The Theory of Endobiogeny: Volume 2: Foundational Concepts for Treatment of Common Clinical Conditions 0128169087, 9780128169087

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Preface for volume 2 When I first encountered the theory of Endobiogeny, I was director of pediatric intensive care and integrative medicine at Sutton children’s hospital. I was steeped in questions of adaptation, survival, and immunity. I was also searching for answers that my training at Stanford University and clinical experience could not answer. I took a chance on Endobiogeny. More than that, I gave notice of resignation to meet my coauthor, mentor, and codeveloper of Endobiogeny, Dr. Lapraz, for the hospital administrators refused to let me attend his course. I had no understanding of what Endobiogeny was—there was nothing to read on the topic. Once at the seminar, I immediately perceived the teachings to be profound, but, lacking systematic organization and scientific references. Over the next 10 years, I set out to remedy both of these insufficiencies, as I perceived them. This four-volume series on the theory of Endobiogeny is the fruit of that determination thanks to the patient guidance and teachings I received from my mentor and friend, Jean-Claude Lapraz. Of the four volumes, this one is perhaps the closest to my original training in intensive care. The theme of this book is the practical application of Endobiogeny to issues such as adaptation and infectious disease. The theory of Endobiogeny is an emerging approach to medicine, at once scientific and humanistic, complex and practical. It is rooted in an integrative vision of physiology while placing the patient's experience of Life at the center of the evaluation. The key to the theory of Endobiogeny is the manner in which experimental and empirical observations are woven together to make sense of a phenomenon that has perplexed clinicians throughout the ages. Clinical Endobiogeny has three components: listening to the patient, examining the patient, and analysis of biomarkers using a modeling system called the biology of functions. Why study and practice Endobiogeny? In the vocation of medicine, it brings the physician a sense of intellectual fulfillment and emotional enrichment thanks to its rational and precise analytical method. In the practice of medicine, it brings satisfaction to doctor and patient by promoting a collaborative decision-making model of health. In the experience of healing, Endobiogeny allows the patient to be heard, understood, and treated as a whole person.

Details of the theory of Endobiogeny were presented in The Theory of Endobiogeny Volume 1: Global Systems Thinking and Biological Modeling for Clinical Medicine. This work, the first of three subsequent volumes, is eminently practical. They are written in a manner that allows you to transform your practice in a gradual way. In this tome, Volume 2, we focus on adaptation, defense and detoxification, and common disorders related to their dysfunction. A curated selection of polyvalent medicinal plants, minerals, and diets are presented that allow for rapid symptomatic relief and the initial treatment of terrain. In this way, you begin addressing disorders for which pharmaceutical treatments do not exist, or, for which they have not proven effective. The Theory of Endobiogeny Volume 2: Foundational Concepts for Treatment of Common Clinical Conditions is organized so that the concepts of preceding chapters are integrated into the teachings of subsequent chapters. Chapters  1 and 2 teach signs, symptoms, and biology of function indexes related to the autonomic nervous system (ANS) and corticotropic axis. These factors are key to regulation of immunity and treatment of immune dysfunction, which are discussed in Chapters 3 and 4. The basic elements of adaptation and immunity are then integrated into the notion of symbiosis, dysbiosis, and the treatment of dysbiosis—beyond probiotics—as presented in Chapters 5 and 6. Chapters 7 and 8 return to key elements of the expression of life: liver, gallbladder, and exocrine (digestive) pancreas. Here, we discuss their key roles in digestion, adaptation, and more. Specific signs and symptoms are correlated to common issues presenting in the clinic. The selection of medicinal plants, diets, and minerals for specific aspects of hepatobiliary and pancreatic dysfunction are presented to allow for a more rational selection of therapeutic interventions. With the understanding of the ANS, corticotropic axis, immunity, symbiosis, liver, and exocrine pancreas, the origin of specific infectious disorders can be explained and treated at the root cause level of dysfunction, as explained in Chapter 9. Chapter 10 introduces a second line of hormonal function: the thyrotropic axis. Along with the ANS and the corticotropic axis, it constitutes the essential trio of regulation of adaptation and immunity. Once again, detailed signs, symptoms, and biology of function indexes are discussed

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to ­recognize clinical conditions related to thyrotropic hormone dysfunction beyond T4 and T3. With this understanding of the thyrotropic axis and its relationship to calcium, Chapter  11 explores the French notion of spasmophilia. Spasmophilia explains a fundamental factor in the development of a host of chronic or degenerative disorders, viz. asthma, colitis, cancer, anxiety, depression, Alzheimer’s disease, and more. Thus, the preceding 10 chapters are integrated into the discussion of what is spasmophilia, what are its signs and symptoms, and how it is treated. To assist the new practitioner of Endobiogeny, this book contains two key resources. Chapter  12 presents a detailed case study that walks you through evaluation, treatment, and follow-up of a case of recurrent pharyngitis. Many of the theoretical concepts presented in The Theory of Endobiogeny Volume 1: Global Systems Thinking and Biological Modeling for Clinical Medicine are on display, practically applied and explained in detail. The precise meaning of aspects of childhood history, clinical ­examination signs, chronobiologic transitions, and, correlation of biology of function indexes to signs, symptoms, and

rational selection of therapeutic interventions. A concise materia medica of plants and their application to specific clinical conditions is presented in the addendum. This work is the continuation of a lineage starting with the developer of the theory of Endobiogeny, the late Christian Duraffourd, to the codeveloper of the teachings and my mentor, Jean-Claude Lapraz, to myself as a systematizer and expander of Christian’s original concepts. It grew out of decades of experience teaching Endobiogeny around the world and is the authoritative teaching on the subject. We believe that the book functions best in two ways. The first is as a desktop reference for those already trained in advanced forms of integrative medicine. The second is a starting point for those seeking a more meaningful way to practice the healing arts without leaving the profession of medicine. Upon completing this book, we hope you consider the other volumes in this series, as well as formal study and certification in clinical Endobiogeny. Kamyar M. Hedayat

Chapter 1

A clinical approach to autonomic nervous system Introduction The autonomic nervous system (ANS) calibrates five key areas: (1) endocrine system, (2) immune function, (3) neurotransmitter activity, (4) metabolism, and (5) tonus. Evaluating the activity of each aspect of ANS function can be done quickly by history, examination, or biology of functions. Because the ANS is reactive in nature, the treatment of acute exacerbations of ANS imbalances can offer rapid symptomatic relief. Chronic entrainment of dysfunction requires long-term treatment, typically with a combination of medicinal plants and psychological/lifestyle interventions. Below we present common history and physical examination findings grouped in two ways: by system and by branch of the ANS. The chapter concludes with a discussion of key indexes of the biology of functions related to ANS activity. Because the ANS, and alpha-sympathetic in particular, is so imbricate in the functioning and relaunching of central and peripheral physiology, one must carefully evaluate not only ANS activity, but also its relationship to other factors. This will more clearly elucidate specific symptoms and signs and allow for a more precise therapy. For example, when evaluating symptoms related to mood and cognition, while alpha is implicated, it is seldom the sole factor. It may be responsible for particular signs or symptoms, but its diverse activities will implicate other systems and processes. The degree to which alpha entrains the expression of one or numerous factors determines the symptom, its threshold, duration, and severity. Returning to the quadratic relationship of alpha, dopamine, thyrotropin-releasing hormone (TRH), and prolactin (The Theory of Endobiogeny, Volume 1, Chapter 3), we can discuss three common scenarios among many possibilities. There are other factors implicated but not shown (histamine, GABA, peripheral hormones as neurosteroids, etc.). In the first scenario, there is a harmonious expression of all four factors (Fig.  1.1). A well-equilibrated expression of all four factors results in optimal adaptation, one in which the organism engages and understands its environment, contextualizes it based on past experiences, ranks its

The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816908-7.00001-3 © 2019 Elsevier Inc. All rights reserved.

existential and emotional values, and then expresses adaptability of the terrain. In the second scenario, there is insufficient inhibition of dopamine. If dopamine cannot sufficiently slow down prolactin, the predominance of dopamine (­dopamine ≫ TRH > PL > alpha > peripheral adaptation response) will lead to an implosive adaptation. The cognitive function becomes disorganized and outpaces both the ability of the organism to give context to perceived or imagined aggressions and the peripheral adaptation response (Fig. 1.2). In the third scenario, there is excess TRH ­activity. When TRH predominates over dopamine: TRH ≫ PL > alpha > dopamine, the response will be an explosive adaptation. The organism will express intense outbursts of activity, emotional in nature, with poor understanding of the directionality or purpose of the behavior due to insufficient dopamine (Fig. 1.3). When reducing alpha using medicinal plants, understanding these relationships allows for a more targeted and synergistic approach to therapy. For example, in the first scenario, inhibiting alpha sympathetic, say, with Lavandula angustafolia (lavender) may be sufficient because it reduces sympathetic tone.1, 2 In the second scenario, inhibiting alpha and prolactin may be necessary. Using Lavandula angustafolia and Poterrium sanguisorba (salad burnet) would be an efficient combination. Poterium sanguisorba inhibits alpha and prolactin.1, 2 In the third scenario, using Lavandula angustafolia with Leonurus cardiaca would be efficient, as Leonorus cardiaca inhibits TRH.3

Historical findings relating to the ANS by system Symptoms related to the autonomic nervous system can be grouped together by system of the body (Table 1.1). In this way, the organic functioning of systems can be evaluated according to the cycling of both branches of the ANS. NB: The role of the factor of the ANS presented may not be the sole or exclusive factor.

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FIG. 1.1  Harmonious relationship between alpha, dopamine, TRH, and prolactin in a quadratic relationship. In the figure, alpha stimulates dopamine (red arrow) to calibrate the quality of cognition and planning in the face of an aggression. Alpha also stimulates TRH, which plays a role in the quality of the emotional perception and response. TRH makes an appeal to dopamine (broken red arrow). One reason is to regulate TRH’s stimulation of prolactin. Alpha and TRH both stimulate prolactin. Prolactin stimulates dopamine and dopamine in turn inhibits (blue arrow) prolactin. The quality of the prolactin regulation ensures adaptability, in part because it turns first to second loop. (© 2015 Systems Biology Research Group.)

FIG. 1.3  Explosive adaptation response predominated by TRH and by extension alpha sympathetic. Alpha’s stimulation of dopamine (thin red arrow) is not as great as its stimulation of TRH (medium red arrow). Alpha and TRH both stimulate prolactin. Prolactin insufficiently stimulates dopamine and dopamine insufficiently inhibits prolactin (thin blue arrow). The net effect is a higher degree of emotionality and emotivity relative to the rational cognition favored by dopamine. The end result is an explosive adaptation response, marked by intense expressions of rage. (© 2015 Systems Biology Research Group.)

Historical findings relating to the ANS by branch of the ANS Symptoms related to the ANS can also be evaluated according to the individual branch: sympathetic alpha and beta, and, parasympathetic. In this way, the totality of expression of each branch can be appreciated throughout the global organism and according to regional tendencies of expression according to the endobiogenic phenotype of the patient (Table 1.2). NB: The role of the factor of the autonomic nervous system presented may not be the sole or exclusive factor.

Physical examination findings relating to the ANS by system FIG. 1.2  Implosive adaptation with a poorly managed quadratic relationship between alpha, dopamine, TRH, and prolactin. Alpha also stimulates TRH, which plays a role in the quality of the emotional perception and response. TRH makes an appeal to dopamine (broken red arrow). Alpha and TRH both stimulate prolactin. Prolactin stimulates dopamine. There is insufficient inhibition of prolactin by dopamine, resulting in prolonged dopamine and implosive adaptation—see text for details. (© 2015 Systems Biology Research Group.)

The various signs of the ANS can be determined during the consultation. Signs related to temperament can be noted by observation (Table  1.3), by examination of the skin (Table 1.4), head (Table 1.5), chest (Table 1.6), cardiopulmonary system (Table 1.7), abdomen (Table 1.8), nervous system (Table 1.9), and miscellaneous observations (Table 1.10). NB: The role of the factor of the autonomic nervous system presented may not be the sole or exclusive factor.

A clinical approach to autonomic nervous system Chapter | 1  3

TABLE 1.1  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.

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TABLE 1.2  Symptoms related to the autonomic nervous system by aspect of the autonomic nervous system Variable

Category

Finding

State

Alpha

GI

Constipation, spasmodic

Elevated

GI

Tendency to easily vomit

Elevated

GI

Stomach ulcer

Elevated

ID

Streptococcus

Elevated

ID

Herpes

Elevated

ID

Psoriasis

Elevated

ID

Eczema

Elevated

Neuro

Migraines

Elevated

Pulm

Asthma

Elevated

Sleep

Insomnia

Elevated

CV

Hypertension

Elevated

CV

Coronary ischemia

Insufficient, blocked or delayed

Derm

Hot flashes

Elevated

GI

Diarrhea

Elevated

GI

Vomiting

Elevated

GU

Libido, absent

Insufficient, blocked or delayed

ID

Herpes, severe outbreak

Insufficient, blocked or delayed

Immune

Allergies

Insufficient, blocked or delayed

Metabolic

Diabetes

Strong

Metabolic

Fatigue, chronic

Insufficient, blocked or delayed

Pulm

Asthma

Insufficient, blocked or delayed

General

Vagal crisis: vertigo, nausea, sweats and vomiting

Strong

CV

Variceal veins

Strong

Derm

Sweat easily, esp. first part of night

Strong

Derm

Psoriasis

Strong

Derm

Eczema

Strong

GI

Aerophagy

Strong

GI

Abdominal bloating

Strong

GI

Gastritis

Strong

GI

Colitis with diarrhea

Strong

GI

insufficient digestive secretions

Weak

GU

Pelvic congestion

Strong

Neuro

Hallucinations

Weak

Pulm

Bronchitis

Strong

Sleep

Nightmares

Weak

Beta

Para

CV, cardiovascular; Derm, dermatologic; ID, infectious disease; Pulm, pulmonary; Neuro, neurological.

A clinical approach to autonomic nervous system Chapter | 1  5

TABLE 1.3  Signs related to the autonomic nervous system by noted by observation Part

Quality

Finding

Factor

Activity

Comment

Temperament

Internal state

Anxious

Alpha

Elevated

Internal state

Emotionally sensitive

Alpha

Elevated

External state

Impulsive

Beta

Elevated

Correlate with strong TRH metabolic, which lowers the threshold for expression of beta

External state

Expansiveness

Beta

Elevated

Correlate with strong GH, strong estrogen, strong androgens for the expression of the expansiveness

External state

Fidgety, can’t sit still

Beta

Elevated

Internal state

Feelings of anguish

Beta

Elevated

Internal state

Mental fatigue that blocks initiative

Beta

Insufficient: blocked or delayed

Correlated with strong histamine and/or weak cortisol; beta may be delayed and strong in its absolute expression but not as strong as beta

Internal state

Day dreams

Beta

Insufficient: blocked or delayed

Correlate with strong TRH

Internal state

Lacking desires and motivation

Beta

Insufficient: blocked or delayed

Correlated with strong histamine and/or weak cortisol; beta may be delayed and strong in its absolute expression but not as strong as beta

Internal state

Smallest effort seems huge

Beta

Insufficient: blocked or delayed

Correlated with strong histamine and/or weak cortisol; beta may be delayed and strong in its absolute expression but not as strong as beta

Internal state

Split personality

Beta

Insufficient: blocked or delayed

Correlated with strong histamine and/or weak cortisol; beta may be delayed and strong in its absolute expression but not as strong as beta

External state

Introverted

Para

Predominant

External state

Avoids speaking in public

Para

Excessive

Internal state

Timid, shy

Para

Excessive

Internal state

Weak temperament

Para

Insufficient

Aggression usually directed towards self due to difficulty expressing feelings

Voice

Volume

Weak, breathy

Beta

Insufficient: blocked or delayed

Beta may be low or merely blocked due to elevated alpha, elevated histamine, low cortisol

Body

Movement

Active with fine movements

Alpha

Elevated

Alpha strong, weak beta

Movement

Active with gross movement

Beta

Elevated

Can arise from elevated but insufficient para or strong alpha

Movement

Still

Para

Elevated

Build

Round

Para

Elevated

Round face, tendency to central abdominal fat

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TABLE 1.4  Signs related to the autonomic nervous system at the level of skin Quality

Finding

Factor

Activity

Comment

Wrinkles

Deep, vertical

Alpha

Elevated

Found on face

Sensitivity

sensitive to touch, pain, cold

Alpha

Elevated

Sensitivity

Erythema with rubbing or rolfing

Alpha

Elevated

Temperature and moisture

Cold

Alpha

Elevated

Hands, feet, knees

Cold and sweaty

Alpha

Elevated

Axillae, palms, souls of feet

Hot and without moisture

Beta

Elevated

Hands, feet, knees

Moist and often hot

Para

Elevated

Often found, correlate with beta

Cold and without moisture

Para

Insufficient

Eczema

Suppurative

Para

Elevated

Weak cortisol permissive also involved

Strength

Thin, damages easily

Para

Elevated

Due to mineral deficiency and exocrine pancreatic insufficiency

TABLE 1.5  Signs related to the autonomic nervous system at the level of head Quality

Finding

Factor

Activity

Complexion

Rosy and cold

Alpha

Elevated

Zygomatic Arch

Erythema

Alpha

Elevated

Complexion

Alternating pale and rosy

Beta

Elevated

Shape

Round

Para

Elevated

Hair quality

Fine

Para

Predominant

Pupil size, baseline

Enlarged

Alpha

Elevated

Iris

Rosette

Para

Elevated

Functionality of structural para without presuming morphologic implications

Spiculated rosette

Alpha

Elevated

An exploded or spiculated rosette around the iris represents a decimation of the parasympathetic system by alpha

Intact rosette around a spiculated rosette

Alpha

Elevated

Alpha is very strong but has not decimated para

Resistant

Beta

Elevated

In the face of elevated TSH

Sinks to pressure

Para

Elevated

Reduced

Para

Elevated

Enlarged

Para

Insufficient

Far sighted

Para

Elevated

Eye pressure

Pupil size, baseline

Vision

Part

Quality

Finding

Factor

Activity

Ears

Color

Rosy

Alpha

Elevated

Cheeks

Complexion

Rosy and warm

Beta

Elevated

Comment

A general tendency, not strictly correlated

May also represent weak alpha

Tendency

Comment

A clinical approach to autonomic nervous system Chapter | 1  7

TABLE 1.5  Signs related to the autonomic nervous system at the level of head—cont’d Part

Quality

Finding

Factor

Activity

Comment

Lips

Size

Small

Beta

Diminished

Weak beta in structure

Moisture

Dry

Alpha

Elevated

With pancreatic and intestinal troubles

Orientation

Introverted upper lip, extroverted lower lip

Alpha, para

Elevated

Lower lip extroverted: very strong baseline para, with exocrine pancreatic and intestinal congestion → strong carnal desires; upper lip introverted: strong reactional alpha with blocked beta: tendency to guard emotions in the interior, to be in a defense state of adaptation, in fear of revealing oneself

Orientation

Extroverted upper lip, introverted lower lip

Alpha, para

Elevated

Para and alpha are both elevated but at a closer level of equilibrium than above; lower lip introverted: suppress their carnal desires; upper lip extroverted: are willing to externalize their emotions but not their desires

Orientation

Extroverted, upper and lower

Beta

Elevated

Beta > alpha, para, with a tendency towards externalizing emotions and carnal desires, with exocrine pancreatic and intestinal congestion, tendency towards womanizing, being hypersexualized extroverted in their receptiveness and tendency towards carnality, but not necessarily extroverted in their physical actions, i.e., they may wish to be seduced, but not be a seducer

Mucosa, oral

Secretions

Increased

Para

Elevated

Palate, hard

Color

Pallor

Alpha

Elevated

Vascularity

Varicosities

Alpha

Elevated

Lymph nodes

Lymph nodes palpable

Alpha

Elevated

Subman-dibular

ANS

TABLE 1.6  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

Orientation

Concave sternum

Beta

Weak

Orientation

Extroverted Xyphoid

Beta

Predominant

Xyphoid

Comment

Structural vagotonia is the initiator; Change: consequence of vagal stimulation of somatotropic axis (without prejudging parts stimulated, level of function or equilibration)

And/or with weak beta in structure

Structural beta

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TABLE 1.7  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

