Medicinal plant
Replacements and alternatives
2. Utero-tissular: 3 mL twice per day in days 1–10, 4 mL three times per day days 11 to menstruation (Table 35.7): Crocus sativa MT 80 mL, Prunus amygdalus root GM 80 mL, Achillea millefolium MT 40 mL, Hamamelis virginiana MT 60 mL, Melaleuca leucadendron EO 3 mL, Cupressus sempervirens EO 1 mL 3. Oligoelement: Zn-Cu oligo daily in AM for 3–4 months 4. Nutrition: Pumpkin seed oil: 15 mL in evening from day 10 to menstruation
TABLE 35.7 Utero-tissular prescription. Medicinal plant Crocus sativa MT 80 mL Prunus amygdalus root GM 80 mL
Prunus amygdalus bud GM 80 mL
Achillea millefolium MT 40 mL
Alchemilla vulgaris
Hamamelis virginiana MT 60 mL
Achillea millefolium, Alchemilla vulgaris
Quercus pedunculata GM 80 mL
Rhodiola rosea
Inula helenium MT 40 mL
Quercus pedunculata GM
Melissa officinalis MT 60 mL
Avena sativa MT
Salvia sclarea MT 60 mL
Salvia officinalis MT
Melaleuca leucadendron EO 3 mL
Lavandula angustifolia EO 4 mL
Citrus bergamia bigarde EO 4 mL
Cupressus sempervirens EO 1 mL
Key: MT, mother tincture; GM, gemmomacerate; EO, essential oil.
Replacements and Alternatives
Foeniculum vulgare EO, Artemisia dracunculus EO
Key: MT, mother tincture; GM, gemmomacerate; EO, essential oil.
Chapter 36
Premenstrual syndromes (PMS) Summary Essence: Estro-progestive imbalance in the late luteal phase of menstruation. Terrain: (1) Estro-progestive imbalance in the late luteal phase: (a) estrogens > progesterone, (b) progesterone > estrogens, (c) mixed type resulting in (2) Symptoms related to relative predominance of estrogens vs. progesterone with (3) Additional symptoms related to (a) genetic factors of FSH vs. LH predominance and feedback sensitivity, (b) upstream adaptative responses, (c) downstream consequences, (d) precritical Endobiogenic terrain of the patient.
anti-inflammatory,
The precritical terrain is highly variable. The historical quality of the late-luteal response, and the installation of adaptative mechanisms used to calibrate this will determine the particular pre-critical terrain. Some common elements include:
GONADO (peripheral): Adapt estrogens and progesterone, quantitatively and/or qualitatively GONADO (central): Adapt FSH and LH to the proper vertical and horizontal levels of activity OTHER: Address related upstream and downstream factors per indication (e.g., sugar cravings, catamenial migraines, acne, etc.—cf. Table 36.1) DRAIN: (1) Pelvis, (2) Liver-gallbladder
1. Disruption of estro-progestive adaptability a. Hormone therapy i. Direct: hormonal contraceptives, hormonal fertility therapies ii. Indirect: glucocorticoids, thyroid replacement, TSH blockers, etc. 2. Congestion a. Pelvic b. Hepatobiliary
Symptomatic: Topical and analgesics Terrain: varies, cf. text
●
●
●
Terrain in detail Precritical terrain
Treatment goals
●
2. Central Gonado-drainage: 4 mL BID, day 14 to menstruation (Table 36.7): Borago officinalis MT 80 mL, Medicago sativa MT 80 mL, Hamamelis virginiana MT 80 mL + Lavandula angustifolia EO 2 mL, Citrus aurantium amara EO 2 mL. 3. Peripheral Gonado-drainage: 4 mL BID day 10 to menstruation (Table 36.8): Vitex agnus castus MT 100 mL, Fragaria vesca MT 80 mL, Matricaria recutita MT 60 mL. 4. Borage oil: 400–800 mg nightly from day 20 to menstruation.
oral
Sample treatment
Agent
Example is given for a young woman with estrogen predominance with absolutely elevated estrogens, progesterone, and gonadal androgen activity.
The agent that provokes the premenstrual syndromes (PMS) is the late luteal attempt to maintain a certain level of estroprogestive activity in anticipation of implantation of a fertilized ovum.
1. Symptomatic: Apply topically every 4 h to breasts and lower abdomen from 5 days before menstruation: Vitex agnus castus EO 2 mL, Lavandula angustifolia EO 1 mL, Matricaria recutita EO 1 mL, Origanum majorana EO 1 mL in 35 mL Sweet almond oil, 15 mL peanut oil, 10 mL wheat germ oil.
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Critical terrain The notion of the critical terrain has a series of bifurcations, which is why we refer to it as a series of heterogeneous s yndromes (Table 36.1). The notion of a relative
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238 SECTION | C Assessment and treatment of common disorders
TABLE 36.1 Critical PMS terrain and terrain of related symptoms. Level
Endo
Symptoms
Ovaries
Progesterone > Estrogens
Breast engorgement, L > R and diffuse Menstrual clots: few but prolonged Breast engorgement resolves with initial menstrual flow Breast tenderness Abdominal cramping Numerous small menstrual clots
Estrogens > Progesterone
Upstream
↑αΣ + ↑Cortisol
Recurrent infections Herpes reactivation Insomnia Catamenial migraines
↑αΣ > ↑πΣ ↑αΣ + ↑CRH, ACTH, Cortisol + ↓Adrenal cortex + Hepatic congestion ↑αΣ + ↑CRH, ACTH, Cortisol + ↓Adrenal cortex + ↓central Serotonin ↑αΣ + ↓ACTH, Cortisol, Adrenal cortex + ↓central Serotonin ↑TRH
Catamenial exogenous depression Aggravation of endogenous depression
↑FSH
Vivid dreams Emotional outbursts Emotional sensitivity
Mixed
Hyperfunctioning: Para, Alpha, FSH, TSH, GH, PL, Pancreas, Estrogens
Growth of ovarian cysts Growth of breast cysts
Downstream
↑Adrenal androgens with insufficient aromatization
Irritability Aggressiveness Growth of uterine fibroids Abdominal bloating Rapid weight gain
↑Gonadal androgens > Estrogens, Hyperinsulinism ↑Aldosterone
Key: αΣ: alpha-sympathetic, ACTH: Adrenocorticotropin hormone; CRH: corticotropin-releasing hormone; FSH: Follicle-stimulating hormone; L: Left; LH: Luteinizing hormone; R: Right; TSH: thyroid-stimulating hormone.
predominance is categorical and at times arbitrary. A woman may have a mixed type, or vary in the predominance based on age, genital recycling, and pregnancy, and birth history.
With changes in calcium availability, there are implications for adaptability, spasmophilia, and neurotransmitter function.
1. Type of predominance: Estrogen vs. Progesterone vs Mixed 2. Quality of predominance: Absolute vs. Relative (cf. Table 36.4) 3. Primary vs. Secondary symptoms due to a. Upstream adaptative compensation vs. b. Downstream consequences of estro-progestive imbalance c. Mixed states 4. Emunctory congestion similar to precritical terrain, but more pronounced a. Pelvic congestion b. Hepatobiliary congestion, possibly insufficiency
Result
Mechanisms Mechanisms vary based on the critical terrain. Typically, they involve fluid retention and proinflammatory factors.
Various premenstrual symptoms.
syndromes
and
associated
History and BoF findings During acute presentation of PMS, some possible correlations between precritical symptoms and Biology of Functions are presented in Table 36.2. A note about the Progesterone index. It describes the level of progesterone activity. When it is low, it witnesses two events: (1) LH favors androgens (presumably because progesterone activity is sufficient or excessive), and (2) the radial appeal by progesterone to FSH did not yield sufficient calibration of endocrinometabolic estrogen activity. When the Progesterone index is low, it favors inhibition of progesterone and/or LH activity,
Premenstrual syndromes (PMS) Chapter | 36 239
TABLE 36.2 Critical terrain symptoms and Biology of Functions correlations. Symptoms
Elements of terrain
Biology of Functions
Breast engorgement, L > R and diffuse Menstrual clots: few but prolonged Breast engorgement resolves with initial menstrual flow Acne after adolescence Breast or uterine fibroids
Progesterone predominance (absolute or relative)
Varies depending on absolute level of activity of progesterone and estrogens; Evaluate: Progesterone (often ↓), and the various estrogen indexes
Breast tenderness Abdominal cramping Multiple small clots during menstruation
Estrogen predominance (absolute or relative)
cf. above + ↑Aldosterone, ↑IL-1, ↑Inflammation
Recurrent infections Herpes reactivation
↑αΣ + ↑Cortisol
↑/↓ LMI, ↓PMI, ↓IL-1, ↑Cortisol
Insomnia
↑αΣ > ↑πΣ
↑Thyroid relaunching corrected, ↑TRH/TSH + ↑ Metabolic yield
Catamenial migraines
↑αΣ + ↑CRH, ACTH, Cortisol + ↓Adrenal cortex + Hepatic congestion
↑/↓ LMI + ↓PMI, ↑Cortisol, ↓Adrenal cortex, ↓Insulin resistance, ↑Insulin
Catamenial exogenous depression
↑αΣ + ↑CRH, ACTH, Cortisol + ↓Adrenal cortex + ↓central Serotonin
↑/↓ LMI + ↓PMI + ↑Cortisol + ↓Adrenal cortex + ↑Serotonin + ↓IL-1
Aggravation of endogenous depression
↑αΣ + ↓ACTH, Cortisol, Adrenal cortex + ↓central Serotonin
↑/↓ LMI + ↓PMI + ↓Cortisol + ↓Adrenal cortex + ↑Serotonin + ↓IL-1
Vivid dreams Prolonged or intense emotional outbursts
↑TRH
↑Thyroid relaunching corrected, ↑TRH/TSH + ↑ Metabolic yield
Emotional sensitivity
↑FSH
↑FSH
Growth of ovarian cysts
Hyperfunctioning: Para, Alpha, FSH, TSH, GH, PL, Pancreas, Estrogens
↓TSH serum, ↓FSH, ↓LH, ↓PL, ↑/↓Somatostatin, ↑Estrogen indexes (varies), ↑Insulin
Growth of fibrocystic cysts
Hyperfunctioning: Para, Alpha, FSH, TSH, GH, PL, Pancreas, Estrogens
↓TSH serum, FSH, LH, PL, ↑/↓Somatostatin, ↑Growth index or ↑Growth index corrected, ↑Estrogen indexes (varies), ↑Gonadal androgen indexes, ↑Insulin
Irritability Aggressiveness
↑Adrenal androgens with insufficient aromatization
↑Rate of adrenal androgens, ↓DHEA
Growth of uterine fibroids
↑Gonadal androgens > Estrogens, Hyperinsulinism
↓TSH serum, ↑Estrogen indexes (varies), ↑Gonadal androgen indexes, ↑Insulin, ↓Pelvic congestion
Abdominal bloating Rapid weight gain
↑Aldosterone
↑Aldosterone
Key: LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
especially when it correlates with clinical symptoms (cf. Table 36.4).
Physical exam and BoF findings During presentation with acute PMS syndromes, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 36.3). Outside of PMS, the key findings will not be present, but emunctory disturbances may be.
Treatment The general emphasis of treatment is: 1. Symptomatic: topical analgesic/decongestants (Table 36.6) 2. Regulation of terrain: The relative and absolute predominance of progesterone to estrogen must be determined in order to select the relevant treatment (Table 36.4)
240 SECTION | C Assessment and treatment of common disorders
TABLE 36.3 Critical terrain signs and Biology of Functions correlations. Area
Finding
Elements of terrain
Biology of Functions
Luteal predominance
Android morphology Asymmetry Left side > Right side Breast or uterine fibroids
LH predominates in structure starting during fetogenesis
Not applicable
Progesterone
Breast engorgement, L > R and diffuse
Progesterone predominance (absolute or relative)
Varies depending on absolute level of activity of progesterone and estrogens; Evaluate: Progesterone (often ↓), and the various estrogen indexes
Estrogens
Breast tenderness Abdominal cramping
Estrogen predominance (absolute or relative)
cf. above
Uterus
Uterine fibroid, palpable
↑Gonadal androgens > Estrogens, Hyperinsulinism
↓TSH serum, ↑Estrogen indexes (varies), ↑Gonadal androgen indexes, ↑Insulin, ↓Pelvic congestion
Depression
Tender: depression point (left medial scapular border, level of T4) Tender: zone of grief Diminished hippus
Depressive terrain
↑/↓ LMI + ↓PMI + ↑/↓Cortisol + ↓Adrenal cortex + ↑Serotonin + ↓IL-1
Pelvis
Tender, superior-medial left tibia
Pelvic congestion
↑/↓Pelvic congestion
Liver
Tender, superior-medial
Vascular congestion
↑/↓ LMI
Liver
Tender, inferior-lateral
Metabolic congestion
↑/↓ LMI
Gallbladder
Murphy’s point tenderness Tender, superior-medial right tibia Green coating on tongue
Gallbladder congestion
Not applicable
Key: LMI: Leukocyte mobilization index; PMI: Platelet mobilization index.
TABLE 36.4 Medicinal plants for neuroendocrine regulation. Level of activity
P2
E2
Action
Medicinal plant
Relative
↓
↓
←→
↓
↑P2 ↑E2 ↑E2
Achillea millefolium Salvia officinalis, Salvia sclarea, Medicago sativa Salvia officinalis, Salvia sclarea
↑
↓
↓LH
↑
←→
↑E2 ↓LH
↑
↑
Medicago sativa, Lithospermum officinale, Lycopus europaeus, GLA oils Salvia officinalis, Salvia sclarea Medicago sativa, Lithospermum officinale, Lycopus europaeus, GLA oils Lithospermum officinale, Lycopus europaeus Vitex agnus castus, Fragaria vesca leafa
Absolute
↓LH, FSH ↓E2
Key: ←→: activity within range; E2: Estrogens, GLA: Gamma linoleic acid, P2: Progesterone. a
Inhibits transformation of androgens to estradiol.
Premenstrual syndromes (PMS) Chapter | 36 241
Exemplary prescriptions
“neuroendocrine” and “drainage,” but into “central regulation with drainage” and “peripheral regulation with drainage,” and even that is somewhat arbitrary. An example is presented of mixed-type PMS with absolutely elevated progesterone, gonadal androgens, and estrogens. She is a 19-year-old college student with a 28day menstrual cycle. From days 24 to 28, she experiences breast engorgement (elevated Progesterone) and breast tenderness (elevated Estrogens) such that she avoids wearing a bra and engaging in exercise. She also experiences an eruption of papular chin acne at this time (elevated Gonadal androgens, and a secondary source of Aromatization to estrogens). In addition, she experiences severe abdominal cramping and 1.4 kg water weight gain (inflammatory prostaglandins + Aldosterone). With the start of menstruation, the breast symptoms and cramping resolves. Menstruation lasts 6 days and the first 2 days are heavy (hyperestrogenism that starts in the follicular phase).
Based on an Endobiogenic approach to PMS, a number of prescriptions can be derived for each of the possible combinations. NB: Because of the polyvalent actions of the plants targeted for PMS, single plant may address n euroendocrine, immune and drainage needs. Thus, the prescriptions are not arbitrarily divided into
1. Symptomatic: Apply topically every 4 h to breasts and lower abdomen from 5 days before menstruation: Vitex agnus castus EO 2 mL, Lavandula angustifolia EO 1 mL, Matricaria recutita EO 1 mL, Origanum majorana EO 1 mL in 35 mL Sweet almond oil, 15 mL peanut oil, 10 mL wheat germ oil
a. Endocrine (Table 36.5) i. Regulate FSH-estrogen and coupled relationships ii. Regulate LH-progesterone and coupled relationships iii. Oligoelement: Zinc-Copper: to improve estrogen production (low estrogen states) b. Immunity (anti-inflammatories): i. Gamma-linoleic acid (GLA) to favor anti- inflammatory prostaglandins 1. Sources: Borage, Black current, Primrose ii. Oligoelement: Selenium 3. Drainage, in order of implication (Table 36.6) a. Pelvic b. Hepatobiliary unit
TABLE 36.5 Gonadotropic regulators and their polyvalent action. Medicinal plant
Endocrine
Immunity
ANS
Other
Achillea millefolium
↑P2
Anti-inflammatory
(–) Para
Pelvic decon., Antiedematous, choleretic
Alchemilla vulgaris
↑P2, ↓LH
Pelvic decon., choleretic
Fragaria vesca
↓E2,a (+) Cortisol, (–) TSH, PL, growth factors
Antalgic
GLA oil
↓LH
Lithospermum officinale
↓FSH, LH, TSH, (+) T4
Medicago sativa
↓LH, (–) Androgens; ↑E2
Salvia officinalis
↑E2, (+): Thyroid, Adrenal cortex
Anti-inflammatory
(+) Sympathetic
Exocrine hepatic stimulator, dual pancreatrope
Salvia sclarea
↑E2, ↓FSH, ↓PL, (+): Thyroid, Adrenal cortex
Anti-inflammatory
(–) Para, Alpha; (+) Beta
Pelvic and pancreatic drainer; Choleretic, (+) flow of exocrine pancreatic secretions
Anti-inflammatory Diuretic
Key: (–): inhibits, or, -lytic; (+) stimulates, or, -mimetic; Decon.: decongestant; E2: Estrogens, GLA: Gamma linoleic acid, P2: Progesterone. a
Inhibits transformation of androgens to estradiol.
242 SECTION | C Assessment and treatment of common disorders
TABLE 36.6 Polyvalent medicinal plants for drainage. Medicinal plant
Pelvis
Hepatobiliary
Neuroendocrine
Other
•
•
Progesteronic (–) Aldosterone
Pelvic anti-inflammatory, Uterine antihemorrhagic
•
•
Progesteronic, (–) LH
Genital antimicrobial
•
Estrogenic, Spasmolytic
Genital antispasmodic, Antimicrobial
Cupressus sempervirens
•
Estrogenic
Uterine anti-spasmodic
Hamamelis virginiana
•
Cortisol stimulant (mild)
Genitourinary anti-inflammatory, splanchnic drainer
Lavandula angustifoliaa
•
•
Sympatholytic, Parasympatholytic, Spasmolytic
Uterotonic, CNS sedative, GABA-ergic
Matricaria recutitaa
•
•
Sympatholytic, Parasympatholytic, Spasmolytic
Hepato-splanchnic drainer, Anti-inflammatory, antalgic, sedative, neurotropic antispasmodic
Achillea millefolium
a
Alchemilla vulgaris a
Artemisia dracunculus
a
Key: (–): Inhibits; CNS: central nervous system. a
Can be used as an essential oil topically, internally, intravaginally.
2. Central Gonado-drainage: 4 mL BID day 14 to menstruation (Table 36.7): Borago officinalis MT 80 mL, Medicago sativa MT 80 mL, Hamamelis virginiana MT 80 mL + Lavandula angustifolia EO 2 mL, Citrus aurantium amara EO 2 mL 3. Peripheral Gonado-drainage: 4 mL BID day 10 to menstruation (Table 36.8): Vitex agnus castus MT 100 mL, Fragaria vesca MT 80 mL, Matricaria recutita MT 60 mL 4. Borage oil: 400–800 mg nightly from day 20 to menstruation
TABLE 36.7 Central gonado-drainage prescription. Medicinal plant
Alternatives
Borago officinalis MT 80 mL
Lithospermum officinale, Lycopus europaeus
Medicago sativa MT 80 mL
Lithospermum officinale, Lycopus europaeus
Hamamelis virginiana MT 80 mL
Alchemilla vulgaris
Lavandula angustifolia EO 2 mL
Matricaria recutita EO 2 mL
Citrus aurantium amara EO 2 mL
Lavandula angustifolia EO 2 mL
TABLE 36.8 Peripheral gonado-drainage prescription. Medicinal plant
Alternatives
Vitex agnus castus MT 100 mL
Rubus idaeus GM 80 mL + Tilia tomentosa MT 20 mL
Fragaria vesca leaf MT 80 mL
Humulus lupulus MT 60 mL + Ribes nigrum GM 20 mL
Matricaria recutita MT 60 mL
Hamamelis virginiana MT 45 mL + Carduus marianus MT 15 mL
Chapter 37
Otitis media Summary Essence: A spasmophilic condition of the middle ear where pathogens flourishes in stagnant serosal fluid and endocrino-immune incompetence. Terrain: (1) Local spasmophilia: Para > Alpha, with (2) endocrino-immune insufficiency in the face of (3) Emunctory participation in overgrowth and autointoxication resulting in (4) Increased serosal fluid and poor ear drainage; in the face of (5) Pathogens, there is abundant proteins for growth and insufficient immune and endocrine response to end the pathogenic growth, resulting in (6) Otitis media.
Treatment goals Symptomatic: locally applied: anti-infectious, antiinflammatory, analgesic, antipyretic Terrain: ● ● ●
● ● ●
●
ANS: ⇓ Para, Alpha, support Beta (to resolve spasmophilia) CORTICO: Support peripheral adrenal cortex activity THYRO: Support peripheral thyroid function, ⇓ central activity SOMATO: Support endocrine pancreas: insulin IMMUNE: Support thymus DRAIN: 1°-Liver 2°-Gallbladder, 3°-Exocrine pancreas, 4° Intestines DIET: Pancreas sparing, Liquid diet: soups, fruit juices rich in Vitamin C
Sample treatment A treatment for children in addition to standard of care treatment protocol; adjust dose according to age. 1. Sympatomatic: Polyvalent application to tympanic membrane Apply every 2–3 h (Table 37.6) 2. Neuroendocrine: 2 mL four times per day × 4 days, then 2 mL three times per day for 6 days: Quercus pedunculata GM 15 mL, Ribes nigrum GM 45 mL 3. Drainage: 1–2 mL four times per day × 4 days, then 1–2 mL three times per day for 6 days: Plantago major 10 mL, Vitis vinifera GM 30 mL, Olea europaea GM 20 mL The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00037-8 © 2020 Elsevier Inc. All rights reserved.
4. Oligoelement: Copper-Gold-Silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Pancreas sparing during acute infection, liquid diet if favored or tolerated by child
Terrain in detail Precritical terrain The precritical terrain is one in which abundant serosal fluid stagnates, favoring a rich medium for the growth of a pathogen 1. ANS: Spasmophilia with hyperfunctioning Para > Alpha 2. Endocrine: a. Corticotropic, peripheral: insufficient b. Thyrotropic, peripheral: insufficient 3. Emunctory (in order of implication): a. Pancreas, exocrine (overgrowth of tissue) b. Liver (autointoxication) c. Gallbladder (autointoxication) d. Intestine (autointoxication)
Agent There are two general categories (cf. The Theory of Endobiogeny, Volume 2, Chapter 9: Infectious diseases of the ear, nose, throat and bronchus). 1. Further impairment of drainage: sudden changes in middle ear pressure a. Inquire about forceful blowing of the nose 2. Increased loco-regional pathogen burden by colonization or chronic infection: i. Rhinopharyngitis ii. Sinusitis iii. Tonsillitis
Critical terrain 1. ANS: further aggravation of spasmophilia: a. Hyper Para and Alpha b. Beta: blocked or delayed; if surges, tympanic membrane ruptures 243
244 SECTION | C Assessment and treatment of common disorders
2. Endocrine: a. Adrenal cortex insufficiency b. Peripheral thyroid insufficiency 3. Emunctories: Liver takes on a greater prominence a. Liver (autointoxication) b. Gallbladder (autointoxication) c. Pancreas, exocrine (overproduction of serosal fluid) d. Intestine (autointoxication)
Mechanisms Diminished or block drainage of serosal fluid allows for proliferation of pathogens in the protein-rich media; the organism mounts a partial, but insufficient immune response.
Result Infection of the middle ear with pressure on the tympanic membrane causing pain, often with fever and secondary symptoms based on comorbidities, such as coryza or sinus pressure: Otitis media.
History and BoF findings During acute otitis media, in addition to the presenting complaint, some possible correlations between elements of the terrain and the Biology of Functions are presented in Table 37.1.
Physical exam and BoF findings During presentation with acute otitis media, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 37.2)
Treatment In addition to standard-of-care treatment, acute symptomatic treatment should focus on relief of pain and congestion locally. In addition, the elements of the critical terrain should be addressed. If the otitis media is chronic or recurrent, long-term drainage emphasizing the hepato-biliary unit is strongly indicated: 1. Symptomatic: Topical anti-infectious, a nti-inflammatory, analgesic/antipyretic/decongestant therapy: a. Pharmaceutical (cf. The Theory of Endobiogeny, Volume 2, Chapter 9: Infectious diseases) b. Essential oils with polyvalent action (Table 37.3) 2. Neuroendocrine-Immunity regulation (Table 37.4) 3. Oligoelements: Copper, Gold, Silver to support immunity 4. Drainage: Polyvalent plants with multiorgan drainage, and ENT-focused actions (Table 37.5)
Diet 1. Pancreas-sparing diet 2. Liquids: soups, fruit juices rich in vitamin C
TABLE 37.1 Elements of the terrain by history and Biology of Functions correlations. Area
Finding
Terrain
ENT
Nasal discharge, sinus pain, congestion, cough, sneezing
cf. precritical terrain
Alpha
GERD, Gastritis, constipation, insomnia
High Alpha
⇑/⇓ LMI
Cortico
Fatigue, prolonged infections
⇓ Peripheral adrenal cortex
⇓: Cortisol ⇓ Adrenal cortex
Thyro
Vivid dreams, nightmares
⇑ TRH
⇑: Thyroid relaunching, Thyroid relaunching corrected
Enlarged tonsils
⇓ Peripheral thyroid
⇓ Thyroid
Somato
Preference for sweets, skin tags, nasal congestion
Hyperfunctioning hyperinsulinism
⇓ Insulin index ⇑ Insulin resistance
Liver
Poor immune response, loss of appetite especially in AM; prominent veins on eyelids, nasal bridge, chest
Hepatic congestion
⇑/⇓ LMI
Exocrine pancreas
Enlarged tonsils, recurrent ear, nose and throat infections
cf. precritical terrain
⇑ Somatostatin
Colon
Constipation
Key: ENT: Ear, nose and throat; Cortico: Corticotropic; Thyro: Thyrotropic; Somato: Somatotropic axis.
BoF
Otitis media Chapter | 37 245
TABLE 37.2 Examination, Critical terrain, and Biology of Functions relationships in Otitis media. Area
Finding
Terrain
Inner ear
Tympanic membrane: erythematous, bulging, decreased mobility
cf. critical terrain
Outer ear
Cerumen, abundant Cerumen, flakey
Hyper Para > Alpha Hyper Alpha > Para
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓: PMI
Cortico
Tender, distal lateral femur
Appeal to cortisol
⇓ Cortisol
Thyro
Brisk DTR, Clonus, Eyelid flutter on Glabella tap Cold extremities, dry skin
⇑ TRH
⇑: Thyroid relaunching, Thyroid relaunching corrected ⇓ Thyroid yield, thyroid metabolic
Immune
Suprasternal notch: Tender on palpation
Thymus congested
⇓: IL-1
Liver
Tender, superior-medial Tender, inferior-lateral
Vascular hepatic congestion Metabolic hepatic congestion
⇑/⇓ LMI ⇑/⇓ LMI
GB
Tender to palpation, Murphy’s point or GB zone
Gallbladder congestion
N/A
Pancreas
Tender, above umbilicus
Congestion: general
N/A
Tender, right and superior to umbilicus
Over-solicitation: exocrine
⇑/⇓ Somatostatin
Tender, left and superior to umbilicus
Over-solicitation: exocrine
⇑/⇓ Insulin
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
⇑/⇓ ACTH, serum TSH, ⇑: TRH indexes: cf. above
Colon
BoF
Low peripheral thyroid
Key: Cortico: Corticotropic; ENT: Ear, nose and throat; GB: Gallbladder; Neuro: Neurologic; Thyro: Thyrotropic axis.
TABLE 37.3 Polyvalent essential oils for symptomatic relief and direct actions against mechanisms of symptoms. Medicinal plant
ANS
Anti-infectious
Lavandula angustifolia
Spasmolytic
•
Cupressus sempervirens
(-) Para
Thymus vulgaris
(-) Para
Eucalyptus ssp.
Antipyretic
Analgesic
Other Hepatobiliary drainer
•
Tonsil drainer; immune stimulant; lymphatic decongestant
•
•
•
Adrenal cortex stimulant
•
•
•
Pancreatic drainer; Nasal decongestant
Syzygium aromaticum
Sympatholytic; Antispasmodic
•
•
Anti-allergic, antiinflammatory
Mentha piperita
Sympatholytic
•
•
Balances enteric flora
246 SECTION | C Assessment and treatment of common disorders
TABLE 37.4 Medicinal plants that regulate the critical terrain. Medicinal plant a
Lavandula angustifolia a
Thymus vulgaris
Cinnamomum zeylanicum
a
ANS
Immunity
(–) alpha, para
•
(–) para
•
(+) beta
•
Rhodiola rosea b
Ribes nigrum GM Avena sativa
indirect
Cortico
Thyro
Somato
• •
• (+ thymus)
•
•
•
•
•
•
a
Efficient as essential oil or bulk herb.
b
Gemmomacerate preparation only.
Key: ANS: Autonomic nervous system; Cortico: Corticotropic; Somato: Somatotropic; Thyro: Thyrotropic axis.
TABLE 37.5 Medicinal plants for critical terrain drainage. Medicinal plant
ENT
Hepatobiliary
Pancreas, Exo
Intestines
Other
Plantago major
•
•
•
•
Antimicrobial, Immuno-stimulant
Agrimonia eupatoria
• (indirect)
•
•
•
Antimicrobial, antihistaminic
Dual pancreatrope
•
Antimicrobial (ENT tropism)
• (+ hypoglycemant)
• (astringent)
Anti-inflammatory
Juglans regia Rubus fruticosus
•
Key: ENT: Ear, nose, and throat.
Lifestyle 1. Avoid rapid changes in altitude 2. Avoid blowing nose aggressively
Mechanical 1. Cranial work 2. Evaluate for short frenulum and oral-motor competency
Exemplary prescriptions Based on an Endobiogenic approach to otitis media, a number of prescriptions can be derived. Dosing is for a 2-yearold child. Adjust accordingly to age of patient.
1. Sympatomatic: Polyvalent application to tympanic membrane Apply every 2–3 h (Table 37.6) 2. Neuroendocrine: 2 mL four times per day × 4 days, then 2 mL three times per day for 6 days (Table 37.7): Quercus pedunculata GM 15 mL, Ribes nigrum GM 45 mL 3. Drainage: 1–2 mL four times per day × 4 days, then 1–2 mL three times per day for 6 days (Table 37.8): Plantago major 10 mL, Vitis vinifera GM 30 mL, Olea europaea GM 20 mL 4. Oligoelement: Copper-Gold-Silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Pancreas sparing during acute infection, liquid diet if favored or tolerated by child
Otitis media Chapter | 37 247
TABLE 37.6 Botanical ear oil with herbs, amounts and instructions for preparation and administration. Ingredients
Instructions
– Slice 1 clove of raw garlic into 3–4 pieces
– Have patient lay on their side, head parallel to the ground
– Simmer at low heat in 2 TBSP olive oil for 10 min
– Lift the affected ear up and out
– Remove from heat and cool until comfortably dripped on back of hand; place in 1 oz glass jar
– Add 3–4 drops of prepared oil
– Optionally add: 1 mL Methylene blue Lavandula angustifolia EO 5 drops Thymus vulgaris, ct linalool EO 3 drops Eucalyptus spp EO 2 drops Clove EO 1 drop Mentha piperita EO 1 drop
– Twist a cotton ball to a tip and insert into ear canal to prevent leakage – Repeat every 2–3 h until relief is achieved Insert in affected during time of administration of tinctures; also, use needed up to every 2 h for pain to affected ear canal
Key: EO: essential oil.
TABLE 37.7 Neuroendocrine prescription. Medicinal plant
Replacements and alternatives
Quercus pedunculata 15 mL GM
Ribes nigrum GM, Rosa canina GM
Ribes nigrum 45 mL GM
Quercus pedunculata GM
Key: GM: gemmomacerate.
TABLE 37.8 Drainage prescriptions Medicinal plant
Replacements and alternatives
Plantago major 10 mL GM
Agrimonia eupatoria MT
Vitis vinifera 30 mL GM
Plantago major MT 15 mL + Olea europaea GM 15 mL, or, Agrimonia eupatoria MT 30 mL
Olea europaea 20 mL GM
Agrimonia eupatoria MT 10 mL + Plantago major MT 10 mL
Key: EO: essential oil, MT: mother tincture, GM: gemmomacerate.
Chapter 38
Prostate enlargement with lower urinary tract obstruction (LUTO) Summary Essence: A urinary-prostatic spasmophilia with enlargement due to adenomatous hypertrophy, edema, or both. Terrain: Various factors result in enlargement of the prostate, Predisposition: (a) Spasmophilia, (b) pelvic congestion, oversolicited pancreas (exocrine and/ or endocrine), (c) adaptation of gonadal androgen regulation that results in excessive production of dihydrotestosterone (DHT), targeting the prostate for: (1) Adenoma: Para initiates, gonado-thyro-somatotropic factors for hypertrophied growth, localizing in prostate during a time of genital recycling with elevated DHT or (2) Edema of prostate from alpha-initiated (a) cortico-thyrotropic hyperfunction and/or (b) thyro- somatotropic hyperfunctioning during a time of during a time of genital recycling with elevated DHT resulting in (3) Prostate enlargement: compressing the prostatic urethra, causing (4) Lower urinary tract obstruction (LUTO).