Rate

Heart rate slow

Para

Elevated

Rhythm

Palpitations

Beta

Elevated

Rhythm

Extrasystolic beats

Para

Elevated

Width

Pulse narrow

Alpha

Elevated

Amplitude

Pulse bounding

Beta

Elevated

Strength

Pulse weak

Para

Insufficient

Width

Pulse full

Para

Elevated

Aorta

Bruit

Bruit, abdominal

Alpha

Elevated

Artery

Blood pressure

Blood pressure weak

Para

Elevated

Systolic and diastolic

Blood pressure

Blood pressure weak

Para

Insufficient

Normal systolic, weak diastolic, wide pulse pressure

Vein

Tone

Veins dilated

Alpha

Insufficient

Veins

Varicosity

Veins varicose

Para

Excessive

Expiration

Duration

Longer than inspiration

Alpha

Elevated

Inspiration

Duration

Longer than expiration

Para

Elevated

Pulse

Comment

Correlate with liver congestion and/or elevated estrogen

TABLE 1.8  Signs related to the autonomic nervous system at the level of the abdomen Part

Quality

Finding

Factor

Activity

Comment

General

Stomach

Bloating

Para

Elevated

Splanchnic

One-third distal between xyphoid and umbilicus, across entire upper abdomen

Pain on palpation

Beta

Elevated

Hepato-pancreatic congestion

Liver

Costal margin, mid-point to distal

Pain on palpation

Alpha

Elevated

Congestion, liver, toxicity

Costal margin, medial to mid-point

Pain on palpation

Alpha

Elevated

Congestion, liver, circulatory

General

Murphy’s point

Pain on palpation

Alpha Para

Elevated

Spasmophilic state with general visceral congestion

Peri-umbilical, right

Two-third distal to dividing line between mid-costal point and umbilicus

Pain on palpation

Alpha

Elevated

A clinical approach to autonomic nervous system Chapter | 1  9

TABLE 1.9  Signs related to the autonomic nervous system at the level of the other aspects of the nervous system Part

Quality

Finding

Factor

Activity

Origin

Glabellar tap

Upper lid

Eyelid response rapid

Alpha

Elevated

ANS

Eye

Pupil

Dilated in ambient light

Alpha

Elevated

ANS

Pupillary light reflex

Hippus, rapid

Alpha, para central

Elevated

ANS

Hippus represents central alpha: central + peripheral para sympathetic activity; compare with peripheral moisture of hands, feet for para

Pupillary light reflex

Hippus, sustained

Alpha, para central

Elevated, in permanent opposition to each other

ANS

Hippus represents central alpha: central + peripheral para sympathetic activity; compare with peripheral moisture of hands, feet for para

Fasciculations

Present

Alpha, para

Disequilibrium

ANS

Implicates a spasmophilia

Tremor

Present

Alpha

Elevated

ANS

fingers

Tremors, gross

Beta

Elevated

ANS

Tongue

Hands

Comment

TABLE 1.10  Signs related to the autonomic nervous system at the level of miscellaneous systems Part

Quality

Finding

Factor

Activity

Hands

fingers

Tremors, gross

Beta

Elevated

Secretions

Mucous membranes

Dry

Alpha

Elevated

Mucous membranes

Increased

Para

Elevated

Sweating

General

Increased

Para

Elevated

Muscle

Development

Underdeveloped

Para

Insufficient

Biology of functions indices related to the ANS There are a number of indexes in the biology of functions that model sympathetic activity. Five key indexes are discussed in Table 1.11.

A discussion regarding key indices Thyroid relaunching and thyroid relaunching corrected indexes These indexes evaluate the role of alpha in central physiology in relaunching TRH. This is discussed in the beginning of the chapter (cf. Figs. 1.1–1.3).

Comment

Particularly in the first part of the evening

The leukocyte mobilization index (LMI), platelet mobilization index (PMI), and starter index evaluate the peripheral roles of alpha- and beta sympathetic in adaptation.

Leukocyte mobilization index It expresses the liberating capacity of leukocyte sequestered in the splanchnic relative to the hepatic space. Leukocytes are liberated by alpha sympathetic activity. The index evaluates the role of alpha sympathetic in immediate adaptation1 (Fig. 1.4). Alpha-sympathetic demarginates leukocytes that are attached to the endothelial lining of the vasculature. This allows for an instantaneous increase in the adaptation capability of the organism without making new white blood cells in the bone marrow. Owing to the volume of

TABLE 1.11  Some indexes of the biology of functions related to the autonomic nervous system Index

Definition

Positive correlation

Inverse correlation

Lymphocytes

ANS: central Thyroid relaunching

It measures the level of reactivation of the thyrotropic axis by the locus ceruleus (origin of alpha sympathetic) due to exogenous demands

Monocytes

Thyroid relaunching corrected

It measures the endogenous part of solicitation of the thyrotropic axis by the locus ceruleus. By extension, it indicates the level of endogenous disadaptation of the organism and be implication, the relative role of emotionality in relaunching TRH

TRH reactivation index

Leukocyte mobilization

It expresses the demargination capacity of leukocytes from the splanchnic bed relative to those in the perihepatic circulation; and by extension the demargination capacity of the elements of reserve relative to the need to produce those elements. The lower it is, the more adaptive alpha sympathetic activity is within the splanchnic bed. The higher it is, the greater the role of alpha sympathetic

Hemoglobin, neutrophils

White blood cells

Platelet mobilization

It expresses the demargination capacity of platelets sequestered in the splanchnic space relative to those sequestered within the spleen. By extension to demargination capacity of the elements of reserve relative to the need to produce those elements. The lower it is, the more dysfunctional the response to an aggression is by beta sympathetic. The higher it is, the greater the role of beta

Platelets

Red blood cells

Starter index

It expresses the relative predominance of glucose mobilization to start the adaptation response, of glucagon relative to adrenaline

Leukocyte mobilization

Platelet mobilization

ANS: peripheral

FIG.  1.4  Schematic representation of the leukocyte and platelet mobilization indexes. The leukocyte mobilization index reflects the role of alphasympathetic in demarginating leukocytes from the splanchnic endothelium. Leukocytes play a role in immunity. Alpha also can stimulate release of leukocytes from the perihepatic circulation. It also stimulates adrenaline, e.g., beta sympathetic. Beta stimulates release of platelets in reserve from the spleen. Platelets carry clotting factors, but also adsorb to their surface calcium and other elements that contribute to the buffering capacity and adaptation. Beta also stimulates glucagon from the pancreas. Glucagon and beta both stimulate the release of glucose from the liver. This assists in adapting the production of ATP at the cellular level, which also assists in adaptation. (Modified and reproduced from Koeppen B, Stanton, B. Berne and Levy Physiology, 6th ed. Elsevier; 2009. © 2015 Systems Biology Research Group.)

A clinical approach to autonomic nervous system Chapter | 1  11

s­planchnic circulation vs. hepatic circulation, the number of sequestered leukocytes in the splanchnic bed is considerably larger. Therefore, it is the preferred source for augmenting circulating leukocytes. Index high ● Alpha liberating leukocytes more from the splanchnic than hepatic circulation Index low ●

● ●

Adaptative alpha soliciting leukocytes from the perihepatic circulation more than from the splanchnic circulation Increased likelihood of hepato-splanchnic congestion Greater reliance on de novo production of leukocytes from the bone marrow than liberation them from splanchnic reserve

Platelet mobilization index It expresses the liberating capacity of platelets sequestered in the splanchnic vs. splenic space1 (Fig. 1.4). As alpha does with leukocytes, so beta liberates platelets. Recall that while platelets are made in the bone marrow, its endocrine regulator, thrombopoietin, is made in the liver. Thus, the liver is implicated when the index is low. Because of the sequential relationship between alpha and beta, platelet mobilization should be evaluated in relationship to both the LMI and the starter index (cf. below). Index high ●

● ●

Beta liberating platelets more from the splanchnic than splenic circulation Favors an acute stress Often seen in children

Index low ●

●

Beta liberates platelets more from the splenic circulation than the global splanchnic, which is not as efficient given the relative circulatory volume and quantity of platelets in each area. Beta is blocked or delayed.

Table 1.12 presents some possible interpretations combinatorial interpretations of various values of the LMI and PMI.

Starter index The starter index evaluates three levels of function, the first directly, the second two indirectly. In both cases, there is an implication of solicitation of the liver for glycogenolysis and production of adenosine triphosphate (ATP) from glucose.

TABLE 1.12  Interpretation of the leukocyte and platelet mobilization indexes LMI

PMI

Interpretation

⇧

⇧

General sympathetic activity increased on splanchnic bed

⇧

⇔

Delayed βΣ

⇧

⇩

Blocked βΣ, favors spasmophilia

⇩

⇩

Adaptative hyper-αΣ state, favors global splanchnic congestion

LMI, leukocyte mobilization index; PMI, platelet mobilization index; ⇧, high; ⇩, low; ⇔, normal.

splenic circulation in response to all aggressions at the tissue level, be it direct or indirect in nature.

Glucagon vs adrenaline By extension, it witnesses the relative functional level of glucagon (pancreas on liver) in relationship to that of adrenaline (beta on liver) in the installation of the general adaptation syndrome, and, as a result, of their respective thresholds of response to these endogenous or exogenous solicitations.

Energy calibration By extension, it witnesses the relative level of priority of the adaptative responses of energetico-metabolic (TRH-glucagon) in relationship to neuroendocrine (sympathetic-cortisol). The formula for the starter index is LMI/PMI. When evaluating the value of the starter index, one must also look at the quantitative value of two indices that make up this index (Table 1.13). NB: normal value for all three indexes is 0.85–1.15. In each case, the value of the starter index is normal. In the first presentation, the value of the LMI and PMI is also normal. The conclusion is that the relative role of the liver, spleen, and splanchnic bed, of glucagon and adrenaline, of TRH and cortisol on the splanchnic system is proportional in relationship to each other in adaptation because the starter index is within normal limits. Because the LMI

TABLE 1.13  A normal starter index due to three different combinations of values

Liver vs spleen It expresses the relative part of hepatic solicitation of the splanchnic system in relationship to its solicitation of

High low values presented in red/blue respectively.

12  The Theory of Endobiogeny

and PMI are also within normal limits, one may conclude that this proportionality is balanced and favorable for the system. No treatment is required. In the second presentation, the LMI is elevated, the PMI within normal limits. The conclusion is that overall, the relative role of glucagon in relationship to adrenaline and of TRH in relationship to cortisol on the splanchnic system is proportion, because the starter index is normal. However, it is not balanced, because it is achieved with elevated alphasympathetic expression to achieve this level of adaptive capability. In the long term, this could have consequences for the organism. Treatment depends on if the alpha-­sympathetic activity is adaptive or adaptative; if adaptative, use alphasympatholytic plants. Many of the signs and symptoms noted earlier in this chapter would be suggestive of an adaptative expression of alpha and hence the need to treat. In the third presentation, both LMI and PMI are critically low and yet the starter index is normal. The conclusion is that the relative role of glucagon in relationship to adrenaline and of TRH in relationship to cortisol on the splanchnic system proportional, again, because the starter index is normal. However, the relationship of alpha and beta is not balanced nor favorable for the organism. It is an adaptative hyper-alpha-sympathetic activity that is constricting the splanchnic bed and actually blocking the demarginating leukocytes and platelets. Or, conversely, the rate of production is diminished, or, the rate of destruction of these elements is increased, or, both. One must evaluate quantitative factors such as the white blood cell count and different by absolute count, as well as the absolute platelet count. Treatment requires the use of plants that are alpha sympatholytic and splanchnic decongestants. German chamomile (Matricaria recutita) and Roman chamomile (Anthemis nobilis) contain both properties. There are numerous medicinal plants that can be used in combination to achieve the same effect. 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 PMI is still low, use beta agonist plants such as cinnamon (Cinnamoma zeylanicum)4 or bogbean (Menyanthes trifoliata).1, 5

Conclusion The ANS plays a role in both the structural foundations of the organism as well as its functional modes of expression. According to the theory of endobiogeny, one may evaluate the levels of ANS activity both centrally and peripherally, in thought, comportment, digestion, respiration, cardiovascular activity, etc. In addition to what is obtained from history and exam, the biology of functions offers several mathematical representations of alpha and beta sympathetic activity in adaptation. With these levels of assessment, personalized and targeted therapies can be selected to treat the levels and areas of autonomic disequilibrium. The efficacy of therapy can be tracked objectively over time with the biology of functions.

References 1. Duraffourd C, Lapraz JC. Traité de Phytothérapie Clinique: Médecine et Endobiogénie. Masson ed. Paris: Masson; 2002. 2. Lapraz  JC, Carillon  A, Charrié  J-C, et  al. Plantes Médicinales: Phytothérapie Clinique Intégrative et Médecine Endobiogénique. Paris: Lavoisier; 2017. 3. Wojtyniak  K, Szymanski  M, Matlawska  I. Leonurus cardiaca L. (motherwort): a review of its phytochemistry and pharmacology. Phytother Res. 2013;27(8):1115–1120. 4. 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. 5. Lapraz J-C, de Clermont Tonnerre M-L. La Médecine Personnalisée: Retrouver et Garder la Santé. Paris: Odile Jacob; 2012.

Chapter 2

A clinical approach to the corticotropic axis Introduction The corticotropic axis is known as an axis of immediate and medium-term endocrine adaptation. In clinical consultation, especially when time is limited, evaluating the expression of this activity can be of value in addressing symptoms. However, the role of the corticotropic axis is much broader (The Theory of Endobiogeny, Volume 1, Chapters 6 and 10). Recalling the fullness of its activities, the Endobiogenist can address multiple areas of disequilibrium and disease at the level of critical terrain. The four general categories of corticotropic activity to evaluate are (1) disorders of adaptation, (2) grand phases of transition, (3) affection, and (4) comportment. In the historical and exam findings, one will find many clues to these states and the implication of this axis. With the indexes of the biology of functions, one will find confirmation and an objective method of evaluating the evolution of the corticotropic axis to treatment. Disorders of adaptation (The Theory of Endobiogeny, Volume 1, Chapter 12) include the critical terrains of allergic asthma (The Theory of Endobiogeny, Volume 3, Chapter 2), ulcerative colitis, and physiologic depression (The Theory of Endobiogeny, Volume 3, Chapters  11 and 14). In these conditions, one sees inappropriate levels of corticotropic solicitation and response. Both adrenocorticotropic hormone (ACTH) and cortisol will be most implicated in these conditions. The grand phases of transition (The Theory of Endobiogeny, Volume 1, Chapters  6 and 13) implicate the role of adrenal androgens in the grand transitions of life: fetal, birth, adolescence, adulthood, gonadopause, and deinstallation of life. Typically, in these states, one will note a disorder of excessive or insufficient adrenal androgen activity. Or, may observe an adaptative alpha sympathetic tone required to achieve an appropriate level of adrenal androgen activity.

The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816908-7.00002-5 © 2019 Elsevier Inc. All rights reserved.

States of affection refer to various conditions of anxiety, fear, and nervous asthenia. Because of the constant and direct relationship with alpha-sympathetic with the corticotropic axis at all levels, these emotional states tend to affect the corticotropic axis. These conditions most often reflect a disadaptation of cortisol in and of itself (excessive or insufficient), or, of the ratio of adaptive cortisol to global output of the adrenal cortex (cf. Biology of Functions later in this chapter). Finally, states and traits of comportment refer to expressed qualities of personality observed through the behavior of the patient.

Historical findings by system Historical findings by systems are presented in Table  2.1. NB: The indication of a single hormone is not indicative of it being the sole determinant of the finding.

Historical findings by hormone Historical findings of the corticotropic axis are presented in the following tables: melanocyte stimulating hormone (Table  2.2), ACTH (Table  2.3), adrenal androgens (Table 2.4), and cortisol (Table 2.5).

Evaluation of the corticotropic axis Evaluation of the corticotropic axis by examination or observation is presented in Tables 2.6–2.14: general observation and temperament (Table  2.6), skin (Table  2.7), head and neck (Table 2.8). chest and cardiovascular (Table 2.9), abdomen (Table  2.10), fat distribution (Table  2.11), back (Table  2.12), extremities (Table  2.13), and miscellaneous findings (Table 2.14).

13

14  The Theory of Endobiogeny

TABLE 2.1  Historical findings of the corticotropic axis by system Category

Finding

Variable

State

Blood

Elevated serum Na

ACTH

Increased

Cholesterol, elevated

Cortisol

Elevated

Dark hair at birth

Adrenal androgens

Increased

In structure, hyperfunctioning, but only if there are other signs of general structural adrenal androgenism, e.g., dark hair, short and stubby fingers, short distal phalanges of fingers, short necked, etc.

Blond hair at birth

Adrenal androgens

Efficient

In structure, it represents efficient adrenal androgen activity, particularly in patients of Northern European heritage who genetically have less sensitivity to adrenal androgens on the skin and hair. In function, in may represent a hyperfunctioning adrenal: hyperfunctioning cortisol that blocks MSH due to anabolic adrenal insufficiency

Fair complexion that darkens

MSH

Increased

To re-adapt the adrenal gland; starts after 10 months of age, includes color of eyes

Darker complexion that lightens

Cortisol

Increased

As adrenals are re-adapted, cortisol blocks MSH hence the reduction of pigmentation

Palpitations

ACTH

Elevated

Hypotension

ACTH

Insufficient

Hypertension, arterial

Cortisol

Elevated

Pruritis on thighs

ACTH

Elevated

Acne, back

ACTH

Elevated

Striae, colored

ACTH

Elevated

Eczema

ACTH

Elevated

Psoriasis

ACTH

Elevated

Endocrine illnesses

ACTH

Elevated

Easy bruising

Cortisol

Elevated

Acne

Cortisol

Insufficient

In its antiinflammatory activity

Eczema

Cortisol

Insufficient

Absolute, or relative to anabolic adrenal steroid activity

Psoriasis

Cortisol

Excessive

But unable to sufficiently adapt the organism to an adaptation demand

Delay in puberty

Cortisol

Insufficient

Cushing’s disease

Cortisol

Elevated

Energy

Easily fatigued, weak

Cortisol

Insufficient or excessive

GI

Congestion of gastric crux

ACTH

Elevated

ID

Mycotic infections

Cortisol

Elevated

Tendency towards infections

Cortisol

Insufficient or excessive

Insufficient: inability to adapt and mobilize immune activity to the adaptation demand Excessive: suppression, sequestration or apoptosis of elements of immunity

Herpes

Cortisol

Excessive

Cf. above, especially on Thymus and T-lymphocytes

Childhood

CV

Derm

Endocrine

Comment

Particularly root of thighs, trunk

Endocrine maladies involving elevated cortisol

Insufficient: inability to adapt the organism to adaptation demands Excessive: suppressed insulin resistance with impaired distribution of sufficient glucose to brain

A clinical approach to the corticotropic axis Chapter | 2  15

TABLE 2.1  Historical findings of the corticotropic axis by system—cont’d Category

Finding

Variable

State

Comment

Metabolic

Hypoglycemia

ACTH

Insufficient

Also evaluate for insufficient cortisol

Thinness

Cortisol

Excessive

Blocks or delays anabolism

Diabetes

Cortisol

Excessive

Due to hyperglycemia and installation of insulin resistance; may be constant or intermittent

Fatigue, chronic

Cortisol

Elevated

Correlate with low insulin resistance (cf. easily fatigued)

Psych

Depression

Cortisol

Insufficient or excessive

Insufficient: inability to adapt the organism to adaptation demands Excessive: excessive adaptation response

Skeletal

Osteoporosis with spinal pain

Cortisol

Excessive

Risk of fracture

Cortisol

Elevated

Early wakening

ACTH

Elevated

Sleep

TABLE 2.2  Historical findings of the corticotropic axis related to MSH Category

Finding

State

Comment

Childhood

Fair complexion darkens

Increased

To re-adapt the adrenal gland; starts after 10 months of age, includes color of eyes

TABLE 2.3  Historical findings of the corticotropic axis related to ACTH Category

Finding

State

Blood

Elevated serum sodium

Increased

CV

Palpitations

Elevated

Hypotension

Insufficient

Pruritis on thighs

Elevated

Acne, back

Elevated

Striae, colored

Elevated

Eczema

Elevated

Psoriasis

Elevated

Endocrine illnesses

Elevated

GI

Congestion of gastric crux

Elevated

Metabolic

Hypoglycemia

Insufficient

Sleep

Early wakening

Elevated

Derm

Comment

Particularly root of thighs, trunk

Endocrine maladies involving elevated cortisol

Tendency; look for low cortisol

16  The Theory of Endobiogeny

TABLE 2.4  Historical findings of the corticotropic axis related to adrenal androgens Category

Finding

State

Comment

Childhood

Dark hair at birth

Increased

In structure, hyperfunctioning, but only if there are other signs of general structural adrenal androgenism, e.g., dark hair, short and stubby fingers, short distal phalanges of fingers, short necked, etc.

Childhood

Blond hair at birth

Efficient

In structure, it represents efficient adrenal androgen activity, particularly in patients of Northern European heritage who genetically have less sensitivity to adrenal androgens on the skin and hair. In function, in may represent a hyperfunctioning adrenal: hyperfunctioning cortisol that blocks MSH due to anabolic adrenal insufficiency

TABLE 2.5  Historical findings of the corticotropic axis related to Cortisol Category

Finding

State

Blood

Cholesterol, elevated

Elevated

Childhood

Darker complexion that lightens

Increased

CV

Hypertension, arterial

Elevated

Derm

Easy bruising

Elevated

Acne

Insufficient

In its antiinflammatory activity

Eczema

Insufficient

Absolute, or relative to anabolic adrenal steroid activity

Psoriasis

Excessive

But unable to sufficiently adapt the organism to an adaptation demand

Delay in puberty

Insufficient

Cushing’s disease

Elevated

Energy

Easily fatigued, weak

Insufficient or excessive

ID

Mycotic infections

Elevated

Tendency towards infections

Insufficient or excessive

Insufficient: inability to adapt and mobilize immune activity to the adaptation demand Excessive: suppression, sequestration or apoptosis of elements of immunity

Herpes

Excessive

Cf. above, especially on Thymus and T-lymphocytes

Diabetes

Excessive

Due to hyperglycemia and installation of insulin resistance; may be constant or intermittent

Fatigue, chronic

Elevated

Correlate with low insulin resistance (cf. easily fatigued)

Psych

Depression

Insufficient or excessive

Insufficient: inability to adapt the organism to adaptation demands Excessive: excessive adaptation response

Skeletal

Osteoporosis with spinal pain

Excessive

Risk of fracture

Elevated

Endocrine

Metabolic

Comment

As adrenals are re-adapted, cortisol blocks MSH hence the reduction of pigmentation

Insufficient: inability to adapt the organism to adaptation demands Excessive: suppressed insulin resistance with impaired distribution of sufficient glucose to brain

A clinical approach to the corticotropic axis Chapter | 2  17

TABLE 2.6  Observational findings of the corticotropic axis Part

Quality

Finding

Factor

Activity

Origin

Comment

Temperament

External state

Extroverted

ACTH

Predominant

Pituitary

Strong CRH relaunching of ACTH with a good cortisol response

Easily irritated and expresses it

DHEA

Excessive

ANS

Correlate with periodic expressions of beta

Easily irritated and cries afterward

DHEA

Excessive

ANS

Correlate with strong estrogen and/ or weak gonadal androgens

Easily irritated but does not express irritation

DHEA

Excessive

Adrenal

With low or blocked beta

Difficult with adaptation

ACTH

Insufficient

Pituitary

Evaluate for signs of Weak cortisol, elevated prolactin

Depressive tendency, severe

ACTH

Elevated or insufficient

Pituitary

Evaluate for signs of Weak cortisol

Easily overreacts

Cortisol

Excessive

Adrenal

The relative rate of rise in time more than the global daily expression of cortisol

Depressive feeling

Cortisol

Disadapted

Adrenal

Anhedonia, lack of reactivity

Cortisol

Insufficient

Adrenal

Corpulent

Cortisol

Elevated

Adrenal

Correlate with strong insulin/low insulin resistance, weak thyroid activity, often with abundant growth factors

Thin

Cortisol

Excessive or insufficient

Adrenal

Excessive: Blocks anabolism Insufficient: Insufficient permissivity of metabolism

Internal state

Body

Build

TABLE 2.7  Observational findings of the corticotropic axis at the level of skin Disorder

Finding

Factor

Activity

Comment

Eczema

Flexor surfaces

ACTH

Elevated

In addition to strong para and pancreatic congestion; Role of ACTH may be witnessing the role of corticotropic development earlier in life

Lesions

Forehead

ACTH

Elevated

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

MSH

Elevated

Hyper, palmar crease

MSH

Elevated

Hyper, striae

ACTH

Elevated

Particularly found on trunk

Hyper, purple

Cortisol

Elevated

Particularly on breasts, flank and abdomen

Hypo

MSH

Insufficient

Depigmentation

ACTH

Insufficient

Correlate with elevated adrenaline and estrogen

Particularly areolae, genitals; correlate with weak cortisol

18  The Theory of Endobiogeny

TABLE 2.8  Observational findings of the corticotropic axis at the level of head and neck Part

Quality

Finding

Factor

Activity

Face

Shape

Full moon

Cortisol

Excessive

Shape

Square and angulated

Androgens

Predominant

Zygomatic arch

Adiposity

Cortisol, adaptative

Elevated

Quantity

Hirsutism

Androgens

Elevated

In women, in an absolute sense; appearance of hair depends on the androgens (adrenal vs gonadic)

Quality

Coarse

Androgens

Predominant

The relationship is specifically adrenal androgens > gonadal androgens

Color

Dark

Androgens

Predominant

The relationship is specifically adrenal androgens > gonadal androgens

Color

Blond

Adrenals

Efficient

In function, hyperfunctioning adrenal activity; may simply represent hyperfunctioning cortisol that blocks MSH with global adrenal insufficiency; look for other signs of cortisol and general adrenal activity

Pilosity

Bushy

ACTH

Elevated

In face of strong TRH and strong GH

Length

Touches at midline

DHEA

Elevated

Correlate with elevated ACTH

Coarseness

Coarse

Androgens

Elevated

Color

Darker

Androgens

Elevated

Eye

Iris

Melanic spots

MSH

Elevated

Ears

Antitragus

Hair

ACTH

Elevated

Lips

Size

Thin

Cortisol

Elevated

Elevated circulating cortisol with poor peripheral cortisol sensitivity in structure

Neck

Posterior adiposity

Adiposity present

ACTH

Strong

Often seen with a strong adrenal response—correlate with elevated cortisol

Thickness

Thick

Cortisol

Strong

Evaluate supraclavicular space and abdominal fat

Length

Short

Androgens

Strong

Look for other signs of structural hyperandrogenism such as shorted distal phalange of fingers, dark hair, thick hair, etc.

Hair

Eyebrow

Eyelashes

Comment

In the face of strong GH, PL, with androgens that predominate, the bones appear angulated

TABLE 2.9  Observational findings of the corticotropic axis at the level of chest and cardiovascular systems Part

Quality

Finding

Factor

Activity

Comment

Clavicle

Supraclavicular space

Filled out, not hollow

Cortisol

Increased

Evaluate thickness of neck and abdominal fat over mid-region

Inferior chest

Hair

Hair, inferior chest

DHEA

Elevated

Breasts

Asymmetry

Right > left

ACTH

Predominant

Coloration

Striae, purple

Cortisol

Excessive

Areola

Coloration

Hypopigmented

ACTH

Insufficient

Artery, carotid

Bruit

Bruit, carotid

Cortisol, lipids

Elevated

FSH also involved in laterality

A clinical approach to the corticotropic axis Chapter | 2  19

TABLE 2.10  Observational findings of the corticotropic axis at the level of abdomen Part

Quality

Finding

Factor

Activity

Comment

Ribs

Left, distal, midaxillary

Painful

Cortisol

Excessive or insufficient

Zone of distress: the closer the tenderness is to the umbilicus, the deeper the installation of distress

Right distal intercostal space, lateral to midline

Painful

Cortisol

Elevated

Intermittent surges in cortisol related to anger and its solicitation of the liver

Ileocecal junction

Pain on palpation

ACTH

Elevated

In structure, for solicitation of aldosterone and absorption of fluid and electrolytes

Rectosigmoid area

Pain on palpation

ACTH

Elevated

In function, for solicitation of aldosterone and absorption of fluid and electrolytes

Colon

N.B.: Anterior projection of organs represents the current anatomical congestion and/or state of dysfunction.

TABLE 2.11  Observational findings of the corticotropic axis at the level of fat distribution Part

Quality

Finding

Factor

Activity

Comment

Viscera

Omental

Increased

Cortisol

Elevated

Hypertrophic obesity

Face

Cheeks

Increased

Cortisol

Elevated

Upper body

General

Increased

Cortisol

Elevated

Ventral

Supra-umbilical

Increased

Cortisol

Elevated

Hypertrophic obesity

TABLE 2.12  Observational findings of the corticotropic axis at the level of the back Area

Quality

Finding

Factor

Activity

Comment

C8-T2

Spine

Buffalo hump

ACTH

Excessive

Strong cortisol activity

T1-T12

Curvature

Scoliosis

Cortisol

Strong

In the face of peripheral hypothyroidism with strong beta and insufficient para-alpha; can be linked in preadolescent girls with a troubled relationship with the father

Scapula, right

Inferiomedial, T10 (scapular tip)

Pain on palpation

ACTH, structure

Elevated

Congestion, Ileocecal junction

ACTH, function

Elevated

Congestion, rectosigmoid area of colon

Level of T4

Pain on palpation

Cortisol

Excessive or insufficient

Wider, deeper the muscular contraction, the deeper the central depression is; recommend massage focused on that area

Scapula, left Scapula, left

N.B.: Posterior projection of organs represents chronic congestion and/or state of dysfunction; C, cervical; T, thoracic.

20  The Theory of Endobiogeny

TABLE 2.13  Observational findings of the corticotropic axis at the level of the extremities Part

Quality

Finding

Factor

Activity

Comment

General

Tissues

Adiposity, general

Cortisol

Elevated

Often seen with muscle wasting

Arm

Proximal

Adiposity

Cortisol

Elevated

Often seen with muscle wasting

Elbow

Adiposity

Cortisol

Elevated

Arm, distal

Hair

DHEA

Predominant

Hand, left

Ring to index finger ratio

>1

Androgens

Elevated

Leg

Leg, distal

Hair

DHEA

Predominant

Distal, 0.5–1 cm lateral from midline, 2 cm above patella

Pain on palpation

Cortisol

Elevated

Relates to fetal androgens; correlates with more “boy-like,” i.e., aggressive play in girls between 3 and 5 years of age

TABLE 2.14  Observational findings of the corticotropic axis at the level of miscellaneous areas Part

Quality

Finding

Factor

Activity

Bone

Facial features

Angulated

Adrenal androgens

Predominant

Muscle

Mass

Wasting

Cortisol

Elevated

Insufficient androgens + hyper-TRH

Memory

Efficiency

Poor

ACTH

Excessive

Correlated with strong MSH, possibly insufficient beta, low or excessive cortisol, hyperalpha with diminished histamines, insufficient dopamine, weak prolactin

Biology of functions indices related to the corticotropic axis Key indexes related to central and peripheral modeling of corticotropic activity is reviewed in Table 2.15.

βMSH/αMSH index This index evaluates the alpha and beta sympathetic like activity centrally in the brain, and by extension, alpha sympathetic and thyrotropin-releasing hormone (TRH) as the central beta analog (The theory of Endobiogeny, Volume 1, Chapter  3). Melanocyte stimulating hormone (MSH) is a derivative of pro-opiomelanocortin (POMC) (The theory of Endobiogeny, Volume 1, Chapter 6). Amongst the various products, two are of relevance here: αMSH and βMSH. αMSH stimulates the pituitary. It regulates the proportionality of cortisol response to ACTH. During sleep, αMSH helps maintain permissive cortisol activity during the refractory ACTH period installed by melatonin. When the index is low (αMSH > βMSH), it suggests an insufficient of GABA, a central neurocalmative (Fig. 2.1). Clinically, it favors the use of GABAergic anxiolytics,1 such as Passiflora

Comment

­incarnata2 (passionflower), Artemisia dracunculus3 (tarragon), and Melissa officinalis4, 5 (lemon balm). βMSH assists in adaptation by amplifying the two catabolic axes. In the corticotropic axis, it is the “companion of ACTH,” rising and falling commensurately with it.6 βMSH amplifies cortisol’s response to ACTH by increasing the number of ACTH receptors on the adrenal cortex, compensating for states of hypocortisolism.6 Similar to ACTH, it is relaunched in the face of diminishing cortisol activity. In the later part of the sleep cycle, as melatonin falls, ACTH is no longer blocked. βMSH’s amplification of the cortisol response helps install a waking state. In the thyrotropic axis, βMSH is stimulated by TRH and acts as a long-acting stimulator of the thyroid gland, avoiding the vertical pathway of TRH → TSH → Thyroid, and thus feedback inhibition. β-endorphin is another derivative of POMC. It reduces TRH activity, and in this way helps reduces the activity of βMSH on the thyroid (but not its actions on the adrenal cortex). When the index is high (βMSH > αMSH), it favors the use of endorphin-like products, such as Eschscholzia californica7, 8 (California poppy) and Papaver rhoeas9–13 (common poppy) (Fig. 2.1).

A clinical approach to the corticotropic axis Chapter | 2  21

TABLE 2.15  Some central and peripheral indexes of the biology of functions related to the corticotropic axes Index

Definition

Positive correlation

Inverse correlation

Beta MSH/alpha MSH

Central beta relative to central alpha; by extension, intensity of thyroid activity outside of central thyrotropic stimulation, by extension relative insufficiency of endorphins in relationship to GABA in downregulation of central adaptation response

Thyroid metabolic

ACTH

It expresses the organo-metabolic activity of ACTH on the adrenal cortex

DHEA index

Cortisol index

Adaptation

It expresses the relative adaptative activity of ACTH in relation to that of FSH

Eosinophils

Monocytes

Adaptogen

It expresses the relative level of participation of the pituitary in the relaunching of noncircular adaptation; by extension it witnesses the relative appeal to endorphins in the central sphere

Potassium

Calcium

Cortisol

It expresses the role of cortisol during the syndromes of adaptation

Catabolism/anabolism index

Adaptation index

Adrenal gland activity

It expresses the level of activity of the adrenal cortex

Cortisol index

Adrenal androgens

Permissivity

It expresses the permissive role of the adrenal cortex on the activity of the other endocrine glands in their sequential and chronologic activity

Adaptation index

Androgenic index

Adaptationpermissivity

It expresses the relative level of adaptative activity of the adrenal cortex in relationship to its permissive activity

Cortisol index

Permissivity

Histamine activity

It expresses the level of circulating, active histamine

Eosinophils

Adrenal gland

Potential histamine

It expresses the level of fixed and mobile histamine receptors

Histamine activity

Thyroid metabolic

Central

Peripheral

FIG. 2.1  Schematic relationship of alpha MSH, beta MSH, GABA, endorphins, the corticotropic, and thyrotropic axes. Alpha MSH (αMSH) and beta MSH (βMSH) represent central alpha and beta activity, respectively. Alpha MSH stimulates (red arrow) the long axis of adaptation. GABA (blue arrow) inhibits it. TRH stimulates beta MSH, which amplified both cortisol and thyroid activity. Ordinarily, the typical thyroid vertical inhibitory feedback loop would regulate thyroid activity. However, since beta MSH acts outside this process, this negative feedback loop is not present (broken blue arrow). Beta endorphin (β-endorphin) inhibits TRH which by extension can regulation beta MSH. (© 2015 Systems Biology Research Group.)

22  The Theory of Endobiogeny

A discussion regarding the adrenal cortex index

diverted from conversion to cortisol. A phenomenon we refer to as “cortisol steal.”

The adrenal cortex index expresses the global level of activity of the adrenal cortex. What determines the global functionality of the adrenal cortex is the relative ­metabolic distribution between cortisol and adrenal androgens (Fig.  2.2). Both adrenal androgens (gray box) and cortisol (end of black arrow) share a common metabolite: 17 α-hydroxy pregnenolone. The greater the production of adrenal androgens (cf. adrenal androgen index), the greater 17 α-hydroxy pregnenolone will be

Cortisol and adrenal cortex indices: Some notes on interpretation When one evaluates the cortisol index, one must evaluate it in and of itself and relative to the adrenal cortex index. The ratio of the two indices is about 2.5:1 to 3:1. That is to say, the value of the cortisol index should be about 2.5–3 times greater than that of the adrenal cortex index in order for there to be a commensurate level of catabolic and

FIG. 2.2  Pathways of metabolism of cholesterol in the production of adrenal cortex steroids. Adrenal steroids can be divided into two general categories: catabolic and anabolic. Glucocorticoids such as cortisol (mid, right) are catabolic. All others are anabolic: aldosterone (upper right), progestanes (upper left), androgens (lower left), and estrogens (lower right). See text for details. (Modified and reproduced from David Richfield (User:Slashme) and Mikael Häggström. Derived from previous version by Hoffmeier and Settersr. WikiJ Med. 2014;1(1). https://doi.org/10.15347/wjm/2014.005. [CC-BY-SA-3.0] via Wikimedia Commons.)

A clinical approach to the corticotropic axis Chapter | 2  23

anabolic activity, regardless of the absolute values of each index. We present four cases of relationships between these two indexes.

Case 1: High ratio, low global output Consider a case where the cortisol index is 6.8 (normal 3–7), and the adrenal cortex index is 1.4 (normal 2.7–3.3). The ratio of cortisol/adrenal cortex = 6.8/1.4 = 4.86. What this indicates is that cortisol is being produced within the normal range but at the expense of other adrenal cortex hormones. In this case, using medicinal plants and/or vitamins that support the global adrenal cortex will be of benefit: Ribes nigrum (cassis bud), Thymus vulgaris (thyme essential oils), Salvia officinalis (Dalmatian sage), especially if it favors adrenal androgens, such as Rosa canina (dog rose bud).

Case 2: Elevated ratio, cortisol elevated, and adrenal cortex low Consider a second case seen with the more common type of physiologic depression (The Theory of Endobiogeny, Volume 3, Chapter 14). The cortisol index is elevated and the adrenal cortex index is absolutely low, e.g., cortisol = 9, adrenal cortex = 1.5 with a ratio of 9/1.5 = 6. The interpretation is that given the level of stimulation, the adrenal cortex excretes cortisol at a greater rate both absolutely and relative to the output of anabolic steroids. In this case, the reduction of general stimulation with alpha-sympatholytic plants is called for (cf. case 4). One may also use plants that support general adrenal cortex activity (case 1)—especially Rosa canina, or, adaptogenic plants (case 3). However, what is most called for is Sequoia gigantea (Sequoia bud), because it diverts cholesterol metabolism away from cortisol. Dr. Duraffourd stated that it is an “adrenal cortex stimulant favoring adrenal androgens and increasing DHEA and that it reduces ACTH by classical inhibition, and reduces aldosterone and cortisol by shifting adrenal metabolism towards Adrenal androgens” (unpublished).

Case 3: Low ratio, both indices normal Consider a third case in which the cortisol index is low normal at 3, and the adrenal cortex is high normal at 3. The ratio is 3/3 = 1. This indicates that global production of hormones is within normal limits, but that the relative distribution favors adrenal androgens at the expense of cortisol. Often one will find in this case a blocked or reduced adaptability (adaptation-permissiveness index absolutely low and/or negative). The adrenal cortex is often more in a permissive mode at the expense of its adaptive capability (permissiveness index normal or elevated). In this case, using more adaptogenic plants, such as Quercus pedunculata

(oak bud), Rhodiola rosea14 (Rhodiola), or Ribes nigrum15, 16 can be helpful. The use of Achillea millefolium (yarrow essential oil) as a progesteronic plant15, 16 can also be helpful as it provides a precursor for cortisol production (Fig. 2.2).

Case 4: Normal ratio, both indices elevated Consider a fourth case in which the cortisol index is 20 and the adrenal cortex index is 7.5. The ratio is normal: 20/7.5 = 2.67. However, both indices are absolutely elevated. This indicates that the global adrenal cortex output is elevated, but that the relative distribution of its metabolic efforts is within normal limits. Whether this is adaptive or adaptative, and how much of it is permissive vs. adaptive depends on the values of other indices (adaptation-permissiveness index, permissivity index). Also, one should also evaluate alpha-sympathetic (βMSH/αMSH, leukocyte mobilization index, thyroid relaunching, thyroid relaunching corrected) and ACTH (ACTH index, adaptation index) to see what level of solicitation is implicated. The use of alpha-sympatholytics and/or plants that inhibit ACTH may be helpful if the elevated peripheral adrenal cortex activity is adaptative and not adaptive. For example, if these results are observed during pneumonia, it is adaptive. This activity should not be inhibited, but sustained. If it is observed 3 weeks after the resolution of pneumonia, it is adaptative, in which case, overstimulation of the adrenal cortex should be downregulated. The most often-used plants in our practice are Passiflora incarnata2, 17 (passionflower), Lavandula angustafolia15, 16 (lavender essential oil), and/or Leonurus cardiaca (motherwort). The later reduces fixation of cortisol to its receptors and can be a favorable adjunct, particularly if the thyroid relaunching or its corrected index are elevated, implicating TRH.18

Conclusions After the autonomic nervous system, the corticotropic axis is the most easily evaluated in clinical practice. There are numerous symptoms and signs that can be readily and quickly identified. Being familiar with expressions of sympatheticocorticotropic activity in the terrain the Endobiogenist can treat the critical terrain or symptomatically address a wide range of conditions related to physiology, behavior, and mood. Modeling of many key indexes of this index can be performed using only a complete blood count with differential and platelets, allowing for inexpensive and frequent evaluation of the adaptability of the terrain at the corticotropic level.