Treatment goals Symptomatic: Decongest pelvis, splanchnic bed, urinary muscular spasmolysis
Adenoma Terrain: ● ●
● ●
ANS: ⇓ Para > Alpha, ⇑ Beta (to resolve spasmophilia) GONADO: Regulate LH-gonadal androgens (based on sub-type), ⇓ conversion of testosterone (T2) ➔ dihydrotestosterone (DHT) THYRO: Improve thyroid responsiveness to TSH SOMATO: Inhibit GH, growth factors, PL
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00038-X © 2020 Elsevier Inc. All rights reserved.
●
●
●
CORTICO: Adapt cortisol to regulates LH; improve aldosterone activity DRAIN: 1°-Pelvis, by extension: splanchnic bed, 2°-Pancreas, 3°-Liver DIET: Low glycemic, increase consumption of fish, fowl, pumpkin seeds, leafy green vegetables, root vegetables (except potatoes); minimize or avoid grains, avoid nonfermented dairy and red meat;
Edema ● ● ●
●
ANS: ⇓ Alpha > Para, ⇑ Beta (to resolve spasmophilia) ENDO: Depends on subtype (cf. text) DRAIN: 1°-Pelvis, by extension: splanchnic bed, 2°-Pancreas, 3°- Liver DIET: Low glycemic, focus on whole, gluten-free grains, fish, fowl, pumpkin seeds, leafy green vegetables; avoid nonfermented dairy and red meat
Sample treatment: Prostatic adenoma 1. Drainage-decongestion: 3 mL AM, 3 mL afternoons, 4 mL 45 min before bed (Table 38.9): Agrimonia eupatoria MT 120 mL, Hamamelis virginiana MT 120 mL, Citrus limon EO 2 mL, Melaleuca leucadendron EO 2 mL 2. Type 1c neuroendocrine: 3 mL AM, 3 mL afternoons, 4 mL 45 min before bed (Table 38.10): Passiflora incarnata MT 80 mL, Medicago sativa MT 80 mL, Urtica dioica MT 80 mL, Lavandula angustifolia 4 mL EO 3. General adenoma: 4 mL AM and before dinner (Table 38.11): NB: This treatment can be used for any adenomatous growth in adults, e.g., pituitary adenoma, breast adenoma, etc. Lithospermum officinale MT 60 mL, Fabiana imbricata MT 60 mL, Fragaria vesca MT 60 mL, Ribes nigrum GM 30 mL, Prunus amygdalus bud GM 30 mL
249
250 SECTION | C Assessment and treatment of common disorders
Sample treatment: Prostatic edema
Agent
Hyperimmune
Alteration in gonadal androgen production:
1a. Symptomatic: 4 mL 3–4 times per day until symptoms resolve: Eleutherococcus senticosus MT 40 mL, Agrimonia eupatoria MT 40 mL, Hamamelis virginiana MT 40 mL, Lavandula angustifolia EO 2 mL 2a. Allergy-Drainage: 4 mL 3 times per day: Agrimonia eupatoria MT 40 mL, Viola tricolor MT 40 mL, Hamamelis virginiana MT 40 mL, Eucalyptus radiata EO 2 mL, Melaleuca leucadendron MT 1 mL 3a. Neuroendocrine: 4 mL 3 times per day: Passiflora incarnata MT 30 mL, Eleutherococcus senticosus MT 30 mL, Menyanthes trifoliata MT 30 mL, Urtica dioica root and leaf MT 30 mL, Lavandula angustifolia EO 2 mL
1. Genital recycling 2. Gonadopause 3. Significant or persistent stressor with adaptative effects on luteal dynamics
Inflammatory 1b. Symptomatic-Inflammatory type: 4 mL 3–4 times per day until symptoms resolve: Arnica montana MT 40 mL, Matricaria recutita MT 40 mL, Hamamelis virginiana MT 40 mL, Lavandula angustifolia EO 1.5 mL, Melaleuca leucadendron EO 1.5 mL 2b. Somato-Drainage: 4 mL 3 times per day: Malva sylvestris MT 40 mL, Menyanthes trifoliata MT 40 mL, Hamamelis virginiana MT 40 mL, Eucalyptus radiata EO 2 mL, Melaleuca leucadendron MT 1 mL 3b. Neuroendocrine: 4 mL 3 times per day: Passiflora incarnata MT 30 mL, Ribes nigrum GM 30 mL, Menyanthes trifoliata MT 30 mL, Alchemilla vulgaris MT 30 mL, Lavandula angustifolia EO 2 mL
Common to all types 4. Oligoelement: Zinc oligo 1 ampule in AM 5. Diet and lifestyle as discussed
Terrain in detail: Prostate adenoma Precritical terrain Adenoma of the prostate is a benign tumorous growth. It occurs in the transition zone of the prostate, which circumferentially encompasses the proximal urethra. The precritical terrain in all adenomas is as follows: 1. ANS: Hyperfunction πΣ > hyperfunction αΣ in metabolism 2. TSH: elevated activity: expressed as serum TSH >3.4 typically with low Thyroid yield on Biology of Functions 3. Somatotropic: a. Hyperfunctioning GH > Hyperfunctioning PL b. Insulin: implicated in its hyperfunction as a reaction to the above 4. Exocrine pancreas: Oversolicited
Critical terrain The response to the change in androgen production results in a response from the gonadotropic axis, which results in disadapted LH-gonadal androgen dynamics, production, and activity. In the face of the general adenomatous tendency, the increased DHT activity focalizes and localizes adenomatous histopathology to the prostate. 1. ANS: Further elevation of Para > Alpha with spasmophilia of urethral sphincter 2. Endocrine: Gonadotropic: End result: T2 ➔ DHT 1a: Primary LH reactivity: a. Mild drop in gonadal androgens ➔ LH overcompensates 1b: Adrenal androgen overcompensation: b. Low T2/DHT + Insufficient LH response c. Adrenal androgens: intracrine conversion to DHT; LH cannot regulate adrenal androgens 1c: Primary LH overstimulation: d. LH overstimulated by other factors: i. Direct: GnRH, ACTH, or FSH ii. Indirect: 1. TRH ➔ PL ➔ GnRH ➔ LH 2. Dopamine ➔ PL ➔ GnRH ➔ LH 3. Alpha ➔ PL ➔ GnRH ➔ LH 1d: Compensatory LH overfunctioning: e. Compensates for chronic thyro-somatotropic anabolic activity 3. Endocrine: Other: a. Thyrotropic: TSH serum elevated b. Somatotropic: Insulin (cf. Emunctories) 4. Emunctories: Compensatory TSH action on pancreas a. Exocrine pancreas: overnutrition: ↑PAP b. Endocrine pancreas: increased glucose for energy: ↑PSA
Mechanisms Adenomatous growth in prostate transitional zone
Result Lower urinary tract obstruction (LUTO): enlarged prostate compresses prostatic urethra; increased resting tone of urethral sphincter
Prostate enlargement with lower urinary tract obstruction (LUTO) Chapter | 38 251
History and BoF findings
Physical exam and BoF findings
There are two levels of history to evaluate with adenoma of the prostate. The first is general to LUTO (Table 38.1). The second is particular to the critical terrain of adenoma. Some possible correlations between precritical symptoms and Biology of Functions are presented in Table 38.2.
During presentation for acute prostatic enlargement, some anticipated physical exam findings are presented in Table 38.3. In addition, a digital rectal prostate examination should be performed. Note the size, lateral asymmetry, density (boggy, firm, etc.), and any nodularity on the surface. Biology of Function correlation for each axis implicated in
TABLE 38.1 Symptoms of lower urinary tract obstruction. Stage
Dysuria
Bladder function
Comment
1
Delayed onset Urgency Frequency Incomplete voiding
Intact
Outlet partially obstructed from hypertrophy in the prostate portion of urinary bladder or due to ANS hyperfunctioning or both Pelvic heaviness Symptoms aggravated by pelvic congestion
2
Stage 1 and: Reduced strength of stream Dribbling
Hyperexcitable
Bladder distended to produce enough force to overcome outlet obstruction
3
Stage 2 and: Passive urination
Hypoexcitable
Damaged reflex arcs
TABLE 38.2 Historical, terrain, and Biology of Functions relationships in prostatic adenoma. Area
Finding
Terrain
PMH
Childhood tonsil enlargement, appendicitis Thick, dark hair at birth
Adenoma tendency Prominence of adrenal androgens in structure Dysregulation of LH-Gonadal androgen relationship
Acne: neonatal, adolescent, adult
BoF
C.f. Chapter 15: Acne
Temp.
Loss of professional competence or confidence
Diminished testosterone activity
⇓ Androgen indexes ⇑/⇓ LH
ANS
Dry mouth, matinal anorexia Sweaty feet, moist hands, nocturnal occipital sweating
Elevated Alpha Elevated Para
⇑/⇓ LMI
Gonado
Acne
Dysregulated androgens
C.f. Chapter 15: Acne
Cortico
Recurrent infections, allergies, fatigue Hair: receding superior-lateral forehead and/or increased growth above temples
Low Cortisol DHEA
⇓: Cortisol ↑DHEA, ↑Rate of adrenal androgens
Thyro
Vivid dreams, nightmares
TRH
Enlarged lymph nodes/tonsils; weight gain—difficult to lose weight
Latent hypothyroidism
↑ Hypothalamo-Metabolic, Thyroid relaunching corrected Serum TSH > 3.3, ↓Thyroid metabolic, ↓Thyroid yield
Skin tags, cracked feet, bulbous nose
Excessive GH
Weight gain, midabdominal
Hyperinsulinism
↑: GH growth score, Growth index, Growth index corrected ↓Insulin, ↑Insulin resistance,
Feet cooler than hands; dilated lowerextremity veins; hemorrhoids
Pelvic congestion
⇓ Pelvic congestion
Somato
Pelvic
Key: ANS: Autonomic nervous system; Cortico: Corticotropic; Gonado: Gonadotropic; Somato: Somatotropic; Temp: Temperament; Thyro: Thyrotropic PMH: Past medical history, BoF: Biology of Functions.
252 SECTION | C Assessment and treatment of common disorders
TABLE 38.3 Critical terrain examination, terrain, Biology of Functions relationships in prostatic adenoma. Area
Finding
Terrain
BoF
Prostate
Enlarged, firm or boggy, lateral asymmetry, and/or nodules
Adenomatous prostate hypertrophy
Cf. Critical terrain, adenoma
ANS
Dry mouth, matinal anorexia Abundant saliva, Sweaty feet, moist hands
Elevated Alpha Elevated Para
⇑/⇓ LMI
Gonado
Acne Structural asymmetry Left > Right: eyes, hands, feet, muscular density Hair: coarse, dark, particularly at midline; distal extremity hair growth Thinning hair Quadriceps dense, well structured
Dysregulated androgens Structural lutealism
C.f. Chapter 15: Acne
Quadriceps poorly structured, diminished in size and/or density
In the face of prostate adenoma, androgens are interiorized and favor DHT > Testosterone and/or DHEA
Hair: receding superior-lateral forehead and/or increased growth above temples Calves dense, well structured
DHEA
Glabellar tap: Fluttering of eyelids Enlarged lymph nodes/tonsils Distal lower extremity edema that narrows at the ankles
TRH
Skin tags, cracked feet, bulbous nose Weight gain, midabdominal
Excessive GH Hyperinsulinism
↑: GH growth score, Growth index, Growth index corrected ↓Insulin, ↑Insulin resistance,
Pelvic
Feet cooler than hands; dilated lower extremity veins; hemorrhoids; Tenderness on palpation of left upper tibia pelvic congestion point
Pelvic congestion
⇓ Pelvic congestion
Pancreas
Tender, above umbilicus Tender, right of umbilicus Tender, left of umbilicus
Congestion: general Oversolicitation: exocrine Oversolicitation: exocrine
N/A ⇑/⇓ Somatostatin N/A
Liver
Tender, superior-medial Tender, inferior-lateral
Vascular hepatic congestion Metabolic hepatic congestion
⇑/⇓ LMI ⇑/⇓ LMI
Colon
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
⇓: ACTH, serum TSH, ⇑: TRH indexes
Cortico
Thyro
Somato
Increased structural gonadal androgens
Increased DHT Prominent gonadal androgens
↑: Comparative genital androgeny, Rate of gonadal androgens ↑Musculotrope + ↑Genital androgens; ↓: Comparative genital androgeny, Rate of gonadal androgens ↑DHEA, ↑Rate of adrenal androgens
Prominent adrenal androgens
Latent hypothyroidism
↑Hypothalamo-Metabolic, Thyroid relaunching corrected Serum TSH > 3.3, ↓Thyroid metabolic, ↓Thyroid yield
Key: ANS: Autonomic nervous system; Cortico: Corticotropic; Gonado: Gonadotropic; Somato: Somatotropic; Temp: Temperament; Thyro: Thyrotropic PMH: Past medical history, BoF: Biology of Functions.
Prostate enlargement with lower urinary tract obstruction (LUTO) Chapter | 38 253
the development of prostatic enlargement is presented in Tables 38.4 and 38.5. The significance of each index is discussed in The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate.
Treatment The standard of care is symptomatic, focusing on inhibition of alpha-sympathetic tone and/or of 5-alpha reductase enzyme activity (cf. The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate). The focus of the
TABLE 38.4 Indexes of endocrine coupling, and gonadotropic function in prostatic adenoma. Endocrine coupling
Gonadotropic
↑Follicular implication
Varies: LH
↑Thyrotropic implication
↑Total androgen rate
↑Hypothalamo-Metabolic implication
↑/Nl: Adrenal androgen rate
↑Global upstream 2
↑/Nl: Genital androgen rate
↑Global upstream 3
↑Genital androgeny
Key: Nl: Normal.
TABLE 38.5 Thyro-, somato-, and corticotropic indexes in prostatic adenoma Thyrotropic
Somatotropic
Corticotropic
Varies: Thyroid
↓Pelvic congestion
Varies: Cortisol
Varies: Thyroid yield
↑Metabolic yield
Varies: Aldosterone
Varies: TRH/TSH
↑Adenosis
↑Evoked histamine
↑/Nl:Global TRH of Adaptation
↑Growth or Corrected growth
↓Platelet mobilization
↓Necrosis
Varies: Inflammation
Varies: Somatostatin ↓Insulin index ↑Insulin resistance ↓Redox Varies: Pancreatic index ↑GH growth score ↑Expansivity index
d iscussion is nonpharmacological in this volume. According to the theory of Endobiogeny, the general emphasis of treatment of the terrain is: 1. Symptomatic, to relieve LUTO symptoms: a. Decongestion: loco-regional and global (Table 38.6), in order of importance: i. Pelvis ii. Splanchnic bed iii. Liver iv. Portal circulation b. ANS: Reduce Alpha and relaunch beta; allow parasympathetic to be passively or indirectly reduced by readaptation of sympathetic tone (Table 38.7) 2. Neuroendocrine regulation (Table 38.7): NB: Correlation of medicinal plants to specific indexes can be found in The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate. a. ANS: Reduce Alpha-sympathic, relaunch beta, and allow for passive adaptation of parasympathetic b. Endocrine i. Androgen regulation Cortico-Gonadotropic and Gonadotropic are primary depending on the subphenotype ii. Regulate the anabolic response from thyro- somatotropic function favoring adenomas c. Oligoelements: Zinc to keep PSA inactive 3. Alimentation a. Foods rich in zinc: sprouted pumpkin seeds, pumpkin oil b. Consume: low-glycemic foods, high-fiber foods; specific strategies vary by other indexes c. Avoid: alcohol, coffee, spicy foods, creamy cheeses, fried foods, animal flesh, animal fats (especially for cooking). 4. Lifestyle: avoid irritation of the prostate (Table 38.8)
Exemplary prescriptions Based on an Endobiogenic approach to prostatic enlargement, a number of prescriptions can be derived. Because of the number of subphenotypes of benign prostatic adenoma, there are numerous possible neuroendocrine treatments. What is presented is a treatment for type 1c: primary LH overstimulation. 1. Drainage-Decongestion: 3 mL AM, 3 mL afternoons, 4 mL 45 min before bed (Table 38.9): Agrimonia eupatoria MT 120 mL, Hamamelis virginiana MT 120 mL, Citrus limon EO 2 mL, Melaleuca leucadendron EO 2 mL 2. Type 1c Neuroendocrine: 3 mL AM, 3 mL afternoons, 4 mL 45 min before bed (Table 38.10): Passiflora incarnata MT 80 mL, Medicago sativa MT 80 mL, Urtica dioica MT 80 mL, Lavandula angustifolia 4 mL EO
254 SECTION | C Assessment and treatment of common disorders
TABLE 38.6 Polyvalent drainage plants for prostatic adenoma. Plant
Pelvic
Splanchnic
Alchemilla vulgaris
•
Achillea millefolium
•
•
Aesculus hippocastanum
•
•
Hepatic
Portal
Other Progesteronic
Agrimonia eupatoria
•
Artemisia dracunculus
•
Carduus marianus
•
Progesteronic, (–) LH • •
•
Dual pancreatrope, Antiallergic Mental antispasmodic
•
•
Hamamelis virginiana
•
Lavandula angustifolia
•
Reduces sympathetic tone, Anti-inflammatory
Melaleuca leucadendron
•
Spasmolytic, Estrogenic
Matricaria recutita
•
Pygeum africana
•
Quercus pedunculata
•
Urtica dioica root
•
•
•
Anti-inflammatory
•
3. General adenoma: 4 mL AM and before dinner (Table 38.11): NB: This treatment can be used for any adenomatous growth in adults, e.g., pituitary adenoma, breast adenoma, etc. Lithospermum officinale MT 60 mL, Fabiana imbricata MT 60 mL, Fragaria vesca MT 60 mL, Ribes nigrum GM 30 mL, Prunus amygdalus bud GM 30 mL 4. Oligoelement: Zinc oligo 1 ampule in AM 5. Diet and lifestyle as discussed
Terrain in detail: Prostate edema Precritical terrain The precritical terrain is one of hypermetabolism with stagnation, implicating mild enlargement of the prostate, which later sensibilizes it to further enlargement in the critical terrain from edema. 1. Hyperandrogenism: various origins; cf. Critical terrain—adenoma 2. ANS: πΣ > αΣ in metabolism 3. Exocrine pancreas: Oversolicited 4. Circulation: Pelvic congestion (αΣ > πΣ)
Agent Adaptive demand involving cortico-thyrotropic yoking 1. Chronobiologic: seasonal, circannual 2. Substantial and sudden conflict or stressor
Anti-inflammatory, antiallergic Cortisol-like activity that (–) LH •
Endocrine redistributor (–) 5α-reductase activity
3. Slow, progressive conflict or stressor that reaches a critical point of fragilization.
Critical Terrain When the adaptive demand, expressed through alpha- cortico-thyrotropic yoking becomes adaptative. The ANS component is common: ● ANS: Hyperfunctioning αΣ > hyperfunctioning πΣ Otherwise, there are three general origins of edema, of which patients will often have a critical terrain for one or two of the three: 1. Hyperimmune: this is similar to the atopic terrain (cf. Part 3, Chapters 16, 17, and 29, and, The Theory of Endobiogeny, Volume 3: Chapters 1 and 2: Allergic disorders and Asthma, respectively) a. Corticotropic: ↑ACTH, ↓Cortisol, ↑Histamines b. Thyrotropic: ↑TRH, ↑Interleukins (proinflammatory series) 2. Inflammatory: this is a neuroendocrine inflammatory terrain arising from somatotropic desynchronization a. Corticotropic: ↑ACTH, ↑Cortisol b. Thyrotropic: ↑TRH, ↓TSH serum, ↑peripheral thyroid (often), ↑Interleukins (proinflammatory series) c. Somatotropic: ↑Insulin, ↓Insulin resistance, ↑free radicals, ↑necrosis 3. Fluid retention: this terrain favors fluid accumulation due to a terrain that shares elements of the first two critical terrain subtypes
Prostate enlargement with lower urinary tract obstruction (LUTO) Chapter | 38 255
TABLE 38.7 Polyvalent medicinal plants for regulation of the prostatic adenoma terrain.
TABLE 38.8 Lifestyle recommendations for prostate enlargement.
Axis
Factor
Therapy
Category
Principle
Example
ANS
↓Alpha
Matricaria recutita MT, EO Lavandula angustifolia EO Passiflora incarnata MT Menyanthes trifoliata EO Cinnamomum zeylanicum EO
Avoid
Inflammation Prostate irritation or injury
Tobacco products Horseback, bicycle riding Constipation Excessive sexual activity Prolonged sitting
↑Beta
Gonadotropic
↓LH
↑Estrogens ↑Progesterone Regulate: Testosterone and DHEA ↓DHT
Lithospermum officinale MT Medicago sativa MT Pygeum africana MT Alchemilla vulgaris MT Avena sativa MT Salvia sclarea MT Achillea millefolium MT Alchemilla vulgaris MT Eleutherococcus senticosus MT
Prostate overactivity Diminishes perineal flow Encourage
Frequent standing Exercise
Prostate emptying
For every 55 min of sitting, walk for 5 min Aerobic exercise: walking, running, elliptical Moderate sexual activity (2–3 times per week)- the more semen demanded, the more pelvic congestion
Urtica dioica root MT
Thyrotropic
↑Thyroid yield
Avena sativa MT Ascophyllum nodosum Selenium, Iodine, Copper oligo
Somatotropic
↓Growth factors ↓Prolactin
Fragaria vesca MT
TABLE 38.9 Drainage-Decongestion prescription for prostatic adenoma.
Poterium sanguisorba MT Fragaria vesca MT Malva sylvestris MT
Medicinal plant
Replacements and alternatives
Agrimonia eupatoria MT 120 mL
Plantago major MT
Hamamelis virginiana MT 120 mL
Alchemilla vulgaris MT 60 mL + Piper methysticum MT 60 mL
Citrus limon 2 mL EO
Mentha spicata EO 2 mL
Melaleuca leucadendron EO 2 mL
Myrtis communis ct. linalool EO 2 mL
↓Insulin Corticotropic
Regulate Cortisol ↓Aldosterone
Ribes nigrum GM Salvia sclarea EO, MT Achillea millefolium MT Borago officinalis MT
Exocrine pancreas
Regulate
Agrimonia eupatoria MT Avena sativa MT
Key: EO: essential oil, GM: gemmomacerate, MT: mother tincture.
a. Corticotropic: ↑ACTH, ↓Cortisol, ↑Histamine receptors > ↑circulating histamine, ↑Aldosterone b. Thyrotropic: ↑TRH, ↓TSH serum, ↑peripheral thyroid (often), ↑Interleukins (proinflammatory series) c. Somatotropic: ↑Insulin, ↓Insulin resistance, ↑free radicals, ↑necrosis
Mechanisms Various inflammatory mechanism resulting in loss of capillary permeability and accumulation of fluid in the extravascular space: cytokines, interleukins, prostaglandins, histamines, aldosterone-mediated fluid retention, etc., which increase interstitial fluid pressure, compressing capillaries, veins and/or lymphatic channels.
Result Lower urinary tract obstruction (LUTO).
History, Physical exam, and BoF findings The history of LUTO is discussed in Table 38.1. Common historical findings shared in all forms of prostate enlargement (except those related to adenoma) are presented in Table 38.2. Common examination findings are presented in Table 38.3. Symptoms and signs and BoF findings specific to prostate edema are presented in Table 38.12. Biology of Functions correlation for each axis implicated
256 SECTION | C Assessment and treatment of common disorders
TABLE 38.10 Neuroendocrine-splanchnic-inflammation prescription for prostatic adenoma. Herb
Replacements and alternatives
Passiflora incarnata MT 80 mL
Scutellaria latiflora MT
Medicago sativa MT 80 mL
Lithospermum officinale MT
Urtica dioica root MT 80 mL MT
Menyanthes trifoliata MT 40 mL + Serenoa repens MT 40 mL
Lavandula angustifolia 4 mL EO
Matricaria recutita EO 2 mL + Melaleuca leucadendron EO 1 mL
Key: EO: essential oil, GM: gemmomacerate, MT: mother tincture, SAMe: S-adenosyl methionine.
TABLE 38.11 General adenoma prescription for prostatic adenoma. Herb
Replacements and alternatives
Lithospermum officinale MT 60 mL
Lycopus europaeus MT 60 mL
Fabiana imbricata MT 60 mL
Leonurus cardiaca MT 60 mL
Fragaria vesca MT 60 mL
Quercus pedunculata GM 30 mL + Menyanthes trifoliata MT 15 mL + Humulus lupulus MT 15 mL
Ribes nigrum GM 30 mL
Fragaria vesca MT 30 mL
Prunus amygdalus bud GM 30 mL
Prunus amygdalus root GM 30 mL
Key: GM: gemmomacerate, MT: mother tincture.
1. Symptomatic, to relieve LUTO symptoms: a. Decongestion: loco-regional and global (Table 38.6), same order of importance b. Address elements of the terrain resulting in edema (Table 38.15). 2. Neuroendocrine regulation (Table 38.7) NB: Correlation of medicinal plants to specific indexes can be found in The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate 3. Oligoelements: Zinc to keep PSA inactive 4. Alimentation: cf. adenoma 5. Lifestyle: cf. adenoma
Exemplary prescriptions Based on an Endobiogenic approach to prostatic enlargement from edema, a number of prescriptions can be derived. Because of the number of phenotypes of edematous prostate enlargement, there are numerous possible neuroendocrine treatments. Targeted prescriptions are indicated.
Hyperimmune 1a. Symptomatic: 4 mL 3–4 times per day until symptoms resolve: Eleutherococcus senticosus MT 40 mL, Agrimonia eupatoria MT 40 mL, Hamamelis virginiana MT 40 mL, Lavandula angustifolia EO 2 mL 2a. Allergy-Drainage: 4 mL 3 times per day: Agrimonia eupatoria MT 40 mL, Viola tricolor MT 40 mL, Hamamelis virginiana MT 40 mL, Eucalyptus radiata EO 2 mL, Melaleuca leucadendron MT 1 mL 3a. Neuroendocrine: 4 mL 3 times per day: Passiflora incarnata MT 30 mL, Eleutherococcus senticosus MT 30 mL, Menyanthes trifoliata MT 30 mL, Urtica dioica root and leaf MT 30 mL, Lavandula angustifolia EO 2 mL
Inflammatory
in prostatic edema is presented in Tables 38.13 and 38.14. The significance of each index is discussed in The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate.
Treatment The standard of care is symptomatic, focusing on inhibition of alpha-sympathetic tone and/or of 5-alpha reductase enzyme activity (cf. The Theory of Endobiogeny, Volume 3, Chapter 7: Disorders of the prostate). The focus of the discussion is nonpharmacological in this volume. According to the theory of Endobiogeny, the general emphasis of treatment depends on the terrain subtype: hyperimmune, inflammatory, or fluid retention.
1b. Symptomatic-Inflammatory type: 4 mL 3–4 times per day until symptoms resolve: Arnica montana MT 40 mL, Matricaria recutita MT 40 mL, Hamamelis virginiana MT 40 mL, Lavandula angustifolia EO 1.5 mL, Melaleuca leucadendron EO 1.5 mL 2b. Somato-Drainage: 4 mL 3 times per day: Malva sylvestris MT 40 mL, Menyanthes trifoliata MT 40 mL, Hamamelis virginiana MT 40 mL, Eucalyptus radiata EO 2 mL, Melaleuca leucadendron MT 1 mL 3b. Neuroendocrine: 4 mL 3 times per day: Passiflora incarnata MT 30 mL, Ribes nigrum GM 30 mL, Menyanthes trifoliata MT 30 mL, Alchemilla vulgaris MT 30 mL, Lavandula angustifolia EO 2 mL
Common to all types 4. Oligoelement: Zinc oligo 1 ampule in AM 5. Diet and lifestyle as discussed
Prostate enlargement with lower urinary tract obstruction (LUTO) Chapter | 38 257
TABLE 38.12 Critical terrain symptoms, signs, and Biology of Functions indexes in prostatic edema. Factor
Symptoms
Signs
Indexes
↑Alpha
Dry mouth Oral herpes or canker sores when stressed Hypertension
Stringy saliva Injected sclera Dilated pupils Cold extremities Rapid lid movement on glabellar tap
↑/↓LMI
↑Histamine
Allergies, dermatitis, pruritis, angioedema Gastric acidity Hypervigilance
Dermatographia Rapid, prolonged, or intense erythema of skin with rolling palpation
↑Histamine (may only be present on exam on the envelope of the organism, not in the interior)
↑ACTH activity
Social, outgoing, determined, or forceful
Bushy eyebrows
↓ACTH: favors comportment
↑Cortisol
Insomnia Early waking with vigorous exercise in morning Oral herpes or canker sores when stressed
Fat deposits on zygomatic arch Striae Cortisol point, distal lateral femur tender
↑Cortisol
↑TRH
Vivid dreams Imaginative, tangential thinker, creative problem solver
Flutter on glabellar tap Very brisk deep tendon reflexes Clonus
↑Thyroid relaunching, ↑Thyroid relaunching corrected, ↑global TRH of adaptation, ↑TRH/TSH (thinking style)
↑Thyroid
Great capacity for work, brightness to the eyes
↑Insulin, ↓Insulin resistance
Intense sugar cravings Susceptibility to hypoglycemia
↑Thyroid, ↑Thyroid yield Edematous, enlarged neck flap Skin tags Midgut doughy adiposity
Key: LMI: Leukocyte mobilization index; TRH: Thyrotropin-releasing hormone.
TABLE 38.13 Indexes of endocrine coupling, and gonadotropic function in prostatic edema Endocrine coupling
Gonadotropic
↑Follicular implication
↓LH
↑Thyrotropic implication
↑/NL: Total androgen rate
↑Hypothalamo-Metabolic implication
↑/Nl: Adrenal androgen rate
↑Global upstream 2
↑/Nl: Genital androgen rate
↑Global upstream 3
↑Comparative genital androgeny
Key: Nl: Normal.
↑Insulin, ↓Insulin resistance
258 SECTION | C Assessment and treatment of common disorders
TABLE 38.14 Thyro-, somato-, and corticotropic indexes in prostatic edema. Thyrotropic
Somatotropic
Corticotropic
Varies: Thyroid
↓Pelvic congestion
Varies by type: Cortisol
Varies: Thyroid yield
↑Growth or Corrected growth
Varies by type: Aldosterone
↑/Nl: TRH/TSH
↓Necrosis
Varies by type: Evoked histamine
↑/Nl: Global TRH of Adaptation
Varies: Somatostatin
↓Platelet mobilization
Varies: Thyroid relaunching corrected
Varies by type: Insulin index
↑Inflammation
Varies by type: Insulin resistance
Varies by type: IL-1
Varies by type: Redox Varies by type: Pancreatic index Varies by type: GH growth score Varies by type: Expansivity index
TABLE 38.15 Polyvalent drainage plants for prostatic edema. Medicinal plant
Antihist.
Antialler.
Agrimonia eupatoria
•
•
Arnica montana
•
•
↓ Alpha, Beta
Delays insulin
Artemisia dracunculus
•
•
↓ Alpha and Para
Estrogenic
Borago officinalis
•
Eucalyptus globulus
•
Lavandula angustifolia
•
Anti-inflam.
•
Plantago major
•
Endocrine
↓ para (indirect)
• •
•
• •
Emunctory Drainage: hepatopancreatic (exocrine, endocrine), portal
(–)FSH > LH, (–) Aldosterone
•
Melaleuca leucadendron Matricaria recutita
ANS
Kidney: Diuretic Exocrine pancreas
↓ Alpha, Beta, Para
Drainage: pelvis
Antispasmodic, ↓ Alpha and Para
Estrogenic (mild)
Drainage: pelvis
↓ Alpha and Para
(–) ACTH
Drainage: pelvic, splanchnic, hepatic
•
(–): Inhibits; Aller.: Allergic; ANS: Autonomic nervous system; Hist.: Histaminic; Inflam.: inflammatory.
Drainage: hepatopancreatic (exocrine, endocrine),
Chapter 39
Prostatitis Summary Essence: Local stagnation favors inflammation and/or infection of the prostate, often asymptomatic unless presenting with pelvic pain Terrain: (1) Hyperandrogenism favoring dihydrotestosterone (DHT) resulting in (2) Focalized hypermetabolism of the prostate soliciting (3) Pelvic congestion with stagnation fragilizing the prostate, favoring (4a) Inflammation and/or (4b) Infection of the prostate from local translocation or acquired sexually resulting in (5) Actue prostatitis which can evolve over time to (6) Chronic prostatitis with various urinary and pelvic symptoms, especially pain in either case.
Treatment goals Symptomatic: Pelvic drainage, antimicrobial medicinal plants, antibiotics Terrain: Varies based on origin of congestion and stagnation ● ●
●
●
●
●
ANS: Resolve spasmophilia: ⇓ Para and Alpha, ⇑ Beta GONADO: Readapt LH-Androgen equilibrium for Endobiogenic terrain of patient (cf. Chapter 38: Prostate enlargement); Adapt FSH and its nutritional congesting role on tissues THYRO: Varies, adapt to avoid inflammation and insufficient utilization of immune elements SOMATO: Varies, adapt to avoid desynchronization and thus inflammation, but also adenoidal and hypertrophic conditions CORTICO: Varies, adapt cortisol regulation LH, histamines, and thyrotropic sensibilization DRAIN: 1°-Pelvis/Splanchnic bed, 2°-Pancreas, 3°-Liver
Sample treatment Month 1: 1. Oligo: a. Mg: 1 dose BID b. Cu-Ag-Au: 1 dose QID × 1 week, then TID × 1 week, then BID × 2 weeks The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00039-1 © 2020 Elsevier Inc. All rights reserved.
2. Rectal application: suppository or infusion: AM, before bed (cf. Exemplary prescriptions in the end of the chapter) 3. Pelvic drainage, Antimicrobial: Ribes nigrum GM 60 mL, Achillea millefolium MT 60 mL, Matricaria recutita MT 60 mL, Hamamelis virginiana MT 60 mL + Melaleuca leucadendron EO 3 mL, Lavender EO 2 mL: 4 mL BID (Table 39.4) 4. Diet: per BoF and PAP/PSA ratio 5. Lifestyle (Table 39.6)
Month 2–3: 1. Rectal application: suppository or infusion (cf. end of the chapter) 2. Pelvic drainage, Antimicrobial: Ribes nigrum GM 60 mL, Achillea millefolium MT 60 mL, Matricaria recutita MT 60 mL, Hamamelis virginiana MT 60 mL + Melaleuca leucadendron EO 3 mL, Lavandula angustifolia EO 2 mL: 4 mL BID 3. Neuroendocrine: Lithospermum officinale MT 60 mL, Medicago sativa MT 60 mL, Salvia sclarea MT 60 mL, Achillea millefolium MT 60 mL: 4 mL BID (Table 39.5) 4. Diet: per BoF and PAP/PSA ratio 5. Lifestyle (Table 39.6)
Terrain in detail Precritical terrain The precritical terrain is similar to the critical terrain of prostatic enlargement (cf. Chapter 38: Prostate enlargement) with elevated DHT. This targets the prostate for congestion and stagnation to meet metabolic demands. The configuration of the remaining endocrine axes is highly variable (cf. also The Theory of Endobiogeny, Volume 3, Chapter 7: Prostate disorders). This determines the vector of fragilization toward congestion, stagnation, inflammation, and immune competency. In addition, there are various metabolic (Table 39.1) and anatomical (Table 39.2) factors that fragilize the pelvis and prostate for inflammation and infection. In the face of all these possible factors, there are two key elements that can be addressed to bring a patient with 259
260 SECTION | C Assessment and treatment of common disorders
TABLE 39.1 Metabolic structuro-functional and functional elements of terrain favoring prostatitis. Factor
Element
Consequence
↑πΣ
Nutritional congestion: Pelvis, Prostate
Hyperemia ➔ distention of tissues, compression: lymphatics, venous outflow
↑αΣ
Vascular congestion: Pelvis, Prostate
Delayed egress of blood ➔ edema, compression: lymphatics, venous outflow
↑FSH, ↑αΣ
Mucosal congestion: urinary bladder, urethra, descending colon
Stasis, favors bacterial overgrowth
↑Thyrotropic
Inflammation
Capillary/Lymphatic leak ➔ translocation of microbial agents
↑Insulin ↑Cortisol
3. Microbial: a. Gram negative > positive: Escherichia. coli, Enterococcus ssp., Pseudomonas ssp., Chlamydia trachomatis, Ureaplasma ssp., Trichomonas vaginalis b. Fungi, Virus: rule out immune compromise, autoimmune disorders
Critical terrain The critical terrain is highly variable based on the precritical terrain. What is key is that the autonomic portion of the response aggravates the precritical congestive and stagnating condition, and the endocrine response dysadapts the immune response. 1. ANS: Hyper elevated Alpha > Elevated Para 2. Emunctory and vasculature (in order of importance): a. Pelvic basin congestion b. Exocrine pancreas oversolicited c. Liver congestion
Mechanisms TABLE 39.2 Anatomic structural and functional elements of terrain favoring prostatitis. Category
Example
Structuro-functional
Urinary bladder voiding dysfunction Bladder neck obstruction Ejaculatory duct obstruction Pelvic side wall tension
Immune compromise
HIV, Iatrogenic (radiation therapy, chemotherapy, post-surgical)
Inflammation and/or sequestered space for microbial growth and/or colonization of prostatic tissue, irritation of local nerves, irritation of aspect of bladder contiguous with prostate.
Result Prostatitis, often silent, but with various urinary symptoms and/or pelvic pain
History and BoF findings chronic prostatitis out of a latency for recurrent infection or inflammation: 1. ANS: a. Metabolic: Elevated Para > Elevated Alpha b. Vascular: Spasmophilia: Elevated Alpha > Para 2. Emunctory and vasculature (in order of importance): a. Pelvic basin congestion b. Exocrine pancreas oversolicited c. Liver congestion
Acute and chronic prostatitis is often silent and thus is diagnosed when there are symptoms. Symptom groups 1–4 may present in acute cases, symptom groups 1–5 in chronic prostatitis. 1. Pain: pelvic, abdominal, low back 2. Urinary: dysuria, lower urinary tract obstruction (cf. Chapter 38: Prostatic enlargement) 3. Systemic, infectious: fever, chills, malaise 4. Systemic, Immune: arthralgias, myalgias 5. Penile: Ejaculatory pain, erectile dysfunction
Agent
Physical exam and BoF findings
The agent with be a critical factor of vulnerability that results in a liminal threshold of inflammation and/or presence of virulent organisms.
Specific exam findings and BoF findings are discussed in Chapter 38: Prostate enlargement. See also The Theory of Endobiogeny, Volume 3, Chapter 7: Prostate disorders).
1. Endocrine: Table 39.1 2. Anatomical: Table 39.2
1. Localized pain in pelvic basin, lower abdomen or low back
Prostatitis Chapter | 39 261
2. Prostate, digital palpation via rectum: a. Acute: prostate hot, boggy b. Chronic: unremarkable, or, nodular and tender to palpation
Treatment Antibiotics are particularly suited for cases that are severe, chronic and/or in immunocompromised patients (cf. The Theory of Endobiogeny, Volume 3, Chapter 7: Prostate disorders). The following medicinal plants can be used according to an Endobiogenic reflection of the terrain: 1. Symptomatic (Table 39.3): a. Antimicrobial i. Plants with genitourinary tropism ii. Cu-Au-Ag oligoelement
b. Anti-inflammatory, anticongestive plants with pelvic tropism c. Antalgics, analgesics 2. Neuroendocrine (Table 39.5): a. ANS: Spasmolytics i. Genitourinary muscular antispasmodics ii. Pelvic circulatory tropism b. Endocrine: Depends on the terrain (cf. Chapter 38: Prostate enlargement) 3. Oligoelements: Mg: muscular spasmolysis to relieve the congesting tendency 4. Diet: See Chapter 38: Prostate enlargement for a full discussion a. General avoidance: Alcohol, coffee, spicy foods, creamy cheeses, fried food, red meat, animal fats
TABLE 39.3 Polyvalent symptomatic medicinal plants for prostatitis. Medicinal plant
Antihist.
Antialler.
Achillea millefolium
Anti-inflam.
Anti-infect.a
Emunctory
Other
•
•
Drainage: pelvic
Vagolytic
Drainage: hepatopancreatic (exocrine, endocrine), portal
↑ Para (indirect)
Agrimonia eupatoria
•
Arnica montana
•
•
Artemisia dracunculus
•
•
•
Drainage: Pelvic, splanchnic, pancreatic
Neurologic antispasmodic
Eucalyptus globulus
•
•
•
Drainage: exocrine pancreas
Antalgic
Hamamelis virginiana
•
•
•
Drainage: pelvis, splanchnic bed
Mild Alpha-mimetic to overcome stagnation
•
Juniperus communis
•
Lavandula angustifolia
•
Matricaria recutita
•
•
•
Syzygium aromaticum Thymus vulgaris
Drainage: Urinary, Hepatorenal (GM) •
•
Melaleuca leucadendron Plantago major
Sympatholytic
•
•
•
•
•
•
•
•
•
Drainage: pelvis
↑ Alpha, Beta, Para
Drainage: pelvic, splanchnic, hepatic
↑ Alpha and Para
Drainage: pelvis
Neuromuscular antispasmodic, ↑ Alpha and Para
Drainage: hepatopancreatic (exocrine, endocrine), ↑ Alpha and Para, Antalgic Drainage: Urinary
Parasympatholytic, Analgesic
(–): inhibits; Aller.: Allergic; ANS: Autonomic nervous system; GM: gemmomacerate preparation; Hist.: Histaminic; Infect.: infectious; Inflam.: inflammatory. a Refers to specific genitourinary tropism.
262 SECTION | C Assessment and treatment of common disorders
b. PAP>PSA—vegan/alkaline diet—avoid red meat, dairy, gluten c. PSA>PAP—Regulation of insulin with medicinal plants and dietary glycemic control measures 5. Lifestyle: avoid activities that promote inflammation or irritation of the prostate (Table 39.6) By far, the most efficient plants are essential oils of Eucalyptus ssp. and Melaleuca leucadendron, and rectal administration is far more efficient than oral administration. See The Theory of Endobiogeny, Volume 3, Chapter 7: Prostate disorders for a discussion of rectal efficiency of administration.
Months 2–3: 1. Rectal application: suppository or infusion (cf. below: Local application of essential oils) 2. Pelvic drainage, Antimicrobial: Ribes nigrum GM 60 mL, Achillea millefolium MT 60 mL, Matricaria recutita MT 60 mL, Hamamelis virginiana MT 60 mL + Melaleuca leucadendron EO 3 mL, Lavandula angustifolia EO 2 mL: 4 mL BID 3. Neuroendocrine: Lithospermum officinale MT 60 mL, Medicago sativa MT 60 mL, Salvia sclarea MT 60 mL, Achillea millefolium MT 60 mL: 4 mL BID (Table 39.5) 4. Diet: per BoF and PAP/PSA ratio 5. Lifestyle (Table 39.6) Local application of essential oils
Exemplary prescriptions Based on an Endobiogenic approach to prostatitis, a general 3-month prescription protocol is presented for acute prostatitis.
TABLE 39.5 Neuroendocrine prescription.
Month 1:
Lithospermum officinale MT 60 mL
Lycopus europaeus MT
Medicago sativa MT 60 mL
Alchemilla vulgaris MT, Pygeum africanum MT
Salvia sclarea MT 60 mL
Salvia officinalis MT, Angelica archangelica MT 30 mL + Avena sativa MT 30 mL
Achillea millefolium MT 60 mL
Alchemilla vulgaris MT
1. Oligo: a. Mg: 1 dose BID b. Cu-Ag-Au: 1 dose QID × 1 week, then TID × 1 week, then BID × 2 weeks 2. Rectal application: suppository or infusion: AM, before bed (cf. below: Local application of essential oils) 3. Pelvic drainage, Antimicrobial: Ribes nigrum GM 60 mL, Achillea millefolium MT 60 mL, Matricaria recutita MT 60 mL, Hamamelis virginiana MT 60 mL + Melaleuca leucadendron EO 3 mL, Lavender EO 2 mL: 4 mL BID (Table 39.4) 4. Diet: per BoF and PAP/PSA ratio 5. Lifestyle (Table 39.6)
TABLE 39.4 Pelvic drainage-antimicrobial prescription. Medicinal plant
Replacements and alternatives
Ribes nigrum GM 60 mL
Fragaria vesca MT
Achillea millefolium MT 60 mL
Alchemilla vulgaris MT
Matricaria recutita MT 60 mL
Hamamelis virginiana MT
Hamamelis virginiana MT 60 mL
Achillea millefolium MT
Melaleuca leucadendron EO 3 mL
Eucalyptus ssp. EO 2 mL + Achillea millefolium EO 1 mL
Lavandula angustifolia EO 2 mL
Matricaria recutita EO 1 mL + Eucalyptus ssp. EO 1 mL
Key: EO: essential oil, MT: mother tincture.
Medicinal plant
Replacements and alternatives
Key: EO: essential oil, MT: mother tincture, GM: gemmomacerate.
TABLE 39.6 Lifestyle recommendations. Category
Principle
Example
Avoid
Inflammation
Tobacco products
Prostate irritation or injury
Horseback, bicycle riding; constipation
Prostate overactivity
Excessive sexual activity
Diminishes perineal flow
Prolonged sitting
Frequent standing
For every 55 min of sitting, walk for 5 min
Exercise
Aerobic exercise: walking, running, elliptical
Prostate emptying
Moderate sexual activity (2–3 times per week)—the more semen demanded, the more pelvic congestion
Encourage
Prostatitis Chapter | 39 263
1. Rectal Suppository formula: Melaleuca leucadendron EO 5%, Lavandula angustifolia EO 5%, Achillea millefolium EO 3%, Syzygium aromaticum EO 0.5% in a base of Shea butter 2. Rectal infusion: Melaleuca leucadendron EO 5 mL, Lavandula angustifolia EO 3.5 mL, Achillea millefolium EO
1 mL, Syzygium aromaticum EO 0.5 mL in 60 mL of mother tincture with pelvic tropism (e.g., Hamamelis virginiana, Achillea millefolium, etc.). Shake well, draw 5–10 mL with a bulb syringe. Lying flat with a folded towel under hips, slowly infuse over 2–5 min. Contract gluteal muscles, wait 15 min or longer before standing erect.
Chapter 40
Rhinopharyngitis Summary Essence: Nasopharyngeal spasmophilia with para > alpha and inefficient cortico-immune adaptation to noxious agent. Terrain: (1) Adaptative nasal congestion: local spasmophilia: Para > alpha, delayed beta favoring (2) Passive local precritical congestion: (a) para, (b) histamine, (c) insulin, (d) emunctories: exocrine pancreas, gallbladder, intestines; when confronted by a (3) Noxious stimulus (infectious, particulate, gaseous) demonstrates (4) Corticoimmune dysadaptability resulting in (5) Nasopharyngeal congestion and infection along with various other symptoms.
Treatment goals Symptomatic: Topical decongestant and antimicrobial. Terrain: ●
● ●
● ● ● ●
ANS: ⇓ Para, Alpha, support Beta (to resolve spasmophilia) CORTICO: Support peripheral adrenal cortex activity THYRO: Support peripheral thyroid function, ⇓ central activity IMMUNE: Support thymus, reduce local histamine SOMATO: Support endocrine pancreas DRAIN: (1) Spleen, (2) Liver-gallbladder, (3) Intestines DIET: Reduce solicitation of exocrine pancreas and gallbladder
Sample treatment For patients 12 and older. Adjust according to age. 1. Topical ANS-immuno-drainer: c.f. text for details Lavandula angustifolia 4 drops; Eucalyptus ssp. 2 drops; Thymus vulgaris, ct. linalool 1 drop; Mentha piperita 1 drop in 14 mL carrier oil; NB: Children 0–5 years: remove Mentha piperita 2. ANS-drainage 3 mL TID × 6–10 days (Table 40.5): Plantago major MT 60 mL, Avena sativa MT 30 mL, Juglans regia GM 30 mL, Lavandula angustifolia EO 1 mL, Thymus vulgaris EO 1 mL 3. Immuno-endocrine: 3 mL TID × 6–10 days (Table 40.6): Rhodiola rosea MT 60 mL, Ribes nigrum GM 60 mL The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00040-8 © 2020 Elsevier Inc. All rights reserved.
4. Oligo: Copper-gold-silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Acute: liquid diet, Chronic: pancreas and gallbladder sparing
Terrain in detail Precritical terrain The precritical terrain of rhinopharyngitis consists of a local congestive spasmophilia of the nasal mucosa and pharynx. 1. ANS: Local nasopharyngeal spasmophilia: Para > alpha, delayed beta 2. Congestion: a. Hyper para b. Local histamine c. Hyperinsulinism: hyperemia, nutritive congestion 3. Emunctory oversolicitation: a. Exocrine pancreas: mucosa production b. Gallbladder: toxin accumulation settling in the nasal passages as a site of hypermetabolism c. Intestines: toxin accumulation settling in the nasal passages as a site of hypermetabolism
Agent and predisposing factors Exposure to a noxious agent: gaseous, particulate, or infectious (c.f. The Theory of Endobiogeny, Volume 2, Chapter 9: Infectious diseases). In addition, there are some predisposing or aggravating factors: 1. Structural blockage of flow of secretions 2. Chronobiologic: 1–7 years (thyrotropic subphase predominance) 3. Gallbladder- and pancreas-straining diet: animal fats, fried foods, high glycemic, red meat
Critical terrain In the face of the noxious or provoking agent, the organism’s response installs the nasopharyngitis, centered around cortico-immune incompetence: 265
266 SECTION | C Assessment and treatment of common disorders
1. Cortico-immune incompetency: a. Peripheral adrenal cortex insufficiency b. Peripheral thyroid insufficiency c. Thymic insufficiency d. Congestion of spleen, local lymphatics (hyperalpha) 2. Congestion: exacerbation of precritical factors + hyper para
2. ANS-immuno-endocrine regulation to resolve the infection (Table 40.3) 3. Drainage with polyvalent plants with antiviral activity (preferable), in order of efficiency (Table 40.4)
Mechanisms
1. Acute state: Liquid diet 2. Subacute and chronic: Pancreas and gallbladder sparing (gluten and dairy avoidance most important)
In cases of viral infections (the most common): 1. Proliferation of virulent organisms in the congested, overnourished tissue 2. Release of immune and inflammatory factors locally in response
Result Rhinopharyngitis: rhinorrhea, sneezing, congestion, sinus pain, headache, anosmia, cough.
History and BoF findings Historical findings during acute rhinopharyngitis along with possible correlations the Biology of Functions of the critical terrain are presented in Table 40.1.
Physical exam and BoF findings During presentation with acute rhinopharyngitis, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 40.2).
Treatment The general emphasis of treatment is: 1. Symptomatic relief of congestion and infection
Diet
Exemplary prescriptions Based on an Endobiogenic approach to rhinopharyngitis, a number of prescriptions can be derived, presented here for patients 12 and older. Adjust according to age. 1. Topical ANS-immuno-drainer: Lavandula angustifolia 4 drops; Eucalyptus smithii 2 drops; Thymus vulgaris, ct. linalool 1 drop; Mentha piperita 1 drop in 14 mL carrier oil; NB: Children 0–5 years: remove Mentha piperita. (1) Mix well in a small glass container; (2) 1–5 years: apply topically 3–4 times per day, 6 and older: saturate cotton-tipped applicator and apply to lower nostrils 4–6 times per day. 2. ANS-drainage 3 mL TID × 6–10 days (Table 40.5): Plantago major MT 60 mL, Avena sativa MT 30 mL, Juglans regia GM 30 mL, Lavandula angustifolia EO 1 mL, Thymus vulgaris EO 1 mL 3. Immuno-endocrine: 3 mL TID × 6–10 days (Table 40.6): Rhodiola rosea MT 60 mL, Ribes nigrum GM 60 mL 4. Oligo: Copper-gold-silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Acute: Liquid diet, Chronic: pancreas and gallbladder sparing
TABLE 40.1 Findings on history, critical terrain, and Biology of Functions. Area
Finding
Terrain
ENT
Nasal discharge, sinus pain, congestion, headache, cough, sneezing
c.f. above
Alpha
GERD, Gastritis, constipation, insomnia
High alpha
⇑/⇓ LMI
Cortico
Fatigue, prolonged infections
⇓ Peripheral adrenal cortex
⇓ Cortisol ⇓ Adrenal cortex
Thyro
Vivid dreams, nightmares
⇑ TRH
Enlarged tonsils
⇓ Peripheral thyroid
⇑ Thyroid relaunching, Thyroid relaunching corrected ⇓ Thyroid
Preference for sweets, skin tags, nasal congestion
Hyperfunctioning hyperinsulinism
Somato
BoF
⇓ Insulin index ⇑ Insulin resistance
TABLE 40.2 Examination, terrain, and Biology of Functions relationships for rhinopharyngitis. Area
Finding
Terrain
BoF
ENT
Boggy, erythematous or pale nasal mucosa, coryza, pharyngeal irritation/cobble stoning
c.f. critical terrain
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓ PMI
Cortico
Tender, distal lateral femur
Appeal to cortisol
⇓ Cortisol
Thyro
Brisk DTR, Clonus, Eyelid flutter on Glabella tap Cold extremities, dry skin
⇑ TRH Low peripheral thyroid
⇑ Thyroid relaunching, Thyroid relaunching corrected ⇓ Thyroid yield, Thyroid metabolic
Immune
Suprasternal notch: tender on palpation
Thymus congested
⇓ IL-1
Pancreas
Tender, above umbilicus Tender, right and superior to umbilicus Tender, left and superior to umbilicus
Congestion: general Oversolicitation: exocrine Oversolicitation: exocrine
N/A ⇑/⇓ Somatostatin ⇑/⇓ Insulin
Spleen
Tender to palpation, or, tenderness along the zone of depression
Splenic congestion
⇓ PMI
GB
Tender to palpation, Murphy’s point or GB zone
Gallbladder congestion
N/A
Liver
Tender, superior-medial Tender, inferior-lateral
Vascular hepatic congestion Metabolic hepatic congestion
⇑/⇓ LMI ⇑/⇓ LMI
Colon
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
⇑/⇓ ACTH, serum TSH, ⇑ TRH indexes: c.f. above
Key: Cortico, corticotropic; ENT, ear, nose and throat; GB, gallbladder; Neuro, neurologic; Thyro, thyrotropic axis.
TABLE 40.3 Medicinal plants that regulate the critical terrain. Medicinal plant
ANS
Immunity
(−) Alpha, para
•
Thymus vulgaris
(−) Para
•
Cinnamomum zeylanicuma
(+) Beta
•
a
Lavandula angustifolia a
Rhodiola rosea b
Ribes nigrum GM Avena sativa
Indirect
Cortico
Thyro
Somato
• •
• (+ Thymus)
•
•
•
•
•
•
Key: ANS, autonomic nervous system; Cortico, corticotropic; Somato, somatotropic; Thyro, thyrotropic axis. a
Efficient as essential oil or bulk herb.
b
Effects are in gemmomacerate preparation.
TABLE 40.4 Medicinal plants for critical terrain drainage. Medicinal plant
ENT
Pancreas, Exo
Plantago major
•
Rubus fruticosus Agrimonia eupatoria
Intestines
Other
•
•
Antimicrobial, immuno-stimulant
•
• (+ Hypoglycemant)
• (Astringent)
Antiinflammatory
• (Indirect)
•
•
Antimicrobial, antihistaminic
•
Antimicrobial (ENT tropism)
Juglans regia Key: ENT, ear, nose, and throat.
Dual pancreatrope
Gallbladder
•
268 SECTION | C Assessment and treatment of common disorders
TABLE 40.5 ANS-drainage prescription.
TABLE 40.6 Immuno-endocrine prescription.
Medicinal plant
Replacements and alternatives
Medicinal plant
Plantago major MT 60 mL
Agrimonia eupatoria MT
Rhodiola rosea MT 60 mL
Eleutherococcus senticosus MT
Ribes nigrum GM 60 mL
Rosa canina GM, Quercus pedunculata GM
Avena sativa MT 30 mL Juglans regia GM 30 mL
Agrimonia eupatoria MT
Lavandula angustifolia EO 1 mL
Matricaria chamomilla EO, Anthemis nobilis EO
Thymus vulgaris EO 1 mL
Cinnamomum zeylanicum EO
Replacements and alternatives
Chapter 41
Sinusitis Summary Essence: Sinus spasmophilia with alpha > para and inefficient adaptation and immune response to noxious agent. Terrain: (1) Adaptative sinus congestion: local spasmophilia: Alpha > para, delayed beta favoring (2) Active and passive precritical congestion: (a) alpha: delays drainage, (b) para, (c) histamine, (d) insulin, (e) emunctories: exocrine pancreas, gallbladder, intestines; when confronted by a (3) Noxious stimulus (infectious, particulate, gaseous) demonstrates (4) Cortico-immune dysadaptability resulting in (5) Infection, sinus pressure and various other symptoms.
Treatment goals Symptomatic: Topical decongestant and antimicrobial (Table 41.3). Terrain: ●
● ●
● ● ● ●
ANS: ⇓ Para, Alpha, support Beta (to resolve spasmophilia) CORTICO: Support peripheral adrenal cortex activity THYRO: Support peripheral thyroid function, ⇓ central activity IMMUNE: Support thymus, reduce local histamine SOMATO: Support endocrine pancreas DRAIN: (1) Spleen, (2) Liver-gallbladder, (3) Intestines DIET: reduce solicitation of exocrine pancreas and gallbladder
Sample treatment Dosing is for 12 years and older. Adjust accordingly to age of patient. 1. Topical: 3–4 times per day during acute sinusitis and 2–3 times per day for chronic sinusitis over affected area: Eucalyptus ssp. 5 drops, Cupressus sempervirens 3 drops, Thymus vulgaris, ct. linalool 2 drop, Citrus limon 1 drop in 14 mL carrier oil. Instructions: (1) Mix well in a small glass container, (2) Apply topically to sinus cavities, avoiding the eyes, (3) Saturate a cotton-tipped applicator and (4) Apply to lower nostrils 2–4 times per day when signs of rhinopharyngitis are also present
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00041-X © 2020 Elsevier Inc. All rights reserved.
2. ANS-gallbladder drainage: 4 mL three times per day × 6–10 days, then 2.5–3 mL twice per day for an additional 6–10 days if season of recurrent sinusitis (Table 41.4): Plantago major MT 60 mL, Raphanus niger MT 60 mL, Cinnamomum zeylanicum EO 1 mL, Thymus vulgaris EO 1 mL 3. Immuno-endocrine: 3 mL TID × 6–10 days (Table 41.6): Rhodiola rosea MT 60 mL, Ribes nigrum GM 60 mL 4. Oligo: Copper-gold-silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Acute: liquid diet, Chronic: pancreas and gallbladder sparing
Terrain in detail Precritical terrain The precritical terrain is identical to that of rhinopharyngitis except for the predominance of alpha over beta in the spasmophilia. This favors stagnation of serosal fluids normally excreted from the sinus cavities: 1. ANS: Local spasmophilia: Alpha > Para, delayed beta 2. Congestion: a. Active: Alpha b. Passive: Hyper para, local histamine, hyperinsulinism: hyperemia, nutritive congestion 3. Emunctory oversolicitation: a. Exocrine pancreas: mucosa production b. Gallbladder: toxin accumulation settling in the nasal passages as a site of hypermetabolism c. Intestines: toxin accumulation settling in the nasal passages as a site of hypermetabolism
Agent It is not uncommon to find various related comorbidities such as chronic nasal congestion and allergies. Exacerbations of these disorders predispose the patient to a sinus infection or inflammation (in the case of a noxious, noninfectious agent
269
270 SECTION | C Assessment and treatment of common disorders
(c.f. The Theory of Endobiogeny, Volume 2, Chapter 9: Infectious diseases). 1. Chronic type 1 allergies 2. Loco-regional obstructions and irritations: polyps, dental infections, chronic rhinopharyngitis 3. Any demand for increased alpha, or in which there is a hyperalpha response, e.g., changes in barometric pressure, seasonal changes, etc.
2. White blood cells release immune factors causing congestion and swelling of the nasal passages. 3. Tissue hypoxia and cilia motility insufficiency
Result Sinusitis with various symptoms: sinus pressure, sinus pain, front headache, fever, green or creamy yellow discharge.
Critical terrain
History and BoF findings
In the face of an aggression, the alpha-sympathetic response reaches a critical level that completely or significantly seals the sinus passages leading to stagnation and an inflammatory response and/or growth of infectious agent with insufficient cortico-immune support.
Historical findings during acute sinusitis along with possible correlations the Biology of Functions of the critical terrain are presented in Table 41.1.
1. ANS: a. Alpha: Hyperfunctioning to isolate the sinuses and protect the regional tissues b. Para: Hyperfunctioning with congestion and hypersecretions c. Beta: Hypofunctioning, Prolongs: congestion, obstruction, stagnation of secretions 2. Cortico-immune incompetency: a. Peripheral adrenal cortex insufficiency b. Peripheral thyroid insufficiency c. Thymic insufficiency d. Congestion of spleen, local lymphatics (hyperalpha) 3. Congestion: exacerbation of precritical factors + hyper para
Mechanisms 1. Proliferation of virulent organisms on sinus tissue, inflammation of the sinuses
Physical exam and BoF findings During presentation with acute sinusitis, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 41.2).
Treatment There is a potential role for the use of antibiotics in acute sinusitis, though even this is questionable, both in adults and children. A majority of cases resolve without pharmacological treatment. Having said that, a symptomatic approach is favored for relief of symptoms. From the endobiogenic perspective, the underlying terrain should be addressed long-term if sinusitis is recurrent or chronic. The general emphasis of treatment of the terrain is as follows, with the top areas of focus being the sinuses and gallbladder: 1. Symptomatic a. Sinus drainage and clearing b. Topical decongestant and antimicrobials
TABLE 41.1 Findings on history, critical terrain, and Biology of Functions. Area
Finding
Terrain
BoF
ENT
Nasal discharge, sinus pain, congestion, headache, cough, sneezing
c.f. above
c.f. above
Alpha
GERD, Gastritis, constipation, insomnia
High alpha
⇑/⇓ LMI
Cortico
Fatigue, prolonged infections
⇓ Peripheral adrenal cortex
⇓ Cortisol ⇓ Adrenal cortex
Thyro
Vivid dreams, nightmares
⇑ TRH
Enlarged tonsils
⇓ Peripheral thyroid
⇑ Thyroid relaunching, Thyroid relaunching corrected ⇓ Thyroid
Preference for sweets, skin tags, nasal congestion
Hyperfunctioning hyperinsulinism
⇓ Insulin index ⇑ Insulin resistance
Somato
Sinusitis Chapter | 41 271
TABLE 41.2 Examination, terrain, and Biology of Functions. Area
Finding
Terrain
BoF
ENT
Boggy, erythematous or pale nasal mucosa, coryza, pharyngeal irritation/ cobble stoning
c.f. above
c.f. above
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓ PMI
Cortico
Tender, distal lateral femur
Appeal to cortisol
⇓ Cortisol
Thyro
Brisk DTR, Clonus, Eyelid flutter on Glabella tap Cold extremities, dry skin
⇑ TRH
⇑ Thyroid relaunching, Thyroid relaunching corrected ⇓ Thyroid yield, Thyroid metabolic
Immune
Suprasternal notch: tender on palpation
Thymus congested
⇓ IL-1
Pancreas
Tender, above umbilicus
Congestion: general
N/A
Tender, right and superior to umbilicus
Oversolicitation: exocrine
⇑/⇓ Somatostatin
Tender, left and superior to umbilicus
Oversolicitation: exocrine
⇑/⇓ Insulin
Spleen
Tender to palpation, or, tenderness along the zone of depression
Splenic congestion
⇓ PMI
GB
Tender to palpation, Murphy’s point or GB zone
Gallbladder congestion
N/A
Liver
Tender, superior-medial
Vascular hepatic congestion
⇑/⇓ LMI
Tender, inferior-lateral
Metabolic hepatic congestion
⇑/⇓ LMI
Tender: ACTH-F, TRH, TSH reflection points
Colon congestion
⇑/⇓ ACTH, serum TSH, ⇑ TRH indexes: c.f. above
Colon
Low peripheral thyroid
Key: Cortico, corticotropic; ENT, ear, nose and throat; GB, gallbladder; Neuro, neurologic; Thyro, thyrotropic axis.
2. ANS-immuno-endocrine regulation to resolve the infection (Table 41.3) 3. Oligoelement: Copper‑gold‑silver 4. Drainage with polyvalent plants with antiviral activity (preferable), in order of efficiency, with strong emphasis on the gallbladder (Table 41.4)
Diet 1. Pancreas and gallbladder sparing 2. Complete avoidance of fried foods, cooked animal fats, and creamy foods
Exemplary prescriptions Based on an endobiogenic approach to sinusitis, a number of prescriptions can be derived. Dosing is for 12 years and older. Adjust accordingly to age of patient. 1. Topical: 3–4 times per day during acute sinusitis and 2–3 times per day for chronic sinusitis over affected area:
Eucalyptus ssp. 5 drops, Cupressus sempervirens 3 drops, Thymus vulgaris, ct. linalool 2 drop, Citrus limon 1 drop in 14 mL carrier oil. Instructions: (1) Mix well in a small glass container, (2) Apply topically to sinus cavities, avoiding the eyes, (3) Saturate a cotton-tipped applicator and (4) Apply to lower nostrils 2–4 times per day when signs of rhinopharyngitis are also present 2. ANS-gallbladder drainage: 4 mL three times per day × 6–10 days, then 2.5–3 mL twice per day for an additional 6–10 days if season of recurrent sinusitis (Table 41.5): Plantago major MT 60 mL, Raphanus niger MT 60 mL, Cinnamomum zeylanicum EO 1 mL, Thymus vulgaris EO 1 mL 3. Immuno-endocrine: 3 mL TID × 6–10 days (Table 41.6): Rhodiola rosea MT 60 mL, Ribes nigrum GM 60 mL 4. Oligo: Copper-gold-silver: Day 1: 1 dropper (or ampule) four times per day, Day 2: 1 dropper (or ampule) three times per day, Days 3–6: 1 dropper (or ampule) twice per day 5. Diet: Acute: liquid diet, Chronic: pancreas and gallbladder sparing
272 SECTION | C Assessment and treatment of common disorders
TABLE 41.3 Medicinal plants that regulate the terrain. Medicinal plant
ANS
Immunity
(−) Alpha, para
•
Thymus vulgaris
(−) Para
•
Cinnamomum zeylanicuma
(+) Beta
•
a
Lavandula angustifolia a
Rhodiola rosea b
Ribes nigrum GM Avena sativa
Indirect
Cortico
Thyro
Somato
• •
• (+ Thymus)
•
•
•
•
•
•
Key: ANS, autonomic nervous system; Cortico, corticotropic; Somato, somatotropic; Thyro, thyrotropic axis. a
Efficient as essential oil or bulk herb.
b
Effects are in gemmomacerate preparation.