References 1. Verburg-Van Kemenade  BM, Jenks  BG, Driessen  AG. GABA and dopamine act directly on melanotropes of Xenopus to inhibit MSH secretion. Brain Res Bull. 1986;17(5):697–704. 2. Akhondzadeh  S, Naghavi  HR, Vazirian  M, Shayeganpour  A, Rashidi H, Khani M. Passionflower in the treatment of generalized

24  The Theory of Endobiogeny

3.

4.

5.

6.

7.

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9.

anxiety: a pilot double-blind randomized controlled trial with oxazepam. J Clin Pharm Ther. 2001;26(5):363–367. Govorko  D, Logendra  S, Wang  Y, et  al. Polyphenolic compounds from Artemisia dracunculus L. inhibit PEPCK gene expression and gluconeogenesis in an H4IIE hepatoma cell line. Am J Physiol Endocrinol Metab. 2007;293(6):E1503–E1510. Awad R, Muhammad A, Durst T, Trudeau VL, Arnason JT. Bioassayguided fractionation of lemon balm (Melissa officinalis L.) using an in  vitro measure of GABA transaminase activity. Phytother Res. 2009;23(8):1075–1081. Yoo  DY, Choi  JH, Kim  W, et  al. Effects of Melissa officinalis L. (lemon balm) extract on neurogenesis associated with serum corticosterone and GABA in the mouse dentate gyrus. Neurochem Res. 2011;36(2):250–257. Abe  K, Nicholson  WE, Liddle  GW, Orth  DN, Island  DP. Normal and abnormal regulation of beta-MSH in man. J Clin Invest. 1969;48(8):1580–1585. Reimeier  C, Schneider  I, Schneider  W, Schafer  HL, Elstner  EF. Effects of ethanolic extracts from Eschscholtzia californica and Corydalis cava on dimerization and oxidation of enkephalins. Arzneimittelforschung. 1995;45(2):132–136. Kleber  E, Schneider  W, Schafer  HL, Elstner  EF. Modulation of key reactions of the catecholamine metabolism by extracts from Eschscholtzia californica and Corydalis cava. Arzneimittelforschung. 1995;45(2):127–131. Pfeifer S. On the occurrence of glaudine in opium and Papaver rhoeas L. Pharmazie. 1965;20(4):240.

10.

Soulimani R, Younos C, Jarmouni-Idrissi S, Bousta D, Khallouki F, Laila  A. Behavioral and pharmaco-toxicological study of Papaver rhoeas L. in mice. J Ethnopharmacol. 2001;74(3):265–274. 11. Saeed-Abadi S, Ranjbaran M, Jafari F, et al. Effects of Papaver rhoeas (L.) extract on formalin-induced pain and inflammation in mice. Pak J Biol Sci. 2012;15(21):1041–1044. 12. Sahraei  H, Faghih-Monzavi  Z, Fatemi  SM, Pashaei-Rad  S, Salimi SH, Kamalinejad M. Effects of Papaver rhoeas extract on the acquisition and expression of morphine-induced behavioral sensitization in mice. Phytother Res. 2006;20(9):737–741. 13. Pourmotabbed  A, Rostamian  B, Manouchehri  G, et  al. Effects of Papaver rhoeas extract on the expression and development of morphinedependence in mice. J Ethnopharmacol. 2004;95(2–3):431–435. 1 4. Kelly  GS. Rhodiola rosea: a possible plant adaptogen. Altern Med Rev. 2001;6(3):293–302. 1 5. Duraffourd  C, Lapraz  JC. Traité de Phytothérapie Clinique: Médecine et Endobiogénie. Masson ed Paris: Masson; 2002. 1 6. Lapraz  JC, Carillon  A, Charrié  J-C, et  al. Plantes Médicinales: Phytothérapie Clinique Intégrative et Médecine Endobiogénique. Paris: Lavoisier; 2017. 1 7. Gazolaa A, Costa G, Castellans L, et al. Involvement of GABAergic pathway in the sedative activity of apigenin, the main flavonoid from Passiflora quadrangularis pericarp. J Ethnopharmacol. 2015;25(2):158–163. 1 8. Wojtyniak  K, Szymanski  M, Matlawska  I. Leonurus cardiaca L. (motherwort): a review of its phytochemistry and pharmacology. Phytother Res. 2013;27(8):1115–1120.

Chapter 3

Immunity Introduction The immune system is a reactive modality that allows the organism to exist in its fundamental quest not only to be alive but also to thrive. It allows the materiality of the system to be materially closed unto to itself and energetically open to the universe. Understanding the true role of the immune system requires a global systems perspective. According to the theory of endobiogeny, this approach offers depth and breadth to the management of numerous states of health and illness. Table 3.1 is a partial listing of conditions evaluated by an endobiogenic approach to the immune system. Capital to the integration of immunity into the concept of terrain is that its formation, organization, maturation, functioning, and regulation are under the constant regulation of the neuroendocrine system. This approach to the immune system reduces the complexity of treatment, allows for root cause treatment, and elucidates the cause vs effect of the immune system in a host of disorders. Thus, this chapter addresses three fundamental issues regarding the immune system: its purpose, function, and integration into global functioning of the organism. This chapter is not meant to be an exhaustive or detailed review of the immune system. It seeks to demonstrate the nature of the relationship of the endocrine system and digestive glands in the structural formation of the immune system and the neuroendocrine relationship with respect to the function of the immune system. Regulation of the immune system from an endobiogenic approach (Chapter 4) and the role of the microbiome in immunity (Chapter 5) are discussed separately.

That which brings about the need for immunity Every organism is a closed unit of function open to its environment. “Closed” refers to its distinct and discrete materiality of structure and function. For example, two individuals standing next to each other have two distinct bodies with two distinct metabolisms. They are closed unto each other. They are not intermeshed or intermixing. One cannot utilize the glucose of the other to generate adenosine triphosphate (ATP). One cannot share the liver of the other in case of toxin overload. Thus, each is a closed system that functions for its intrinsic

benefit. “Open” refers to its receptivity to and engagement with its environment.1 Every organism is subjected to exogenous energy: ultraviolet rays, gamma radiation, geomagnetic influences, etc.2–5 However, organisms also exchange electrochemical (i.e., pheromones6–10) and ­electromagnetic11–14 information that influence the behavior of other organisms. Organisms are open to the physical movement of nutrients for metabolism.1 Finally, they must be open to the egress of metabolic waste. To be alive is to be open. To be open is to risk one’s integrity. To risk one’s integrity is to risk death. To be alive, ergo, means to risk death. In safeguarding its material constitution, the organism must maintain some mechanism by which it can interact with the external world. That mechanism is the immune system—generated, mobilized, and regulated by the neuroendocrine system.

Immune system: Definition and general function The immune system is described as a physiologic system of resistance. The term “immune,” derived from the Latin “in” and “-munia,” means “not obligated to service.” Male Roman citizens were obliged to engage in certain duties related to the state. Those who were immune were exempt from this service. To be immune, then, means to be free of what is considered to be a natural consequence of belonging to something larger than oneself. For the individual organism, to be part of the universal expression of Life is to be subjected to the potential for harm, for one cannot survive without being open. Thus, immunity is the state of being free of the natural consequences of being open. Thus, the immune system is a system of protection more than resistance. More accurately, it is a manager of self vs nonself, of friend vs foe. From this perspective, we see that there are four basic roles of the immune system: vigilance, tolerance, defense, and attack.

Vigilance Vigilance is by far the most important function of the immune system. Being aware of the possibility of risk and avoiding harm is far more prudent that reacting to it. Vigilance requires a system of surveillance, a h­ ierarchization of values,

1. One should not forget that gases such as oxygen and energetic solar emanations (for the production of vitamin D) are also nutrients. The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816908-7.00003-7 © 2019 Elsevier Inc. All rights reserved.

25

26  The Theory of Endobiogeny

TABLE 3.1  A partial Endobiogenic consideration of immunity in clinical practice Optimal functioning

Disorders implicating immunity

Disorders affected by the immune system

Chronobiologic seasonal adaptation

Atopy: asthma, allergies, eczema

Infertility

Chronobiologic unfolding of genetic programs: grand phase adaptation through birth, puberty, and gonadopause

Hashimoto’s thyroiditis

Depression

Meteorological and geopathic adaptation

Myasthenia gravis

Atherosclerosis

Tolerance of a wide variety of foods

Infections

Arthritis

Hemolytic anemia

Inflammatory bowel disease

Glomerulonephritis

Obesity

and a means to meet a threat. The highest level of surveillance is maintained by the nervous system. It calibrates the threshold of reactivity of the immune system within the larger context of global functioning via the limbic area. This is why elevated sympathetic tone is implicated in autoimmune disorders from Hashimoto’s thyroiditis to ulcerative colitis, and hyperimmune disorders such as asthma.

Tolerance The vast majority of nonself-entities are not harmful. They are either neutral (i.e., ambient nitrogen) or beneficial (i.e., nutrients, commensal flora). Thus, after vigilance, tolerance is the second most important function of the immune system. The thymus maturates lymphocytes, which play a key role in determining self from nonself. Thus, the thymus sits at the crossroad of identity. Its dysfunction is implicated is dysthymia (literally improper function of the thymus) and depression. Tolerance allows for the binary hierarchization of: self = safe nonself = threat to be expanded into a triune hierarchy of: self = safe nonself , nonaggressive = tolerated nonself , aggressive = threat

Defense

making it harder for them to colonize or invade the host. Autoimmune antibodies can be a type of defense against dysregulated neuroendocrine solicitation of an organ or gland. They are a naturally occurring phenomenon.15 It slows down the over activity of its target. In the precritical phase, it is protective and beneficial (i.e., thyroglobulin antibodies). However, as a modality of adaptability (cf. The Theory of Endobiogeny, Volume 1, Chapter 12) it can lead to an autoimmune state in its chronicity.15

Attack Attack refers to the mobilization of the immune system in response to a true or perceived threat to the organism. Attack requires material, energy to use that material, and a plan on how to use the energy and material. The material is derived from the immune system (phagocytes, cytokines, immunoglobulins, etc.). The energy and direction of the immune response is managed by the neuroendocrine system (cf. The Theory of Endobiogeny, Volume 1, Chapter  12). Because of its considerable energy costs, the organism engages in attack only when required to. Autoimmune disease is also a type of attack response.

Relationship of the immune system to the global system The asking of ultimately serious questions, which means to be seized in turn by an ultimately serious quest, reshapes our concepts in favor of the kinds of perceptions needed to “see” the desired answer…A question determines and brings about its answer just as the desired end shapes the nature of the kind of question asked. This is the way by which science synthetically creates that which it then ‘discovers’ out there in nature.

Defense is a proactive mechanism that reduces the possibility of harm. Two good examples are commensal organisms Joseph Chilton Pearce.16 and certain types of autoimmune antibodies. Commensal According to the theory of endobiogeny, the immune organisms have several mechanisms that create an in-­ hospitable environment for noncommensal organisms, system is not a principle system of the organism. It lacks the

Immunity Chapter | 3  27

criteria of a manager. It does not manage the materialization and intrinsic functioning of the organism. It does not regulate itself through hierarchical feedback loops. For example, cortisol mobilizes neutrophils but neutrophils do not inhibit cortisol in term to regulate their mobilization. Finally, it is not an actor in the hierarchization process regulated by the central nervous system. It neither plans nor strategizes, it neither calibrates nor initiates anything. It is a reactive modality in the service of the global system for the purposes noted above. Both its materialization and actions are regulated by the endocrine system. In the general role of surveillance, there is a constant interaction between alpha-sympathetic, adaptive functions of the corticotropic axis and the immune system. The less competent one aspect of the triad is, the greater one or both of the other aspects will become. For example, according to the theory of endobiogeny, in atopic disorders such as eczema, it is the adaptive aspects of the

corticotropic axis which are insufficient (The Theory of Endobiogeny, Volume 3, Chapters  1 and 2). A hyperalpha, hyperimmunity state is installed to compensate. Conversely, in peripheral depression alpha and cortisol are overadapted and the immune system (particularly thymic assessment of self vs other) is impaired. Each axis of the endocrine system plays a role in the structure and function of the immune system. However, this triadic relationship between autonomic nervous system (ANS)corticotropic axis-immunity is a functional relationship in permanent dynamism. Many researchers continue to study the immune system as an isolated system, as if it functions independent of other activities in the organism. Or, it is studied in vivo in artificial models of complex human disorders that do not reflect human physiology (Fig. 3.1).17 One of the tragic results of this reductionist approach is the study of septic shock. Animal trials of pharmaceutical therapies for sepsis have shown

FIG. 3.1  Correlations of the gene changes among human burns, trauma, and endotoxin and the corresponding mouse models. Scatter plots and Pearson correlations (R2) of the log twofold changes of 4918 human genes responsive to trauma, burns, or endotoxemia (FDR  TRH

•

TRH/TSH low

Thyrotropic

Cortisol elevated

PTH Somatotropic

Somatostatin Glucagon

Emunctory

Diet

Drugs

PTH high (−) CCK •

Somatostatin high or low Starter

Insulin

Insulin low or high

Liver, metabolic

Starter index high

Exocrine pancreas

•

Small intestines

Symbiosis

Colon

Normal stool transit

Somatostatin high or low

Hyperalimentation

•

Fasting

↑

Endocrine

Octreotide

Neurologic

Opiates

Endocrine

Anticholinergics (diphenhydramine, atropine), bupropion

Immune

Cyclosporine

80  The Theory of Endobiogeny

TABLE 6.1  Elements of the terrain effecting choleresis and biliary stasis

Disorders of dysbiosis Chapter | 6  81

TABLE 6.2  Indexes favoring hyperimmunity

TABLE 6.3  Indexes favoring hypoimmunity

Category

Index

Value

Category

Index

Value

Corticotropic

ACTH + adaptation

↓

Corticotropic

ACTH

↑

Cortisol to adrenal cortex ratio

> 4:1

Cortisol

↓

↓

Adrenal cortex

Evoked histamine

Varies, often ↓

Leukocyte mobilization

↑

Leukocyte mobilization

Varies, often ↓

Platelet mobilization

Varies, ↑ is more deleterious

Platelet mobilization

Varies, often ↓

Adaptation permissivity of the adrenal cortex

↑, may also be negative

Adaptation permissivity of the adrenal cortex

Varies, often ↓

Inflammation

↑

Inflammation

Varies, often ↓

Gonadotropic

Estrogen index corrected

↑

Gonadotropic

Estrogen index corrected

↓

Thyrotropic

Genito-thyroid

↑

Thyrotropic

Genito-thyroid

↓

Thyroid index

Varies, often ↑

Thyroid index

Nl/↓

Thyroid relaunching corrected

↑

Varies

Insulin

↑

Thyroid relaunching corrected

Somatostatin (exocrine pancreas)

↓

Insulin

Nl/↓ Nl/↑

Redox

↑

Somatostatin (exocrine pancreas)

Noxious free radicals

↑

Redox

↓

Interleukin (IL-1) index

↑

Noxious free radicals

↓

Interleukin (IL-1) index

↓

Somatotropic

Carcinogenesis

Somatotropic

Carcinogenesis

Diet The influence of diet occurs at several stages of life. Key among them are nutrient exposure in perinatal diet and birth method, weaning, and childhood diet. In addition to what is eaten, the proximity of consumption of food to its cultivation, and the pattern of consumption are also important.

Initial diet Diet is the principle factor that contributes to the diversity of intestinal flora. From birth, the infant’s diet (breast milk vs formula, time of introduction of solid foods) profoundly influences immunity and the composition of the microbiome (Fig. 6.1).3, 4, 10 What’s more, composition of the microbiome influences the development of childhood disorders, which can impact lifelong health (Fig. 6.2).10 Whatever the causes of dysbiosis, various types of imbalances are associated with numerous disorders in adult life. We are not claiming causation, but there is emerging

evidence that addressing the dysbiosis can bring the patient out of the critical terrain and liminal expression of disease.11 In Fig.  6.3A shows a proposed normal diversity of phyla on various parts of the body. Fig. 6.3B shows the relative proportions of these phyla of microorganisms in healthy cohorts and those with disease. Distinct disorders appear to have distinct ecosystems of flora in healthy controls vs those with liminal disease. Again, we are not assuming causation, but note the correlation and observe the importance of understanding the endobiogenic terrain that has contributed to this dysbiosis.

Regional nutrient predominance Stable populations with monodiets (high consumption of specific nutrients) develop a microbiome specialized in the metabolism of nutrients highly concentrated in the diet. Thus, the consumption of local and traditional foods

82  The Theory of Endobiogeny

FIG. 6.1  Influence of delivery method and infant feeding on the microbiome. The amniotic fluid, once thought to be sterile, is the fetus’ first exposure to flora. The method of birth, the endobiogenic equilibrium of the mother’s vaginal and skin flora are the second exposure. After this, method of nutrition is third. Fourth is the introduction of foods during the weaning period. Finally, the choice of refined vs whole foods, processed vs minimally processed foods influences a critical bifurcation in the prevalence of certain flora over others. (Reproduced from Tanaka M, Nakayama J. Development of the gut microbiota in infancy and its impact on health in later life. Allergol Int 2017;66(4):515–522. © 2017 Japanese Society of Allergology.)

FIG. 6.2  Dysbiosis and childhood disease. There is a continuous interaction between symbionts that affects host immunity. There is host-bacteria interaction (upper left), which plays a role in regulation of intestinal bacteria. This in turn, influences bacteria-bacteria interaction with respect to the ecology of substrates (lower left), such as short-chain fatty acids (SCFA). This in turn creates an endobiogenic equilibrium that further influences host immunity (top right). This triadic relationship will determine if an optimal calibration of immunity develops (upper right after arrow), or a dysbiotic terrain with various disorders of dysregulated immunity (lower right after arrow). (Reproduced from Tanaka M, Nakayama J. Development of the gut microbiota in infancy and its impact on health in later life. Allergol Int 2017;66(4):515–522. © 2017 Japanese Society of Allergology.)

(i.e., seaweed for Japanese, sorghum for Africans) even when they have to be imported, offers optimal nutritional balance.4 However, it should be noted that local or regional foods are rich in nutrients that allow the plants to adapt to their environment. We hypothesize that they may allow the consumers of the plants to similarly adapt to ­local

e­nvironmental conditions. Soil quality and by extension total atmospheric quality also affect composition of the microbiome.12 In conclusion, we favor the consumption of local or regional foods if the growing conditions are favorable. In the case of humans living far from their ancestral environment, the consumption of foods grown local to their

Disorders of dysbiosis Chapter | 6  83

External auditory canal

Hair on the head

Mouth

Healthy control

Patient

Inflammatory bowel disease

Nostril

Oesophagus

Skin

Gastrointestinal tract

Type 2 diabetes

Vagina

Penis

Necrotizing enterocolitis

(A)

(B) Firmicutes

Bacteroidetes

Fusobacteria

Actinobacteria

Verrucomicrobia

Proteobacteria

FIG. 6.3  Microbial diversity in various areas of the body and dysbiosis associated with various diseases. See text for details. (Reproduced from Blum HE. The human microbiome. Adv Med Sci 2017;62(2):414–420. doi:10.1016/j.advms.2017.04.005. Elsevier.)

place of birth and development may also confer benefits. It is not clear what the impact will be of cultivating and consuming foods not native to the area of consumption but native to the genetic heritage of the patient. The history of humanity is one of migration and intermixing of growths, with transpositions of foods one region to another, such as potatoes from Peru to Ireland, or pomegranates from Iran to California.

Alimentary patterns A high-energy diet low in dietary fiber, rich in animal fats, refined carbohydrates and other high glycemic foods is ­perhaps the most detrimental to the general well-being of the enteric flora.13 The implications for regional and systemic dysfunction are considerable: 1. Pancreas, endocrine: diminished beta islet cells and insulin production 2. Liver: inflammation, reduced insulin sensitivity, lipogenesis, and steatosis 3. Muscle: inflammation, reduced insulin sensitivity 4. Adipose: inflammation, lipogenesis, hyperplasia The particular role of specific nutrients is noted in Fig. 6.4.14 Gluten and salt may have a contributory role in human dysbiosis. Pro-inflammatory foods such as red meat,

s­ aturated fats, and refined sugars also play a role contribute.14 The precise role of artificial sweeteners and gluten is disputed in the research literature at this time. We do not encourage its consumption for various reasons. The general type of diet (vegetarian vs omnivorous) also influences the composition of the enteric microbiota, which can influence weight gain.15 The consumption of more animal flesh requires a greater number of flora that consume proteins more than carbohydrates. Fig. 6.5 summarizes variation in flora diversity overtime, and the influences of diet, region, and ethnicity.

Noncommensal organisms The presence of noncommensal organisms is itself the result of a disturbance of the endobiogenic equilibrium of the individual. However, the degree of pathogenicity depends on three general factors: (1) the intrinsic qualities of the pathogen, (2) the commensal microbiota, and (3) the host. With respect to the pathogen, we can observe three general factors: (1) intrinsic virulence, (2) relative virulence, and (3) quantity of organisms. The pathogen has its own intrinsic virulence and tropism not only for a specific species (i.e., human vs chicken) but also a specific tissues within an organism. This is determined by the genetic composition and

84  The Theory of Endobiogeny

the adaptation response. Once again, we find three factors: (1) buffering capacity, (2) quality, intensity, and duration of the adaptive response, (3) quality of the compensatory and restorative mechanisms. These nine factors of the three elements create a probability field that determines the actual risk of dysbiosis and infectious disease.

Chronobiologic impositions Age

FIG. 6.4  Diagrammatic overview of the current mechanisms for macrocomponents of the modern diet altering susceptibility to infection, allergy, and autoimmunity. Solid black lines indicate direct human evidence for enhancement is present; solid red lines indicate direct human evidence of inhibition exists; gray lines indicate only in vitro or animal model evidence exist currently; dotted lines indicate significant disagreement within the scientific literature. TLR4, toll-like receptor 4; IL, interleukin; TNF, tumor necrosis factor; Treg, T-regulatory cell. All clip art and images sourced from free-for-us online repositories. (Reproduced from Myles IA. Fast food fever: reviewing the impacts of the Western diet on immunity. Nutr J 2014;13:61. doi:https://doi.org/10.1186/1475-2891-13-61. © Myles; licensee BioMed Central Ltd. 2014.)

phenotypic expression of the microorganism. It includes its ability to produce endotoxins, to live in a secluded area (i.e., the gallbladder), or its ability to evade certain defense measures. The relative virulence is related to the quality of the local terrain in which it enters. The quantity of organisms is also important. For example, it is clear that a pathogen of high virulence can overwhelm an initially competent endobiogenic terrain in moderately elevated concentrations. However, a pathogen of low virulence enters can still cause disease with a high enough inoculation load in an initially competent endobiogenic terrain. In both cases, it’s a question of time and loss of buffering capacity. With respect to the enteric microbiota, there are again three factors: (1) diversity of flora, (2) quality of the diet, and (3) quality of local terrain based on the functioning of the noted emunctories and the neuroendocrine equilibrium. Host factors play an important role in the ultimate pathogenicity of organisms and the symptomatic expression of

Chronobiologic programming through the grand phases of life imposes certain demands on the organism. They require certain levels of particular hormones, which require an alteration in the metabolic activity of enteric flora in specific areas of the intestines (cf. above: endobiogenic cartography). Assuming optimal flora at birth, the general evolution of various phyla and genera of the enteric microbiota will occur throughout life. At birth, facultative anaerobes such as Escherichia coli and Enterococcus predominate. Actinobacteria such as Bifidus genera then start to populate the organism. As children start to consume solid foods, certain species come into prominence and remain that way for the duration of life (Bacteroides ssp., Streptococcus, etc.). As we age, Firmicutes such as Lactobacilli and Clostridium ssp. increase in number as Bifidus species decline. It is becoming increasingly clear that part of the general shift in microbiota reflects a “catastrophic success” of human society16 (Fig. 6.6). According to the extant records from paleomicrobiology and paleoanthropology, the paleoathropocene era of an agricultural diet led to a certain microbiome. This was altered during the industrial revolution and the introduction of processed foods. In the shortest period known of human cultural shifts, there has been an acceleration over the last 4–5 decades in the human microbiome thanks to the use of antibiotics, cesarean section births, and bottle feeding. Along with this is a rise of environmental toxins of industrial origin.

Seasons Longitudinal studies of the microbiome of individuals demonstrate variations in the relative predominance of various genera over “brief” periods of time such as 6–18 months (Fig.  6.7). Based on an endobiogenic reflection, one concludes that these intrapersonal variations are due to seasonal adaptation demands (The Theory of Endobiogeny, Volume 1, Chapter 12).9 During prespring, there is a brief period of thyroid relaunching. This leads to a catabolic predominance that induces a physiologic “spring cleaning.” It results in an increased elimination of accumulated biologic products from the tissues. However, it is also the time of lowest intestinal absorption. Thus, during this time, proper functioning of emunctories (liver, exocrine pancreas, kidney, colon) and proper colonic transit time are key (alpha- and parasympathetic).

Disorders of dysbiosis Chapter | 6  85

Age

Dietary habits

First days of life

Vegetarian diet

Mostly Bifidobacteria Human microbiota

1. Increase Bacteroidetes 2. Decrease Clostridia

Stable: Firmicutes (64%) Bacteroidetes (23%) Proteobacteria (8%) Actinobacteria (3%)

1. Increase Bacteroidetes 2. Decrease Bifidobacteria

Increase Bifidobacteria

Different species level

Elderly

1. Increase Actinobacteria and Bacteroidetes 2. Decrease Firmicutes and Proteobacteria

Southern vs northern Europeans Origin

Chinese vs Americans

Adults

Europeans vs Africans

FIG. 6.5  Factors related to microbial population and diversity. Upper right: general trends in diversity over the life span. Upper left: influence of a vegetarian diet. Bottom: variations based on the region of population studied. (Reproduced from Angelakis E, Armougom F, Million M, Raoult D. The relationship between gut microbiota and weight gain in humans. Future Microbiol 2012;7(1):91–109. doi:https://doi.org/10.2217/FMB.11.14.)

Paleoanthropocene

Industrial revolution

Great acceleration

Processed foods

Antibiotics Cesareans Bottle feeding

Human microbiome Shift to agricultural diet

Dysbiosis Microbiomics

Resistance Black death

Pollution Evolvability

Mercury Arsenic

Antibiotics Disinfectants Heavy metals

Age of exploration Epidemics

Vaccination Emerging disease Tourism/transport

Dispersal/disease Migration with parasites

Zoonoses Agricultural mutualisms

600

Tg p.a.

Nitrogen fixation

Tg p.a.

Methanogenesis

Antibiotic failure Pandemics

Megafaunal extinctions

300 0 400

Agricultural methane: ruminants, rice paddies

Landfill

Legume cultivation

Fossil fuels

↑ Methanogenesis

200 0

Hd

8.3 8.2 8.1 8.0 7.9

pCO2

Oceanic pH, Atmospheric [CO2]

100,000

1775

1953

Holocene 10,000

↑ N2 fixation ↑ Denitrification Selection ↑ temp ∆ Climatic zones

450 400 350 300 250

11700 bp

Pleistocene

Haber process

1,000 years bp

Present

∆ Marine symbiosis Selection ↓ pH

Anthropocene 100

0

FIG. 6.6  Human influence on human microbiome and global atmospheric conditions. (Reproduced from Gillings MR, Paulsen IT. Microbiology of the anthropocene. Anthropocene 2014;5:1–8. doi:10.1016/j.ancene.2014.06.004.Elsevier.)

86  The Theory of Endobiogeny

FIG. 6.7  The relative abundance of various species and phyla vary from season to season. For example, Baceteroides are more prevalent in summer than in winter. The specific change in prevalence varies from individual to individual. (A) Abundance (y-axis) of the 25 bacterial phyla that were detected (only the most common bacteria are indicated in the legend) by individual (x-axis). Individual's order along the x-axis is identical in both panels. Phyla that are significantly differentially abundant between seasons (FDR 18 months)

Methods of food preparation that are taxing on the exocrine pancreas Cooking with saturated animal fats is hard on the pancreas. Ghee may be an exception to this if the food is sautéed. Fried foods are taxing on the exocrine pancreas (and the gallbladder) because it requires an increased amount of fat emulsion (bile) and lipolysis (lipase).

Foods that increase demand on the exocrine pancreas Regardless of the method of preparation, the following foods are demanding on the pancreas. When they are ­prepared by the methods noted above to be hard on the pancreas, their negative impact is further augmented. 1. Refined grains 2. Saturated fats 3. Uncultured dairy products

Case study History A 10-year-old girl presented with a 2.25-year history of migratory joint pain diagnosed at idiopathic juvenile arthritis. It started 2 weeks before her eighth birthday. At that time, she was positive for streptococcal pharyngitis and received treatment with penicillin, amoxicillin/clavulanic acid, and amoxicillin. The joint pain started during the active infection. The initial workup was positive lupus factor, but negative for rheumatoid factor. RAST test was positive. She was treated with antihistamines to which she experienced adverse effects. At presentation, at 10 years of age, the migrating joint pain as follows: ●

Foods that are pancreas sparing 1. High purine fish a. Sardines b. Herring c. Anchovies d. Salmon 2. Whole ancient grains and seeds a. Brown rice b. Quinoa c. Buckwheat d. Millet 3. Leafy green vegetables

● ● ●

Pain: ● Still: throbbing ● Moving: sharp, occasionally shooting like electricity from wrists to elbow, and knees to feet ● Hands: numbness of fingers ● Feet: like sharp hot knives Duration: 3 weeks Ameliorating: acupuncture, ice/heat, rest Aggravating: nonsteroidal antiinflammatories

Two months prior to presentation her mother removed gluten, dairy, and nightshade vegetables from the diet. This helped expand the frequency of the cycles to every 4–5 weeks from every 3 weeks. Review of systems: (1) cutaneous dermatitis touching certain foods, (2) food allergies to gluten, dairy, and nightshade vegetables, and (3) failure to thrive: height and weight well below fifth percentile.

126  The Theory of Endobiogeny

Past medical history: (1) eczema, age 6, resolved before the onset of the joint pain, (2) perinatal trauma: (a) maternal preterm labor at 20 weeks on bedrest, (b) premature rupture of membranes at 35 weeks, and (c) induced vaginal birth, and (3) postnatal complications: hypothermia, hypoglycemia: 4-day hospitalization. Social: Per parental report: type-A personality, internally driven, does not cooperate well with peers on projects, dissatisfied with high marks on homework, more mature than her 15-year-old sister. Assessment of history: (1) not autoimmune (insufficient autoimmune factors), (2) hyperimmune allergic terrain with history of atopia (implication: liver, gallbladder, exocrine pancreas), (3) dysbiosis (perinatal events, antibiotic during onset of current illness), (4) chronobiologic: type-A personality with onset in birth month, on eve of eighth birthday: transition from thyrotropic tissular to corticoid metabolic, and (5) cosmobiologic component: cyclicity of pain.

TABLE 8.5  Polyvalent drainage and antiallergic treatment for a child with joint pain Treatment

Agent

Key actions

Drainage 1 tincture

Cornus sanguinea GM

Antinecrotic, slows TSH and thyroid, endocrine drainer, stimulates hepatic Kupffer cells

Alnus glutinosa GM

Antiinflammatory to mucosa and synovia, tissue drainer, drainer of the MPS (liver, spleen, lymphatics), diuretic

Ampelopsis weitchii GM

Cicatrant for ligamentous and cartilaginous structures, antifibrotic

Cnicus benedictus MT

Stimulates general drainage of the liver, antalgic, antineuralgic, antiallergic, eupeptic, antirheumatic, volumetric diuretic, supports, general hepatic drainage capability and organizes coherence of hepatic function, antimicrobial regulator of dysbiosis

Drainage 2 tincture

Arctium lappa MT

Immuno-modulating, antiallergic (leukotriene inhibitor), pancreatic stimulant (exocrine and endocrine), prebiotic (inulin), hepato-protectant, cholagogue, volumetric diuretic, blood cleanser

Dysbiosis

Aqueous humic substances

Regulator of dysbiosis

Mitochondria

Coenzyme Q10

Essential cofactor in cellular respiration

Examination Her exam was significant for the following, organized by emunctory significance (other signs omitted for clarity of the case study): ●

● ●

● ● ●

Liver: prominent veins on face and chest; tender to palpation upper and lower portions Gallbladder: gallbladder point tender Pancreas: tenderness on general, exocrine, and endocrine points Splanchnic: congestion from hepatopancreatic blockage Kidney: bluish tinge to sclera Musculoskeletal: no edema, limited range of motion with tenderness and clicking of affected joints

Biology of functions Confirmed all the assessments above (see Table 8.6).

Diagnosis Hyperimmune arthritis with immune complex deposition in the joints.

Treatment The patient was started on a drainage treatment with topical treatment for her joints since she did not tolerate nonsteroidal antiinflammatories. On follow-up, a treatment for dysbiosis and mitochondrial support was added, along with referral for mindfulness and breathing techniques for stress management (Table 8.5).

Results Within 4 months, she experienced a reduction in anxiety and joint pain. The intensity of pain and frequency diminished. Nine months into treatment, before her 11th birthday, she had better regulation of emotional outbursts, improved

a­ ppetite and growth, and improved recovery from exercise. The episodes of joint pain were reduced to 3 days. Hand pain was reduced by 50% and the electrical shock sensation was occasional and intermittent. Within 1 year, she had near complete resolution of upper and lower-extremity joint pain. By 18 months, the joint pain had completely resolved and the patient had learned to share her emotions with her mother when feeling stressed. By 2-year followup, she still had no joint pain, was fully active in gymnastics, was learning how to cooperate with others in-group projects and continued to gain weight ( right

TSH

Predominant

Instructure, in response to the basic influence of LH on laterality

Heart

Rate

Heart rate rapid

Thyroid

Augmented

May be absolutely elevated or augmented by TRH and/or cortisol

Finding

Level

Activity

TSH demand greater than T4 response

Thyroid gland congestion from oversolicited

TABLE 10.10  Others signs by region3 Part

Quality

Comment

Anterior projection of organs represents the current anatomical congestion and/or state of dysfunction Colon

Transverse, distal, left

Pain on palpation

TSH

Strong

Oversolicitation of thyroid and splenic flexure for nutrient reuptake

Colon

Transverse, distal, right

Pain on palpation

TRH

Predominance

Relative to TSH

Posterior projection of organs represents chronic congestion and/or state of dysfunction T4, left

Para spinal, 2.5 cm lateral

Pain on palpation

TRH

Scapula, right

Inferior-medial, T7-T8

Pain on palpation

FSH, TRH

Congestion, colon

Scapula, left

Inferior-medial, T7-T8

Pain on palpation

TSH, PL

Congestion, colon

General

Extremities

Lymphatic congestion

Thyroid

Latent hypothyroidism

Palm

Central

Erythematous

Thyroid

Strong

Oversolicitation of exocrine pancreas

TRH role implicated; direct interpretation: Congestion, lung, bronchial involvement

A clinical approach to the thyrotropic axis Chapter | 10  151

TABLE 10.10  Others signs by region—cont’d Part

Quality

Finding

Level

Activity

Comment

Leg

Medial to ankle, bilateral

Adiposity

TSH

Elevated

Compensated hypothyroidism

Leg

Proximal tibia, most medial aspect

Pain on palpation

T4

Diminished efficiency

LH implicated in strong TSH, pain L > R on exam

Leg

Proximal tibia, most medial aspect

Pain on palpation

TSH

Strong

LH more easily disturbed than FSH by strong TSH, pain L > R on exam

Ankle

Superior to ankle

Fat pad

TSH

Reactive

Compensation attempt for weak T4

A discussion of key thyrotropic indexes of the biology of functions When approaching an evaluation of the thyrotropic indexes, first review quantitative biomarker measurements: serum TSH, free T4, free T3, thyroid antibodies, etc. This information will contextualize the interpretation of indexes, especially since serum TSH is used to calculate a number of indexes. What is presented here is not comprehensive. It is a discussion of key indexes for students working with the elementary

concepts of endobiogeny. The indexes are d­ ivided into groups based on the area of origin and area of action that the indexes represent. It is arbitrary and there are some overlaps that are not presented to avoid redundancy. Conceptually, we have grouped the indexes as ­follows: ­central indexes with peripheral impact (Table  10.11; Fig.  10.1), radial gonado-­ thyrotropic (Table 10.12), those evaluating the thyroid gland and its threshold of response (Table 10.13), and, parathyroid and bone indexes (Table 10.14).

TABLE 10.11  Central thyrotropic indexes with peripheral impact Relationship Index

Definition

Import

Direct

Thyroid relaunching

It measures the level of reactivation of the thyrotropic axis by the locus ceruleus (Fig. 10.1)

It witnesses the degree of disadaptation of the organism, implicating the solicitation of TRH for central and/or peripheral activity and all that that implies

Thyroid relaunching corrected

It measures the endogenous part of solicitation of the thyrotropic axis by the locus ceruleus. By extension, it indicates the level of endogenous disadaptation of the organism (Fig. 10.1)

It witnesses the degree of disadaptation arising specifically from endogenous causes of disadaptation

Thyroid relaunching

TRH/TSH

It measures the relative level of tissular activity of TRH in relation to that of TSH

Indirectly it evaluates the relative part of congestion vs hyperplasia in anabolic adaptation, the relative part of nutrition vs metabolic production, the relative part of neuroendocrine vs organo-metabolic adaptation, and the relative part of the elaboration of potential vs structural realization, and thus of the imaginary relative to the material realization

Amylosis index, demyelination index

Inverse

Correlations Adaptation index, genito-thyroid, beta-MSH/alphaMSH Adaptation index, genito-thyroid, beta-MSH/alphaMSH

Adenosis index, serum TSH

Estrogen index, organotissular estrogen yield index, prolactin index

152  The Theory of Endobiogeny

FIG. 10.1  Thyroid relaunching and thyroid relaunching corrected indexes. Center: the locus ceruleus, in the brain stem, is the origin of noradrenalin (NA), the neurotransmitter of alpha-sympathetic. The thyroid relaunching index evaluates the degree to which alpha stimulates TRH in the parvoventricular nucleus of the hypothalamus. TRH relaunches thyroid activity (left). The thyroid relaunching index corrected corrects the basic evaluation for the degree that this occurs due to endogenous threats, be they real or perceived, mental or emotional aggressions. In this example, the limbic area (right), stimulates alpha in the locus ceruleus, which then stimulates TRH and relaunches the thyroid. (© 2015 Systems Biology Research Group.)

TABLE 10.12  Radial gonado-thyrotropic index Relationship Index

Definition

Import

Direct

Genito-thyroid

It measures the part played by the gonads in the appeal to and response by both metabolic and endocrine thyroid activity in the functional adaptation of structure

High: Thyroid activity is efficient relative to the estrogen demand. Favors inflammation and autoimmunity Low: TSH is not able to adapt the thyroid relative to the degree of estrogen demand. Favors hyperimmunity

Cortisol

Inverse

Correlations Adaptation index, cortisol index, corrected estrogen index IL-1, thyroid index, thyroid yield

TABLE 10.13  Indexes evaluating the thyroid gland and its activity Relationship Index

Definition

Import

Direct

Inverse

Correlations

Thyroid index

It measures the effective metabolic activity of peripheral thyroid hormones

High: Thyroid metabolic activity is elevated without conclusion regarding the degree of solicitation, rate of response or requirements of the organism Low: Thyroid metabolic activity is diminished without conclusion to the degree of solicitation, rate of response or requirements of the organism

LDH

CK

Genito-thyroid, thyroid yield, metabolic yield

Thyroid yield

It measures the relative part of the thyroid’s metabolic contribution in comparison with the level pituitary stimulation

High: The thyroid is easily relaunched when its metabolic effects decline Low: There is a delay in the readaptation of thyroid metabolic activity by the pituitary

Thyroid index

Serum TSH

Genito-thyroid, thyroid yield, metabolic yield

A clinical approach to the thyrotropic axis Chapter | 10  153

TABLE 10.14  Parathyroid and bone indexes Relationship Index

Definition

Import

Direct

Inverse

Correlations

Para-thyroid hormone index (PTH)

It measures the endocrinometabolic activity of PTH

High: There is a prolonged appeal to PTH to solicit bone for adaptation due to the inefficiency of thyroid activity in regulating cellular respiration and/ or the efficiency of thyroid response to stimulation Low: The inverse holds true

Serum calcium

Thyroid metabolic index

Bone remodeling

Bone remodeling

It measures bone remodeling activity and the extent of bone impairment. It also bears witness to the general level of metabolism, and specifically to its adaptation activity

High: The bone is being solicited in its turnover activity to participate in adaptation as a source of calcium for adaptation and osteocalcin for metabolism Low: Favors a more efficient peripheral metabolic activity that does not require a strong appeal to bone

Serum TSH

Estrogen activity

PTH, adrenal cortex, estrogen index, corrected estrogen index

References 1. Duraffourd C, Lapraz JC. Traité de Phytothérapie Clinique: Médecine et Endobiogénie. Paris: Masson; 2002. 2. Lapraz  JC, Carillon  A, Charrié  J-C, et  al. Plantes Médicinales: Phytothérapie Clinique Intégrative Et Médecine Endobiogénique. Paris: Lavoisier; 2017.