TABLE 41.4 Drainage of organs implicated in the critical terrain. Medicinal plant
ENT
Gallbladder
Pancreas, Exo
Intestines
Other
Raphanus niger
•
Antifungal, antibacterial; immune stimulant; fluidifies secretions
Cynara scolymus
•
Hepato-detoxifier, eupeptic
Plantago major
•
Agrimonia eupatoria
• (Indirect)
Rubus fruticosus
•
•
•
•
Antimicrobial, immunostimulant
•
•
Antimicrobial, antihistaminic
• (+ Hypoglycemant)
• (Astringent)
Antiinflammatory
Key: ENT, ear, nose, and throat.
TABLE 41.5 ANS-gallbladder drainage prescription. Medicinal plant
Replacements and alternatives
Plantago major MT 60 mL
Agrimonia eupatoria MT
Raphanus niger MT 60 mL
Cynara scolymus MT
Cinnamomum zeylanicum EO 1 mL
Satureja montana EO 1 mL
Thymus vulgaris EO 1 mL
TABLE 41.6 Immuno-endocrine prescription. Medicinal plant
Replacements and alternatives
Rhodiola rosea MT 60 mL
Eleutherococcus senticosus MT
Ribes nigrum GM 60 mL
Rosa canina GM, Quercus pedunculata GM
Chapter 42
Tonsillitis Summary Essence: Infection of tonsils due to stagnation of flow and overproliferation of lymphoid cells. Terrain: (1) Adenoidal hypertrophy of tonsils: (a) Para hyperfunctioning, (b) Lymphoid hypertrophy: overadapted FSH, estrogens, TSH, (c) Lymphocyte overproduction, residing in tonsils, (d) Hyperinsulinism, (e) Emunctory congestion: exocrine pancreas, gallbladder; in the face of (2) Microbial aggression, (3) Hyperalpha and/or para (congestion of tonsils, pus) with (4) Corticothyrotropic insufficiency to mobilize immune cells and reduce inflammation results in (5) Tonsillitis.
Treatment goals Symptomatic: antibiotics, inflammatory, tonsillectomy. Terrain: ●
● ●
●
● ●
●
ANS: ⇓ Para and Alpha (predominance based on erythematous vs pustular tonsillitis; adapt Beta as indicated CORTICO: Support peripheral adrenal cortex activity THYRO: Support peripheral thyroid function, ⇓ central activity as indicated SOMATO: Improve insulin sensitivity, reduce insulin resistance IMMUNE: Support thymus DRAIN: (1) Exocrine Pancreas, (2) Liver-gallbladder, (3) Tonsils DIET: Pancreas sparing
Sample treatment Dosing is presented for children 2–5 years of age. Adjust dosing according to age and severity of illness, noting caveats throughout; This protocol is presented as an addition to standard of care treatment. 1. Topical/Gargle antimicrobial, antalgic: Apply directly to tonsils every 4 h while child awake: Lavandula angustifolia EO 1 drop, Mentha piperita EO 1 drop, Atomidine (Trichloro-Iodine) 4 drop, Methylene blue 5 mL (may substitute with Gentian violet or carrier oil): saturate cotton tipped-applicator, apply to tonsils. See end of chapter for gargle instructions and caveats. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00042-1 © 2020 Elsevier Inc. All rights reserved.
2. Endocrino-immunity: 1.5 mL four times per day × 10 days (Table 42.5): Ribes nigrum GM 20 mL, Vitis vinifera GM 30 mL, Olea europaea GM 10 mL, Cinnamomum zeylanicum leaf EO 6 drops 3. ENT drainage-immunity: 1.5 mL four times per day × 10 days (Table 42.6): Plantago major MT 30 mL, Rubus fruticosus GM 10 mL, Avena sativa MT 20 mL, Eucalyptus ssp. EO 4 drops 4. Diet: Pancreas sparing
Terrain in detail Precritical terrain The tonsils experience passive congestion from two sources: increased metabolism and increased lymphocytes residing in the tonsils: 1. ANS: Para > Alpha 2. Endocrine: adenoidal tissular growth focused on follicular cells of tonsils: a. Gonadotropic i. Hyper FSH 1. Congests mucosal tissue 2. Stimulates estrogens by vertical stimulation 3. Stimulates TSH by horizontal stimulation ii. Hyperestrogenism 1. Favors overproliferation of immune cells, housed in lymphoid tissues 2. Makes an appeal to TSH b. Thyrotropic i. TSH, elevated: 1. Due to: peripheral thyroid: relative or absolute insufficiency of response to TSH, estrogens and/or FSH 2. Results in: increased production of T-lymphocytes in thymus ii. Peripheral thyroid: latent hypothyroidism c. Somatotropic i. Pancreas, Endocrine: Hyperinsulinism with elevated insulin resistance: increased nutrition for growth of cells
273
274 SECTION | C Assessment and treatment of common disorders
3. Emunctory a. Pancreas, Exocrine: Oversolicitation participates in adenoidal growth and proteins for lymphocyte production b. Congestion of other lymphoid tissue (e.g., lingual, adenoids, spleen) favors a greater reliance on tonsils for immune defense c. Gallbladder: insufficient toxin elimination
2. Endocrine: insufficient response to that required for the infection a. Corticotropic, peripheral b. Thyrotropic, peripheral 3. Emunctories: a. Exocrine pancreas further oversolicited, p articipates in immune cell production along with estrogens and TSH
Agent
Mechanisms
Microbial actor, by direct entry and/or local circulation invades enlarged and congested tonsils (c.f. The Theory of Endobiogeny, Volume 2, Chapter 9: Infectious diseases)
Invasion and proliferation of microorganisms within tonsils with inflammatory and/or exudative response.
1. De novo exogenous pathogen 2. Translocation of colonizers of nose, sinuses, or pharynx
Result
Critical terrain In the face of a microbial aggression, the host’s response allows the infection to develop and participates in the presentation of specific symptoms. The hyperfunctioning sympathetic activity is an attempt to yoke the cortico-thyrotropic response. The parasympathetic elevation is reactive to the sympathetic activity. The predominance of alpha in relationship to para will determine if the tonsillitis is exudative or not. 1. ANS hyperfunctioning a. Para > Alpha: exudative b. Alpha > Para nonexudative c. Beta: varies
Tonsillitis: inflammation, with or without exudate, fever, pain on swallowing, etc.
History and BoF findings During acute tonsillitis, some possible correlations between precritical and critical terrain symptoms and Biology of Functions are presented in Table 42.1.
Physical exam and BoF findings During presentation with acute tonsillitis, the following may be observed on physical exam with some possible Biology of Functions correlations (Table 42.2).
TABLE 42.1 Historical, terrain and Biology of Functions relationships in tonsillitis. Area
Finding
Terrain
BoF
Exocrine pancreas
Recurrent sinusitis, tonsillitis, eczema, mucus production with dairy/gluten, bloating, anus fissures
Oversolicited
⇑ Somatostatin
Alpha
GERD, constipation, insomnia, dry, flakey cerumen
High alpha
⇑/⇓ LMI
Para
GERD, shyness, abundant, moist cerumen
Hyper parasympathetic
Cortico
Fatigue, prolonged infections
⇓ Peripheral adrenal cortex
⇓ Cortisol ⇓ Adrenal cortex
Thyro
Vivid dreams, nightmares
⇑ TRH
⇑ Thyroid relaunching, Thyroid relaunching corrected
Enlarged tonsils
⇓ Peripheral thyroid with elevated TSH serum
⇓ Thyroid
Preference for sweets, skin tags, nasal congestion
Hyperfunctioning hyperinsulinism
⇓ Insulin index ⇑ Insulin resistance
Somato
Key: Cortico, corticotropic axis; Somato, somatotropic axis; Thyro, thyrotropic axis.
Tonsillitis Chapter | 42 275
TABLE 42.2 Examination, terrain, and Biology of Functions relationships for tonsillitis. Area
Finding
Terrain
BoF
ENT
Enlarged tonsils (>2+), ± erythematous, ± exudate; Boggy, erythematous or pale nasal mucosa, coryza, pharyngeal irritation/cobble stoning
c.f. above
c.f. above
Behavior
Shy, spasmophilic (e.g., tantrums)
Vagotonia with spasmophilia
Neuro
Chvostek
Spasmophilia
⇑/⇓ LMI + ⇓ PMI
Cortico
Tender, distal lateral femur
Appeal to cortisol
⇓ Cortisol, or ⇑/normal cortisol + ⇑ACTH
Thyro
Brisk DTR, Clonus, Eyelid flutter on Glabella tap
⇑ TRH
⇑ Thyroid relaunching, Thyroid relaunching corrected
Cold extremities, dry skin
Low peripheral thyroid
⇓ Thyroid yield, Thyroid metabolic
Immune
Suprasternal notch: tender on palpation
Thymus congested
⇓ IL-1
Pancreas
Tender, above umbilicus
Congestion: general
N/A
Tender, right, and superior to umbilicus
Oversolicitation: exocrine
⇑/⇓ Somatostatin
Tender, left, and superior to umbilicus
Oversolicitation: exocrine
⇑/⇓ Insulin
Spleen
Tender to palpation, or, tenderness along the zone of depression
Splenic congestion
⇓ PMI
GB
Tender to palpation, Murphy’s point or GB zone
Gallbladder congestion
N/A
Key: Cortico, corticotropic axis; ENT, ear, nose and throat; GB, gallbladder; Somato, somatotropic axis; Thyro, thyrotropic axis.
Treatment The general emphasis of treatment is to support what the organism was not able to efficiently perform: 1. Symptomatic (Table 42.3) a. Antimicrobial action focused on ear, nose and throat region b. Pancreato-tonsil drainage c. Febrifuges 2. Endocrino-immune adaptation (Table 42.4) a. Pituitary b. Adrenal cortex c. Peripheral thyroid d. Immune function 3. Downregulation of exocrine pancreatic activity a. Pancreas-sparing diet
Exemplary prescriptions Based on an endobiogenic approach to tonsillitis, a number of prescriptions can be derived. Dosing is presented for children 2–5 years of age. Adjust dosing according to age and severity of illness, noting caveats throughout; This protocol is presented as an addition to standard of care treatment.
1. Topical/Gargle antimicrobial, antalgic: Apply directly to tonsils every 4 h while child awake: Lavandula angustifolia EO 1 drop, Mentha piperita EO 1 drop, Atomidine (Tricloro-Iodine) 4 drop, Methylene blue 5 mL (may substitute with Gentian violet or carrier oil): saturate cotton-tippedapplicator, apply to tonsils. NB: (1) In children 6 and older, OK to dilute 3 drops in 30 mL Plantago major tisane and use as gargle; (2) In children 2 and younger, do not use Mentha piperita; (3) When applying topically, apply before meals to avoid gag-reflexinduced vomiting 2. Endocrino-immunity: 1.5 mL four times per day × 10 days (Table 42.5): Ribes nigrum GM 20 mL, Vitis vinifera GM 30 mL, Olea europaea GM 10 mL, Cinnamomum zeylanicum leaf EO 6 drops 3. ENT drainage-immunity: 1.5 mL four times per day × 10 days (Table 42.6): Plantago major MT 30 mL, Rubus fruticosus GM 10 mL, Avena sativa MT 20 mL, Eucalyptus ssp. EO 4 drops 4. Diet: Pancreas sparing
276 SECTION | C Assessment and treatment of common disorders
TABLE 42.3 Polyvalent symptomatic plants. Medicinal plant
Antimicrobial
ENT
Exocrine pancreas
Other
Agrimonia eupatoria
• (Gram +)
ENT drainer
•
Pancreatic drainer, dual pancreatrope, antiinflammatory
Lymphatic drainer
•
Thyroid stimulant, reduces FSH overactivity
Avena sativa Cupressus sempervirens (EO only)
• (Antiviral)
Tonsil drainer, Lymphatic decongestant
Eucalyptus ssp. (EO only)
• (Bacteria, viruses)
Nasal decongestant
Juglans regia
Antalgic, immunestimulating •
Febrifuge, inhibits inflammatory cytokines, antalgic
•
•
Antiseptic; dual pancreatrope
Olea europaea GM
• (Bacteria, viruses)
•
Dual pancreatrope
Plantago major
• (β-Hemolytic Streptococcus)
ENT drainer
•
Immuno-stimulant; Hepato-renal drainer
Rubus fruticosus
• (Group B Streptococcus)
Astringent
Vitis vinifera (GM only)
• (Strep. and Staph.)
Pancreatic drainer Febrifuge; hepatorenal drainer
TABLE 42.4 Endocrino-immune support. Medicinal plant
Pituitary
Rhodiola rosea
•
Inula helenium
•
Ribes nigrum GM
Quercus pedunculata GM
Adrenal gland
Thyroid
Immune
Other
•
•
Supports thymus
•
ENT antiinfectious
Antiallergic
Endocrine adaptogen
•
•
Antiallergic; drains extracellular matrix
Polyendocrine redistributor
•
•
Febrifuge
Indirect
Cinnamomum zeylanicum
•
Zingiber officinale
•
•
l-Tyrosine
• (Production of adrenaline)
• (Production of T4)
Olea europaea GM
• (T4 to T3 conversion)
Avena sativa
•
Febrifuge, antiinflammatory
•
Febrifuge, pancreatic drainer Lymphatic drainer
Tonsillitis Chapter | 42 277
TABLE 42.5 Infection-endocrine prescriptions. Herb
Replacements and alternatives
TABLE 42.6 ENT drainage-immunity. Herb
Replacements and alternatives
Ribes nigrum GM 20 mL
Quercus pedunculata GM, Rosa canina GM
Plantago major 30 mL MT
Agrimonia eupatoria MT, Juglans regia GM
Vitis vinifera GM 30 mL
Olea europaea GM 20 mL + Avena sativa MT 10 mL
Rubus fruticosus GM 10 mL
Agrimonia eupatoria MT
Avena sativa 20 mL MT
Zingiber officinale MT 20 mL + Rubus fruticosus GM 10 mL
Eucalyptus spp. 4 drops EO
Lavandula angustifolia EO, Cupressus sempervirens EO
Olea europaea GM 10 mL
Vitis vinifera 5 mL + Avena sativa MT 10 mL
Cinnamomum zeylanicum leaf EO 6 drops
Citrus limon EO 4 drops + spearmint EO 2 mL
Key: EO, essential oil; MT, mother tincture; GM, gemmomacerate.
Key: EO, essential oil; MT, mother tincture; GM, gemmomacerate.
Chapter 43
Materia Medica Introduction
Medicinal plants
The Endobiogenic approach to usage of medicinal plants is rooted in an approach called “rational clinical phytotherapy.” Rational because it is based on a rational, scientific understanding of the physiologic actions of the plants, not solely symptomatic actions. It is clinical because the selection occurs only after a careful clinical evaluation, matching the combination of medicinal plants to the totality of who the patient is, and the implications of their disorder(s). Seventy-nine medicinal plants are presented in summary form, focusing on the essence of what the plant represents, summary of its actions and best usage, parts used and galenic form, methods of preparation, and notes and precaution (Table 43.1). The specific actions of the plants are discussed in The Theory of Endobiogeny, Volumes 2 and 3, and in innumerable scientific publications, some of which are cited under Appendix 2: References and resources. This Materia Medica plays three different roles, based on the reader’s current level of knowledge: (1) For those familiar with the Endobiogenic approach to phytotherapy: This Materia Medica will evoke key insights and create a vector for application of medicinal plants in the moment, (2) Those learned in other approaches to phytotherapy: gain a new perspective on familiar plants, (3) For those novice to phytotherapy: the Materia Medica displays the dazzling horizon of what is possible in the use of the intelligence of these polyvalent entities. Table 43.1 explains how to read each entry. NB: Not every entry contains all headings. Table 43.2 presents our general approach to dosing of mother tinctures and gemmomacerates for adults. Table 43.3 presents recommended dosing for children.
Abies balsamea or pectinata (Balsam fir, Silver fir)
Key BH: Bulk herbs; BID: bis in die: twice per day; ct.: chemotype; CV: Cardiovascular; DE: dry extract; ENT: Ear, nose, and throat; EO: essential oil; GI: Gastrointestinal; GM: gemmo (embryonic) macerate; GU: genitourinary; H: Hydrolat; IBS: irritable bowel syndrome; MT: mother tincture; PMS: premenstrual syndrome; PO: per orum: by mouth; TID: ter in die: three times per day; qHS: quaque hora somni: at bedtime; QID: quater in die: four times per day; qOD: quaque altera die: every other day. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00043-3 © 2020 Elsevier Inc. All rights reserved.
Essence: A plant that assists the organism in retaining essential vitality of defense and restoration through the osteocortico-immune axis. Summary: A restorative plant for immuno-corticotropic exhaustion. Use in chronic recurrent infections rooted in low cortisol activity, spasmophilias (esp. acute extrinsic asthma attacks) and childhood disorders of bone. Parts used: Bud, needles; Galenic: GM, EO.
Achillea millefolium (Yarrow) Essence: A plant the fosters the fractal possibilities of assimilation, growth and adaptation. Summary: A polyvalent plant for cortico-gonado-genital and digestive conditions, it is an essential plant for women, and for GI, GU, and infectious disorders, especially rooted in vagotonia in men and women. Use with high Progesterone index. Parts used: Whole plant; Galenic: MT, EO, DE, BH, infused oil. Method: Tisane: 10 g flowering tops/liter water, steeped 10 min; 3–4 cups per day between meals; Sitz bath: 100 g flowering top/liter water, steeped 10 min, diluted in 19 L water; sit for 10–20 min; EO: Dilute in carrier oil 3%–30% for topical application. Notes and precautions: Hypersensitivity to yarrow or other flowers in the Asteraceae family (sesquiterpene lactones), pregnancy (except weeks 36–40—EO potentially abortifacient), young children, epileptics (EO potentially neurotoxic in elevated internal doses); augments effects of anticoagulants, antihypertensives, sedatives. Do not apply topically to open wounds.
Agrimonia eupatoria (Agrimony) Essence: A plant that conditions the quality of nutrient intake, and which drains and defends the midline structures affected by infection or excess apportment of nutrient. Summary: The essential plant for digestive regulation and renewal of the adaptive dynamism of the buffering 281
282
SECTION | D Essentials of therapeutics
TABLE 43.1 Sections of each heading. Heading
Significance
Latin binomial, common name in parenthesis
Avoids confusion between variations in common names
Essence
Presents the core concept of the totality of the plant
Summary
Presents an Endobiogenic recapitulation of areas of most effective clinical usage
Parts used
Different parts of plants can have different properties; the parts used are indicated to provide clarity when selecting various preparations of the plant
Galenic forms
A list of commonly available preparations of plants in the United States of America
Method
Offers instructions on preparation bulk dry plant material and/or essential oils for tisanes, balneotherapy, inhalation, rectal application, etc.
Notes and precautions
Notes and precaution regarding the usage, dosage and/or clinical populations for whom the plant should not be used, or, used with caution
TABLE 43.2 Dosing of tinctures for variable effects. Effect
Dose
Frequency
Moderating
1–3 mL
1–3 times per day
Regulating
3–5 mL
2–4 times per day
Controlling
4–15 mL
2–4 times per day
TABLE 43.3 Suggested dosing for children based on therapeutic aim. Weight
Moderating
Regulating
Controlling
3–6 kg
2–6 drops
6–10 drops
8–20 drops
7–9 kg
4–10 drops
8–16 drops
12–30 drops
10–14 kg
0.5–1 mL
0.75–1.25 mL
1–2.5 mL
15–19 kg
1–1.5 mL
1.5–2 mL
2–4 mL
19–24 kg
1–2 mL
1.5–2.5 mL
2–6 mL
≥25 kg
1–3 mL
3–5 mL
4–15 mL
capacity. #1 Plant for digestion, h epatobiliary-pancreatic drainage. Use in infectious, allergic, autoimmune states, and conditions affecting ENT, GI, and pulmonary systems. Parts used: Leaf and flower; Galenic: MT, BH. Method: Tisane: 1 tsp. steeped in 200 mL water for 4–8 min, drink 2–4 times per day; Compress: 2–3 tsp. steeped in 100 mL water for 10–12 min, apply to affected areas; Tincture: 0.75–2 mL per dose, before meals and before bed as needed. Notes and precautions: At high doses can cause convulsions, anaphylactic and cardiogenic shock.
Alchemilla vulgaris (Lady’s mantle) Essence: A polyvalent plant for cortico-gonado-genital and digestive regulation that stands guard against luteal excess. Summary: A superb genital-intestinal plant for luteal patients with dysregulated LH and/or gonadal androgens; use in all genito-pelvic disorders implicating LH, progesterone and/or gonadal androgens, and digestive disorders. Use with low LH index where progesteronic activity is still required to regulate gonadal androgens. Parts used: Whole herb; Galenic: MT, FE, DE, BH.
Materia Medica Chapter | 43 283
Method: Internal: Tisane: 5 g/1 cup water, infused 10– 15 min/3–4 cups daily; External: Decoction or infusion of 50–100 g/1 L water; use as a gargle, douche, for lavage of sores and lacerations.
Notes and precautions: Contraindicated in hyperestrogenism, illnesses with an estrogenic component: cancers, mastopathies, disorders aggravated by vagolysis; potentizes the effects of anticoagulants, photosensitizing in high doses.
Alnus glutinosa (Black Alder)
Anthemis nobilis (Roman Chamomile)
Essence: A mucosal-immuno-inflammatory regulator of the hollow organs and cavities. Summary: A targeted therapy for inflammation of mucosal and serosal cavities and its origins in dysfunction of the macrophage-phagocyte system. Use in all disorders of hollow cavities: airways, sinuses, digestive tract where inflammation and/or infections are at play. Parts used: Buds; Galenic: GM.
Essence: A plant that returns all physiologic function to its essential and intrinsic function through entrainment of the proper frequencies of function. Summary: A refined and polyvalent neuro-autonomic regulator useful in patients of all ages. It assists infectious and spasmophilic disorders of GI tract and CNS. Parts used: Flower; Galenic: BH, EO. Method: Tisane: 1 tsp. dried flowers steeped 5 or more min in 200 mL water, drink ad libitum, at least 3 cups per day, EO: Children: 1 drop neat on pulse points or palms of feet, EO: all ages: diffused, inhaled, neat; EO: 12 and older: 1 mL per 120 mL tincture.
Althea officinalis (Marshmallow) Essence: A superb antiinflammatory plant for cases of mucosal congestion and inflammation. Summary: An efficient antiinflammatory for hollow structures and cavities that are affected by inflammation arising from direct injury to the mucosal surface, with tropism for the digestive tract, sinuses, and airways. Parts used: Leaf, blossom, root; Galenic: FE, DE, BH. Notes and precautions: Can retard absorption of medications taken simultaneously.
Ananassa sativa (Pineapple, Ananas) Essence: A cooling plant for stagnant, inflammatory conditions rooted in exocrine pancreatic insufficiency and neuroendocrine compensation. Summary: A targeted plant for inflammatory conditions rooted in exocrine pancreatic dysfunction. Use in primary digestive inflammatory conditions: IBS, Crohn’s disease, ulcerative colitis, celiac disease, etc. Parts used: Fruit; Galenic: MT, DE.
Angelica archangelica (Angelica) Essence: A transformative and interconnecting plant whose regulation of spasmophilic and hypoestrogenic conditions allow proper flow of structural and functional activities. Summary: A truly useful plant for vagotonic spasmophilics, especially women with estrogen insufficiency relating to menstrual or structuro-functional spasmophilias. Parts used: Root, seeds; Galenic: BH, EO, MT. Method: Infusion (root) 1 tsp. in 1 cup water; steep 5–15 min, drink three times per day around meal time; Decoction (root): ¾ tsp. finely chopped in 8 oz water; bring to a boil and simmer 10 min, filter and drink 2–3 cups per day.
Arctium lappa (Burdock) Essence: A plant that establishes core drainage and buffering capacity while expelling toxins through emunctory channels. Summary: A polyvalent drainer and depurative ideal for immuno-dermatologic disorders. Use in all disorders of immunity and infections, active or latent, blood toxicity and metabolism, especially those affecting the skin, ENT, and pulmonary spheres. Parts used: leaf, root; Galenic: MT, DE, BH. Method: Decoction of root: 2–3 g, minced, in 5 oz water: boil 1 h, filter and drink TID; Poultice: Infuse 20 g leaves in 8 oz water 15 min. Notes and precautions: Synergistic with hypoglycemants and diuretics, can augment activity of vagolytics such as Thyme.
Arnica montana (Arnica) Essence: A plant that redistributes energy to the center while ensuring regulated ANS-Somatotropic-inflammatory equilibrium. Summary: A cardiometabolic plant ideal for anxious patients in an inflammatory terrain. It is helpful in allergic/anxiety states with tachycardia, insomnia, etc. and in all disorders of inflammation rooted in a hyperinsulinism with somatotropic desynchronization. Use with a low Insulin resistance or high Insulin indexes with elevated Noxious free radicals. Parts used: Flower; Galenic: MT, BH, Oil. Notes and precautions: Cardiotoxic and hallucinogenic at high doses, can diminish the activity of antihypotensive and anticoagulant medications. Avoid during pregnancy and nursing.
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Artemisia dracunculus (Tarragon) Essence: A unique plant of neuro-digestive-pelvic regulation, imparting a feeling of freshness and clarity in states of anxious fatigue and agitation. Summary: An excellent plant for vagotonics with psycho-neuro-digestive spasmophilias, best used in mental, muscular, and pelvic conditions such as anxiety, muscular spasms, prostatic enlargement, and menstrual disorders, as well as infections. Parts used: Leaf; Galenic: EO, BH. Method: EO, internal: 1/2–1 drop 2–3 times per day, preferably diluted in tincture; EO, topical: 5%–50% dilute applied to affected area; Tisane: 25–30 g/1 L water, infuse 10 min, drink in 3–4 divided doses after meals. Notes and precautions: Disorders worsened by vagolysis, relative or absolute hyperestrogenism, estrogen-dependent cancers; EO can be irritating to the skin and mucous membranes when used undiluted; use with caution in first trimester of pregnancy; avoid prolonged use.
Avena sativa (Milky Oat) Essence: A harmonizer of gonado-thyrotropic coupling and the implications of immuno-pancreatic competency. Summary: Use in Hashimoto’s thyroiditis, children with recurrent ENT infections and any pulmonary or ENT disorder marked by a low Genito-thyroid index. Parts used: Fruit, arial parts, seeds; Galenic: MT, FE, DE, bulk herb. Method: Tisane (Neuro): 1 tbsp. leaves in ¼ L water, 10 min; drink throughout day; decoction of grain: 20 g/1 L water: boil 15–20 min (laxative, diuretic). Notes and precautions: Hyperthyroid Grave’s disease, other hyperthyroid states; hyperestrogenic states, hyperinsulin states.
Betula pubescens (Birch) Essence: A revitalizer rooted in hepato-renal drainage and osteo-immune support. Summary: Use in all conditions requiring blood cleansing, restoration of liver, bone marrow, immune function and stabilization of bone architecture (osteomalacia, osteoporosis). Parts used: Buds, leaf; Galenic: GM, FE, DE, BH, EO.
Borago officinalis, leaf (Borage) Essence: A plant that re-establishes the proper role of nutrition and defense rooted in the folliculo-estrogen dynamism and its implication in allergies and perceived need for defense. Summary: An efficient pituitary regulator that restores central-peripheral estro-luteal balance. A cortico-gonadotropic harmonizer and restorative of dys
function installed by this relationship. Use when the imperative is to inhibit FSH > LH, to regulate estrogens > luteal hormones, and in allergic states. Parts used: Leaf, flower, stems; Galenic: MT, FE, BH. Notes and precautions: Contraindicated in pregnancy and nursing, in epilepsy as it may interact with antiepileptics; may cause hepatotoxicity with prolonged or acute high dose use of an infusion due to presence of pyrrolizidine alkaloids.
Borago officinalis, seed (Borage oil) Essence: A revitalizer of tissues and their capacity to expel interstitial waste products based on regulation of disturbed immunity rooted in pro-inflammatory prostaglandins. Summary: Use in pelvic and menstrual disorders, and hypercoagulable states. Parts used: seed; Galenic: Oil.
Carduus marianus (Milk thistle) Essence: The plant for clearance of material impairing the functions of hepatocytes, returning the liver to an essential state of intrinsic harmonics of endocrino-immuno-nutritional-buffering capacity. Summary: The essential plant for restoration of the filtration capacity of the liver and its role in buffering and detoxification. #1 Hepato-protective and hepato-regenerative plant, especially with porto-splanchnic congestion, useful in all conditions requiring reintegration of the liver into adaptation, immune and detoxification responses and by extension efficient nutrition. Parts used: Aerial parts, fruit, seed; Galenic: MT, DE, BH. Method: Tisane (aerial): ½ tsp./250 mL water, infuse 10 min; 2–3 cups/day; seed, ground: 1 tsp. 4 times daily before meals and before bed. Notes and precautions: May cause mild GI upset, allergies associated with Asteraceae family; may interfere with medications that use CYP450 enzymes for metabolism at high doses.
Carica papaya (Papaya) Essence: A plant that hydrates stressed pancreatic tissues, restoring the productive capacity of the exocrine pancreas. Summary: A targeted plant for gastro-pancreatic dysfunction and metabolic implications. Use in intestinal disorders where exocrine pancreatic dysfunction affects gastric emptying, nutrient absorption, or microbiotic population. It is particularly indicated in a low Somatostatin index. Parts used: Fruit; Galenic: MT, DE.
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Carum carvi (Caraway)
Citrus limon (Lemon)
Essence: A plant that restores the forward momentum of physiologic processes in their sequential action and centralperipheral coordination. Summary: A digestive and estro-androgenic regulator at central and peripheral levels. It is a most effective neurodigestive and pelvic antispasmodic and in stagnant states: flatulence, dyspepsia, IBS, hypervagal states. Use in all disorders rooted in hyperandrogenism and/or estrogen insufficiency: acne, metrorrhagia, progesterone-predominant PMS symptoms, infertility, amenorrhea, oligomenorrhea, prostatic adenoma, etc. Parts used: Seed; Galenic: EO, BH, H.
Essence: Promotes movement and flow through enhancement of buffering capacity and improved rheology of fluids. Summary: Use in all states of stagnation, acidosis and infection related to stagnation or congestion. Parts used: Fruit; Galenic: EO, GM, FE, FP. Method: Cellulitis, superficial circulation: Essential oil: Topical: 4 mL per dose and/ or >12 mL per day of mother tincture); discontinue 3 days prior to elective surgery.
Melissa officinalis (Melissa, Lemon balm) Essence: A plant that re-establishes thyrotropic integrity and its integration into CNS, immune and adaptation dynamics through a nurturing of the neuro-thyrotropic relays and circuits. Summary: #1 Neuro-thyroid adaptogen, use in Hashimoto’s thyroiditis, labile thyrotropic function (hypoand hypermania or anxiety states), spasmophilia: central and peripheral, structural, and functional. Parts used: Stem with leaves; Galenic: MT, BH, DE, EO. Method: Tisane: 3 g leaves/1 cup water, steep 10 min for digestive issues and drink after meals, steep 15 min for nervous system/insomnia and drink before bed; Compress: 50 g leaves/liter of water; infuse 15 min, use in bath or as a compress; EO, internal: 1–2 drops 1–3 times per day diluted and encapsulated, EO, topical: 5%–30% diluted in carrier oil, apply 2–3 times per day to affected area; Hydrolat: 1–3 tsp. in water, 1–3 times per day. Notes and precautions: Contraindicated in central hypothyroidism; severe bradycardia.
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Mentha piperita (Peppermint) Essence: A plant that favors calibrated management of input, throughput and output. Summary: Excellent digestive tonic, antiinfectious, and antalgic for superficial neuromuscular and dermatologic disorders. Parts used: Leaf and flower; Galenic: EO, BH, H. Method: EO: Analgesic: 0.1%–1% (2–20 drops/5 mL carrier), Nasal or buccal application: 0.25%–1% (5–20 drops/5 mL carrier): Antalgic: 1%–5% (1–5 mL/5 mL carrier); Hydrolat: PO: 1–3 tsp. bid; Diffusion, compress or tisane: 1 tsp. dry leaves in ¾ c. water, 10-min infusion (keep covered), before meals. Notes and precautions: Menthones in high dose can be neurotoxic; can cause glottic closure in high doses, esp. infants; irritating to the skin in infants and small children; can be irritating to the eyes if applied close to the eyes above a dilute concentration; avoid in gastro-esophageal reflux originating in weak gastro-esophageal sphincter and/or hiatal hernia.