3. Lapraz J-C, Clairemont de Tonnerre M-L. La Médecine Personnalisée: Retrouver Et Garder La Santé. Paris: Odile Jacob; 2012.

Chapter 11

Spasmophilia Nothing is exactly as it seems, nor is it otherwise. Attributed to Alan Watts (1973), rooted in the teachings of the Lankavatsra Sutra.

Introduction Spasmophilia is not a disorder, nor is it not a disorder. It is a latent terrain of probabilistic incapacity of response to solicited demands. Thus, it is a state of discrepancy between the potentiality of the organism and the expressed capacities in its adaptive modalities. To understand spasmophilia is to hold the key to a thousand doors that have no locks and embrace that which has no form. To treat spasmophilia is to have answers to questions not yet conceived and dispel that which is not present—but which is not absent either. Spasmophilia emerges when there is a disadaptation of calcium metabolism in states of normal serum calcium levels. Calcium is a crucial mineral regulated by numerous factors for numerous processes in numerous tissues. The etiology of the precritical terrain and inciting factors of spasmophilia are therefore complex and varied. The first documented spasmophilic disorder is hysteria, attributed to a woman’s womb, and documented in a 1900 BCE papyrus.1 Spasmophilia can be mental (indecision, panic attacks, bipolar depression), neurologic (migraine), neuromuscular (muscle spasms, asthmatic bronchospasms), digestive (abdominal cramps, gastric reflux), urinary (urgency, voiding difficulties), etc. Spasmophilic conditions are functional in nature, not structure. Thus, it can be challenging to demonstrate pathology when the patient is in a latent or precritical state. This is why historically, the response to spasmophilia has been to diminish, dismiss, deny, or dominate the patient. Diminishment, dismissal, and denial of symptoms are expressed through nosologic terms such as “psychosomatic,” “idiopathic,” “hypochondriac,” and “malingering.” Domination has been expressed in three ways: isolation, control, and cutting—sometimes all three in the same patient. Isolation of patients occurs in mental wards. Control is the use of physical or chemical restraints (psychiatric medications). Cutting involves various disorders from trephination (since the Neolithic era),2, 3 to hysterectomy,1 lobotomy, and leucotomy.3–5 The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816908-7.00011-6 © 2019 Elsevier Inc. All rights reserved.

According to the late Dr. Duraffourd, up to 85% of given population have latent spasmophilic tendencies. We theorize that contemporary, industrialized societies express a greater spasmophilic tendency than preindustrial ones.1 Functional spasmophilia can touch anyone at any time due to a fragilization of the terrain. The electrification of civilization has favored an unprecedented chronobiologic disruption in complex organisms. This, along with increasingly frequent exposure to man-made electromagnetic fields has impaired chronobiologic regulation.6–13 Thus, one finds an increasing number of diseases of cortico-thyrotropic disequilibrium: autoimmune disorders, insomnia, depression, schizophrenia, etc. Spasmophilia can be divided into three categories: structuro-functional, functional, and chronobiologic. Structuro-functional spasmophilia is rooted in genetic and epigenetic inheritance of particular endocrine function in adaptive modalities. There is unprecedented exposure of organisms to xenoendocrine products. This has revealed latent genetic tendencies, altering endocrine thresholds of activity.14–16 Our time is that of degenerative and self-destructive disorders: cardiovascular disease, cancer (more advancedstage cancer in younger patients), precocious puberty, allergies, autoimmune, and rheumatic disorders. Functional spasmophilia is situational and can occur in anyone with a fragilized terrain. Chronobiologic spasmophilia is related to specific phases of development, such as phases of childhood or genital recycling (The Theory of Endobiogeny, Volume 1, Chapter 13). Perhaps as a patrimony of the 18th-century French medical tradition of considering mental disorders as organic, perhaps due to the genius of Dr. Duraffourd, the approach of endobiogeny is to respect the report of the patient and seeks out physiologic imbalances of the terrain. The goal of treatment is to compensate and correct imbalances not control the patient. It is to return the patient to a latent state, restoring their endobiogenic terrain and adaptive capabilities in the face of Life and all its many splendors and travails.

Role of calcium in the organism The dialectic of calcium The great dialectic tension between material structure and functionality is that of form and fluidity, static, and dynamic. 155

156  The Theory of Endobiogeny

But this dialectic is the sound of one hand clapping, as it has but one interlocutor: calcium. Within bone marrow lie the cellular elements of adaptation: erythrocytes, leukocytes, and platelets, under management of the gonadotropic axis. Within cortical bone lies the vast majority of calcium in reserve. Calcium is the most important mineral of adaptation. Bone, under thyrotropic regulation, is the reservoir of the potentiality, intensity, gain,1 and sustain of adaptation. Bone is the great modifier of adaptability. It represents the most solid, powerful, and stable tissue in the body. And yet, from this rigidity arises the fluid adaptability of the organism through the agency of calcium.

Five stages in the sequence of events According to the theory of endobiogeny, there are five stages in the sequence of events: (1) cause, (2) agent, (3) response, (4) mechanism, and (5) effect (The Theory of Endobiogeny, Volume 1, Chapter 13). The great challenge we face in contemporary medical science is that the focus is primarily at the level of mechanism and effect. Worse, mechanisms are referred to as causes. In either case, the terrain and reality of living systems have been removed from the analysis and the treatment is geared toward mechanisms and not causes. With respect to spasmophilia, the sequence is as follows: 1. Cause (precritical terrain): Latent mismanagement of free calcium 2. Agent: Aggression (varies based on the type of spasmophilia) 3. Response (critical terrain): Neuroendocrine activity that does not sufficiently mobilize and distribute calcium for adaptation 4. Mechanism: Calcium insufficiency 5. Effects: Varied (based on the type of spasmophilia and location), the sum of the neuroendocrine response, its degree of efficiency and efficacy in mobilizing and delivering calcium and the tissue most in need We start our discussion at the fundamental level of agent and mechanism, reflect on causes then conclude with the bookends of response and effect.

Roles of calcium Mechanical structural Calcium is the element par excellence of mechanical structure. Bone is 70% inorganic calcium salts and associated minerals, 30% organic material such as collagen.17 The structural role of calcium in bone confers functional benefits. The functional role confers structural integrity (Table 11.1). Calcium’s dual roles are nested within each other. 1. Gain refers to the ability to increase power or amplitude.

TABLE 11.1  Six roles bone arising from the structural role of calcium Structure

Role

Support

Support against gravity, multiplanar mobility, greater degrees of freedom of movement

Movement

Leverage for muscle: input force amplification that makes output force more efficient and thus improves torque (force × distance). Bone functions without skeletal muscle; the inverse is not true

Adaptation

Protects and nourishes marrow for production of red and white blood cells and platelets used in adaptation

Electrolytes

Participates in electrolyte balance: calcium, phosphate, magnesium, etc.

pH

Participates in alkalization via calcium carbonate

Protection

Protects vital structures (brain, lungs, heart, kidneys, liver, marrow), reducing risk of injury and death during existential aggressions

Of the six roles of the skeletal system, five have direct nested activity with function. The sixth, protection, is implicitly related to function. There is on average 1000 g of calcium in the adult human body, 99% of which is stored. The 1% (10 g) free calcium is distributed between serum, interstitial tissue, and cells. Thus, the skeletal system represents a major well of calcium in reserve for the organism. Calcium also plays a role in all three levels of metabolism: structural (i.e., basal), structuro-functional, and functional (cf. below).

At the threshold of structure and metabolism: Free vs bound calcium Bone is a living and dynamic tissue that uses inorganic mineral salts, primarily calcium, to create a light, shock-­absorbent structure. The turnover of calcium in bone is constant and permanent throughout life. Thus, bone is not a calcified tissue, which refers to deposition of calcium in soft tissues. Between hard and soft tissue lies liquid tissue: blood. Blood is the most fluid tissue born of the most rigid. Bone is the house of marrow, the womb of the cellular elements of blood. Blood serves as the interface between hard and soft tissues, between form and function, and between structural and functional metabolism. Calcium travels the sanguine highway like a dharma bum in a permanent peregrination. However, the laws of chemistry and demands of adaptation

Spasmophilia Chapter | 11  157

seek to constrain its movement in blood. On the one hand, the greater the availability of calcium in the blood is, the greater its potential role in adaptation. However, this also poses a risk for calcification of soft tissue. Thus, the organism must constantly seek a point of equilibrium that maximizes adaptation and minimizes calcification. The answer lies in the dynamic equilibrium of bound vs free calcium. Approximately 40%–45% of all circulating calcium is free or ionized. The majority remains bound to carrier proteins, chiefly albumin. When we discuss calcium’s role in metabolism, we explicitly refer to free calcium. Total serum calcium refers to free plus bound calcium. It is not only the factors that mobilize calcium that are key to the efficiency of adaptation but also those that ensure calcium’s bioavailability and utilization by cells.

Structural metabolism In structural metabolism, calcium is once again the most important mineral as it has the greatest number of roles. We can categorize calcium’s roles by location and activity. Calcium acts in all areas: intracellular, transmembrane, interstitial, and humoral. Its modalities of action are two: electrical and electro-structural. Electrical activity is transmembrane propagation of electrical charges such as neuronal impulses and cardiac rhythms (Fig. 11.1). Electro-structural effects refer to conformational changes that calcium exacts on various protein species through its binding to negatively charged domains. This

occurs at all levels of the organism. Within the cell, several enzymatic activities are calcium dependent in what is referred to as second messenger pathways. The first messenger is the primary signal or information carrier. It binds to a receptor, translocates, etc. to activate a first response. The first response, for example, the production of inositol tri-phosphate (IP3) stimulates the release of calcium stores from the endoplasmic reticulum of the cell, resulting in various effects thanks to special intracellular proteins, chief amongst them the calmodulin and annexin family of proteins, both highly conserved. For example, calcium binding to calmodulin results in a conformational state from closed to open. Calmodulin then plays a role in activities as far ranging as brain, cardiac rhythmicity, and circadian rhythms at the mechanistic level.18 By these mechanisms, both electrical and electrostructural roles of calcium act in a complimentary and additive fashion. For example, contractility of the heart relies on transmembrane calcium movement and depolarization. However, the response of the calcium channel within the cell membrane depends in part on calmodulin, activated by calcium. Considering the various genetic polymorphisms in the subunits of calmodulin, as one example, one can see how the general spasmophilic precritical terrain produces specific illnesses in one patient vs another. Thus, we find that at the downstream mechanistic level, calmodulin is implicated in cardiac dysrhythmias, Parkinson’s disease (dopamine dysregulation), and global system chronobiologic disorders such as insomnia and seasonal dysfunctions.18

• K+, Cl– (out) • lto1,2 (transient outward)

• Ca2+ (in), K+ (out) • lCa-L (Ca long) • lKS (K slow delayed rect.)

1

+52 mV

2

• K+ (out) • lKS (K slow delayed rect.) • lKR (K rapid delayed rect.) • lK1 (inward rect.)

• Na+ (in)

3

0

• lNa (rapid)

4

–96 mV

• K+

4 200 ms

• lK1 (inward rect.)

FIG. 11.1  Electrical activity of fast-response ventricular myocytes of the heart. The ingress of sodium (Na: phase 0) initiates depolarization, but it is calcium (Ca: phase 2) ingress that determines the amplitude and duration of the depolarization. (Reproduced from Quasar derivative work: Mnokel (talk) derivative work: Silvia3 (Action_potential2.svg) [CC-BY-SA-3.0] via Wikimedia Commons.)

158  The Theory of Endobiogeny

Annexins also play profound and fundamental roles in cellular activity (Fig.  11.2). One example is endocytosis, such as cholesterol incorporation into cells for steroid hormone production. A second example is exocytosis, such as hormone glandular excretion. Annexins help anchor receptors across the cell membrane, organize the lipid membrane as well as the cytoskeleton. The antiinflammatory response of cortisol is mediated through annexins. Annexins also play a mechanistic role in apoptosis and cancer development. They also help regulate coagulation and fibrinolysis.19 Returning to the general discussion of calcium’s electrostructural activity, at the tissular level we have the contraction of muscle. At the serum level, once may consider the activation of clotting proteins.20 For example, prothrombin circulates in the serum. It contains glutamate receptors that bind calcium to particular residues. Prothrombin is activated to thrombin when calcium binds to tight binding receptors. There are four additional weak-binding sites to which calcium may also bind. This allows for interaction of thrombin with proteins and phospholipids. From the endobiogenic perspective, while calcium is crucial in all these activities, long-term calcium administration is not a panacea to “cure” or regulate the constitutive activities related to calcium. It is the terrain as regulated by the endocrine system that creates the demand for calcium. And it is the same terrain that determines the quantity, distribution, timing, and mobilization of stored calcium, be it

from bone or intracellular sources. Thus, the import of this discussion is only to contextualize the role of calcium in structural and adaptive states of metabolism and thus highlight its role as a buffering agent of the terrain.

Structuro-functional metabolism Structuro-functional activity refers to the adaptation of basal cellular endocrinometabolic and organotissular demands. This can be an alteration in the rate or intensity of function. With respect to minerals, calcium plays a constitutive role. Recall that bound structural calcium in bone is a force multiplier allowing for efficient physical movement. Free ionic calcium is a force multiplier of adaptation allowing for efficient movement of Life within the organism. With respect to the autonomic nervous system (ANS), the para-sympathetic nervous system is most implicated as the regulator of the rate of metabolism. Within the endocrine system, the gonadotropic axis is most implicated— namely estrogens, as the initiators of metabolism. The structuro-functional demand can be intrinsic to the cell, such as growth or mitosis. It can be organo-metabolic, such as increased production of hormones. As we will discuss later in the chapter, there are particular structuro-functional phenotypes related to dysregulation of estrogens. Thus, the gonadotropic axis is the initiating axis in structurofunctional spasmophilic conditions.

FIG. 11.2  Various roles of annexins. Numbers in parenthesis refer to references from the text from which the image was taken. (Reproduced with permission from D’Acunto CW, Gbelcova H, Festa M, Ruml T. The complex understanding of Annexin A1 phosphorylation. Cell Signal 2014;26(1):173–178. https://doi.org/10.1016/j.cellsig.2013.09.020.)

Spasmophilia Chapter | 11  159

Functional metabolism Functional adaptation is adaptation of the regional or global metabolism of the organism during the various adaptation syndromes (The Theory of Endobiogeny, Volume 1, Chapter 12). Thus, alpha-sympathetic and the corticotropic axis are implicated as the response elements to the adaptation demand. In cases of both structuro-functional and functional spasmophilia, various emunctories and adaptative congestive states are implicated. Table 11.2 summarizes the general relationship of types of spasmophilia and elements of the terrain implicated.

Relationship of calcium to elements of the terrain Minerals Calcium acts synergistically and typically in concert with other minerals (cf. Fig. 11.1). They have additive, additivecompetitive, competitive, and complimentary functions, summarized in Table 11.3. Part of the contextualization of

the sufficiency of calcium in adaptation is its qualitative relationship with these other minerals with respect to concentration, localization, availability, and sequencing of function. Calcium, sodium, and potassium are the three most important cations in the body. The basal dialectic is between sodium and potassium. Recall that sodium is the primary extracellular cation, potassium the primary intracellular one. Calcium, though its concentrations are relatively low compared to sodium and potassium, serves as a pivot or, quite literally, a spark between the two. Na/Ca pumps regulate the concentration of sodium and calcium, which regulates membrane depolarization (cf. above, structural metabolism). Calcium also acts as a spark to stimulate transient potassium egress from the cell, allowing cells to have a lower threshold for depolarization (Fig. 11.3).21 The relationship of calcium to phosphorous maintains a particular logic in the regulation of the adaptation response. When calcium is released from bone, it is released largely as calcium phosphate. Thus, both calcium and phosphorous levels rise in the serum. Phosphorous stimulates calciuria, which safeguards the organism against rapid, prolonged, or excessive adaptation response, and hence, against soft tissue calcification.

The special role of magnesium TABLE 11.2  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

TABLE 11.3  Role of minerals in the regulation of serum calcium availability Factor

Location

Action

Effect

Sodium, chloride, potassium

Kidney

Retention of calcium

↑ Serum calcium

Magnesium, lithium, cobalt

Intestines

Absorption of calcium

↑ Serum calcium

Phosphorous

Kidney

Calciuria

↓ Serum calcium

Magnesium (Mg2+) is the doppelgänger of calcium. It has additive, inhibitory, and complimentary effects in structure and function. Like calcium, functional central TRH + histamines as neurotransmitter

Lifestyle

Insufficient sleep Altered diurnal rhythms Insufficient hydration Poor alimentary quality and hygiene

Environment

Cosmobiologic stress Geopathic stress Chronic exposure to power lines Early (viz., perinatal or childhood) exposure to endocrine disruptors and xenohormones Chronic adult exposure to endocrine disruptions and xenohormones

Epigenetics

Generational exposure to factors noted above

in organized, urban societies to autonomic function that ­exceeds the ­actual survival and adaptation requirements of the organism. Because of this reality of the dynamics of the human personality, ANS dysfunction is quite often that which initiates or aggravates the terrain. Therefore, if one is in doubt as to the type of spasmophilia, regulate the ANS.

Autonomic spasmophilia is a state in which the timing of beta is abnormal. This can occur in two ways. The first is nonsequential or blocked beta (Fig. 11.9). In this case, para and alpha relay back and forth without allowing sufficient time for beta to express. An example of this is atrial fibrillation. The active phase of atrial contraction is absent due to the fibrillation, a type of para-alpha-para cycling. The second ANS spasmophilia is delayed beta. Fig. 11.10 shows the ANS function of a 33-year-old woman with infertility and progesterone-predominant premenstrual syndrome. In the late follicular phase, she has a true deficiency of progesterone. There is a moderate augmentation of para-sympathetic activity to readapt the organometabolic ovarian production of progesterone (The Theory of Endobiogeny, Volume 3, Chapters 4 and 5). However, due to a genetically inherited tendency of the ovary to respond insufficiently to LH in the face of estrogen activity to excrete progesterone, alpha is (over) solicited to adapt the time for production of progesterone. The sustained intensity and duration of alpha favors increased production of progesterone but delayed release. Her progesterone is released late (after the optimal timing for ovulation) and is excessive, resulting in infertility and engorgement of her breasts. There are a number of physiologic consequences from this sequence of events with symptomatic implications. First, the total drop in pressure from zenith to nadir is greater in a spasmophilic terrain, submitting the organism to cycles of excess and insufficiency, be it of nutrients, tonus, pressure, etc. (Table  11.9). While the total duration of the cycle has increased in time and intensity, the absolute time of recovery has been reduced, in this case by 15%. As a result, the organism has less time to recover, to reestablish its buffering capacity, electrical gradients, adenosine diphosphate (ADP) conversion to ATP, glucose storage, etc. A spasmophilic terrain degrades the organism and favors the development of various types of disorders. According to the particular endobiogenic terrain of the organism, there are various permutations of alteration of pressure, time and rate of rise for each segment of the cycle, as well as recovery time. Because of the inheritable and epigenetic influences on distribution and function of ANS neurotransmitters, receptor isoforms, and second messenger responses, the particular symptoms will vary from patient to patient.

Functional spasmophilia Functional spasmophilia is a reactional compensatory response to exogenous adaptation demands (Table 11.11). It occurs when an alternation of the rhythms of life are imposed or must be installed. There are four general initiatory events: shock, lifestyle, cosmobiologic, and geopathic events (Fig.  11.11). All are interconnected to varying degrees. A single event or more commonly, multiple different events may occur at once.