Menyanthes trifoliata (Bogbean) Essence: A plant that resolves issues of sequestration and stagnation through restoring the proper dialectical of adrenaline and gonadal androgens. Summary: An excellent regulator of disadaptation through restoration of ANS sequencing (beta-relaunching), estro-androgenic balance, and regulation of inflammation, immune activity and tumoral growth. Parts used: Leaf; Galenic: MT, BH, FE.
Passiflora incarnata (Passionflower) Essence: A plant that dampens the intensity of the organism’s perception of and resistance to what is. Summary: #1 Sympatho-Corticotropic regulator in cases anxiety (insufficient GABA as noted by low βMSH/αMSH index + high Noxious free radicals), posttraumatic stress, and any disorder with elevated cortisol (high Cortisol index). Parts used: Flower; Galenic: MT, BH, DE. Method: Tisane: 2 g (1 tsp.)/150 mL water, steep 10– 15 min, drink 2–3 times per day. Notes and precautions: Excessive doses can cause headaches and altered vision; can augment the effect of hypnotics.
Pinus sylvestris (Pine) Essence: An erectifying rectifier that redistributes energy to the periphery through adaptation of the sympathetic ganglia and its privileged relationship to the entire adrenal gland as well as the osteo-energetic matrix of structuro-functional vitality.
Summary: A revitalizer in asthenic patients with cortico-immuno-insufficiency. Parts used: Bud (GM), needles (EO, Hydrolat); Galenic: EO, GM, H. Method: Essential oil: Inhaled or Nebulized: Ear, nose, throat, lower respiratory infections 1 drop/3 mL 0.9%–3% normal saline or albuterol according to indication, Topical: Chest, joints: 1%–15% adults (1–15 mL/5 mL carrier oil), Bath: 2%–5% (2–5 drops/5 mL carrier), Internal 1–3 mL/250 mL tincture; Hydrolat: 1–4 tbsp. 3–4 times per day for acute infections, 1–4 tbsp. 2–3 times per day for chronic asthenia.
Plantago major (Plantain) Essence: A plant that returns the distressed and overburdened central structures to essential structurofunctional functionality. Summary: #1 Polyvalent drainer for disorders of ear, nose, throat, upper and lower airways, and GI. Parts used: Leaf; Galenic: MT, DE, BH. Method: Tisane: 2–3 tsp./1 c. water, steeped 5 min, 3–4×/day; Compress for eye disorders: infuse 2 tbsp. in ¾ cup water for 15 min.
Populus nigra (Black poplar) Essence: A plant that allows for adaptative responses to break through internally imposed restrictions arising from incompetency of response. Summary: A supreme aid in treatment of spasmodic neuro-cardio-vascular conditions and inflammation of airways. Use as a companion to primary treatments, especially Ribes nigrum and Alnus glutinosa. Parts used: Buds; Galenic: GM.
Poterium sanguisorba (Salad Burnet) Essence: A plant that stanches the hemorrhaging of metabolic efficiency arising from CNS, thyro-somatotropic, digestive, tissular, or sanguine dysfunction, it resolves the fear of mental and tissular disintegration or loss of constitutional integrity. Summary: #1 Somato-metabolic regulator, with farreaching implications in human health. Parts used: Root, leaf and flower; Galenic: MT, FE, BH. Method: Decoction: 5 min, 25–30 g of root/500 mL water, 1–3 times/day. Notes and precautions: Contraindicated in pregnancy, nursing, failure to thrive in children.
Quercus pedunculata (Oak) Essence: A plant of stability through redistributive equity of endocrine function in the short and long circuits of adaptation.
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Summary: An excellent polyendocrine plant that redistributes the general endocrine activity allowing for a general regulation of the organism. Use when cortico-pituitary regulation is needed to harmonize permissive cortisol activity with the other three endocrine axes. Parts used: Bud; Galenic: GM.
Raphanus niger (Black radish) Essence: A cosmobiologic regulator of seasonal movement through the thyrotropic-hepatobiliary-pulmonary relationship. Summary: #1 Prespring adaptation and detoxifier, disorders of digestive-pulmonary stasis. Parts used: Root; Galenic: MT, DE, syrup. Method: Mother tincture: no more than 2 mL TID; Juice (fresh): 1–2 oz before main meal (add olive or flax oil or honey to reduce risk of heart burn); Simple syrup: slice a whole black radish in fine slices. Layer in a pot alternating with crystallized sugar. Let sit for 24 h, strain and refrigerate. Take 4–6 tbsp. per day in divided doses. Notes and precautions: Contraindicated in biliary obstruction; Relative: latent or frank hypothyroidism, Use with precautions in gastritis.
Rhodiola rosea (Goldenroot) Essence: A true adaptogen across the lifecycle for survival, reproduction, and durability. Summary: Use when regulation and support is required across multiple areas of function: central or peripheral, basal or adaptive activity, cognitive function, circulation, reproduction, etc. Parts used: Root; Galenic: MT, DE, BH. Notes and precautions: Can worsen Bipolar disorder or high-strung people if they have low beta-sympathetic and elevated and unregulated TRH.
Ribes nigrum (Cassis) Essence: A true cortico-tissular adaptogen rooted in the natural simplicity of the flow of Life. Summary: The most versatile corticotropic regulator. Benefits disorders in which corticotropic, cortico-somatotropic, or cortico-gonadotropic activity is implicated in dysdapated permissive or adaptive function. Parts used: Bud, leaf, fruit; Galenic: GM, MT, DE, BH, fruit.
Rosa canina (Dog rose) Essence: An essential revitalizer and nourisher for children and adults in the vector of ensuring the persistence of Life.
Summary: An excellent sympathetico-corticotropic support in children, asthenia, acute and chronic ENT infections and/or food allergies. Parts used: Bud; Galenic: GM. Notes and precautions: Use during day for stamina, use in evenings for restoration and reparative actions; may cause excitation in evenings in some patients.
Rosmarinus officinalis (Rosemary) Essence: Polyvalent plant offering a freshness to the organism through the return of both hyper- and hypofunctioning states to equilibrium. Summary: Use in patients with allergic or autoimmune disorders with inflammation rooted in adrenal cortex insufficiency. Parts used: Flower, young shoots; Galenic: EO, GM, MT, DE, HL, BH. Method: EO, internal (chemotype 1,8 cineole or verbenone): don’t exceed 300 mg/day, hydrolat: 1–3 tsp. BID to TID; EO external (ct. camphor): musculo-articular 2%–10% (2–10 drops/5 mL carrier); EO external (ct. 1,8 cineol): pulmonary: 2%–10% (2–10 drops/5 mL carrier); Tisane: 5–10 g/1 L water, 15 min steep, 1–3 cups/day; Bath: EO: 10–20 drops in excipient, Decoction: 50 g/1 L, decoct 10 min, add to bath water (avoid before bed). Notes and precautions: Contraindicated (EO primarily): chemotypes verbenone and camphor in: pregnancy, small children, and epileptics; beware of possible risk of adrenal-overstimulation. Use essential oil with precaution in GI irritation, nephritis, dermatitis, allergic reactions.
Rubus fruticosus (Blackberry) Essence: A plant that regulates the consequences of somatopancreatic oversolicitation and hyperfunction. Summary: An excellent plant for the treatment of metabolic, immune, and inflammatory disorders rooted in exocrine or endocrine pancreas overactivity. Parts used: Shoots, leaf, fruit; Galenic: GM, MT, DE. Method: Decoction of leaf: 2 tsp./1 c. water, decoct 3 min, then infuse 10 min, drink; Compress: decoct 1 tbsp./ cup water; apply to skin or add to bath. Notes and precautions: Contraindicated in hypoglycemia states.
Salvia officinalis (Sage) Essence: A plant that unfolds the involuted spheres of potentiality in central and peripheral function, in adaptation, in structure and in structurofunctional activity. Summary: A nearly perfect plant for central and peripheral neuroendocrine and emunctory regulation
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ensuring longevity and clarity of mind. Use in cases of peripheral cortico-gonado-thyrotropic insufficiency with hepato-pancreatic oversolicitation. Parts used: Leaf; Galenic: EO, MT, DE, BH. Notes and precautions: Possible interaction with certain antiepileptic medications, may exacerbate hypertension, especially with arteriosclerosis.
Salvia sclarea (Clary Sage) Essence: A plant the brings clarity of physiologic regulatory imperatives during the unfolding and in the unfolded spheres of potentiality of central and peripheral function, in adaptation, in structure and in structurofunctional activity. Summary: A neuroendocrine harmonizer and deepacting polyendocrine revitalizer. Use in all states of corticotropic, gonadotropic, and thyrotropic deficiency, as well as their coupled and yoked relationships: cortico-gonadotropic, gonado-thyrotropic, or cortico-thyrotropic. Parts used: Whole plant; Galenic: EO, DE, FE, BH, MT. Method: Tisane: 5–10 g/L water; infuse 10–15 min, drink in 3–4 divided doses daily; EO, internal: 2–6 drops/ day in divided doses; EO, external: 5%–10% applied to affected area 1–2 times per day. Notes and precautions: Contraindicated in hyperestrogenic states, estrogen-dependent cancers, pregnancy (except after 37 weeks gestation), lactation; use caution with children ages 6–7 during the end of the thyroid tissular growth phase.
Satureja montana (Winter Savory) Essence: A promoter of stamina, perseverance, and adaptability in the face of aggressions. Summary: It is most indicated for advanced cases of asthenia and adrenal insufficiency, when infections play a prominent role in inciting an asthma attack and in patients with strong spasmophilic tendencies or comorbidities such as arthritis or intestinal candidiasis. Parts used: Leaf and flower; Galenic: EO, BH. Method: EO: PO: 0.5–5 drops per day diluted in tincture, optimal: 15 US drops (750 μL) per 125 mL due to phenolic compounds, Topical: mix with other EO’s, dilute and use in localized areas only; Hydrolat: PO 1–3 tsp. bid, as gargle, nebulized, compress; Tisane: 1–2 tsp. in ¾ c. water, infuse 10 min, 2–3 cups per day. Notes and precautions: Contraindicated in pregnancy, nursing, hemorrhoids, hemorrhagic disorders, Crohn’s (esp. rectal EO). Relative: Adrenal overstimulation, hypertension, gastritis, hepatic failure. NB: Rich in phenols such as carvacrol, thymol, etc., which can be muco-irritating in moderate to high doses.
Secale cereale (Rye) Essence: A subtle yet effective reintegrator and reparative of the hepato-pancreatic axis affected by intake and impaired in excretion. Summary: A hepatobiliary-pancreatic restorative. Use in cases of elevated liver enzymes in the recuperative phase, or, with dermatologic conditions rooted in h epato-pancreatic dysfunction. Parts used: Rootlets; Galenic: GM.
Sequoia gigantea (Sequoia) Essence: A revitalizer founded on the durability and persistence of Life in the face of adversity, also a tonic for involescence. Summary: Use in cases of peripheral adrenal overstimulation where Cortisol-to-Adrenal cortex ratio is >5, with absolute global adrenal cortex insufficiency, and to restore bone after catabolic activity. Parts used: Young shoots; Galenic: GM.
Taraxacum officinale (Dandelion) Essence: A plant that pierces through the blockages of drainage and accumulation of metabolic heat. Summary: A superb drainer in conditions involving excess heat and dysmetabolic conditions. Use in all conditions requiring quick drainage due to metabolic, rheumatic, and allergic conditions, as well as certain states of depletion with stagnation. Parts used: Whole plant; Galenic: MT, FE, DE, BH. Notes and precautions: Can increase the effects of antihypertensives, diuretic and hypoglycemiant medications.
Thymus vulgaris (Thyme) Essence: A global neuroendocrine and immune regulator through organization of the self-correcting capacity of the organism. Summary: #1 Immuno-adrenal support for vagotonics with atopia, infectious or digestive complications. Parts used: Stem and flowers; Galenic: EO, BH, MT. Methods: EO: topical, internal (PO) Acute: 2 drops TID; Nonacute: 0.5–2 drops/day; EO-rectal: 0.1%; Tisane (general use): ½ tsp./cup water, infuse 5 min; Neutropenia: 2 tsp. of Thymus vulgaris herb in 6 cups water. Boil 7 min, steep 7 min. Drink throughout the day. Compress, Oral rinse: 1 tbsp./1 cup water; Bath: 1 cup in 4 L water; add to bath. Notes and precautions: Contraindicated in pregnancy, HTN, Glaucoma, hyposecretory states.
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Tilia tomentosa (Linden) Essence: A gentle plant of downregulation, and clearance of accumulated emotional or physical toxins. Summary: Especially helpful in children and sensitive adults, use in anxious patients and in any condition aggravated by anxiety, and in any patient with latent neurologic spasmophilia rooted in insufficient GABA (low βMSH/αMSH index) and/or excess central relaunching (high Thyroid relaunching or Thyroid relaunching corrected indexes). Parts used: Bud, leaf, flower; Galenic: GM, BH, H.
Urtica dioica, root (Stinging nettle) Essence: A plant that arrests the excess of androgenic sequestration and closure, thus allowing for drainage and depuration. Summary: A depurative that regulates peripheral gonadal androgen metabolism and associated factors. Use in all cases of gonadal androgen excess, especially when genital, cardiac, or joint issues are comorbid factors: uterine fibroids, enlarged prostate, lower urinary tract obstruction, atherosclerosis, psoriatic arthritis, etc. Parts used: Root; Galenic: MT, DE, BH. Method: BH: 3–5 tbsp. dry root in 4 c. water; decoct 3 min AND steep 10 min, drink in 3 even doses/day.
Urtica dioica, leaf (Stinging Nettle)
whose nocturnal installation of relaxation sends us to the little death of sleep and sweet reprieve of dreams, quenching the quest for “that sleep of death, [and] what dreams may come/when we have shuffled off this mortal coil.”a Summary: A grand regulator of central-overstimulation, redirecting metabolism to the periphery. #1 Plant for acute spasmophilia and chronic regulation of spasmophilic terrain. Parts used: Rhizome, roots, stolons; Galenic: BH, EO, DE, MT. Method: Tisane: 2.5 g root (1 heaping tsp.) per 150 mL water, 10–15 min steep; 1–4 cups per day; Cold maceration: same recipe, let sit 12 h; Bath: 100 g (3.5 oz = 3/4 c.) root/2 L water, steep 15 min, add to a hot bath and rest 10– 15 min; EO: 8 gtt in 1 tsp. sesame oil, mix and add to bath; Compress; 100 g root/1 L water, steep 10 min, apply to contusions and sore joints. Notes and precautions: Valerian has a strong smell, which may limit its use with sensitive patients; Bath: acute exacerbation of eczema, psoriasis, etc.; fevers, congestive heart failure, hypertonia; pregnancy and nursing (United Kingdom, none noted for rest of Europe), may cause somnolence and GI irritation in higher doses, may augment the effects of other hypnotic plants or benzodiazepines.
Vinca minor (Periwinkle)
Essence: A plant that revitalizes and adapts the organism to accommodation with the external environment. Summary: An antiallergic, antiinflammatory that revitalizes tissues. Use in cases of allergies, autoimmunity, and rheumatic conditions. Parts used: Leaf; Galenic: MT, DE, BH. Method: Fresh plant: decoct 10 min in 4 c. water, drink in 3–6 even doses/day).
Essence: A plant that regulates mental and physical consumption and the process of assimilation in both cases. Summary: A regulator of spasmophilic, and neurologic dysfunction rooted in vasculo-pancreatic dysfunction. Use in neurologic and cardiac disorders related to mental or vascular spasmophilia and metabolic dysfunction rooted in pancreatic dysfunction. Parts used: Petals; Galenic: MT, FE, DE, BH. Notes and precautions: Avoid in lactating women.
Vaccinium myrtillus (Bilberry)
Viscum album (Mistletoe)
Essence: A plant that helps to retain what is essential and dispel what is not. Summary: A firm and dependable tonifier and circulator. Use in disorders of microcirculatory dysfunction, ocular, metabolic, and infectious conditions. Parts used: Berry, leaf, young shoots; Galenic: DE, FE, GM, BH, MT, fruit. Method: Berry Decoction: 3 tbsp. in 3 c. water, boil 10 min, drink in 4–6 doses/day; Leaf tisane: 1 tbsp. in 4 c. water, steep 10 min, drink in 2–3 even doses/day.
Valeriana officinalis (Valerian)
Essence: A plant to reduce neuro-sympathetic guardedness by improving the organism’s structural cellular coherence and organization, and which calls forth the deus ex-cerebri of endorphins. Summary: Re-establishes buffering capacity in the face of pain and hyper vigilance. Use in cancer and chronic pain where there is insufficient endorphin activity. Parts used: Leaf, bud; Galenic: GM, DE, BH. Notes and precautions: Contraindicated in pregnancy, nursing, chronic infections (Tuberculosis, AIDS), cerebral tumors, lymphoma, and leukemia; NB: Can augment the effect of central nervous system depressants
Essence: A tonic whose diurnal yarn wanes the engrams of resistance to what is, what was, and what will be. A tonic
a. Shakespeare, W. Hamlet, Act 3, Scene 1, To be or not to be soliloquy.
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and antihypertensive medications. High doses: diarrhea, vomiting, anemia, leukopenia, purpura; berries are toxic. Chemotherapy dosing may need to be reduced if used simultaneously.
Viola tricolor (Wild pansy) Essence: A plant that assure material integrity through the axis of immuno-pulmonary competency and polyvalent drainage, thus allowing the organism to be flexible and dynamic in the face of external aggressions. Summary: A supreme depurative and drainer. #1 Antiallergic polyvalent therapeutic: use in all cases of allergy and polyemunctorial congestion. Parts used: Flower; Galenic: MT, BH. Method: Tisane or Compress: Infuse 1 tsp. in 8 oz water 10 min, drink TID before meals or apply to affected area.
Vitex agnus castus (Chaste Tree) Essence: A plant assuring the central-gonadotropic vector of structurofunctional capability and the tension contained within the dialectic of fertility and nonfertility and its cyclical turnover. Summary: The supreme regulator of peripheral and central gonadotropic function as well as relative gonado-thyrotropic and gonado-somatotropic relationships. #1 Plant for regulation of neuro-gonadotropic excess: diminishes peripheral and central gonadotropic activity but favors catabolic thyroid activity to support peripheral gonadotropic factors. A truly superb plant for women through childbearing and menopausal years, and for men with estrogen excess. Parts used: Berry, flowering tops; Galenic: MT, FE, BH, fruit. Notes and precautions: Contraindicated (Standard and high dose): Pregnancy, nursing, conditions in which relaunching of ACTH is undesirable.
Zea mays (Corn) Essence: It restores the fundamental buffering capacity and rooted stability that allows the organism to resume the natural geometric process of function and restitutio ad integrum. Summary: A hepatorenal drainer and analgesic best suited for complications of inflammatory disorders. Use for hepatorenal drainage compromised by the volume or duration of inflammatory material and partial proteins, especially when rooted in low serum TSH, elevated Cortisol, and low Insulin resistance: brain fog, chronic fatigue, fibromyalgia, etc. Also useful for cardiovascular and metabolic disorders. Parts used and galenic: Rootlets (GM), Silk (FE, BH, MT).
Zingiber officinale (Ginger) Essence: A plant the localizes the essential vitality of the organism where it faces stagnation, ischemia, lassitude, or insufficiency, be it endocrine, digestive, or immune in nature. Summary: An effective restorative and revitalizer of corticotropic, gonadotropic, and thyrotropic function focusing more on second-loop completion than first-loop adaptation. Use in states of insufficiency or deficiency of cortisol, adrenal or gonadal androgens and T4 and for digestive disorders. Parts used: Rhizome; Galenic: EO, DE, FE, MT, BH.
The special role of medicinal clay Medicinal clays, also known as diatomaceous earth, are a rich source of minerals. We prefer Illite clay, a green clay, mined and manufactured for internal use in France for two reasons. First, it has a high quality, as it is prepared according to European pharmacopeia standards. Second, it is less astringent and irritating to the mucosa than other types of clay. Clays have six major properties: 1. Adsorption: Endotoxins, biologic and environmental toxins 2. Absorption: Regulates composition of stool 3. Antimicrobial, broad-spectrum action 4. Antiinflammatory 5. Endocrine: Balances insulin levels and peripheral serotonin 6. Nutritional: Natural source of minerals: Silica, lithium, magnesium, and iron Notes on using clay 1. Preparation: Soak 15 min or longer, mix with nonmetallic spoon, e.g., AM: Soak overnight, stir in AM and drink, PM Use: Soak in AM, stir before bed or a meal and drink 2. Optimization: a. Liquid: Prepare with spring or purified water, or tisane that complements indication for use of clay, e.g.,: Althea officinalis for inflammation of intestines, Plantago major for bronchitis. b. Taste: Add 2–5 drops of fresh lemon juice or ¼ tsp. apple cider vinegar c. Essential oils: Add when clay is still dry 3. Adverse reactions: a. Rapid detoxification: Use less clay, prepare with tisane of Taraxacum officinale b. New onset-constipation: Use more water, or, add dissolvable fiber
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Adults:
Recipes with clay Constipation Ingredients: 1 tsp. clay, 1 heaping tablespoon inulin, Optional: 1 tsp. ground cardamom or caraway or fennel seed, or, 1 drop Origanum vulgare essential oil. Instructions: Mix in 2–4 cups water in the evening. Let sit 15 min. Drink at the time of sleep.
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Equilibration of intestinal flora ●
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Ingredients: Clay, 1 tsp., Mentha piperita (Peppermint) EO, 1 drop, Cichorium intybus (Chicory) hydrolat, 1 tbsp., Probiotics, ¼ tsp., 1 cup water Instructions: Prepare in AM. At the time of sleep, stir and drink on an empty stomach
Food poisoning Start using clay with the FIRST signs of food poisoning.
Ingredients: 1–2 tbsp. clay, Mentha piperita EO 1 drop, one of the following: Thymus vulgaris, Satureja montana, Origanum vulgare EO 1 drop, Optional: Rose water, 1 capful Instructions: Mix in the smallest amount of water tolerable to patient. Drink right away, or wait 15 min, mix again and drink. Repeat every 2–4 h until diarrhea and discomfort resolved Children:
●
●
●
Ingredients: 1–2 tbsp. clay, Mentha piperita EO 1 drop, Optional: Rose water, 1 capful, 1 tsp. stevia or xylitol— sweeten to taste Instructions: Mix, and let sit 15 min. If 2 years, stir and give entire mixture. Administer 2–4 oz every 1–2 h as needed. Note: If not well tolerated, chill to reduce taste. If patient vomits, reduce dose to 1 tsp. every 10 min
Chapter 44
Endobiogenic diets and nutrition Introduction to alimentation according to Endobiogeny According to the theory of Endobiogeny, the neuroendocrine system, as the manager of metabolism, determines the quality of nutrient digestion, extraction, and distribution based on local and global indicators of metabolic demand and requirements (c.f. The Theory of Endobiogeny, Volume 3, Chapter 9: Motricity of the bowel). Within the context of genetic inheritance, epigenetic modification and a person’s place in space and time (c.f. The Theory of Endobiogeny, Volume 1, Chapter 13: Art of the History), the quality, quantity, and timing of alimentation solicits specific types of digestive and neuroendocrine responses that have implications in all states of illness and wellness. Consider how both a rabbit and a cow are vegetarians yet have completely different habitus. In considering different types of dietary approaches, one must consider a number of factors. The first is stage of chronobiologic unfolding. For example, a child during a growth spurt vs a child who has plateaued, a woman at 40 years vs in menopause, etc. The second is adaptation syndrome: e.g., acute adaptation vs restitution phase. The third is heritage. For example, a first-generation Japanese-American may do better with a greater amount of seaweed, fish, and fermented soy in their diet all things considered than an American of Northern European descent due to historical differences in the microbiome. The fourth is the accessibility to regional foods, being those within a 100-km distance, assuming similarity and contiguity of geographical terrain and weather patterns. The fifth are the indications derived from the Biology of Functions indexes related to somatotropic function: oxidative state, cellular permeability, insulin sensitivity, metabolic rate, etc. This chapter offers a broad array of dietary approaches, discussed in Volumes 2 and 3 of The Theory of Endobiogeny. In addition, there are some new recommendations to allow for a greater diversity of patients and clinical conditions to be addressed within the outpatient setting. The chapter is divided into four sections: (1) a general approach to alimentation, (2) special regimens, (3) m onodiets,
The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00044-5 © 2020 Elsevier Inc. All rights reserved.
(4) targeted nutrient consumption. The first is a general approach to healthy eating and improving longevity. The second refers to diets meant to be consumed possibly indefinitely or long periods of time in order to address particular chronic issues of the terrain. Examples include pancreas-sparing and alkaline diets. The third are specialized and time-limited regimens. They involve high consumption of a single or limited number of foods in order to provide a therapeutically significant amount of whole nutrients for acute benefit. This occurs on an order of days, as with the 10-day Apple-Sardine diet. The fourth are guides to targeted nutrient consumption, e.g., calcium-rich foods, magnesium-rich foods, etc. Together, this chapter allows for a rational, clinical approach to dietary recommendations rather than a capricious or fad-based approach.
A general guide to healthy eating We believe that there is a generally healthy approach to eating. Not all recommendations are applicable to all people all the time, but most are applicable to most people, most of the time. Our considerations are derived by syncretic consideration of (1) traditional, preindustrial dietary practices, (2) large-scale, crosscultural, longitudinal epidemiological studies, (3) prospective clinical trials. We find that this approach is applicable to three types of patients: (1) in good health, wishing to prolong wellness, (2) for whom a specific diet cannot be identified, (3) for whom a paradigm shift is needed in food culture and hygiene prior to instituting a restrictive diet some time in the future. Guidance is listed in order of importance of introduction. Work with the patient to apply each point over a period of time, for example, 2–4 weeks for each point. 1. Culture of eating: (a) gratitude for meal, (b) awareness of implications of consumption, (c) start with bitter or sour food, (d) masticate 30 s per morsel, (e) set utensils down until prior morsel swallowed, (f) drink 15 min before or 1 h after meal, (g) stop before feeling full, (h) lunch largest meal, (i) dinner 3–5 h before sleeping, (j) fast 12 h starting from end of dinner
299
300 SECTION | E Essentials of alimentation
2. Caloric intake: 80% of stated requirements: (1) portion reduction, (2) intermittent fasting (14–16 h) 3. What to eat: preindustrials, whole foods, prepared in traditional methods and eaten seasonally unless otherwise indicated by clinical condition 4. Food types by frequency of consumption: a. Frequent: i. Spring water, Herbal teas ii. Pancreas-sparing foods (in order of preference, frequency and volume of consumption): 1. Soups (vegetable broth-based) 2. Vegetables (in descending order of preference): sprouts, bitter, and fragrant herbs (e.g., cilantro, parsley, tarragon, basil, mint, etc.), leafy greens and sea vegetables (c.f. alkaline diet), resistant starches (yams, sweet potatoes) 3. Bone broths made from the bones of: duck, turkey, chicken, wild game, pastured, grassfed animals 4. Ancient grains and seeds: brown rice, basmati rice (aged and soaked), quinoa, buckwheat, millet (in moderation) 5. High purine fish: sardines, herring, anchovies, salmon 6. Dairy, cultured: yoghurt, kefir, buttermilk (traditional) 7. Fruits: low glycemic: wild forest berries (strawberries, lingonberry, cloud, bilberry, cranberry, etc.), apples, pineapple, papaya, guava 8. Honey 9. Meats (in descending order of ease of digestion): the flesh of: pheasant, turkey, chicken, duck iii. Fermented foods: 1. Europe: Jamón ibérico (Iberian ham), Pepperoni, Salami, Sauerkraut, Prosciutto, Crème fraîche, Skyr (Icelandic w hey-yoghurt), Kvass (fermented rye beverage), Cidre poiré, Cornichons 2. Americas: sourdough bread, buttermilk 3. Caucuses: kefir, yoghurt 4. Asia: tempeh, miso, soy sauce, tamari, natto, kimchi (cabbage); Pu-erh tea, kombucha; 5. India, Middle east, Africa: idli, dosas, torshi (pickled, fermented vegetables), dugh (fermented yoghurt drink), kashk (fermented whey made from dugh), shubat (fermented camel milk); injera (bread made from teff— only if pure teff) iv. Prebiotics (6 g per day): 1. Root vegetables: onion (raw > cooked), jicama root, dandelion root, burdock root, leeks, asparagus
2. Cultured dairy: yoghurt, kefir 3. Misc.: miso, high fiber foods b. In moderation: i. Drinks: coffee (cold > hot brewed), tea (white > green > black) ii. Nuts: almonds, walnuts, hazelnut, Brazil nut iii. Meats: wild game, pastured, grass-fed (in descending order of preference): lamb, beef, pork iv. Dairy: hard cheeses aged 18 months or longer (excludes cave-aged) v. Alcohol: 3–4 servings per week c. Infrequently: cured meats (traditional, nitrite-free): 2–3 servings per month, cave-aged cheeses, soft cheeses, unfermented dairy d. Avoid: high glycemic foods, gluten-containing grains, saturated fats, nonpastured, nongrass-fed meat, animals raised with antibiotics, hormones, or genetically modified corn and/or soy 5. Methods of cooking: raw, steamed, boiled, broiled, or braised, grilled 6. Food preparation a. Grains: soaking and sprouting b. Meats: soak in vinegar or pomegranate paste c. Fowl: marinate in yoghurt, buttermilk, citrus, vinegar d. Fish: marinate in vinegar-based sauces, mustard, or citrus-oil mixture
Special regimens Alkaline diet Purpose: Acidity affects all aspects of biology and physiology. The primary source is biologically derived metabolic waste due to three factors: (1) adaptative global neuroendocrine regulation of metabolism, (2) quality of digestive juices, (3) choices made by each individual in consumption. Returning tissues to a more pH neutral state optimizes buffering capacity, resolves adaptative states, and allows for greater capacity for health and wellness. Clinical indication: All disorders of chronic inflammation: pain, fibromyalgia, autoimmune and atopic conditions, musculoskeletal disorders, myalgia, poor tolerance of massages or vigorous exercise, cancer (active or remission), etc. Biology of Functions: ↑ Cortisol + ↓ TSH + ↑ insulin + ↓ insulin resistance + ↑ noxious free radicals, or, ↓ Cortisol + ↑ TSH + ↓ insulin + ↑ insulin resistance + ↓ Redox.
Phase 1: Preparation Week 1: Start juicing, stop dairy, alcohol, and fried foods 1. Remove from diet: Dairy products (except where noted above), fried foods, alcohol 2. Add greens in liquid form, 2–3 times per day, before meals, in divided doses: You can choose one, two or all three of these for variety
Endobiogenic diets and nutrition Chapter | 44 301
a. Fresh green juice: 6 green apples, 4 stalks celery with greens, 2 dandelion leaves, 1 handful parsley, 1 handful cilantro, 2 pickling cucumbers, skin on, 1 fennel bulb, 2 in. ginger, ½ organic lemon with skin and pith b. Fresh green smoothies: 1 cup Swiss chard or Kale or Spinach, 1 handful parsley, 1 cup fermented Sauerkraut in brine, ½ cup water, beet, cabbage or carrot juice c. Alkalizing powder: greens or mixture of sodium and potassium salts of citrate or carbonate Week 2: Stop grains 1. Remove from diet: Grains and nuts, except as noted 2. Drink 6 cups of spring water + lemon or herbal teas throughout day: a.m.: 2 cups upon waking, 10 a.m.: 1 cup, 2 p.m.: 2 cups, 8 p.m.: 1 cup 3. Drink the green juice three times per day, before each meal: a.m.: 30 min before breakfast, Noon: eat 30 min later, at 6 p.m.