166  The Theory of Endobiogeny

FIG. 11.9  ANS spasmophilia due to blocked beta. The dot and dash blue line represents the normal sequencing of the ANS. The red line shows a schematic representation of para-alpha-para cycling without time for para. See text for details. (© 2015 Systems Biology Research Group.)

FIG. 11.10  ANS spasmophilia due to delayed beta. The dot and dash blue line represents the normal sequencing of the ANS. The red line shows a schematic representation of slightly elevated para with excessively elevated alpha. Beta is delayed but proportional to alpha intensity and duration when it occurs. Since alpha is prolonged, beta is greater than normal. See text for details. (© 2015 Systems Biology Research Group.)

TABLE 11.9  Physiologic consequences of a spasmophilic terrain Condition

Excess

Consequence

Insufficiency

Consequence

Perfusion

Hyper perfusion of nutrients

Inflammation, hyperanabolism, altered cerebral-mediated consciousness

Hypoperfusion

Glucose

Hyperglycemia

Hypoanabolism, acidity, ketosis, altered cerebralmediated consciousness

Calcium

Hypercalcemia

Soft-tissue calcification

Hypocalcemia

Muscle tone

Hypertonicity

Hypertension, contractions, reduced range of movement

Hypotonicity

Hypoglycemia

Hypotension, flaccidity, weakness

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FIG. 11.11  Functional spasmophilia events are four: shock, lifestyle, cosmobiologic, and geophysical. Each has subcategories. See text for details. (© 2015 Systems Biology Research Group.)

Shock Definition A shock is defined as a sudden, intense, and existential threat to the organism. It can be due to exogenous or endogenous causes. It can be physical in nature, such as sudden exposure to cold or intense exertional demands. More often it is emotional in nature. Thus, the existential nature can be real, probable, or perceived. A significant burn injury is a real existential threat. In the moment of a motor vehicle accident, existential demise is a probability. A traumatic recall of survival of such an event is an imagined existential threat. Perceived existential threats are based on the cognitive framework, internal and external resources, and prior experience of the organism. It can be in anticipation of a recurrence of prior shocking events, such as verbal or sexual

abuse or accidents. The organism can be exposed to chronic, repetitive aggressions of a lower intensity. This includes work (i.e., job loss) and family-related stresses (i.e., divorce, drug use by a child), environmental, and circumstantial issues. The endobiogenist must be aware of these events in a patient’s life and its relationship to the onset of disease, even if it is not in their training to address the trauma (cf. The Theory of Endobiogeny, Volume 1, Chapter 13).

Pathophysiology The pathophysiology of shock states is rooted in the general adaptation syndrome with an evolution to an adaptative state (cf. The Theory of Endobiogeny, Volume 1, Chapter 12). The chronic, repetitive stressors initially solicit immediate and chronic adaptation responses but may evolve into adaptative states (Fig. 11.12). Recall that the sympathetic nervous

FIG. 11.12  Adaptation according to the theory of endobiogeny. There are various types of adaptation and adaptability states. A shock state evokes the general adaptation syndrome, which can devolve into chronic adaptation syndrome or an adaptative state if the perception or recall or the presence of the aggression persists. (© 2015 Systems Biology Research Group.)

168  The Theory of Endobiogeny

FIG. 11.13  The organism and its engagement with the external milieu. The organism (large triangle, right), engaged with the external milieu (smaller triangle, left). The general options or the organism are entrainment (i.e., of rhythms), engagement (i.e., external threats), or entry (i.e., of a foreign entity or substance). The organism utilizes three general faculties, which are linked through their exchange within the limbic area. These faculties are the central and autonomic nervous systems, various states of consciousness, and endocrine management of metabolism and the terrain. (© 2015 Systems Biology Research Group.)

system and the corticotropic axis are the initiators of these responses with a relaunching of thyroid activity via the alpha-TRH relationship. Overtime, these events will degrade the terrain through exhaustion of buffering agents such as magnesium, calcium, gamma-aminobutyric acid (GABA), hepatic congestion, etc. Recall the relationship between the external and internal worlds, between the central nervous system (CNS), ANS, and endocrine system, is linked by the limbic area’s processing of internal and external events at deep animal-like levels of evaluation (Fig. 11.13).

Biology of functions There are two ways of evaluating the indexes of the biology of function. The first is the pre-critical and critical terrain of spasmophilia, namely the leukocyte mobilization index (LMI) and platelet mobilization index (PMI). The PMI will

be low in spasmophilia. If the LMI is normal, beta sympathetic activity is delayed. If the LMI is high or low, then beta is blocked, in Endobiogenic parlance. In addition, a number of indexes can be related to the consequences of spasmophilia (Table 11.10). The function values are more relevant than the structure values in spasmophilia.

Associations Shock states alter lifestyle choices (cf. below). Once again, one sees bimodal responses, i.e., hypersomnia and insomnia. Both alter physiologic rhythmicity and relationship to the external rhythms. Shock states alter dietary choices due to the nutritional value and quality of particular foods vis-à-vis central and peripheral demands. For example, in a high-cortisol, high-thyroid adaptation state, the consumption of whole grain foods and root vegetables can

TABLE 11.10  Some BoF indices to evaluate during shock states Axis

Index

Value

Comment

ANS

Starter index

↑

Alpha predominant response: typically, in adults

↓

Beta predominant response: typically, in children

↑

βMSH predominant: favors excessive TRH relative to endorphins

↓

αMSH predominant: evaluate dopamine and alpha-sympathetic activity

ACTH

↓

Intense ACTH solicitation and action with quick inhibition

Cortisol

↑

May be adaptive if evaluated shortly after onset of acute stressor, if chronically elevated, likely adaptative and reflective of a resistance to what is

↓

May indicate poststressor compensatory recover to allow for anabolic predominance; chronically, favors degraded adrenal output state

CNS

Corticotropic

βMSH/αMSH

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TABLE 11.10  Some BoF indices to evaluate during shock states—cont’d Axis

Index

Value

Comment

Thyrotropic

Thyroid relaunching

↑

It witnesses the degree of disadaptation of the organism

Thyroid relaunching corrected

↑

As above, from specifically endogenous causes such as due to reactive modalities of cognitive-emotional states

TRH/TSH

↑

Indirectly suggests a tendency to run through exhaustive permutations of events, asking “What if this…” to several degrees of relatedness, or several degrees of absurdity

↓

Indirectly suggests a tendency to become process oriented, to make inflexible plans of action and response that may be contrary to the best interests of self

↑

May be adaptive if evaluated shortly after onset of acute stressor, if chronically elevated, tends to be adaptative; evaluate relative to adrenal cortex function—it may represent an adaptive strategy to limit metabolic rate to preserve or protect the organism

↓

May indicate poststressor depletion of thyroid activity or resistance of the organism to movement in chronic cases. Evaluate relative to adrenal cortex function—it may represent an adaptive strategy to limit metabolic rate to preserve or protect the organism

Thyroid

prove beneficial to shift global energy distribution from central to peripheral metabolism and reduce inflammation. Cosmobiologic events can induce existential threats (i.e., motor vehicle accidents, suicide attempt, myocardial infarctions, cancer metastasis, etc.).7, 32–37 They, like all four categories of initiators of functional spasmophilia can degrade the terrain, reduce buffering capacity and diminish the adaptability of the organism to additional aggressions (cf. below).

Lifestyle Lifestyle choices regarding work, sleep, and alimentation may also fragilize the terrain and favor spasmophilia. Nocturnal work and onset of sleep after midnight both alter melatonin output and rhythmicity, which disrupts the important restorative activities of melatonin and other hormones, degrading the terrain.38, 39 Certain seasons, phases of life, and states of aggression require particular nutrients to address the needs of solicited organs and endocrine glands. For example, there is a catabolic cleansing of the organisms during prespring initiated by a peak in thyroid function (Fig. 11.14). It requires proper gallbladder activity to accomplish the removal of winter-accumulated waste products. The consumption of bitter and sour foods aids this process. An alimentary lifestyle that favors foods rich in animal fats is contrary to the endobiogenic nutritional demands of this time of year, as it congests the gallbladder. The adverse dietary regimen, repeated over a number of years, results in autointoxication, acidity, and degradation of the terrain. Thus, lifestyle choices are affected and affect the other three external factors.

Cosmobiologic Cosmobiologic demands are a frequent source of functional spasmophilia. It does the endobiogenic physician well to anticipate the chronobiologic adaptive demands of their patients. Changes during the spring and autumn are times of sensibilization for the organism that can initiate spasmophilia (Fig.  11.14). Spring-induced spasmophilia originates from a vertical thyrotropic disadaptation. On the far right of Fig. 11.4 is the prespring time. Peripheral thyroid function diminishes and is relaunched before the first day of spring, March 20–21 in the Northern hemisphere. If T4 activity declines below the endobiogenic threshold of the organism, TRH is relaunched to readapt TSH and the thyroid equilibrium. If the TRH action exceeds peripheral thyroid response, a centrally induced hyperthyroid spasmophilia ensues. The hyperfunctioning TRH stimulates myolysis. The resulting increase in glutamic acid binds serum calcium. TRH’s conversion of T4 to T3 favors calcitonin release and storage of calcium over T4-mediated osteoclasty. In toto, there is reduced ionic calcium for adaptation demands. Autumn spasmophilia lies within sympatheticocorticotropic activity (center of chart, preautumn). There is a rise in global adrenal cortex function and adrenaline to readapt body heat in the face of declining temperatures. If the rise in adrenaline is excessive, it fixes calcium to glutamate, setting off a spasmophilia. Increased cortisol participates in this action by its genomic upregulation of beta-receptors. The earth’s mean geomagnetic activity, functions inversely with that of peripheral thyroid activity, except during the prespring decline in thyroid activity. In general, the lower the geomagnetic activity, the greater

170  The Theory of Endobiogeny

FIG. 11.14  Seasonal chronobiologic adaptation syndrome according to Dr. Duraffourd, with geomagnetic data provided by and used with permission of Professor Alfonsas Vainoras, MD, Habil. Dr., Lithuania State Medical University Institute of Cardiology, mean magnetometer readings from Lithuania, January–December 2015. Endocrine function is shown in relative levels of fluctuation. Geomagnetic data are shown in absolute value, in pico Teslas (pT). Dates are shown in the US system where the month precedes the day of the month. Dates apply for the Northern hemisphere. From the left, geomagnetic activity is the highest line, followed by peripheral thyroid. The lowest line is the adrenal cortex. See text for details. (© 2016 Systems Biology Research Group.)

thyroid activity needs to be to readapt the internal heat and metabolic rate of the organism. While the activity shown is mean data, there are daily fluctuations. If geomagnetic activity surges during a time of strong thyroid activity, such as winter, it can disturb the endobiogenic equilibrium of the organism though a state of hyperfunctioning and consumption of calcium. Conversely, when geomagnetic activity declines during states of low thyroid activity, such as summer, it can lead to a state of insufficiency of metabolism that can similarly precipitate a spasmophilic state in latent spasmophilics. In addition to seasonal changes, there are other cosmobiologic interactions that can initiate spasmophilia. These include fluctuations in solar and lunar electromagnetic activity, which also affect geomagnetic output. This disadaptation of rhythm is rooted in the pineal axel and its regulating effects on peripheral corticothyrotropic activity (cf. The Theory of Endobiogeny, Volume 1, Chapter 5). Table 11.11 presents a summary of events that initiate functional spasmophilia.

Structuro-functional spasmophilia

TABLE 11.11  Summary of events that initiate a functional spasmophilia Event

Example

Subexample

Exogenous shocks

Physical

Unique, massive Death of loved one Traffic accident, etc.

Emotional

Unfavorable personal environment (war, work, domicile) Lifestyle

Cosmobiologic

Introduction There are 10 types of structuro-functional spasmophilics (Fig. 11.15). They can be divided into two general groups: constitutional and chronobiologic unfolding. The constitutional types related to excess estrogens (calcium pooling) or insufficient androgens (calcium management). Types 1–3 exclusively affect women and type 4 affects men. The chronobiologic unfolding types are still rooted in imbalances in estrogens and androgens. However, they occur during childhood or genital recycling in adults and hence have to do with particular states of equilibrium rooted in time and space.

Repetitive shocks Relationship issues (children, parents, divorce, etc.)

Geophysical

Work schedule

Night shift work

Sleep

Sleeping after midnight

Diet

Inappropriate diet for endobiogenic terrain and nutrient demand according to adaptation demand

Seasonal adaptation

Spring Autumn

Diurnal adaptation

Insomnia, difficulty waking up

Existential

Birthday

Meteoric

Weather changes

Geopathic stress

Fluctuations in Earth’s electromagnetic output

Time changes

Daylight savings Air travel (crossing multiple time-zones)

Spasmophilia Chapter | 11  171

FIG. 11.15  Schematic of spasmophilia nosology. There are 10 types of spasmophilia subphenotypes based on constitutional or time-related genetic changes. (© 2016 Systems Biology Research Group.)

Type 1: Pure hyperfolliculinic hysteroid women Pure hyperfolliculinic hysteroid women have a defect in pituitary FSH receptors. They are insensitive to estrogen feedback, indicated by a broken blue arrow (Fig. 11.16). Thus, one finds hyper-FSH and hyperestrogen activity. Based on the genetic polymorphisms, there is relaunching of LH horizontally by FSH and radially by estrogen. Initially, this is to make an appeal for progesterone (cf. The Theory of Endobiogeny, Volume 1, Chapter 7). The rise of progesterone is not able to sufficiently inhibit estrogens because FSH stimulation is not sufficiently responsive. While progesterone makes an appeal to LH to relaunch androgens, gonadal androgens cannot meet the level of estrogen or androgen activity. This is because the prolonged and elevated estrogen activity stimulates sex hormone-binding globulin (SHBG) to bind androgens and keep the active levels diminished relative to estrogens. This constant hyperfunctioning of the gonadotropic axis submits the organism to a constant structuro-functional adaptation demand that fragilizes the terrain overtime with progressive congestion of associated organs and emunctories. There is a particular morphology and comportment to these types of women (Table  11.12). The term “hysteroid” refers to the comportmental aspects of the hyperfolliculinic type. The term is regrettable, rooted in ancient

Greek ­notions of the role of the uterus and the weakness of women.1 Nonetheless, it is the term of record. Treatment goals are inhibition of FSH and decongestion of the uterus.

Type 2: Hyperfolliculinic hyperthyroid hysteroid women In this second type, the primary hyperfunctioning of FSH and estrogens solicits and entrains hyperfunctioning of gonado-thyrotropic activity. The physiology of this relationship as related to calcium metabolism was noted earlier (cf. Figs.  11.5–11.7). The goal of treatment is to address both central and peripheral gonado-thyrotropic imbalances.

Type 3: Androgenic women Androgenic women are normally less susceptible to structuro-functional spasmophilia as their androgenic predominance favors a more stable calcium metabolism and more efficient levels of circulating free calcium. Androgenic women who exhibit spasmophilia exhibit a conflict between their estrogens and androgens. That is to say, the established mechanisms of regulation of peripheral gonadotropic activity do not occur in the typical rhythmic cybernetic fashion. Based on the genetic and epigenetic

FIG. 11.16  Type 1 Spasmophilia: pure hyperfolliculinic hysteroid women. See text for details. (© 2016 Systems Biology Research Group.)

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TABLE 11.12  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.

factors, they have improper regulation of central and peripheral folliculo-luteal dynamics. Endogenous reasons can arise from a variety of factors that augment estrogen expression, such as TRH during seasonal changes or emotional and physical stressors (Table  11.13). Use of estroprogestive medications for conception, contraception, medical disorders (i.e., acne), and sexual lifestyle choices is a common source of disequilibrium of the terrain of

TABLE 11.13  Some potential sources of spasmophilia in androgenic women Origin

Event

Seasonal

Spring readaptation of T4 by TRH

Emotional stress

TRH relaunching by locus ceruleus

Menstrual cycle

FSH peaks on menstrual days 7–9, and 12–13a Estrogen peaks: D10–18, D21–23 TRH peaks: Ovulation, D21–23

Iatrogenic

a

Estro-progestive therapies Thyroid supplementation with estrogen relaunching

Assumes a 28-day menstrual cycle with ovulation on days 12, 13, or 14. See The Theory of Endobiogeny, Volume 3, Chapters  4 and 5 for a full discussion of the menstrual cycle.

these women. Children born to mothers treated with estroprogestive therapies during pregnancy can also express a spasmophilic terrain after birth. Their spasmophilic comportment is labile because they exhibit intermittent androgenism. As their estrogens and androgens are in conflict in the periphery, they are also in conflict in the brain as neurosteroids related to mental and emotional response patterns. Because of their natural androgenic nature, these women guard their independence in relationships. However, during times of estrogen predominance, they seek a strong man but are not satisfied with them for long. When they also exhibit an inverse relationship of evoked to potential histamine, it indicates emotional vulnerability and sensitivity. In the face of emotional stress, these women aggressively resist and attack their male partners, only to feel contrite later when their estrogens resurge. The goal of treatment is to balance estroluteal activity and regulate the adrenal cortex. The latter assists in achieving the former by delaying the secretion and excretion of estrogens and by increasing estrogen binding to SHBG.

Type 4: Constitutional hypoandrogenism: Men As noted, men less frequently exhibit structuro-functional spasmophilia. The natural androgenic predominance of the male terrain allows for a more stable regulation of calcium by men. Men who suffer from constitutional hypoandrogenism typically exhibit a relative hyperestrogenism. This favors the type of calcium consumption noted above and thus reduction in available free serum calcium. The goal of therapy is to relaunch androgen production.

Type 5: Vagotonia of childhood: 1.5–6 years Infants and toddlers are vagotonic as part of the chronobiologic programming of rapid growth (cf. The Theory of Endobiogeny, Volume 1, Chapter  13). There are two ­subtypes of vagotonia of childhood. Type 5a is a physiologic vagotonia that resolves by 3–4 years of age. During this time, given the relative estrogenism of children, they are susceptible to spasmophilic episodes. Type 5b is a constitutional vagotonia that persists into school age. These are children whose vagotonia extends beyond 4 years of age due to a genetic predisposition. Examples include a sweet and docile comportment, prolonged periods of sleep and napping, enuresis, elevated calorie-to-weight ratio,2 and preference for sweet foods. Recall that a thyrotropic subprogram runs in childhood from 1 to 7 years of age (Table 11.14), which can further fragilize the child, especially type 5b if they

2. The caloric requirements of humans are 50 kcal/kg for 1–9 kg of weight, 20 kcal/kg for the next 10 kg of weight (10–19 kg) but only 10 kcal/kg for every kg of body weight >19.