Phase 2: Induction
10. Fruit: Lemon, cherries (black or red), blueberries, raspberries, strawberries, papaya, grapes (black or red), pomegranate
Phase 3: Evolution Weeks 8–12 1. Reduce the amount of green juice if desired to before lunch and dinner 2. Add a breakfast of porridge + honey 3. Continue water, fruit juices as above
Phase 4: Months 4–6: Introduction of neutral foods 1. Root vegetables: Beet, burdock, celery root, parsnip, turnip 2. Mushrooms 3. Nuts 4. Fruits: melons, mango, papaya, avocado 5. All white fish 6. Sweeteners: Honey, agave, stevia
Weeks 3–7: The alkaline diet 1. Remove from diet: Red meat, chicken, fish except where noted otherwise 2. Drink 8 cups of water per day + lemon or herbal teas: a.m.: 2 cups upon waking, 9 a.m.: 1 cup, 10 a.m.: 1 cup, 2 p.m.: 2 cups, 4 p.m.: 1 cup, 8 p.m.: 1 cup 3. Green juice + 2 scoops protein List of permissible foods 1. Protein: Whey protein, tempeh, miso, cottage cheese (4 cups per week), egg whites (baked) 2. Fish: Salmon, tilapia, ono, flounder, sea bass, trout 3. Salad dressing: 1 tbsp. lemon juice, 2 tsp. olive oil, spices to taste 4. Drinks: Spring water, kombucha, pomegranate juice, tart cherry juice, herbal teas: chamomile, dandelion, ginseng, burdock, slippery elm, butcher’s broom, sage, meadowsweet, strawberry leaf, plantain, agrimony 5. Potassium-rich foods: Swiss chard, Spinach 6. Phosphorous-rich foods: Pumpkin seeds, hemp hearts, squash seeds, salmon, tempeh, mustard seed 7. Greens: Sprouts, spinach, kale, Swiss chard, beet greens, mustard greens, collard greens, broccoli, cauliflower, cabbage, lettuce, watercress, alfalfa, kohlrabi, garlic, carrots, asparagus, squash, zucchini, parsnips, pumpkins, tomatoes, sauerkraut (in brine), pickles (in brine) 8. Nuts and Seeds: Sprouted seeds (best), pumpkin seed, squash seed, chestnuts, flax seeds, almonds (raw), almond butter, sunflower seeds, sunflower butter, hemp hearts 9. Grains: Quinoa, amaranth, millet, brown rice, black rice, red rice
Pancreas-sparing diet Purpose: The pancreas is integrated into structural and adaptation demands. It provides material for buffering capacity and tissular growth. Neuroendocrine regulators on the pancreas include: parasympathetic tone, cortisol, TSH, TRH, somatostatin, and prolactin. In disorders of accumulation, both pancreas and neuroendocrine factors are implicated. Sparing solicitation of exocrine and endocrine pancreas diminishes the material and driving factors of incorporation of this material in states of hypertrophy and hyperplasia. Clinical indication: Any condition affected by simple carbohydrates (inflammatory conditions), animal proteins (autoimmune, atopic, inflammatory conditions, uterine fibroids, prostate enlargement, etc.), TSH (adenoidal disorders: enlarged tonsils, adenoidal tumors, adenocarcinomas, etc.), TRH (amyloidal disorders: atherosclerosis, Alzheimer’s disease, type 2 diabetes, etc.) or prolactin (certain states of metastasis, hyperestrogenism, or hyperandrogenism). Biology of Functions: varies; general: ↑ active membrane permeability, ↑/↓ TRH/TSH; one of the following two patterns: ↑ cortisol, ↓ somatostatin, ↑ insulin, ↓ insulin resistance index or ↓ cortisol, ↑ somatostatin, ↓ insulin, ↑ insulin resistance index. The pancreas-sparing foods are listed under “A general guide to healthy eating”. It can be recommended as a medium (3–6 months) or long-term strategy (years) depending on various factors. If liberalization is indicated later one, start by introducing foods 1 month at a time by category, e.g., grass-fed red meat, cane sugar, gluten-containing products, nonfermented dairy, etc.
302 SECTION | E Essentials of alimentation
Constipation
Vegetables
Purpose: The consistence of stool and motricity of the bowel can be affected by foods that are hyperosmotic, contain fiber, or are lubricating. In addition, an Endobiogenically regulated microbial terrain improves digestive efficiency and nutrient extraction, which reduces dwell time. Clinical indication: Constipation. Biology of Functions: Not applicable. Dietary approach: 1. Fiber: a. Normal transit: Soluble (c.f. Table 44.1): start at 5–10 g per day, increase to a goal of 30–40 g per day. Drink 6 glasses of water per day, add 1 additional glass (250 mL) per 10 g fiber after the first 10 g per day for a goal of 8 glasses (2 L per day). b. Slow transit: Nonsoluble fiber: edible skins of fruits and gourds, leafy green vegetables 2. Fruit: whole fruit with skin on if organic (c.f. Table 44.2) 3. Honey (as a demulcent and hyperosmotic food) 4. Fermented foods (c.f. A general guide to healthy eating)
TABLE 44.1 High-fiber foods by category. Category
Food
Serving
Fiber (g)
Grains
Bran Cereal
1 cup
20
Barley
1 cup
14
Bulgur
1 cup
8
Freekeh
1 cup
7
Flax seeds*
3 tsp.
7
Quinoa*
1 cup
6.5
Whole wheat spaghetti
1 cup
6
Buckwheat*
1 cup
4.5
Groats (Kasha)*
1 cup
4.5
Ezekiel bread
2 slices
4
Oats, raw*
1 cup
4
Corn*
1 cup
4
Brown rice*
1 cup
3.5
Lentils*
1 cup
15
Black beans*
1 cup
15
Pinto beans*
1 cup
15
Kidney beans*
1 cup
13
Lima beans*
1 cup
13
Navy beans*
1 cup
11
Chick peas*
1 cup
6
Legumes
Nuts
Fruits
Split peas*
1 cup
16
Green peas*
1 cup
9
Kale*
1 cup
7
Yam*
1 cup
6
Broccoli*
1 cup
4
Spinach, cooked*
1 cup
4
Pistachios*
4 oz
12
Hazelnuts*
4 oz
9
Pumpkin*
4 oz
4
Almonds*
4 oz
2.5
Grapefruit*
1
14
Avocado*
1, med
12
Raspberries*
1 cup
8
Pear*
1
5
Apple*
1
5
Banana*
1
4
Blueberry*
1
4
Orange*
1
4
Figs, dry*
2
4
Dates*
4
3
Key: * = gluten-free, bold = high in protein.
5. Probiotic supplements 6. Cleansing diets rich in fiber and oils: Grape cure, apple-sardine, brown rice diet 7. Oils: a. Choleretic: Olive oil b. Lubricating: Olive: best general oil, Sesame: for children full of energy and anxious adults, Borage oil: for obese individuals, Flax oil: for obese individuals, asthmatics, inflammatory disorders c. Dose: 0–11 months: ¼ tsp., 12–23 months: ½ tsp., 2–4 years: 1 tsp., 5–7 years: ½ tbsp., 8 years and older: 1 tbsp. d. Frequency: 1–2 times per day followed by 250 mL of spring water if it does not interfere with sleep and urinary habits: a.m. before breakfast, before bed
Immunity modulation diet Purpose: In states of debilitation, the presentation of immune-boosting foods as broths and juices can offer nutrients in a form easy to assimilate. In states of convalescence, the same foods can be blended, steamed, or eaten raw. Perhaps the most beneficial of all foods is raw garlic, swallowed whole. A general list of foods with nutrients favorable for support of immunity is listed in Table 44.3.
Endobiogenic diets and nutrition Chapter | 44 303
TABLE 44.2 Best fruits for constipation by season of growth. Spring
Summer
Autumn
Winter
All year juices
Grapes
Strawberries
Apples
Grapefruit
Prune
Watermelon
Figs
White grape
Watermelon juice
Pomegranate
Apple
Pears Quince
TABLE 44.3 Foods containing nutrients that support immunity. Zn
Se
S
Fruits
Apples
•
•
Avocados
•
•
Berries
•
•
•
•
Bananas Vegetables
B vitamins
Phytonutrients
Food
Kiwi
Mg
Vitamins A, E
Class
•
•
•
Sprouts
•
•
•
•
Endive
•
•
Tomato
•
•
Carrots
•
Gourds
•
Dark leafy greens (best: spinach, collard greens, kale)
•
•
Onions, garlic
•
•
Cabbage, broccoli
•
•
Grains
Buckwheat
•
Nuts and seeds
Flax, sesame, pumpkin, sunflower
•
Spices
Turmeric, ginger
Others
Brewer’s yeast Fermented drinks Fermented foods
Probiotics
•
•
•
•
• •
•
•
•
•
• •
304 SECTION | E Essentials of alimentation
Clinical indication: Hypoimmune and hyperimmune disorders (atopy, autoimmune). Biology of Functions: Varies, according to disorder; c.f. The Theory of Endobiogeny, Volume 2, Chapter 3: Immunity, Volume 3, Chapters 1–2: Allergic disorders and Asthma, and Volume 4, section 3: Asthma and Eczema.
Monodiets Apple-sardine diet Purpose: The Apple-Sardine diet is a special form of a pancreas-sparing diet that focuses on a limited number of foods for a defined period of time. It provides large amounts of calcium, omega-threes, easily assimilable proteins, bioflavonoids and hydration. A full explanation of the role of each food is discussed in The Theory of Endobiogeny, Volume 1, Chapter 17: Therapeutics according to an Endobiogenic reflection. Clinical indication: Any conditions rooted in spasmophilia, inflammation, and/or accumulation of toxins due to emunctory congestion, from acute parotitis to bronchitis to weight gain (c.f. The Theory of Endobiogeny, Volume 2, Chapter 11: Spasmophilia, and, Volume 4, Chapter 12: Spasmophilia). Biology of Functions: Varies according to the condition. The specific methodology of the diet is presented in Table 44.4. In acute states, one can start immediately with day 4 and then proceed to day 10. In chronic states, the patient should be advised to follow the full 10-day procedure. We have accommodated the diet to include brown rice in cases of hypoglycemia or intolerable hunger. For those who cannot tolerate sardines, canned herring or fresh anchovies may be used.
Brown rice diet Purpose: Regulation of the sensitivity of the endocrine pancreas to the excretion of insulin based on diet or stressors, and all that that implies in the genesis and continuation of myriad disorders. Clinical indication: Inflammatory conditions arising from somatotropic desynchronization, autoimmune conditions, metabolic disorders arising from insulin resistance, postindulgences (vacations, holidays, stress eating), cellulites. Biology of Functions: Varies; ↑ insulin + ↓ insulin resistance, or, ↓ insulin + ↑ insulin resistance. Similar to the apple-sardine diet, it is a mirror diet in which the second half of the diet is the inverse of the first half (Table 44.5). Day 1 is a complete rest day for the endocrine pancreas, as it involves nothing by vegetables steamed or raw, ad libitum. The second day is a mild demand on the endocrine pancreas from the presence of nonfructose disaccharides present in fruit. Days 3 and 4 solicit a moderate and calibrated demand for insulin thanks to the complex carbohydrates mixed with fiber in brown rice. Day 5 is the same as day 2, and day 6 the same as day 1. Throughout the 6 days, mountain, spring, or purified water, as well as unsweetened herbal teas or unsweetened kombucha can be consumed ad libitum. 6–8 glasses per day is highly recommended.
Grape cure Purpose: To improve the quality of chronobiologic adaptability, especially during the winter months and to improve cardiovascular health and longevity. This occurs thanks to the high intake of grapes, rich in phytonutrients, resveratrol,
TABLE 44.4 Apple-sardine diet day-by-day instructions. Day of diet Food
1
2
3
4
5
6
Chicken/fish—all types
•
•
Vegetables
•
•
•
Fruits—all types
•
•
•
Apples
•
•
•
•
•
•
Sardines
•
•
•
•
•
Brown rice
•
•
•
•
•
7
8
9
10
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Notes Days 1–10: (1) Brown rice is the only grain allowed, not required, (2) Olive oil is the only oil permissible, (3) Drink as much water with lemon juice as desired, (4) Avoid: egg yolks, fried foods, sugars, nuts, beans, dates. Days 4–7: (1) Eat as many sardines and apples as desired, (2) Organic apples only. Eat when oxidized and browned. Nonorganic apples either do not oxidize or oxidize very slowly. You can grate them, cut into slices, bruise with a fork or a meat tenderizer (in a 1-gal freezer bag to prevent splatter), (3) Apples can be eaten 30 min before sardines or 3 h after sardines but in no other order, (4) Judicious consumption of brown rice is permitted on these days (1–2 cups total throughout the day). Days 8–10: Adding foods from later days too early will upset your stomach and ruin the effects of the diet.
Endobiogenic diets and nutrition Chapter | 44 305
TABLE 44.5 Brown rice diet summary. Day Food
1
Vegetables
•
2
3
4
5
6 •
Fruits
•
•
Brown rice
•
vitamin K, copper, riboflavin, and melatonin. This diet should be practiced in the end of August or early autumn. Clinical: Dysbiosis, rheumatic diseases, metabolic syndrome (obesity), hypercholesterolemia, hypertriglyceridemia, thrombotic disorders, pancreatic rest (important to eat every 1.5 h to prevent insulin response to glycolysis from fasting), detoxification from drugs, anesthesia, medications, etc. Biology of Functions: Varies. It is a diet of mirror symmetry, as seen in the apple-sardine and brown rice diets. One proceeds to simplify one’s diet on days 1–4, then spends days 5–14 eating nothing but grapes, then gradually re-introducing other foods over the next 4 days (Table 44.6).
Nutrient-rich foods
•
Biology of Functions: varies. Latent spasmophilia: ↑/↓/ normal Leukocyte mobilization + ↓ Platelet mobilization (and no spasmophilic disease); Adrenal insufficiency: ↓ Adrenal cortex, or, Cortisol/Adrenal cortex 17 months
1 oz
311
121
Yoghurt, Kefir
1 cup
296
149.4
Beets
1 cup
520
Collard greens
1 cup
268
62.7
Papaya
1 med.
500
Spinach
1 cup
245
41.4
Brussels sprouts
1 cup
500
30
Turnip greens
1 cup
197
28.8
Broccoli
1 cup
450
30
Cottage cheese
1 cup
174
206
Cantaloupe
1 cup
425
20
Mustard greens
1 cup
165
36.4
Tomato
1 cup
425
Asparagus
1 cup
400
Beet greens
1 cup
164
38.9
Barley
1 cup
240
Bok choy
1 cup
158
20.4
¼ cup
190
Cow’s milk
4 oz
138
74.4
Pumpkin seed
Swiss chard
1 cup
102
35
Quinoa
1 cup
145
Kale
1 cup
94
36.4
Sesame seed
¼ cup
125
Cabbage
1 cup
63
43.5
Black bean
1 cup
120
Broccoli
1 cup
62
54.6
Cashew
¼ cup
117
Brussels sprouts
1 cup
56
56.2
Sunflower seeds
¼ cup
114
Green beans
1 cup
55
43.8
Buckwheat
1 cup
85
Summer squash
1 cup
49
36
Brown rice
1 cup
84
Millet
1 cup
77
Parsley
0.50 cup
Flax seed
2 tbsp.
55
42
Calories
10.9
155
40
Key: dairy in bold.
Biology of Functions: varies. Active spasmophilia: ↑/↓/normal Leukocyte mobilization + ↓ Platelet mobilization (expressed spasmophilia); Adrenal overstimulation: ↑ Cortisol index, or, Cortisol/Adrenal cortex >4, regardless of absolute value of either index.
The following foods offer an excellent combination of magnesium and potassium to complement calcium intake (Table 44.8). Most can be eaten raw or lightly cooked except where indicated. All are easily digestible.
Endobiogenic diets and nutrition Chapter | 44 307
Vitamin E-rich foods Purpose: A general increase in the consumption of vitamin E-rich foods to improve the balance of antiinflammation overinflammation, and reduction of overoxidation. Clinical: All disorders where inflammation, oxidation, free radicals, hypercholesterolemia, thrombosis, or necrosis are implicated. Biology of Functions: Varies. Any of the following elevated: IL-1, redox, oxidation, noxious free radicals, proinflammatory, inflammation, necrosis. The richest sources of dietary vitamin E are listed in the Table 44.9.
TABLE 44.9 Vitamin E-rich foods. Source
Per 100 g serving
Wheat germ oil
150 mg
Almond oil
95 mg
Canola oil
44 mg
Sunflower oil
41 mg
Hazelnuts
20 mg
Almonds
15 mg
Olive oil
14 mg
Appendix 1
Essential physical exam images Introduction The physical exam is one of the key areas of the Endobiogenic assessment, along with a careful history and laboratory analysis. Below we reproduce images that summarize key physical exam findings and their relationship to the terrain.
Oral There are numerous findings in the mouth. A key finding related to insufficiency of amylase enzyme from the exocrine pancreas is swelling of the papilla of the canal of Stensen. This canal carries parotid amylase in saliva to assist in hydrolysis of starches prior to entry into the small intestines. It is located bilaterally on the buccal surface of the mouth, across from the second upper molars. For a visual image of this finding, as well as the papilla of the canal of Wharton, and other oral findings, see The Theory of Endobiogeny, Volume 2, Chapters 1, 2, 7, 8, and 10, and, Volume 3, Chapter 6.
Abdomen Some points relate to the anatomical position of the organ and its direct palpation, such as the liver, others are projections of glands, such as the points related to gallbladder and pancreas (Fig. A1.1). Clockwise from bottom, center: Grayed zone: when tender to palpation: 1. Grayed zone: when tender with light palpation: Hepatic congestion of extrahepatic origin: spasm of sphincter of Oddi (biliary-pancreatic congestion), splanchnic congestion, etc. 2. Red hexagon in grayed zone: when tender with light palpation: sphincter of Oddi is congested: evaluate gallbladder 3. Liver, right lower costal margin: a. inferior-lateral: when tender on deep palpation under the costal margin indicates hepatic secretory congestion, with implications of difficulty with detoxification
b. superior-medial: when tender on deep palpation under the costal margin indicates hepatic congestion due to elevated alpha-sympathetic tone on the hepatic venules and hepatic vein 4. Below Xyphoid process: when tender on moderate palpation indicates gastric inflammation 5. In midline, two fingers width below gastric point: when tender on moderate palpation indicates duodenal inflammation 6. In midline, below small intestinal point: when tender on deep palpation indicates splanchnic congestion resulting in hepato-pancreatic blockage 7. Zone of distress: when tender on light palpation indicated an installation of grief and a depressive tendency; the closer it is to the umbilicus, the more deeply installed the feeling of grief will be 8. Center, midline: when tender on moderate palpation indicates general pancreatic congestion due to over- solicitation and favors drainage of the gland 9. Center, right, and slightly superior to general pancreatic point: when tender on moderate palpation indicates exocrine pancreatic congestion due to oversolicitation, evaluate for dilation of opening of canal of Stensen in mouth. 10. Center, left, and slightly superior to general pancreatic point: when tender on moderate palpation indicates endocrine pancreatic oversolicitation 11. Center, left of umbilicus: when tender on deep palpation with movement toward the umbilicus indicated jejunal dysbiosis; evaluate for presence of coating on tongue A second level of abdominal exam relates specifically to the colon (Fig. A1.2). All findings are obtained by deep palpation and applied pressure. The various points of the colon, according to the theory of Endobiogeny, are rich in certain types of receptors, which play a role in nutrient reclamation from stool (Table A1.1). The relevance of this is discussed in The Theory of Endobiogeny, Volume 2, Chapter 5: Symbiosis, and, Volume 3, Chapter 11: Inflammatory bowel diseases. 309
310 Appendix 1
Liver congestion: Secretory
Liver congestion: Circulatory
Splanchnic congestion ® hepato-pancreatic blockage
Zone of distress Murphy’s Point: Congestion: Sphincter of Oddi
Hepatic congestion, extra-hepatic: Sphincter of Oddi, Splanchnic congestion, Duodenal plexus
Endocrine pancreas overtaxed
General pancreatic congestion
Exocrine pancreatic congestion FIG. A1.1 Endobiogenic abdominal visceral exam. See text for details. (© 2015 Systems Biology Research Group.)
FIG. A1.2 Cartography of central endocrine receptors on the colon according to the Theory of Endobiogeny. See text for details. (© 2015 Systems Biology Research Group.)
Appendix 1 311
TABLE A1.1 Endo-Enteric relationships by location, receptor, hormone, and, metabolites. Location
Microbiotic metabolism
Metabolites reclaimed
Central receptor
Peripheral hormone
Ileocecal junction
Fermentation: polysaccharides, cellulose, pectins, oligosaccharides Carbohydrates→short chain fatty acids, iodine scavenging
Water Electrolytes
ACTH: Structural adaptation
Adrenal cortex: Aldosterone
Ascending right colon
As above + Muscle fibers, mucous, desquamated cells Lipid hydrolysis
Proteins
FSH
Gonads: Estrogens
Hepatic flexure
Bile acids: Enterohepatic recycling
Lipids
TRH/TSH
Pancreas: Insulin, glucagon Gallbladder
Right transverse colon
Deamination of proteins Short chain fatty acids (SCFA) Phenols, indoles Lipid fermentation
Proteins
FSH
Gonads: Estrogens
Left transverse colon
Lipid fermentation: desaturated fatty acids, sterols
Proteins
LH
Gonads: Androgens
Iron, proteins
TSH
Spleno-humoral immunity
Lipids Trace metals
GH Prolactin
Pancreas: Insulin; Relaunching of second loop of adaptation and augmentation of ACTH
Water Electrolytes
ACTH: Functional adaptation
Adrenal cortex: Aldosterone
Splenic flexure Descending colon
Recto-sigmoid
Flora putrification Final reduction of nondigested, nonmetabolized material pH neutral
Leg On the leg, various findings can be interpreted in light of endocrine, abdominal, and pelvic elements of the terrain. The image shows the anterior view of patient’s left leg (Fig. A1.3). All findings are symmetrical except for “painful crow’s feet.” 1. Lateral, distal femur: when tender on deep palpation indicated a prolonged appeal to cortisol, but does not indicate what the cortisol response is
2. Medial, Painful crow’s feet, fibula a. Left leg, closer to midline: pelvic congestion b. Right leg, closer to midline: gallbladder congestion c. Common, more medial: TSH appeal to T4 that is insufficient in timing and/or response to the TSH demand without presupposing the quantitative or effective tissular actions of either
312 Appendix 1
Medial
Lateral
Cortisol
Painful “crow’s foot” - left: pelvic congestion - right: gall bladder
TSH T4 ¯ (left > right as LH more easily distributed than FSH) FIG. A1.3 Some relevant findings on the leg related to the global terrain. (Used with permission from an original drawing by Duraffourd and Lapraz, unpublished. © 2019 Systems Biology Research Group.)
Appendix 2
References and resources Introduction The theory of Endobiogeny developed in the crucible of three currents: traditional, empirical, and scientific knowledge. There is a long history of medical herbalism and scientific experimentation within France that influenced the development and application of Endobiogeny to clinical medicine. A full but not exhaustive list of references can be found in the first three volumes of The Theory of Endobiogeny. In this handbook, we have avoided specific references to maintain a manageable size of the book as a bedside reference in the clinical setting. Here you will find key peer-reviewed scientific references on Endobiogeny and the use of medicinal plants. The list, again, is neither definitive nor exhaustive, but may be considered demonstrative of the volume of scientific research that supports the logical and physiologic basis of Endobiogeny as well as a rational clinical approach to phytotherapy.
Articles Endobiogeny Buehning LJ, Hedayat KM, Sachdeva A, Golshan S, Lapraz JC. A novel use of biomarkers in the modeling of cancer activity based on the theory of endobiogeny. Glob Adv Health Med. 2014;3(4):55-60. Hedayat K, Lapraz JC, Schuff BM, et al. A novel approach to modeling tissue-level activity of cortisol levels according to the theory of Endobiogeny, applied to chronic heart failure. J Complex Health Sci. 2018;1(1):3-8. Lapraz JC, Hedayat KM. Endobiogeny: a global approach to systems biology (part 1 of 2). Glob Adv Health Med. 2013;2(1):64-78. Lapraz JC, Hedayat KM, Pauly P. Endobiogeny: a global approach to systems biology (part 2 of 2). Glob Adv Health Med. 2013;2(2):32-44.
Medicinal plants Articles are listed in order of the medicinal plants discussed, by Latin binomial.
Iaremii IM, Meshchyshen IF, Hrihor'ieva NP, Kostiuk LS. [Effect of Arnica montana tincture on some hydrolytic enzyme activities of rat liver in experimental toxic hepatitis]. Ukr Biokhim Zh. 1998;70(6):88-91. Kavvadias D, Abou-Mandour AA, Czygan FC, et al. Identification of benzodiazepines in Artemisia dracunculus and Solanum tuberosum rationalizing their endogenous formation in plant tissue. Biochem Biophys Res Commun. 2000;269(1):290-295. Cefalu WT, Ye J, Zuberi A, et al. Botanicals and the metabolic syndrome. Am J Clin Nutr. 2008;87(2):481S-487S. Harada M, Hirayama Y, Yamazaki R. Pharmacological studies on Chinese cinnamon. V. Catecholamine releasing effect of cinnamaldehyde in dogs. J Pharmacobiodyn. 1982;5(8):539-546. Anderson RA. Chromium and polyphenols from cinnamon improve insulin sensitivity. Proc Nutr Soc. 2008;67(1):48-53. Chen TS, Liou SY, Chang YL. Antioxidant evaluation of three adaptogen extracts. Am J Chin Med. 2008;36(6):1209-1217. Davydov M, Krikorian AD. Eleutherococcus senticosus (Rupr. & Maxim.) Maxim. (Araliaceae) as an adaptogen: a closer look. J Ethnopharmacol. 2000;72(3):345-393. Pearce PT, Zois I, Wynne KN, Funder JW. Panax ginseng and Eleuthrococcus senticosus extracts—in vitro studies on binding to steroid receptors. Endocrinol Jpn. 1982;29(5):567-573. Wright CI, Van-Buren L, Kroner CI, Koning MM. Herbal medicines as diuretics: a review of the scientific evidence. J Ethnopharmacol. 2007;114(1):1-31. Skakun NP, IKh P. [Fragaria vesca as a Cholagogue.]. Vopr Pitan. 1964;23:75-76. Bondarenko AS, Zelepukha SI. [Antimicrobial properties of Fragaria vesca and Fragaria grandifolia.]. Mikrobiol Zh. 1962;24:41-45. Visen P, Saraswat B, Visen A, et al. Acute effects of Fraxinus excelsior L. seed extract on postprandial glycemia and insulin secretion on healthy volunteers. J Ethnopharmacol. 2009;126(2):226-232. 313
314 Appendix 2
Birdsall TC. 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Altern Med Rev. 1998;3(4):271-280. van Vliet IM, Slaap BR, Westenberg HG, Den Boer JA. Behavioral, neuroendocrine and biochemical effects of different doses of 5-HTP in panic disorder. Eur Neuropsychopharmacol. 1996;6(2):103-110. Wheatley D. Medicinal plants for insomnia: a review of their pharmacology, efficacy and tolerability. J Psychopharmacol. 2005;19(4):414-421. Yamaguchi N, Satoh-Yamaguchi K, Ono M. In vitro evaluation of antibacterial, anticollagenase, and antioxidant activities of hop components (Humulus lupulus) addressing acne vulgaris. Phytomedicine. 2009;16(4):369-376. Alkharfy KM, Frye RF. Effect of valerian, valerian/hops extracts, and valerenic acid on glucuronidation in vitro. Xenobiotica. 2007;37(2):113-123. Milligan S, Kalita J, Pocock V, et al. Oestrogenic activity of the hop phyto-oestrogen, 8-prenylnaringenin. Reproduction. 2002;123(2):235-242. Hosseini S, Jamshidi L, Mehrzadi S, et al. Effects of Juglans regia L. leaf extract on hyperglycemia and lipid profiles in type two diabetic patients: a randomized double-blind, placebo-controlled clinical trial. J Ethnopharmacol. 2014;152(3):451-456. Sourgens H, Winterhoff H, Gumbinger H, Kemper F. Effects of Lithospermum officinale and related plants on hypophyseal and thyroid hormones in the rat. Int J Crude Drug Res. 1986;24(2):53-63. Auf'mkolk M, Kohrle J, Gumbinger H, Winterhoff H, Hesch RD. Antihormonal effects of plant extracts: iodothyronine deiodinase of rat liver is inhibited by extracts and secondary metabolites of plants. Horm Metab Res. 1984;16(4):188-192. Wojtyniak K, Szymanski M, Matlawska I. Leonurus cardiaca L. (motherwort): a review of its phytochemistry and pharmacology. Phytother Res. 2013;27(8):1115-1120. Ovanesov KB, Ovanesova IM, Arushanian EB. [Effects of melatonin and motherwort tincture on the emotional state and visual functions in anxious subjects]. Eksp Klin Farmakol. 2006;69(6):17-19. Beer AM, Wiebelitz KR, Schmidt-Gayk H. Lycopus europaeus (Gypsywort): effects on the thyroidal parameters and symptoms associated with thyroid function. Phytomedicine. 2008;15(1-2):16-22. Bora KS, Sharma A. Phytochemical and pharmacological potential of Medicago sativa: a review. Pharm Biol. 2010;49(2):211-220. Logan AC, Beaulne TM. The treatment of small intestinal bacterial overgrowth with enteric-coated peppermint oil: a case report. Altern Med Rev. 2002;7(5):410-417. Kuduk-Jaworska J, Szpunar J, Gasiorowski K, Brokos B. Immunomodulating polysaccharide fractions of Menyanthes trifoliata L. Z Naturforsch C. 2004;59(7-8):485-493.
Bennani-Kabchi N, Fdhil H, Cherrah Y, El Bouayadi F, Kehel L, Marquie G. [Therapeutic effect of Olea europea var. oleaster leaves on carbohydrate and lipid metabolism in obese and prediabetic sand rats (Psammomys obesus)]. Ann Pharm Fr. 2000;58(4):271-277. Bennani-Kabchi N, Fdhil H, Cherrah Y, et al. Effects of Olea europea var. oleaster leaves in hypercholesterolemic insulin-resistant sand rats. Therapie. 1999;54(6):717-723. Grundmann O, Wang J, McGregor GP, Butterweck V. Anxiolytic activity of a phytochemically characterized Passiflora incarnata extract is mediated via the GABAergic system. Planta Med. 2008;74(15):1769-1773. Dhawan K, Kumar S, Sharma A. Comparative anxiolytic activity profile of various preparations of Passiflora incarnata linneaus: a comment on medicinal plants' standardization. J Altern Complement Med. 2002;8(3):283-291. Hussan F, Mansor AS, Hassan SN, Tengku Nor Effendy Kamaruddin TN, Budin SB, Othman F. Anti-inflammatory property of plantago major leaf extract reduces the inflammatory reaction in experimental acetaminophen-induced liver injury. Evid Based Complement Alternat Med. 2015;2015:347861. Mello JC, Guimaraes NS, Gonzalez MV, et al. Hydroxyl scavenging activity accounts for differential antioxidant protection of Plantago major against oxidative toxicity in isolated rat liver mitochondria. J Pharm Pharmacol. 2012;64(8):1177-1187. Kelly GS. Rhodiola rosea: a possible plant adaptogen. Altern Med Rev. 2001;6(3):293-302. Pooja, Bawa AS, Khanum F. Anti-inflammatory activity of Rhodiola rosea—"a second-generation adaptogen". Phytother Res. 2009;23(8):1099-1102. Alonso R, Cadavid I, Calleja JM. A preliminary study of hypoglycemic activity of Rubus fruticosus. Planta Med. 1980;Suppl:102-106. Lima CF, Andrade PB, Seabra RM, Fernandes-Ferreira M, Pereira-Wilson C. The drinking of a Salvia officinalis infusion improves liver antioxidant status in mice and rats. J Ethnopharmacol. 2005;97(2):383-389. De Leo V, Lanzetta D, Cazzavacca R, Morgante G. [Treatment of neurovegetative menopausal symptoms with a phytotherapeutic agent]. Minerva Ginecol. 1998;50(5):207-211. Viola H, Wolfman C, Levi de Stein M, et al. Isolation of pharmacologically active benzodiazepine receptor ligands from Tilia tomentosa (Tiliaceae). J Ethnopharmacol. 1994;44(1):47-53. Urtica dioica; Urtica urens (nettle). Monograph. Altern Med Rev. 2007;12(3):280-284. Roschek B, Jr., Fink RC, McMichael M, Alberte RS. Nettle extract (Urtica dioica) affects key receptors and enzymes associated with allergic rhinitis. Phytother Res. 2009;23(7):920-926.
Appendix 2 315
Farzami B, Ahmadvand D, Vardasbi S, Majin FJ, Khaghani S. Induction of insulin secretion by a component of Urtica dioica leave extract in perifused Islets of Langerhans and its in vivo effects in normal and streptozotocin diabetic rats. J Ethnopharmacol. 2003;89(1):47-53. Nahata A, Dixit VK. Ameliorative effects of stinging nettle (Urtica dioica) on testosterone-induced prostatic hyperplasia in rats. Andrologia. 2011;44 Suppl 1:396-409. Durak I, Biri H, Devrim E, Sozen S, Avci A. Aqueous extract of Urtica dioica makes significant inhibition on adenosine deaminase activity in prostate tissue from patients with prostate cancer. Cancer Biol Ther. 2004;3(9):855-857. Chopin Lucks B. Vitex agnus castus essential oil and menopausal balance: a research update [Complementary Therapies in Nursing and Midwifery 8 (2003) 148-154]. Complement Ther Nurs Midwifery. 2003;9(3):157-160. Wuttke W, Jarry H, Christoffel B, Spengler B, SeidlovaWuttke D. Chaste tree (Vitex agnus-castus)-pharmacology and clinical indications. Phytomedicine. 2003;10:348-357. Dante G, Facchinetti F. Herbal treatments for alleviating premenstrual symptoms: a systematic review. J Psychosom Obstet Gynaecol. 2010;32(1):42-51. van Die MD, Burger HG, Teede HJ, Bone KM. Vitex agnus-castus (Chaste-Tree/Berry) in the treatment of menopause-related complaints. J Altern Complement Med. 2009;15(8):853-862. Xu H, Fabricant DS, Piersen CE, et al. A preliminary RAPD-PCR analysis of Cimicifuga species and other botanicals used for women's health. Phytomedicine. 2002;9(8):757-762. Loch EG, Selle H, Boblitz N. Treatment of premenstrual syndrome with a phytopharmaceutical formulation containing Vitex agnus castus. J Womens Health Gend Based Med. 2000;9(3):315-320. Milewicz A, Gejdel E, Sworen H, et al. [Vitex agnus castus extract in the treatment of luteal phase defects due to latent hyperprolactinemia. Results of a randomized placebo-controlled double-blind study]. Arzneimittelforschung. 1993;43(7):752-756.
Books Books are listed in alphabetical order by first author and in descending order of date in cases of multiple works by the same author(s). Andrianne, P. Treatise on Gemmotherapy. The Therapeutic Use of Buds. Brussels: Editions Amyris; 2012. Charrié J-C, de Clairemont Tonnerre M-L. Se soigner toute l’année au naturel. France: Prat Editions; 2017. Charrié J-C, Souffland-Groussard M, Bartczak S, Paslin D, Lapraz JC. Les clés de l’alimentation Anti-Cancer et Maladies Inflammatoires, Infectieures, Auto-Immune. France: Terre Vivante Editions; 2017. Duraffourd C, Lapraz JC. Traité de Phytothérapie Clinique: Médecine et Endobiogénie. Paris: Masson; 2002. Duraffourd C, Lapraz J-C. Cahiers de Phytothérapie Clinique Vol 1-5. Paris: Masson; 1984. Duraffourd C, Lapraz JC, Valnet J. ABC de Phytothérapie dans les Maladies Infectieuses. Paris: Editions J. Grancher; 1998. Hedayat K, Lapraz JC. The Theory of Endobiogeny: Global Systems Thinking and Biological Modeling for Clinical Medicine. vol. 1. Philadelphia: Academic Press; 2019. Hedayat K, Lapraz JC. The Theory of Endobiogeny: Foundational Concepts for Treatment of Common Clinical Disorders. vol. 2. Philadelphia: Academic Press; 2019. Hedayat K, Lapraz JC. The Theory of Endobiogeny: Advanced Concepts for Treatment of Complex Clinical Conditions. vol. 3. Philadelphia: Academic Press; 2019. Hedayat K, Lapraz JC, Schuff BM. The Theory of Endobiogeny: A Bedside Handbook. vol. 4. Philadelphia: Academic Press; 2019. Lapraz JC, Carillon A, Charrié J-C, et al. Plantes Médicinales: Phytothérapie Clinique Intégrative et Médecine Endobiogénique. Paris: Lavoisier; 2017. Lapraz J-C, de Clairemont Tonnerre M-L. La Médecine Personnalisée: Retrouver et Garder la Santé. Paris: Odile Jacob; 2012.
Index Note: Page numbers followed by f indicate figures and t indicate tables.
A
Abdominal examination, 309, 312f auscultation, 46 colon, 309 corticotropic axis evaluation, 76t duodenum, 311t dysbiosis, 309 endo-enteric relationships, 311t exterior, 46 gallbladder, 309 hepato-splanchnic congestion, 309 interior structure, 46 liver, 309 middle structure, 46 palpation, 46 pancreas, 309 percussion, 46 stomach, 309 xyphoid process, 309 zone of distress, 309 Abies balsamea/pectinata (Balsam fir, Silver fir), 281 Absorption, dysbiosis, 195 Achillea millefolium (Yarrow), 152, 233, 259, 263, 281 Acne agent, 123 BoF findings examination and, 124, 124t history and, 123, 124t chronic acne recurrent, 126 sample prescriptions in, 126 clay mask prescription, 125t cortico-gonadotropic, 123 critical terrain, 123 drainage, 123 drainage support, 126t face mask, 123 mechanism and response, 123 medicinal plants for neuroendocrine regulation, 126t symptomatic treatment with, 125t neuroendocrine regulation, 126, 126t oligoements, neuroendocrine and emunctory regulation, 126t precritical terrain, 123 symptomatic treatment, 123 medicinal plants with, 125t terrain, 123 treatment acute relief, 125–126
sample, 123 symptomatic, 123 ACTH. See Adrenocorticotropic hormone (ACTH) Adaptation adaptability, 32 adaptative state, 32 adrenal cortex, 11 autonomic nervous system (ANS), 4 chronic adaptation, 32 chronobiologic adaptation, 32 corticotropic activity in, 13 corticotropic axis, 74 cortisol and adrenal cortex index interpretation, 78 dehydroepiandrosterone (DHEA), 12 endocrine system, 4, 4f explosive, 26 immediate adaptation, 31 immune system, 6 implosive, 26 short-term adaptation, 31 Adaptation syndromes and adaptability general adaptation syndrome of endobiogeny, 32 mechanisms and actions, 31 Adenoma, prostate, 249 agent, 250 BoF findings examination and, 251–253, 252t history and, 251, 251t critical terrain, 250 drainage-decongestion prescription, 255t drainage plants for, 254t exemplary prescriptions, 253–254 lifestyle recommendations, 255t mechanisms, 250 medicinal plants for, 255t neuroendocrine-splanchnic-inflammation prescription, 256t precritical terrain, 250 prescription, 256t result, 250 sample treatment, 249 treatment, 253–254 Adipose tissue distribution, 76t Adolescence, 37 Adrenal cortex hormones aldosterone, 12–13 cortisol, 12–13 dehydroepiandrosterone (DHEA), 12 functions, 11 mechanisms and actions, 11
Adrenal cortex index, 77 Adrenocorticotropic hormone (ACTH) corticotropic axis, 73 cortisol, intrinsic overstimulation, 226 mechanism and action, 10 regulation, 10 role in disease, 10 ulcerative colitis, 174 Adulthood, 39, 39t Adverse childhood events (ACE), 41 Affective states corticotropic axis, 73 thyrotropic axis, 87 Agrimonia eupatoria (Agrimony), 133, 137, 139, 152, 206–207, 249–250, 281–282 Alchemilla vulgaris (Lady’s mantle), 137, 282–283 Aldosterone mechanisms and actions, 12 regulation, 12 treatment, 12–13 Alfalfa (Medicago sativa), 15, 237, 249, 289–293. See Medicago sativa (Alfalfa) Alimentation cycle, 62–63 dysbiosis, 195 endobiogeny, 299 Alkaline diet evolution, 301 induction, 301 months 4–6, 301 preparation, 300–301 Alkaline phosphatase bone isoenzyme, 104 Allergic asthma aggravating factors, 128 allergens asthmatic episode response, 128 critical terrain response, 128 mechanisms, 128 BoF history and, 128, 129t physical examination, 128, 129–130t critical terrain, 127 diet, 128, 131 environment, 128, 131 epigenetics, 128 exemplary prescriptions, 131–132 geography and, 128 lifestyle, 131 medicinal plants for drainage, 130t for neuroendocrine regulation, 131t with polyvalent symptomatic actions, 130t
317
318 Index
Allergic asthma (Continued) oligoelements, 131 precritical terrain, 127–128 protective factors, 128 sample treatment along with standard-of-care therapy, 127 symptomatic treatment, 127 treatment, 128–131 Allergic disorders, topology of, 204t Almond bud (Prunus amygdalus), 233 Alnus glutinosa (Black alder), 283 Alpha sympathetic (αΣ) nervous system autacoid of, 4, 4f excretion, stimulation of, 13 general concept of, 5t during metabolism, 4f Alpha-TRH-pancreas tincture, 106 Althea officinalis (Marshmallow), 283 Alzheimer’s disease, 42 Amino acid therapy, rapid transit diarrhea, 187–188 Anabolism, 229 Anal fissures treatment, 155 Ananassa sativa (Pineapple, Ananas), 283 Androgens acne, 123 activity, 16 genomic and nongenomic actions, 16t gonadotropic axis, 79 mechanisms and action, 16 regulation, 16 Angelica archangelica (Angelica), 132, 188, 223, 283 ANS. See Autonomic nervous system (ANS) Anthemis nobilis (Roman Chamomile), 283 Antiallergic, medicinal plants, 207t Anticipatory anxiety, 187 Antihemorrhagic, cicatrizant, 173 Antihistaminic, medicinal plants, 207t Antipruritic eczema, 207–208 Anxiety-drainage prescription, intrinsic asthma, 137t Apple-sardine diet, 304 day-by-day instructions, 304t Arctium lappa (Burdock), 283 Arginine vasopressin. See Vasopressin Arnica (Arnica montana), 11, 283–284 Arnica montana (Arnica), 11, 283–284 Artemisia dracunculus (Tarragon), 133, 137, 185, 188, 284 Artichoke (Cynara scolymus), 286 Asthenia, dysbiosis and, 200, 201t Asthma allergic type aggravating factors, 128 allergens, 128 critical terrain, 127 diet, 131 environment, 131 exemplary prescriptions, 131–132 history and BoF, 128, 129t lifestyle, 131 oligoelements, 131 physical examination, BoF findings, 128, 129–130t precritical terrain, 127–128
protective factors, 128 sample treatment along with standard-ofcare therapy, 127 symptomatic treatment, 127 treatment, 128–131 exercise-induced, 133 extrinsic, 131, 134 intrinsic agent, 133–134 causes, 133–134 critical terrain response, 134 historical and biology of functions correlations, 134, 135t history, 134 mechanisms, 134 medicinal plants, 136t physical examination, biology of functions, 134, 135t precritical terrain, 133–134, 134t prescriptions, 137, 137t symptomatic treatment goals, 133 terrain, 133–134 treatment, 134–137 Atopic disorders, 78 asthma, 78 allergies, 78 eczema, 78 Auscultation, 44t Autacoids, 67 ANS regulation, 4 Autonomic disturbance, 114 Autonomic nervous system (ANS) acne, 123 adaptation, 4 ANS-cortico-gonado-thyrotropic, Crohn’s colitis, 165 ANS-cortico-thyrotropic, ulcerative colitis, 173 ANS-corticotropic, allergic asthma, 127, 131, 131t ANS-corticotropic regulator, exerciseinduced asthma, 133, 137 ANS-drainage, rhinopharyngitis, 268t ANS-drainage-vascular, esophageal varices, 211–212 ANS precritical subtypes, allergic asthma, 127t approaches, 67 autacoids, 4, 4f, 67 cardiopulmonary system, 71t chest, 71t clinical pearls, 69 dermatologic findings, 70t dysbiosis, 195 eczema, 203 edema, 254 function, 4 general concept of, 5t head, 70t historical findings, 69 indexes of biology of functions, 69, 72t intrinsic asthma, 133 lower esophageal sphincter, 214 lower urinary tract obstruction (LUTO), 249 nervous system, 71t
normal transit constipation, 153 physical examination findings, 69 rapid transit diarrhea, 187 role in spasmophilia, 101 secretory diarrhea, 189 signs related to, 69–70t symptoms related to, 68t ulcerative colitis, 174 wet cough, acute bronchitis, 145 Autopathogenecity, 40–41 Avena sativa (Milky oat), 133, 137, 273, 284–286
B
Back, findings on corticotropic axis evaluation, 76t Balsam fir (Abies balsamea/pectinata), 281 Benign prostatic hypertrophy (BPH), 59 Beta-melanocyte stimulating hormone (βMSH), 10 Beta-MSH/alpha-MSH index, 10 Beta sympathetic (βΣ) nervous system ANS function, 4, 4f during metabolism, 4f Betula pubescens (Birch), 284 Bilberry (Vaccinium myrtillus), 293 Biology of functions (BoF), in disorders allergic asthma, 128, 129–130t acne examination and, 124, 124t history and, 123, 124t Crohn’s colitis examination and, 166–167 history and, 166 dry cough, acute bronchitis examination and, 140, 140–141t history and, 140, 140t dysbiosis, 196 intrinsic asthma, 134, 135t lower esophageal sphincter, 214 normal transit constipation examination and, 154, 154t history and, 154, 154t oligomenorrhea examination findings, 228t history and, 228–229, 228t otitis media examination and, 244, 245t history and, 244, 244t premenstrual syndromes examination and, 239, 240t history and, 238–239, 239t pyloric sphincter, 215 rhinopharyngitis examination and, 266, 267t history and, 266 slow transit constipation examination and, 160 history and, 160 wet cough, acute bronchitis examination and, 146, 147t history and, 146, 146t Biology of functions (BoF), general biomarker panels in clinical practice, 51–52, 51t biomarkers, 49–50 in clinical practice, 50–52
Index 319
concept of terrain, 49 description, 49 diet alkaline diet, 300 apple-sardine diet, 304 brown rice diet, 304 calcium-rich foods, 305 immunity modulation diet, 304 pancreas-sparing diet, 301 vitamin E-rich foods, 307 direct indexes, 50 discrepancies between history, exam and, 53–54 future risk of illness, 51 genital ratio, 50 history and exam validation, 50–51 indirect indexes, 50 interpreting indexes, 52–53 issues in data entry, 52 magnesium- and potassium-rich foods, 306 metabolic activity of terrain, 49 selection of medicinal plants, 51 state of known illness, 51 thyroid index, 50 words of caution about indexes, 53 Biology of functions (BoF), indexes corticotropic axis adaptation response, 78 adrenal cortex index, 77 atopic disorders, 78 βMSH/αMSH index, 74–75 depression, 78 insomnia, 78 oligomenorrhea, 229t polymenorrhea, 234t somatotropic axis, 95–98 cellular metabolic activity, 100t peripheral somatotropic indexes, 98, 99t prolactin index, 98, 99t somatotropic hormones effect on metabolism, 99–100t thyrotropic axis, 91 Birch (Betula pubescens), 284 Black alder (Alnus glutinosa), 283 Blackberry (Rubus fruticosus), 291 Black poplar (Populus nigra), 290 Black radish (Raphanus niger), 291 Black walnut (Juglans regia), 288 BoF panels, 51–52 BoF cancer female, 52 BoF cancer male, 52 BoF Mini, 52 BoF standard, 52 Bogbean (Menyanthes trifoliata), 290 Bone, 45 Borage leaf (Borago officinalis), 284 Borage oil (Borago officinalis seed), 284 premenstrual syndromes, 237, 242 Borago officinalis, 15, 237, 284 Borborygmus critical terrain, 151 exemplary prescriptions, 152 precritical terrain, 151 treatment, 152t Bronchial hyper-reactivity, allergic asthma, 128
Bronchial-inflammation-drainage, allergic asthma, 127, 131, 131t Bronchitis, acute dry cough agent, 139 critical terrain, 139–140 examination and BoF findings, 140, 140–141t exemplary prescriptions, 142–143 history and BoF findings, 140, 140t mechanisms, 140 precritical terrain, 139 sample treatment, 139 symptomatic treatment, 139 terrain, 139 treatment, 141–143 wet cough, 3 agent, 145 critical terrain, 145–146 examination and BoF findings, 146 exemplary prescriptions, 148 history and BoF findings, 146 mechanisms, 146 precritical terrain, 145 sample treatment, 145 symptomatic treatment, 145 treatment, 146 Brown rice diet, 304, 305t Buffering capacity, 6 Burdock (Arctium lappa), 283 Burping (eructation) agent, 151 chronic treatment, 151 critical terrain, 151 dietary modification, 151 exemplary prescriptions, 152 precritical terrain, 151 symptomatic treatment, 151 treatment, 151, 152t
C
Cajeput (Melaleuca leucadendron), 289 Calcitonin, 23t Calcium rich foods, 305, 306t spasmophilia, 109 uptake, regulating exogenous, 109 Caloric intake, 300 Cananga odorata, 188 Caraway (Carum carvi), 285 Cardiothoracic findings, 76t Cardiovascular system, 45 Carduus marianus (Milk thistle), 212, 284 Carica papaya (Papaya), 284 Carum carvi (Caraway), 152, 285 Cassis (Ribes nigrum), 291 Catabolic axes, emunctories by, 5 Catabolism, 228–229 Cell energy peripheral thyrotropic axis, 21–22 somatotropic axis, 24 Cell structure gonadal androgens, 16 somatotropic axis, 24 Cellular metabolism, 8t
Cellulite, 12–13 Central gonado-drainage, premenstrual syndromes, 237, 242 Central nervous system (CNS), 6–7 Cervix day 5-10, 219 day 11-13, 219 day 14, 219 day 15-20, 220 day 21-24, 220 day 25-menstruation, 220 Chaste tree (Vitex agnus castus), 294 Chicory (Cichorium intybus), 285 Childhood, 37, 38t Cholestasis, 113–114 symptoms of, 113t Chronic adaptation, 32 Chronobiologic adaptation, 32 Chronobiologic hypoandrogenism in adolescents, 107 in adults, 107 Chronobiology and cosmobiology, 61, 63t Chvostek, 103 Cichorium intybus (Chicory), 285 Cinnamomum zeylanicum (Cinnamon), 139, 269, 273, 285 Circulation, edema, 254 Citrus aurantium amara (Bitter orange), 188, 237 Citrus limon (Lemon), 212, 249, 269, 285 Citrus reticulata (Mandarin orange), 133, 137 Clary sage (Salvia sclarea), 292 Clay preparation, ulcerative colitis, 173, 174t Colitis Crohn’s (see Crohn’s colitis) ulcerative (see Ulcerative colitis) Complexity theory, 3 Congestion, acne, 123 Constipation diet, 302 fruits by season of growth, 303t normal transit agent, 153 anal fissures treatment, 155 chronic treatment, 155 critical terrain, 153 examination and BoF findings, 154, 154t exemplary prescriptions, 155–158 glycerin suppository, 155 high-fiber foods, 156t history and BoF findings, 154, 154t hydration and hyperosmotics, 155 lubricants, 155 mechanisms, 153 precritical terrain, 153 result, 153 sample treatment, 153 stimulant laxatives, 155 symptomatic treatment, 153 treatment, 154–158, 155t slow transit agent, 159 chronic treatment, 161 critical terrain, 159 examination and BoF findings, 160 exemplary prescriptions, 161–162
320 Index
Constipation (Continued) history and BoF findings, 160 mechanisms, 160 precritical terrain, 159 result, 160 sample treatment, 159 symptomatic treatment goals, 159 timely treatment, 160 treatment, 160–162 urgent treatment, 160 Copper-gold-silver (Cu-Au-Ag), oligoelement allergic asthma, 131 otitis media, 243, 246 rhinopharyngitis, 266 secretory diarrhea, 189 sinusitis, 269 Corn silk (Zea mays), 294 Cornus sanguinea, 139 Corpus luteum, 220 Cortico-gonadotropic axis, acne, 123 Cortico-gonadotropic coupling, 74 Cortico-immune incompetency, 270 Cortico-thyrotropic disorders, 29–30 Corticotropic axis acute change, 73 adaptation, 13, 74 affective states, 73 allergic asthma, 128 biology of functions (BoF) indices adaptation response, 78 adrenal cortex index, 77 atopic disorders, 78 βMSH/αMSH index, 74–75 cortisol index, 11–12, 21, 54 depression, 78 insomnia, 78 cortico-gonadotropic coupling, 74 cortisol, 12–13 disorders of adaptation, 73 disorders related to, 74 evaluation of, 74 abdominal findings, 76t adipose tissue distribution, 76t back, findings on, 76t cardiothoracic findings, 76t dermatologic findings, 75t extremities, findings of, 77t head and neck findings, 75t temperament and build, 75t grand phases of transition, 73 historical findings by system, 74, 74t hypothalamus, 10 intrinsic asthma, 133 major corticotropic hormones, interaxial relationships of, 73, 73f peripheral hormones, 11–12 pituitary, anterior, 10 pituitary, posterior, 10–11 rapid transit diarrhea, 188 role, 73 somato-corticotropic coupling, 74 ulcerative colitis, 174 Corticotropin-releasing hormone (CRH) alpha-MSH, 10 beta-MSH, 10
Cortisol acne, 123 allergic asthma, 127 corticotropic axis, 12–13 dry cough, acute bronchitis, 139 estrogen diminishment by, 223 intrinsic asthma, 133 mechanisms and actions, 12 permissive function, 12 regulation, 12 ulcerative colitis, 173 wet cough, acute bronchitis, 145 Corylus avellana (Hazelnut), 285 Crataegus oxyacantha (Hawthorn), 285 Creatine phosphokinase (CPK), 50 Critical terrain acne, 123 adenoma, lower urinary tract obstruction (LUTO), 250 adenoma, prostate, 250 allergic asthma, 128 asthma, 128 borborygmus, 151 burping (eructation), 151 constipation normal transit, 153 slow transit, 159 Crohn’s colitis, 166 dry cough, acute bronchitis, 139–140 dysbiosis, 196 eczema, 204 edema, prostate, 254–255 esophageal varices, 211 flatus, 151 gastroesophageal reflux disease (GERD) lower esophageal sphincter, 214 pyloric sphincter, 215 intrinsic asthma, 134 metrorrhagia, 226 oligomenorrhea, 228 otitis media, 243–244 polymenorrhea, 233 premenstrual syndromes, 237–238, 238t prostatitis, 260 rapid transit diarrhea, 187–188 rhinopharyngitis, 265–266 secretory diarrhea, 189 sinusitis, 270 tonsillitis, 274 ulcerative colitis, 173–175 wet cough, acute bronchitis, 145–146 Crocus sativa (Saffron), 233, 236 Crohn’s colitis agent, 166 ANS-cortico-gonado-thyro-somatotropic, 170–171t BoF findings examination and, 166–167 history and, 166 criteria of indexes deranged per stage of terrain, 167t critical terrain, 166 drainage prescription, 172t exemplary prescriptions, 172 gonadotropic terrains, 168t
mechanisms, 166 medicinal plants for drainage, 171t neuroendocrine regulation, 171t neuro-corticotropic terrains, 168t neuroendocrineimmunity-pain prescription, 172t neuroendocrine terrain support, 170–171t precritical terrain, 165–166 psychological indexes related, 169t result, 166 sample treatment, 165 somatotropic terrains, 169t symptomatic, antihemorrhagic prescription, 172t symptomatic treatment goals, 169–172 thyrotropic terrains, 168t treatment symptomatic treatment, 170t Crohn’s disease, 115, 120 Cupressus sempervirens (Cypress), 148, 233, 269, 285–286 Cynara scolymus (Artichoke), 286 Cypress (Cupressus sempervirens), 285–286
D
Dandelion (Taraxacum officinale), 292 Dehydroepiandrosterone (DHEA) adrenal DHEA, 79, 83 DHEA index, 16 mechanisms and actions, 12 regulation, 12 vs. testosterone, 12 Depression cortisol and adrenal cortex index interpretation, 78 dysbiosis with, 200, 201t Dermatologic findings, corticotropic axis evaluation, 75t Diagnosis of origin of disorder and objective baseline, 36t Diarrhea malabsorption (see Malabsorptive diarrhea) rapid transit (see Rapid transit diarrhea) secretory (see Secretory diarrhea) tincture, 185t Diet alkaline diet evolution, 301 induction, 301 months 4–6, 301 preparation, 300–301 allergic asthma, 128, 131 apple-sardine diet, 304 brown rice diet, 304 burping, 151 constipation, 302 esophageal varices, 212 GERD type 2, 217 immunity modulation diet, 304 lower urinary tract obstruction (LUTO), 250 otitis media, 243–244 pancreas-sparing diet, 301 prenatal diet, 128
Index 321
rhinopharyngitis, 266 secretory diarrhea, 189, 191 sinusitis, 271 slow transit constipation, 159 spasmophilia, 101 tonsillitis, 273 wet cough, acute bronchitis, 148 Digestion, dysbiosis, 195 Digestive flora balance, dysbiosis and, 200t Dihydrotestosterone (DHT), 249 Disorders, related to corticotropic axis, 74 Dog rose (Rosa canina), 291 Dopamine inhibition, 226 Drainage acne, 123 adenoma, prostate, 255t allergic asthma, 130t Crohn’s colitis, 165, 169, 172t dry cough, acute bronchitis, 142t dysbiosis and, 200, 200t edema, prostate, 258t hepato-pancreatic-dermal, 209 hepatobiliary-pancreatic-intestinal, 173 metrorrhagia, 224t oligomenorrhea, 227 otitis media, 243, 247t premenstrual syndromes, 237, 242, 242t slow transit constipation, 159 tonsillitis, 273 Dry cough, acute bronchitis agent, 139 BoF findings examination and, 140, 140–141t history and, 140, 140t critical terrain, 139–140 emollient-drainage-infectious prescription, 143t exemplary prescriptions, 142–143 mechanisms, 140 medicinal plants with drainage and pulmonary tropism, 142t neuroendocrine regulation, 142t with polyvalent symptomatic actions, 141–142t neuroendocrine-infectious prescription, 142, 143t precritical terrain, 139 sample treatment, 139 symptomatic treatment, 139 terrain, 139 treatment, 141–143 Dysbiosis agent, 196 and asthenia, 200, 201t critical terrain, 196 with depression, 200, 201t and drainage tisane, 200, 200t and dyspepsia, 200, 201t emunctory drainers with, 199t equilibration, 200 examination and boF findings, 196 exemplary prescriptions, 198–200 history findings, 196 indexes favoring hyperimmunity, 197t
indexes favoring hypoimmunity, 197t mechanisms, 196 medicinal plants, 199t with nervous disposition, 200, 201t normal transit constipation, 153 precritical terrain, 195 result, 196 sample treatment, 195 symptomatic treatment goals, 195 terrain with intestinal tropism, 200t treatment, 196–200 Dyspepsia, dysbiosis and, 200, 201t
E
Ear oil with herbs, otitis media, 247t Eczema agent, 203 critical terrain, 204 examination and BoF findings, 206, 206t exemplary prescriptions, 207–209 global terrain, 208t history, 205, 205t mechanisms, 205 medicinal plants antiallergic, 207t antihistaminic, 207t dual antihistaminic, antiallergic, 208t precritical terrain, 203 result, 205, 205t sample treatment, 203 symptomatic treatment goals, 203 treatment, 206–209 Edema endocrine regulation, 29t treatment, 12–13 Edema, prostate, 249 agent, 254 critical terrain, 254–255 drainage plants for, 258t exemplary prescriptions, 256 history, 255–256 hyperimmune, 250, 256 inflammatory, 250, 256 mechanisms, 255 precritical terrain, 254 result, 255 treatment, 256 Elecampane (Inula helenium), 287 Electrocardiogram (ECG), 104 Electromyogram (EMG), 104 Eleutherococcus senticosus (Eleuthero), 132, 250, 286–287 Emancipation, 107 Embryogenesis, 37, 37t Embryology gonadotropic axis, 13–14 somatotropic axis, 24 thyrotropic axis, 18 Emunctories, 5–6 catabolic axes, 5 Crohn’s colitis, 166 with dysbiosis, 199t dysfunction, allergic asthma, 128 endocrine system, 101–102 hormones and, 5t
intrinsic asthma, 133 lower urinary tract obstruction, 250 metrorrhagia, 223 otitis media, 244 spasmophilia, 101–102 terrain, 5–6 thyrotropic axis, 5 tonsillitis, 274 ulcerative colitis, 175 wet cough, acute bronchitis, 145 Endobiogenic assessment, thyrotropic axis, 87 Endobiogenic review of systems, 35 for adults, 37t for children, 36t Endocrine system and acne, 123 adaptation, 4, 4f Crohn’s colitis, 166 coupling indexes adenoma, 253t edema, 257t dysbiosis, 195 eczema, 203 hypothalamic-pituitary, 9 importance of endocrine assessment, 4 intrinsic asthma, 133 loops, 32–33 loops, progression of prolactin activity, 24 somatotropic axis, 24 lower urinary tract obstruction, 250 metabolism, 4, 4f otitis media, 243 pancreas glucagon, 27 insulin, 28 pineal, 8–9 rapid transit diarrhea, 188 recycling phases, 11–12t, 14t, 16–17t regulation endocrine-endocrine coupling, 29–30 endocrine-organ couplings, 30–31 loops assist, to identify disorder, 33 role in spasmophilia, 101–102 somatotropic axis, 95 tonsillitis, 273 ulcerative colitis, 174 wet cough, acute bronchitis, 145 Endocrinoemunctory dysfunction, and acne, 124 Endocrino-immunity, tonsillitis, 273 Endometrium day 1-4, 219 day 5-10, 219 day 11-13, 219 day 14, 219 day 15-20, 220 day 21-24, 220 day 25-menstruation, 220 distribution of nutrition to, 233 Endorphins, 75 ENT drainage-immunity, tonsillitis, 273 Environment, allergic asthma, 128, 131 Epigenetics, allergic asthma, 128
322 Index
Esophageal varices agent, 211 critical terrain, 211 exemplary prescriptions, 212 mechanisms, 211–212 medicinal plants, 212t precritical terrain, 211 result, 212 sample treatment, 211 symptomatic treatment goals, 211 treatment, 212 Essential oils, otitis media, 245t Estrogens actions, 15 diminishment by cortisol, 223 evaluating the activity, 16 follicular metrorrhagia types, 223–225 follicular phase, 219 gonadotropic axis, 79 mechanism, 15 particularities of, 15–16 production interruption, 223, 226 regulation, 15 Eucalyptus smithii (Gully gum), 139, 266 Eucalyptus ssp., 127, 132, 262, 269, 273, 286 Exercise dyspnea during, 137 induced asthma, 133 Exocrine pancreas allergic asthma, 128 biology of functions, 119 congestion, 119 edema, 254 and endocrine pancreas, 117 historical findings, 119 insufficiency, 119 neuroendocrine actions on, 118t oversolicitation, 119 physical examination, 119 structure and function, 117 therapeutics, 120 units of function, 117–118 Extremities, 46 findings of, corticotropic axis evaluation, 77t Extrinsic asthma, 131, 134 Eyelids, response of, 103
F
Fabiana imbricata (Pichi), 21, 139, 148, 286 Face, 43–45 Fermented foods, 300 Fertility estrogens, 15 follicle-stimulating hormone, 14t gonadotropic activity, 13 luteinizing hormone, 15 oxytocin, 11 Fetogenesis, 37, 37t Ficus carica (Fig), 286 Flatus critical terrain, 151 dysbiosis prescription for, 152t exemplary prescriptions, 152 precritical terrain, 151
treatment, 152t Follicle-stimulating hormone (FSH) Crohn’s colitis, 165–166 follicular phase, 219 gonadotropic axis, 79 relaunching-cortico-gonado, 223 Follicular phase metrorrhagia estrogens diminishment by cortisol, 223 estrogens production interruption, 223, 226 pituitary activity, dopamine inhibition, 225–226 sex hormone binding globulin’s (SHGB) binding, 226 normal menstruation, 219 early follicular phase (day 1-4), 219 late follicular phase (day 11-13), 219 midfollicular phase (day 5-10), 219 oligomenorrhea, 227 Food poisoning, acute, 199 Fragaria vesca (Strawberry), 26, 185, 237, 286–287 Fumaria officinalis (Fumitory), 287 Function, terrain, 3
G
Galenic forms, 57 Gallbladder examination, 309 normal transit constipation, 153 Gastro-duodenal-pancreatic, 117 Gastroesophageal reflux disease (GERD) lower esophageal sphincter agent, 214 critical terrain, 214 essence, 213 examination and BoF findings, 214 exemplary prescriptions, 214–215 history and BoF findings, 214 mechanisms, 214 medicinal plants, 214t precritical terrain, 213 result, 214 treatment, 213–215 pyloric sphincter agent, 215 critical terrain, 215 essence, 213 examination and BoF findings, 215 exemplary prescriptions, 217 history and BoF findings, 215 mechanisms, 215 medicinal plants, 216t precritical terrain, 215 result, 215 treatment, 213, 216–217 symptomatic treatment goals, 213 Gastrointestinal (GI) tract, 6 General timeline, 35 Genital pauses, 39 Genital ratio, 50 Genito-thyroid index, 52–53 Geography, and allergic asthma, 128 German chamomile (Matricaria recutita), 289
Ginger (Zingiber officinale), 294 Glabella tab, 103, 104t Global systems approach, of endobiogeny, 3 Glucagon endocrine pancreas, 27 somatotropic axis, 95 Glycyrrhiza glabra (Licorice), 287 Goldenroot (Rhodiola rosea), 291 Gonadal androgens, 16–17 Gonadopause, 39, 40t Gonado-somatotropic disturbances, 30 Gonadotropic axis central hormone, 79 common symptoms, 80, 80–81t disorders, 18 embryology, 13–14 endocrinology, 13–14 estrogen production site and method, 84t FSH and LH indexes, 83 function/role of, 79 gonadotropic imbalances, types of, 80 gonadotropic pituitary indexes, 84t hypothalamus, 14 intrinsic asthma, 133 metabolism, 13 metabolites and minerals, 13 normal transit constipation, 153 pathophysiology, 80 peripheral gonadotropic activity, 83, 84t peripheral hormone, 79 pituitary, 14–18 premenstrual syndromes central, 237, 242t peripheral, 237, 242t regulators, 241t regulation of, 79f signs associated with abdomen and genitals, 83t adiposity, 83t breasts and areola, 82t hair, 82t head and neck, 82t muscles and ligaments, 83t skin, 82t temperament, 81t voice and morphology, 81t treatment, 13–14 Gonadotropic imbalances, types of, 80 Gonadotropic pituitary indexes, 84t Gonadotropin-releasing hormone (GnRH) clinical implication, 14 desynchronization, 14 high-frequency GnRH, 15 low-frequency GnRH, 15 mechanisms and actions, 14 regulation, 14 Grape cure, 304–305, 305t Growth hormone (GH) mechanisms and actions, 25 regulation, 25 somatotropic axis, 95 Growth-hormone-releasing hormone (GHRH) mechanisms and actions, 24 regulation, 24
Index 323
restorative sleep, 24 somatotropic axis, 95 Gypsywort (Lycopus europaeus), 288
H
Hair, 45 Hamamelis virginiana (Witch hazel), 185, 233, 237, 249–250, 259, 287–288 Hawthorn (Crataegus oxyacantha), 285 Hazelnut (Corylus avellana), 285 Head and neck findings, corticotropic axis evaluation, 75t Healthy eating, 299–300 Hepatic insufficiency biology of functions, 114 cholestasis, 113t and congestion, 111 exocrine, 113 functions, 111–113, 112t physical exam findings, 113–114 post-prandial signs, 113t relaunching parasympathetic activity, 113t therapeutic approach, 115 units of function, 112–113 Hepatic steatosis, 211 Hepatobiliary, 112 Hepatobiliary-pancreatic, 112, 117, 173 Hepatocytes, 3 Hepato-gastric, 113 Hepato-intestinal, 113 Hepato-pancreatic-dermal drainage, 209 Hepato-splanchnic, 113 Hepato-splenic, 113 High-fiber foods by category, 302t Hippus, 103 Histamine, in ANS function, 4 Holly (Ilex aquifolium), 287 Hops (Humulus lupulus), 287 Hormones and emunctories to various disorders, 5t function, 8t stimulation and regulation, 8t Humulus lupulus (Hops), 133, 137, 287 Hydration, secretory diarrhea, 191 Hydroelectric integrity, aldosterone, 12–13 Hyperaldosteronism treatment, 12–13 Hyper alpha, allergic asthma, 127 Hyperandrogenism, edema, 254 Hyperestrogenism, 107 allergic asthma, 128 Hyperimmunity allergic asthma, 128 indexes favoring, dysbiosis, 197t Hyperprolactinemia, 26 Hyperthyroidism, thyrotropic axis role in, 89t Hypoimmunity, indexes favoring, 197t Hypothalamus corticotropin-releasing hormone (CRH), 10 gonadotropin-releasing hormone (GnRH), 14 growth-hormone-releasing hormone, 24 pituitary hormones, 9 somatostatin, 24 Hypothyroidism, thyrotropic axis role in, 89t
I
Ilex aquifolium (Holly), 188, 287 Illite clay, malabsorptive diarrhea, 181 Immediate adaptation, 31 Immune system, 6 adaptation, 6 BoF indexes and treatment, 4 cortisol activity, 12t FSH function, 14t gonadal androgens, 16t secretory diarrhea, 189 wet cough, acute bronchitis, 145 Immunity modulation diet, 302–304 nutrients that support, 303t Immuno-endocrine prescription, rhinopharyngitis, 268t Infancy, 37, 38t Inflammation, acne, 123 Inflammatory bowel disease (IBD), 165 Initiating factor of structure, 40–41 Insomnia, cortisol and adrenal cortex index interpretation, 78 Insufficient beta, allergic asthma, 127 Insulin BoF index, 301 endocrine pancreas, 28 resistance, somatotropic axis, 98 somatotropic axis, 95 Insulin-like growth factor-1 (IGF-1), 27 somatotropic axis, 95 Insulin resistance, BoF index, 25 Intense alpha, ulcerative colitis, 174–175 Intestinal tropism, terrain with dysbiosis, 200t Intrinsic asthma agent, 133–134 biology of functions historical and, 134, 135t physical examination, 134, 135t causes, 133–134 critical terrain response, 134 history, 134 mechanisms, 134 medicinal plants for drainage, 136t for emotional shock, 134–137, 136t neuroendocrine regulation, 136t with polyvalent symptomatic actions, 136t neuroendocrine regulation, 136t precritical terrain, 133–134, 134t prescriptions, 137, 137t symptomatic treatment goals, 133–134, 136t terrain, 133–134 treatment, 134–137 Inula helenium (Elecampane), 10, 148, 233, 287 Iso-osmotic fluid replacement, secretory diarrhea, 191
J
Juglans regia (Black walnut), 288
K
Knowing in practice, to physicians, 33–34
L
Lactate dehydrogenase (LDH), 49–50 Lady’s mantle (Alchemilla vulgaris), 282–283 Lamium album (White Deadnettle), 25–26, 288 Lavandula angustifolia (Lavender), 127, 132–133, 137, 139, 148, 223, 233, 237, 249–250, 263, 266, 273, 288 Leg examination, 311, 312f Lemon (Citrus limon), 285 Lemon balm (Melissa officinalis), 233, 289 Leonurus cardiaca (Motherwort), 188, 288 Leukocyte, interpretation of, 115t LH. See Luteinizing hormone (LH) Licorice (Glycyrrhiza glabra), 287 Lifestyle, allergic asthma, 131 Ligusticum porteri (Bear root), 57 Linden (Tilia tomentosa), 293 Lithospermum officinale (Stoneseed), 15, 21, 288 Liver, 111 elements of terrain, 111t endocrinometabolic oversolicitation, 128 functions, 111–113, 112t insufficiency and congestion, 111 units of function, 112–113 Lower urinary tract obstruction (LUTO) adenoma, 249 agent, 250 critical terrain, 250 drainage-decongestion prescription, 255t drainage plants for, 254t exemplary prescriptions, 253–254 lifestyle recommendations, 255t mechanisms, 250 medicinal plants for, 255t neuroendocrine-splanchnic-inflammation prescription, 256t precritical terrain, 250 prescription, 256t result, 250 sample treatment, 249 treatment, 253–254 diet, 250 edema, 249 agent, 254 critical terrain, 254–255 drainage plants for, 258t exemplary prescriptions, 256 history, 255–256 hyperimmune, 250, 256 inflammatory, 250, 256 mechanisms, 255 precritical terrain, 254 result, 255 treatment, 256 oligoelement, 250 sample treatment, 249–250 symptomatic treatment goals, 249 symptoms, 251t Luteal insufficiency, acne, 123 Luteal phase metrorrhagia central luteal regulation, 225, 225t luteal predominance inhibits estrogens, 226
324 Index
Luteal phase (Continued) peripheral estrogen-progesterone regulation, 225, 225t zinc-copper oligoelements, 225 normal menstruation, 220–221 early luteal phase (day 15-20), 220 late luteal phase (day 25-menstruation), 220 mid-luteal phase (day 21-24), 220 Luteinizing hormone (LH) follicular phase, 219 gonadotropic axis, 79 in prostatic adenoma, 249 Lycopus europaeus (Gypsywort), 21, 133, 137, 288
M
Magnesium, 104 allergic asthma, 127–128, 131 spasmophilia, 109 Magnesium chelate, slow transit constipation, 159 Magnesium-rich foods, 305–306, 306t Malabsorptive diarrhea agent, 182t BoF findings examination and, 181, 182t history and, 181, 182t diet carbohydrates, 184 fats, 184 proteins, 184–185 exemplary prescriptions, 185 low-fructose foods, 183t mechanisms, 181 medicinal plants with emunctory and other properties, 183t local intestinal flora, epithelial regeneration, and global neuroendocrine function, 181, 184t substitutive pancreatic actions of, 184t precritical terrain, 181 result, 181 sample treatment, 181 short- and medium-chain fatty acids, 183t symptomatic treatment goals, 181 treatment, 181–185 Malva sylvestris (Mallow), 139, 288–289 Manganese (Mn) eczema, 203 Manganese-copper (Mn-Cu) eczema, 207 polymenorrhea, 236 Manganese-Copper-Cobalt (Mn-Cu-Co), eczema, Marshmallow (Althea officinalis), 203, 207, 283 Materia medica dosing for children, 282t dosing of tinctures, 282t Materia medica, 61 Matricaria recutita (German chamomile), 132, 188, 212, 237, 259, 289 Medicago sativa (Alfalfa), 15, 237, 249, 289–293 Medicinal clay constipation, 295
food poisoning, 295 intestinal flora equilibration, 295 recipes, 295 secretory diarrhea, 189, 193t special role of, 294–295 Medicinal plants dosing considerations with, 59–60 dosing tinctures in children, 60 galenic forms, 57 parts used, 57 phytotherapy, 59 plant-drug interactions, 60 routes of adminstration, 59 spasmophilia, 109 uses, 57 Melaleuca leucadendron (Cajeput), 233, 249, 263, 289 Melanocyte-stimulating hormone (MSH) alpha-MSH, 10 beta-MSH, 10 beta-MSH/alpha-MSH index, 10, 74–75 Melilotus officinalis (Yellow sweet clover), 289 Melissa officinalis (Melissa, Lemon balm), 188, 233, 289 Menstrual cycle, normal early follicular (day 1-4), 219 early luteal (day 15-20), 220 follicular phase, 219 late follicular (day 11-13), 219 late luteal (day 25-menstruation), 220 luteal phase, 220–221 midfollicular (day 5-10), 219 mid-luteal (day 21-24), 220 ovulation (day 14), 219 Menstruation disorder, of oligomenorrhea. See Oligomenorrhea Mentha piperita (Peppermint, Spearmint), 152, 185, 196–197, 266, 273, 290 Mentha viridis, 212 Menyanthes trifoliata (Bogbean), 133, 137, 290 Mercurialis annua (Annual mercury), 26 Metabolism corticotropic, 9 endocrine system, 4, 4f gonadotropic, 13 hormone classification by, 8t peripheral gonadotropic hormones, 15 thyrotropic axis, 18 Metabolites corticotropic axis, 18 gonadotropic axis, 13 mobilization and utilization of, 88t thyrotropic axis, 18 Metrorrhagia abnormal uterine bleeding, 226 agent, 226 critical terrain, 226 drainage, 224t exemplary prescriptions, 226 follicular phase estrogens diminishment by cortisol, 223 estrogens production interruption, 223, 226 pituitary activity, dopamine inhibition, 225–226
sex hormone binding globulin’s (SHGB) binding, 226 luteal phase central luteal regulation, 225, 225t luteal predominance inhibits estrogens, 226 peripheral estrogen-progesterone regulation, 225, 225t zinc-copper oligoelements, 225 mechanisms, 226 necrosis, 226 neuroendocrine prescription, 224t precritical terrain, 225–226 result, 226 sample treatments per type, 223–225 treatment, 223 Milk thistle (Carduus marianus), 284 Milky oat (Avena sativa), 284–286 Minerals corticotropic axis, 18 gonadotropic axis, 13 thyrotropic axis, 18 Mistletoe (Viscum album), 293–294 Motherwort (Leonurus cardiaca), 288 Multiple sclerosis, 67 Muscles, 45
N
Nails, 45 Necrosis, metrorrhagia, 226 Nervous disposition, dysbiosis with, 200, 201t Neuro-digestive-anxiety/anger, GERD type 2, 217 Neuroendocrine adult, eczema, 209 otitis media, 243, 247t Neuroendocrine-antiinfectious -astringentemunctory, 181 Neuroendocrine-anxiolytic, 187 Neuroendocrine-anxiolytic essential oil blend, 187 Neuroendocrine axis drainage prescription, 163t slow transit constipation, 159, 162, 163t Neuroendocrine-immunity-drainage, secretory diarrhea, 189, 194t Neuroendocrine-infectious prescription dry cough, 139, 142, 143t wet cough, 148t Neuroendocrine-pancreatic, 118 Neuroendocrine, pediatric, 209 Neuroendocrine prescription metrorrhagia, 224t Neuroendocrine regulation acne, 126 chronic, 126 medicinal plants, 126t oligoements, 126t prescription for, 126t allergic asthma, 131t Crohn’s colitis, 171t dry cough, acute bronchitis, 142t dysbiosis, 198 eczema, 206 edema, 256 intrinsic asthma, 136t
Index 325
premenstrual syndromes, 240t wet cough, acute bronchitis, 148t Nocturnal dyspnea, allergic asthma, 132, 132t Normal menstruation early follicular (day 1-4), 219 early luteal (day 15-20), 220 follicular phase, 219 late follicular (day 11-13), 219 late luteal (day 25-menstruation), 220 luteal phase, 220–221 midfollicular (day 5-10), 219 mid-luteal (day 21-24), 220 ovulation (day 14), 219 Normal transit constipation agent, 153 anal fissures treatment, 155 BoF findings examination and, 154, 154t history and, 154, 154t chronic treatment, 155 critical terrain, 153 exemplary prescriptions, 155–158 glycerin suppository, 155 high-fiber foods, 156t hydration and hyperosmotics, 155 lubricants, 155 mechanisms, 153 medicinal plants ANS regulation and drainage, 157t for dysbiosis, 157t with polyvalent symptomatic actions, 157t precritical terrain, 153 result, 153 sample treatment, 153 stimulant laxatives, 155 symptomatic treatment, 153 treatment, 154–158, 155t Nosologic timeline, 35 Nutrients management, somatotropic axis, 24
O
Oak (Quercus pedunculata), 290–291 Ocimum basilicum (Basil), 10 Olea europaea (Olive), 246, 273 Oligoelements, 61–62, 63t, 109–110 allergic asthma, 131 Crohn’s colitis, 169 eczema, 209 esophageal varices, 211–212 lower urinary tract obstruction (LUTO), 250 oligomenorrhea, 227, 231 otitis media, 243, 246 polymenorrhea, 233 rapid transit diarrhea, 187 secretory diarrhea, 189 slow transit constipation, 159 ulcerative colitis, 173 wet cough, acute bronchitis, 148 Oligoements acne, neuroendocrine and emunctory regulation, 126t Oligomenorrhea agent, 227 alkaline diet, 231 BoF findings
examination findings, 228t history and, 228–229, 228t critical terrain, 228 drainage-decongestion-endocrine prescription, 231t exemplary prescriptions, 231 mechanisms, 228 medicinal plants, 230–231t neuroendocrine, 227, 231, 231t oligoelement, 227, 231 precritical terrain, 227 result, 228 sample treatment, 227 symptomatic, 227 symptomatic and critical terrain actions, 229–230t treatment, 227, 229 TSH-drainage, 227, 231 vaginal dysbiosis douche, 227, 229 Oral examination, 309 Oregano (Origanum vulgare), 152 Organization frameworks, 36t Origanum majorana (Marjoram), 188, 237 Origanum vulgare (Oregano), 152 Oro-pancreatic, 117 Osteocalcin, 104 Otitis media agent, 243 BoF findings examination and, 244, 245t history and, 244, 244t critical terrain, 243–244 diet, 243–244 drainage, 243, 247t essential oils, 245t exemplary prescriptions, 246 lifestyle, 246 mechanisms, 244, 246 medicinal plants, 246t neuroendocrine, 243, 247t oligoelement, 243, 246 precritical terrain, 243 result, 244 sample treatment, 243 symptomatic treatment goals, 243 Ovaries day 1-4, 219 day 5-10, 219 day 11-13, 219 day 14, 219 day 15-20, 220 day 21-24, 220 day 25-menstruation, 220 Ovulation (day 14), normal menstruation, 219 Oxygen availability, intrinsic asthma, 134 Oxytocin mechanisms and actions, 11 regulation, 11 vs vasopressin, 11
P
Pancreas examination, 309 Pancreas-sparing diet, 300–301 acne, 125
Pancreato-central nervous system, 118 Pancreato-dermato-articular, 118 Pancreato-immunity, 118 Pancreato-metabolism, 118 Pancreato-pulmonary, 118 Papaya (Carica papaya), 284 Para-alpha topical aromatherapy, 106 Para-gonadotropic axis, 133 Para-gonadotropic prescription, intrinsic asthma, 137t Parasympathetic (ρΣ) nervous system autacoid of, 4, 4f general concept of, 5t during metabolism, 4f Parasympathetic system (Para), 67 Parathyroid hormone, 23t Passiflora incarnata (Passionflower), 133, 137, 139, 249, 290 Passionflower (Passiflora incarnata), 133, 137, 139, 249, 290 Patient autonomy, 6 Pelvic basin, 46 Peppermint (Mentha piperita), 290 Peripheral axis, ulcerative colitis, 175 Peripheral glands, 21–22 Peripheral gonado-drainage, premenstrual syndromes, 237, 242 Peripheral gonadotropic hormones estrogens, 15–16 gonadal androgens, 16–17 metabolic action, 15 progesterone, 17–18 treating origin of hyperfunctioning, 15 Peripheral hormones, 27 corticotropic axis, 11–12 Peripheral thyrotropic axis, 21–22 Periwinkle (Vinca minor), 293 Permissive functions, of adrenal cortex, 11 Personality, 41 Pharmaceuticals, 64 Phosphorous, 104 Physical examination, 43 abdomen, 46, 309, 310f, 312f endo-enteric relationships, 311t approaches in daily practice, 47 auscultation, 44t bone, 45 cardiovascular system, 45 extremities, 46 face, 43–45 hair, 45 interpreting information from, 47 leg, 311, 312f methods of evaluation, 43, 44t muscles, 45 nails, 45 neurologic system, 46–47 oral, 309 pelvic basin, 46 skin, 45 temporality of exam findings, 43 thorax, 45 time scale of findings, 44t Phytotherapy, 59
326 Index
Pichi (Fabiana imbricata), 286 Pine (Pinus sylvestris), 290 Pineal gland importance, 8 indications for addressing, 9 melatonin activity, 9f treatment options, 9 Pineapple/ananas (Ananassa sativa), 283 Pinus sylvestris (Pine), 290 Pituitary activity, dopamine inhibition, 225–226 Pituitary hormones adrenocorticotropic hormone (ACTH), 10 arginine vasopressin, 10–11 follicle-stimulating hormone (FSH), 14–15 growth hormone (GH), 25 luteinizing hormone (LH), 15 oxytocin, 11 oxytocin vs vasopressin, 11 prolactin (PL), 26–27 Plantago major (Plantain), 127, 185, 246, 269, 273, 290 Platelet mobilization indexes, 115t PMS induced with anxiety asthma, 133 Polymenorrhea biology of function indexes, 234t critical terrain, 233 exemplary prescriptions, 236, 236t history and examination, 233–234, 234t mechanism, 233 medicinal plants, 235t neuroendocrine, 233 neuroendocrine regulators, 235t oligoelement, 236 polymenorrhea, 233 pre-critical terrain, 233 result, 233 sample treatment, 233 symptomatic treatment, 233, 235 terrain, 235 treatment, 235–236 utero-tissular, 233 utero-tissular prescription, 236t Polyvalent symptomatic-digestiveneuroendocrine-drainage dysbiosis, 195 dysbiosis and, 200 Populus nigra (Black poplar), 127, 290 Potassium-rich foods, 305–306, 306t Poterium sanguisorba (Salad burnet), 26, 290 Precritical terrain acne, 123 adenoma, 250 allergic asthma, 127–128 borborygmus, 151 burping (eructation), 151 Crohn’s colitis, 165–166, 167t dry cough, acute bronchitis, 139 dysbiosis, 195 eczema, 203 edema, 254 esophageal varices, 211 intrinsic asthma, 133–134, 134t lower esophageal sphincter, 213 metrorrhagia, 225–226
normal transit constipation, 153 oligomenorrhea, 227 otitis media, 243 polymenorrhea, 233 premenstrual syndromes, 237 pyloric sphincter, 215 rapid transit diarrhea, 187 rhinopharyngitis, 265 slow transit constipation, 159 tonsillitis, 273–274 wet cough, acute bronchitis, 145 Premenstrual syndromes agent, 237 BoF findings examination and, 239, 240t history and, 238–239, 239t borage oil, 237, 242 central gonado-drainage, 237, 242 critical terrain, 237–238, 238t drain, 237 exemplary prescriptions, 241–242 gonadotropic central, 237, 242t peripheral, 237, 242t regulators, 241t mechanisms, 238 medicinal plants for drainage, 242t neuroendocrine regulation, 240t peripheral gonado-drainage, 237, 242 precritical terrain, 237 result, 238 sample treatment, 237 symptomatic treatment goals, 237 treatment, 239–242 Prenatal diet, allergic asthma, 128 Prepuberty, 37 Present illness, 35 Progesterone gonadotropic axis, 79 mechanisms and actions, 17 regulation, 17–18 Prolactin, 226 in adaptation, 26 in disorders, 26 mechanisms and actions, 26 peripheral activity, 26t regulation, 27 somatotropic axis, 95 Prolactin index, 98 Prostatic enlargement LUTO (see Lower urinary tract obstruction (LUTO)) treatment, 253–254 Prostatitis agent, 260 BoF findings examination and, 260–261 history and, 260 critical terrain, 260 essential oils applications, 262 exemplary prescriptions, 262–263 lifestyle recommendations, 262t mechanisms, 260
medicinal plants, 261t neuroendocrine prescription, 262t pelvic drainage-antimicrobial prescription, 262t precritical terrain, 259–260 result, 260 sample treatment, 259 symptomatic treatment goals, 259 treatment, 261–263 Protective factors, allergic asthma, 128 Prunus africanus (African prune), 15 Prunus amygdalus (almond bud), 233 Puberty, 37, 38t Pumpkin seed oil, 233, 236
Q
Quantitative electroencephalogram (QEEG), 104 Quercus pedunculata (Oak), 10, 133, 137, 233, 246, 290–291
R
Radial gonado-thyrotropic index, 93t Raphanus niger (Black radish), 269, 291 Rapid transit diarrhea agent, 187 critical terrain, 187–188 exemplary prescriptions, 188 history, 188 lifestyle, 188 mechanisms, 188 medicinal plants, 188 precritical terrain, 187 result, 188 sample treatment, 187 symptomatic treatment goals, 187 treatment, 187 Rectal infusion, 263 Rectal suppository formula, 263 Recurrent pharyngitis, 115 Rhinopharyngitis agent, 265 BoF findings examination and, 266, 267t history and, 266 critical terrain, 265–266 diet, 266 exemplary prescriptions, 266 mechanisms, 266 medicinal plants, 267t precritical terrain, 265 predisposing factors, 265 result, 266 sample treatment, 265 symptomatic treatment goals, 265 treatment, 266 Rhodiola rosea (Goldenroot), 10, 127, 131, 133, 137, 265, 291 Ribes nigrum (Cassis), 10, 12, 127, 131, 133, 137, 148, 246, 259, 265, 273, 291 Roman Chamomile (Anthemis nobilis), 283 Rosa canina (Dog rose), 11–12, 291 Rosa damascena (Damascus rose), 16 Rosmarinus officinalis (Rosemary), 291 Rubus fruticosus (Blackberry), 273, 291 Rye (Secale cereale), 292
Index 327
S
Saffron (Crocus sativa), 233 Sage (Salvia officinalis), 291–292 Salad burnet (Poterium sanguisorba), 290 Salvia officinalis (Sage), 291–292 Salvia sclarea (Clary sage), 16, 21, 188, 233, 292 Sambucus nigra (Elderberry), 26 Satureja montana (Winter Savory), 148, 292 Sebum production, and acne, 123 Secale cereale (Rye), 292 Secretory diarrhea agent, 189 BoF findings examination and, 191, 192t history and, 191, 191t critical terrain, 189 exemplary prescriptions, 192 mechanisms, 191 neuroendocrine characteristics, 190–191t precritical terrain, 189 result, 191 sample treatment, 189 symptomatic treatment goals, 189 treatment, 191–192, 192–193t Selenium (Se) allergic asthma, 127, 131–132 polymenorrhea, 236 Selenium + Sulfur, secretory diarrhea, 189 Sequoia (Sequoia gigantea), 292 Sequoia gigantea (Sequoia), 292 Serotonin, in ANS function, 4 Serum, 104 Sex hormone binding globulin’s (SHGB) binding, 226 Sexual evolution and devolution, dehydroepiandrosterone (DHEA), 12 Short-term adaptation, 31 Silver fir (Abies balsamea/pectinata), 281 Sinusitis agent, 269–270 ANS-gallbladder drainage, 269, 272t BoF findings examination and, 270, 271t history and, 270, 270t critical terrain, 270 diet, 271 exemplary prescriptions, 271 immuno-endocrine prescription, 272t mechanisms, 270 medicinal plants, 272t precritical terrain, 269 result, 270 sample treatment, 269 symptomatic treatment goals, 269 treatment, 270–271 Skeletal muscle fasciculations, 103 Skin, 45 manifestation, acne, 123 Sleep restoration, 24 Slow transit constipation agent, 159 ANS-drainage prescription, children, 162t ANS prescription, children, 162t
BoF findings examination and, 160 history and, 160 chronic treatment, 161 critical terrain, 159 exemplary prescriptions, 161–162 mechanisms, 160 medicinal plants, ANS regulation, 162t neuroendocrine, 159 precritical terrain, 159 result, 160 sample treatment, 159 symptomatic treatment goals, 159 timely treatment, 160 treatment, 160–162 urgent treatment, 160 Somato-corticotropic coupling, 74 Somato-corticotropic indexes in prostatic adenoma, 253t in prostatic edema, 258t Somatostatin, 95 mechanisms and actions, 24 regulation, 24 Somatostatin index, 119, 120t Somatotropic axis, 95 biology of function (BoF) indexes, 95–98 cellular metabolic activity, 100t peripheral somatotropic indexes, 98, 99t prolactin index, 98, 99t somatotropic hormones effect on metabolism, 99–100t cell energy, 24 cell structure, 24 embryology, 24 glucagon, endocrine pancreas, 27 hypothalamic hormones, 24 insulin, endocrine pancreas, 28 insulin-like growth factor-1 (IGF-1), 27 insulin resistance, 25, 98 intrinsic asthma, 133 metabolism, 24 nutrients, 24 pathophysiology, 95, 96t peripheral hormones, 27 pituitary hormones, 24–27 progression of endocrine loops, 24 secretory diarrhea, 189 signs related to abdomen, 98t back, extremities, and bones, 98t chest and breast, 97t dermatologic signs, 97t head, 97t mouth, 97t temperament, 96t somatotropic endocrine function central, 95 peripheral, 95 storage of energetic material, 24 symptoms related to, 95, 96t Somatotropic weakness, 41 Spasmophilia, 67 ANS role in, 101 asthma, 128
buffering capacity, 101 constitutional hypoandrogenism, 106 diagnostic studies, 104 diet, 101 differential diagnosis, 104 electrophysiologic, 104 emunctories role in, 101–102 endocrine system role in, 101–102 evaluating, 102–103 examination, 103 functional, 107–108 GERD type 2, 216 hippus, 103, 103t hyperfolliculinic hyperthyroid hysteroid women, 105 iatrogenic causes, 109 material elements, 101 neuroendocrine adaptability, 101 observation, 103 origins of, 101 pharmaceutical treatments, 109 physiologic consequences of, 102t pure hyperfolliculinic hysteroid women, 104–105, 105t review of systems, 102 rhythmic living, 101 structuro-functional, 104–107 sympathetic dysfunction in, 102t terrain management, 102t treatments, 108–110 types of, 102 vagotonia of childhood, 106–107 Sphincter of Oddi, 114 Splanchnic congestion, 114, 309 Standard-of-care therapy, allergic asthma, 127 Stinging nettle (Urtica dioica), 293–294 Stoneseed (Lithospermum officinale), 288 Stool transit, dysbiosis, 195 Storage of energetic material buffering capacity, 6 somatotropic activity, 24 Strawberry (Fragaria vesca), 286–287 Structure, terrain, 3 Sulfur (S) allergic asthma, 131 eczema, 207 esophageal varices, 211 Syzygium aromaticum, 263
T
Taraxacum officinale (Dandelion), 5–6, 11, 292 Tarragon (Artemisia dracunculus), 133, 137, 185, 188, 284 Temperament, 41, 41t and build, corticotropic axis evaluation, 75t Terrain, 49 autonomic nervous system as calibrator, 4 buffering capacity, 6 central nervous system, 6–7 definition of, 3 emunctories, 5–6 endocrine system as regulator of, 3–4, 6 function, 3 gastrointestinal tract, 6
328 Index
Terrain (Continued) immune system, 6 metabolic activity, 49 structure, 3 treatment, 3 Testosterone adenoma, 249 vs dehydroepiandrosterone (DHEA), 12 Therapeutics, 61 aims, 61 alimentation, 62–63 chronobiology and cosmobiology, 61 clinical therapy, 61 indications for selection of, 62t lifestyle recommendations, 63–64, 64t medicinal plants, 61 oligoelements, 61–62, 63t pharmaceuticals, 64 spectrum of therapy selection, 62f Thorax, 45 Thymus, 22 Thymus vulgaris (Thyme), 6, 127, 131, 133, 137, 152, 266, 269, 292 Thyro-corticotropic indexes in prostatic adenoma, 253t in prostatic edema, 258t Thyro-drainage-digestion, exercise-induced asthma, 133 Thyroid function, otitis media, 243 Thyroid gland, 22 significance of antibodies, 22 thyroxin (T4), 22 triiodothyronine (T3), 22 Thyroid index, 50 Thyroid Mini, 52 Thyroid-stimulating hormone (TSH) drainage, oligomenorrhea, 227 endobiogenic treatment, 21 mechanisms and actions, 21 thyrotropic axis, 87 physiology and pathophysiology, 89t regulation of, 90 Thyrotropic axis acute change, 87 adaptability and growth, 18 affective states, 87 allergic asthma, 128 biology of functions (BoF) indexes, 91 calcitonin, 23t catabolic and proanabolic activity, 23–24 central thyrotropic indexes with peripheral impact, 92t central vs peripheral thyroid dysfunction, 19 disorders of adaptation, 87 disorders of growth, 87 embryology, 18 endobiogenic assessment, 87 intrinsic asthma, 133 key hormones, review of, 87 metabolism, 18 metabolites and minerals, 18 metabolites, mobilization and utilization of, 88t parathyroid and bone indexes, 93t parathyroid hormone, 23t
peripheral glands, 21–22 radial gonado-thyrotropic index, 93t rapid transit diarrhea, 188 role of, 87 in hyperthyroidism, 89t in hypothyroidism, 89t signs of, 90 head, ears, eye, nose, and throat, 91t neurologic signs, 91t by region, 92t temperament and internal mental life, 91t thyroid gland and chest, 92t symptoms related to, 90, 90t thymus, 22 thyroid gland, 22 thyroid gland and activity, index evaluating, 93t thyroid-stimulating hormone (TSH), 21, 87 physiology and pathophysiology, 89t regulation of, 90 thyrotropin-releasing hormone (TRH), 19–21, 87 physiology and pathophysiology, 88t regulation of, 90 ulcerative colitis, 174–175 vitamin D3, 23t Thyrotropic axis, emunctories by, 5 Thyrotropic disequilibrium, 107 Thyrotropin-releasing hormone (TRH) mechanisms and actions, 19–21 physiology and pathophysiology, 20t role during adaptation, 7f thyrotropic axis, 7f, 87 physiology and pathophysiology, 88t regulation of, 90 treatment, 21 Thyroxin (T4), 22 Tilia tomentosa (Linden), 293 Tissular metabolism, 8t Tongue fasciculation, 103 Tonsillitis agent, 274 BoF findings examination and, 274, 275t history and, 274 critical terrain, 274 endocrino-immune support, 276t ENT drainage-immunity, 277t exemplary prescriptions, 275 infection-endocrine prescriptions, 277t mechanisms, 274 medicinal plants, 276t precritical terrain, 273–274 result, 274 sample treatment, 273 symptomatic treatment goals, 273 treatment, 275 Topical face mask, 125, 125t Topical prophylaxis, allergic asthma, 127, 132, 132t Trauma history, 41 Triiodothyronine (T3), 22 Trousseau’s sign, 103 Tympanic membrane, polyvalent application to, 243
U
Ulcerative colitis agent, 174 ANS-cortico-thyrotropic prescription, 174t BoF findings examination and, 176, 176t history and, 175–176, 175t critical terrain, 173–175 exemplary prescriptions, 179 gonadotropic terrains, 177t hepatobiliary-pancreatic-intestinal drainage prescription, 174t mechanisms, 175 neurocorticotropic terrains, 176t precritical terrain, 173–174 psychological indexes related to, 177t result, 175 sample treatment, 173 somatotropic terrains, 177t symptomatic and somatotropic prescription, 174t symptomatic treatment goals, 173, 178t thyrotropic terrains, 177t treatment, 176–179, 178–179t Urtica dioica (Stinging nettle) leaf, 293–294 root, 293
V
Vaccinium myrtillus (Bilberry), 212, 293 Vaginal dysbiosis douche, oligomenorrhea, 227, 229 Vagotonia, 4, 106–107 allergic asthma, 127 Valeriana officinalis (Valerian), 293 Vasopressin (AVP) mechanism and actions, 11 vs. oxytocin, 11 regulation, 11 Vibernum lantanum, 21 Vinca minor (Periwinkle), 293 Viola tricolor (Wild pansy), 6, 127, 294 Viscum album (Mistletoe), 293–294 Vitamins vitamin A, ulcerative colitis, 173, 180t vitamin D, 23t Crohn’s colitis, 165 spasmophilia, 109 ulcerative colitis, 173 vitamin E rich foods, 307, 307t ulcerative colitis, 173, 180t Vitex agnus castus (Chaste tree), 133, 137, 237, 294 Vitis viniferis (Grape), 246, 273
W
Wet cough, acute bronchitis, 3 agent, 145 BoF findings examination and, 146, 147t history and, 146, 146t critical terrain, 145–146
Index 329
diet, 148 drainage prescription, 149t exemplary prescriptions, 148 mechanisms, 146 medicinal plants with for drainage, 148t for neuroendocrine regulation, 148t polyvalent symptomatic actions, 147t neuroendocrine-infection prescription, 148t precritical terrain, 145 sample treatment, 145
symptomatic treatment, 145 treatment, 146 White Deadnettle (Lamium album), 288 Wild pansy (Viola tricolor), 294 Winter savory (Satureja montana), 292 Witch hazel (Hamamelis virginiana), 287–288
Y
Yea millefolium (Yarrow), 281 Yarrow (Achillea millefolium), 281 Yellow sweet clover (Melilotus officinalis), 289
Z
Zea mays (Corn silk), 6, 21, 294 Zinc (Zn) adenoma, 254 eczema, 207 Zinc-copper (Zn-Cu) oligoelements luteal phase, 225 polymenorrhea, 233, 236 Zingiber officinale (Ginger), 21, 294