Spasmophilia Chapter | 11  173

TABLE 11.14  Recapitulation of the childhood endocrine programming

have latent hypothyroidism (cf. The Theory of Endobiogeny, Volume 1, Chapter 8 and Volume 2, Chapter 10). The thyrotropic influence on metabolism solicits an adaptive vagotonia and estrogenism. The comportment is similar to the folliculinic hysteroid type though with a different pathophysiology (Table 11.15). First, the FSH-estrogen activity is induced by TRH (TRH → FSH → Estrogens), not FSH. Second, the pronounced activity of estrogens on metabolism is due to sensibilization by TRH and to a degree by prolactin, not a quantitative increase in estrogens. Estrogens of childhood are dedicated to the exterior, not secondary sex characteristics. In type 5a, latent spasmophilia arises from the 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. Thus, we understand that the tantrums of the “terrible two’s” originate in the thyrotropic subprogramming related to physical, emotional, and intellectual growth. But it also originates in the interaction between the child and

TABLE 11.15  Morphologic and comportmental characteristics of children during early toddlerhood Endocrine

Morphology

Comportment

FSH

N/A

Hyperemotive, emotionally labile Seduces by helplessness or cuteness to manipulate the behavior of others Unstable relationship with mother: attachment and dependence with periodic fight and flight (i.e., running away to play or hiding)

Estrogens

Smooth skin Silky hair

Open Participatory and communicative

the caregiver. The development of the child is inevitable but conflict is not. It arises from a lack of alignment between the expectations of the child and caregiver, between the personality of the child and the personality of the caregiver. Teaching caregivers how to be more aware of this and to learn to bring greater alignment to caregiving should be considered a part of the endobiogenic treatment.40–42 The transition from metabolics to endocrinotissular activity of the thyrotropic axis reduces the sensibilization to estrogens and thus the emotional lability and tantrums by 3–4 years of age. The therapeutic aims are two. First, offer low-glycemic easy to digest foods. Second, respect the emotional and intellectual integrity of the child by offering firm yet flexible and loving support. The use of medicinal plants or oligoelements should be restricted to cases of comportmental discrepancies between the caregiver and child, or destructive behavior by the child to themselves, others or to valuable property. In type 5b, the vagotonia and thus the emotional lability persist beyond 4 years of age because the vagotonia is constitutional. That is to say, the genetic and epigenetic thresholds of para-sympathetic and insulin activity, receptor isoforms and densities as well as insulin resistance are intrinsically more pronounced. These children exhibit elevated para and insulin resistance with hyperinsulinism and diminished insulin sensitivity. The goal of therapy is similar to type 5a but with more prolonged emphasis on digestive support. It is recommended to start with oligoelements such as magnesium, then spasmolytic gemmotherapy such as Ilex acquafolium (holly), Tilia tomentosa (linden bud) or with Melissa officinalis (lemon balm), or, aromatherapy such as with Lavandula angustafolia (lavender) or chamomile varieties (Anthemis nobilis, Matricaria recutita). The use of medicinal plants that regulate TRH activity such as Leonurus cardiaca or Vibernum lantanum or the homeopathic remedy Lac caninum 3×–6× can be used as a second line of treatment. Self-awareness and self-regulation techniques can also be taught to children typically from 5 to 6 years of age.43

Type 6: Hyperestrogenism, thyrotropic disequilibrium: Emancipation Emancipation is the period of completion of physical and moral development of the organism that occurs between 28 and 32 years of age. It is the time that represents (1) completion of external and internal physical growth and fashioning, (2) completion of moral growth through individuation from family, friends, and societal influence, (3) establishment of romantic ties: marriage, reproduction, and establish of a new nuclear family unit, (4) establishment of a professional career, and (5) economic independence. Emancipation occurs during a re-equilibration of estrogen activity. A spasmophilic crisis can occur when this estrogen appeal is met with thyrotropic disequilibrium. This can be due to endogenous

174  The Theory of Endobiogeny

dysfunction of the gonado-thyrotropic function, or, more typically, due to a crisis in one or more of the five lines of development. The goal of treatment is gonado-thyrotropic equilibrium and to assist the patient in identifying the aspects of emancipation that have not been met. To avoid the emancipation spasmophilia, we prefer to help patients identify and develop these lines of development between 22 and 25 years.

TABLE 11.17  Summary of initiating events in structurofunctional spasmophilia Event

Example

Subexample

Gonadotropic

Genital activity

Menstruation Ovulation Pregnancy Emancipation Genital pause

Grand phases of life

Puberty Gonadopause

Childhood Individuation

Thyrotropic growth Thyrotropic readjustment related to gonadotropic readjustment during emancipation

Type 7: Chronobiologic hypoandrogenism in adolescents During the chronobiologic unfolding of pubertal development, there is a prolonged period of repeated gonadotropic adjustments through metabolic, then tissular then endocrine activity (Table  11.16). During this time, adolescents, boys and girls, can develop altered rates of estrogenic vs androgenic activity. Androgen activity can be delayed in time relative to estrogens, insufficient, or deficient, resulting in relative or absolute hypoandrogenism. The estrogenic predominance favors a structuro-functional spasmophilia. The goal of therapy is to relaunch androgen production. One must be careful not to induce closure of the epiphyseal growth plates during therapy. Thus, a gonadotropic regulator such as Lepidium meyeneii (maca root) or adaptogens like Panax ginseng (ginseng) or cortico-gonadotropic androgenic harmonizers such as Eleuthrococcus senticossus (eleuthero) or Sequoia gigantea (sequoia bud) GM can be of benefit. TABLE 11.16  Recapitulation of pubertal programming

Thyrotropic

of therapy is to relaunch androgen production and reduce SHGB binding of androgens. Table 11.17 summarizes the initiating events of structuro-functional spasmophilia.

Pituitary-parathyroid The evolution of the successful treatment of the spasmophilic terrain results in a latent pituitary-parathyroid axis of regulation. Thus, the patient in this state will require occasional and targeted oligoelement therapy, or plants that regulate general pituitary function or specific vertical axes according to the specific imbalances of each patient.

Iatrogenic causes of fragilization of terrain There are a number of iatrogenic (Table 11.18) that can fragilize the terrain acutely or chronically by altering ­endocrine

TABLE 11.18  Iatrogenic factor that degrade the terrain and favor spasmophilia

Type 8: Chronobiologic hypoandrogenism in adults Type 8 spasmophilia is a hypoandrogenic spasmophilia similar to types 4 and 6. However, the time of chronobiologic unfolding is the time of postpubertal gonadotropic readjustments. There are two subtypes. Type 8a occurs during gonadopause. In women, it reflects a readjustment in peripheral gonadotropic activity induced by diminished fertility potential with the atrophy of ova. In men, it tends to be more gradual and is related to diminishing testicular androgen production and increasing SHBG binding of androgens. Type 8b occurs during genital recycling. The goal

Example

Subexample

Endocrine medication

Oral contraceptives Thyroid medication Glucocorticoids

Vitamin therapy

Rapid IV injections: Ca, Mg, K, etc.

Loss of electrolytes

Diuretics Chelation High-dose vitamins (i.e., ascorbic acid, zinc, etc.) Laxatives

Psychiatric medications and therapies

Sedatives Antidepressants Misdirected psychoanalysis

Spasmophilia Chapter | 11  175

and mineral balance in the organism. It’s important to evaluate the potential role of these agents in each patient’s terrain. This can play a role in both functional and structuro-­ functional spasmophilia. The use of sedatives and antidepressants diminishes the patient’s ability to be aware of and address the emotional and existential concerns that are in turn degrading the terrain. The use of these medications does not diminish the degradation, they only dissociate the patient from their internal life, ultimately stunting or thwarting the potential for personal development and human potential. Misdirected psychotherapy focusing on perpetuation of a victim narrative or failing to direct the patient to existential and spiritual considerations of personal growth have an effect similar to the use of psychoactive medications.

TABLE 11.19  Summary of spasmophilia symptoms on review of systems System/organ

Symptoms

Meta state: Lipothymia

Derealization Dissociation Disequilibrium Weakness or emptiness Hot flushes Narrow vision Seeing stars Dyspnea

Neurologic

Vertigo Paresthesia

Musculoskeletal

Diffuse pain Diffuse tenderness Spasms Patient does not retain effects of manual therapy

Cardiovascular

Rhythm disturbances Arterial disturbances

Gastrointestinal

Hyperacidity Spasms Aerophagia

Urinary

Cystitis Spasms: Urinary disturbances

Genital

Frigidity Uterine spasms Erectile spasm Dysmenorrhea Premenstrual dysphoria

Comportment

Asthenia Hyperemotional states Depressive tendencies

Review of systems Patients can exhibit various types of spasmophilic conditions throughout their life. For example, they may have a history of infantile colic, then adolescent asthma that they outgrow at the end of puberty. They may go two decades before the onset of additional spasmophilic disorders. Thus, a history of prior spasmophilia, the age of onset and resolution, the season, geographic location, inciting, aggravating, and ameliorating factors can all be significant.

Symptoms of Spasmophilia The symptoms of spasmophilia are numerous and typically functional in nature, though they can alter the physical musculo-skeletal structure of the organism. Symptoms are summarized in Table 11.19.

Lipothymia Lipothymia is a French medical term for a syndrome that does not have an English equivalent. It is an acute, evanescent multisystem disorder. The criteria for diagnosis are not clearly defined in the French literature. We put forward endobiogenic criteria for the diagnosis of lipothymia: 1. Derealization: A feeling that things are not entirely real or coherent, but, not quite a dream And simultaneously, 1 or more of the following: 2. Dissociation: being acutely aware of being an observer of one’s own speech or movement 3. Imminent feeling of losing consciousness which never occurs 4. Disequilibrium 5. Intense and sudden weakness or feeling of emptiness 6. Hot flushes 7. Narrowed field of vision 8. Seeing stars (points of light) in the field of vision 9. Dyspnea, such as difficulty taking a satisfying breath despite normoxia

Lipothymia is ruled out if the symptoms occur 3–4 h postprandial. It is ruled out if there is diminishment of cerebral blood flow and/or loss of consciousness, which is related to syncope.

Neurologic 1. Vertigo 2. Paresthesia: they reflect local acidification with partial degradation of the myelin sheath. Phosphorous insufficiency is typically implicated. Rule out diabetes mellitus and demyelinating disorders

Musculoskeletal 1. Diffuse pain or tenderness: often the muscles undergo spasmodic contractions, resulting in paravertebral tenderness; they can result in recurrent vertebro-ligamentous displacements which do not respond in a durable f­ ashion

176  The Theory of Endobiogeny

to manual therapies such as chiropractic, osteopathy, massage, etc. 2. Muscular spasms

Cardiovascular 1. Palpitations 2. Tachycardia 3. Bradycardia 4. Extrasystolic beats 5. Dysrhythmias 6. Arterial spasms

Gastrointestinal 1. Matinal nausea 2. Gastric spasms 3. Aerophagia 4. Biliary dyskinesia: spasm of sphincter of Oddi 5. Intestinal spasms a. Colitis b. Enterocolitis c. Infantile colic

d­ isadaptation with low self-esteem and an autonomic spasmophilia. Certain spasmophilics can have both corticotropic disadaptation and autonomic dysfunction with delayed or blocked beta.

Observation Respiration Spasmophilics may exhibit a rapid and shallow breathing pattern at rest. This is a compensatory response to one of two typical causes. The first is a permanent psychic aggression. Rapid, shallow breathing induces hypocapnia, which reduces cerebral blood flow and hence cerebral metabolism. The second is a respiratory alkalosis, which is increases calcium binding to its carrier proteins, slowing down the intensity of adaptation.

Posture Posture favors the relative predominance of para vs alphasympathetic tone on the paravertebral muscles and core muscles. The patient may appear slumped (para > alpha) or erect and stiff (alpha ≫ para).

Urinary

Signs diagnostic of spasmophilia

1. Cystitis 2. Cystalgia 3. Dysuria 4. Polyuria 5. Enuresis

The diagnostic signs of spasmophilia were developed in the mid-to-late 19th century44 in an environment of experimental physiology that respected the concept of the milieu intérieur. The onset of analytical quantitative biochemistry led to an erroneous association of spasmophilia with frank hypocalcemia. We return to the original qualitative concept of neuromuscular hyperexcitability rooted in a dysfunctional terrain of calcium metabolism.

Genital 1. Premenstrual dysphoria 2. Dysmenorrhea 3. Uterine colic 4. Frigidity 5. Erectile dysfunction

Comportment Asthenia Asthenia is a feeling of lassitude, of general weakness, malaise, or ennui. It is quasiconstant and worse in morning upon waking.

Hyperemotional states This can be a structural tendency in folliculinics, or an adaptive reactional state rooted in central mechanisms related to the hierarchization of internal and external states and events.

Depressive tendency Spasmophilics are submitted to a permanent stress due to the degradation of their terrain. According to the theory of endobiogeny, depression is a peripheral corticotropic

Chvostek’s sign: General neuromuscular response to aggressions Pathophysiology Chvostek’s sign is described as a tetany that results from quantitative hypocalcemia. However, the sign is absent in 30% of patients with hypocalcemia and present in up to 25% of patients with normocalcemia.45–47 According to the theory of endobiogeny, it is a sign of neuromuscular excitability due to an insufficiency of free tissular calcium. This is consistent with our theory of spasmophilia and the clinical observations noted prior. Thus, Chvostek’s sign represents the general compensatory response of the organism in the face of aggressions.

Technique Chvostek’s sign involves attempting to elicit a response by cranial nerve VII, the facial nerve (Fig. 11.17). Chvostek I involves tapping the facial nerve as it exits the skull (A) at a point 0.5–1 cm below the lateral zygomatic arch and 2 cm anterior to the ear lobe. Twitching of facial muscles is a positive sign (Fig. 11.18). Chvostek II involves tapping

Spasmophilia Chapter | 11  177

FIG. 11.17  Chvostek’s sign: neuroanatomy. The right image shows the course of cranial nerve VII and its egress from the skull. The left image shows two areas of the face where the nerve can be provoked. See text for details. (Reproduced from (Left) Hoffman E. The Chvostek sign; a clinical study. Am J Surg 1958;96(1):33–37 and (Right) Patrick J. Lynch, medical illustrator [CC BY 2.5], via Wikimedia Commons.)

Technique The technique involves inflating a sphygmanometer on the proximal upper extremity. The pressure is retained for 3–4 min at a pressure greater than the patient’s current systolic pressure. Occlusion of the brachial artery and the ensuing ischemia elicits carpopedal spasm of the hand in positive cases. The hand takes on a swan-like contortion (Fig. 11.19). Other observed signs can be associated with additional insufficiencies of elements related to calcium function: (1) paresthesias: phosphorous, (2) fasciculation: magnesium, and (3) cramping of ipsilateral fingers: potassium.

Hippus: Mental spasmophilia Pathophysiology FIG. 11.18  Chvostek I. The ipsilateral facial muscles contract, most noticeably with closure of the eyelids and elevation of the upper lip. (Netter medical illustration used with permission of Elsevier. All rights reserved.)

the distal facial nerve (B). With the patient lying supine, mouth passively open and relaxed, one follows a line joining the corner of the mouth to the zygomatic prominence. Two-thirds of the distance from the corner of the lip to the arch one finds the egress of the nerve. Twitching of the upper lip on the ipsilateral side is a positive sign.44

Trousseau’s sign: Neuromuscular response to ischemia Pathophysiology Trousseau’s sign reflects the compensatory capabilities of the organism during states of hypoperfusion or ischemia.

The pupillary light reflex evaluates the response of the pupils to light. A sudden increase in light presented to the retina elicits a para-sympathetic response to constrict the pupil and reduce the amount of light entering the eye. This response is regulated by the ciliary ganglion of cranial nerve III, the oculomotor nerve (Fig. 11.20). The sudden rise in para-sympathetic activity elicits a compensatory alpha response, which vasodilates the pupil despite the persistence of focused light entry on to the pupil. The para-alpha reaction continues for some time as long as the light continues to be shined into the eye. Hippus refers to this spasmodic contraction and dilation of the pupillary muscle in the para-alpha volley. The paraelement indirectly reflects the relative level of serotonin activity, the alpha that of dopamine. The rate of response refers to the rapidity of the initial contraction (para) and dilation (alpha). The more rapid the response, the lower the threshold of stimulation and the greater the reactional

178  The Theory of Endobiogeny

FIG. 11.19  Performing Trousseau’s sign. See text for details. (Netter medical illustration used with permission of Elsevier. All rights reserved.) Ciliary ganglion

Oculomotor nerve Optic tract

Constrictor muscle of iris

Edinger - Westphal nucleus

Optic chiasm

Aqueduct

(of III nucleus complex)

Optic nerve Preganglionic parasympathetic part of oculomotor III

Pretectal nucleus

FIG. 11.20  Hippus and the light reflex. See text for details. (Courtesy of http://www.tedmontgomery.com/eye.)

compensatory nature of the organism in its central cognitive activity. The degree of response refers to millimeters of change in diameter of the pupil overtime. The greater the degree of dilation and/or constriction, the greater the quantitative amount of para and alpha expressed (cf. Table 11.20). A right pupillary response greater than left favors a spasmodic mental response to anticipation of events to a greater degree than rumination over past events. A left response greater than right favors the opposite.

Technique 1. Place the patient is a supine position 2. Diminish or turn off the lights in the examination room 3. Holding a bright, focused beam of light to the lateral aspect of the eye, rapidly move the light into the field of view directing it toward the pupil

TABLE 11.20  Interpreting hippus Observation

Increased

Diminished

Rate of response

↑ Qualitative para/alpha

↓ Qualitative para/alpha

Degree of response

↑ Reactivity of para/alpha

↓ Reactivity of para/alpha Evaluate for depressive terrain

Duration of response

↑ Severity of spasmophilia

Evaluate for ketosis, iatrogenic sedatives, disorders of dopamine insufficiency (Parkinson’s, mental retardation— certain types, etc.)

Spasmophilia Chapter | 11  179

4. Hold the light for up to 1 min, or, as long as the patient can tolerate 5. Observe the: a. Rate of initial constriction and dilation b. Rate and degree of subsequent response c. Duration of response d. Laterality of the response (right vs left pupil)

Glabella tap: Ratiocination capability in the face of aggressions Pathophysiology

Consider two cases. Both have the same initial response: rapid and strong pupillary constriction followed by a rapid and significant pupillary dilation. This indicates that the patient has a strong central para (i.e., serotonin: first response) and a strong and reactionary central alpha (i.e., dopamine: second response).

The glabella tap evaluates the efficiency of the organism’s ratiocination capabilities in the face of an aggression. It evaluates the relative role of thyroid relaunching and ­central regulation of the adaptation response of (1) alpha (noradrenaline): rapid movement of lower eyelid, (2) central alpha (dopamine): rapid movement of upper eyelid, and (3) TRH: flutter of both eyelids postpercussion (Table 11.21). The longer the flutter, the greater the solicitation and expression of TRH by alpha.

Case 1

Technique

Pathophysiology: the subsequent spasmodic movement of the pupil is very small with the pupil more dilated than constricted. This indicates that once elicited, the central ­alpha (dilation) is greater than the para (constriction). Alpha dominates para. Clinical: The patient is reactive to psychic aggression but quickly plans a response (dopamine) to their initial impression of aggression (serotonin) without taking the time to gather additional information or verify what they have experience. This patient may be perceived as jumping to conclusions or having a “hair trigger” for getting worried about events.

Case 2 Pathophysiology: The second constriction is substantial but further dilations are small. The pupil remains more constricted than dilated. This indicates that once elicited, the central para (constriction) is greater than the alpha (dilation) activity. Para dominates alpha. Clinical: The patient is reactive to psychic aggression but mentally “freezes.” They are awash in information (serotonin) with a relative insufficiency of planning (dopamine) in relationship to the amount of information received. This type of patient tends to emotionally “shutdown” in the face of confrontation and will often seek to avoid confrontation when possible.

1. Place the patient is a supine position 2. Ask them to focus on the ceiling, eyes open 3. Without indicating the procedure, briskly strike the midpoint of the brow just above the nasal bridge 4. Observe the response of the a. Upper eyelid b. Lower eyelid c. Postpercussive response of both lids The glabella tap adds important information to the observation of hippus. First, it distinguishes the relative degree of origin of dopamine from alpha vs serotonin (cf. Chapter  1 and The Theory of Endobiogeny, Volume 1, Chapter 3). Second, it provides information regarding the role of TRH in general with respect to the sequencing of serotonin-dopamine-TRH-histamine and alpha-dopamineTRH-thyroid relaunching. Combining the information of glabella tap and hippus, one can evaluate the relative degree of central vs peripheral physiology in the adaptation response.

Tongue fasciculation: Reticular activating system Pathophysiology The intrinsic and support muscles of the tongue are innervated by cranial nerve (CN) XII, the hypoglossal.48 Fasciculations

TABLE 11.21  Interpreting the glabella tap Speed of response

Upper (dopamine) vs lower lid (alpha)

Flutter (TRH)

Interpretation

Rapid

Upper > lower

−

Potential for efficient planning

Rapid

Lower > upper

+

Anxious, tangential planning

Normal

Lower ≫ upper

+

Panic with inefficient planning

180  The Theory of Endobiogeny

are spontaneous spasmodic partial contractions of muscle fiber groups. CN XII originates in the lower pons near the area of the RAS. The RAS regulates the general level of awareness of the organism. According to the theory of endobiogeny, glossal fasciculations reflect a general disorganization of the coherence and rhythmicity of central-peripheral activity.

Technique 1. The patient is requested to open their mouth a. Observe for fasciculations while the tongue rests in its neutral state 2. The patient is requested to extend their tongue a. Observe for fasciculations of the intrinsic muscles b. Observe for tremors of the tongue originating from the hypoglossal and genioglossal muscles

Fasciculations of skeletal muscles: TRH and spine Fasiculations are spontaneous contractions of skeletal muscle fibers when the patient is at rest. They have a similar pathophysiology as tongue fasciculation, but implicate the spinal motor neurons. The sum of factors implicated are a general spasmophilia in a terrain of increases activity of the reticular activating system, TRH and serotonin.

Hypoandrogenism, gonadal Evaluate for signs of gonadal androgen insufficiency (The Theory of Endobiogeny, Volume 3, Chapter 3.

Diagnostic studies: Serum biomarkers Alkaline phosphatase bone isoenzyme It evaluates the relative solicitation of bone and rate of calcium turnover.49–51 When the bone isoenzyme it is elevated it signifies a relative predominance of bone turnover in relationship to that of liver or intestine.52 When total alkaline phosphate is also elevated, it is more indicative of spasmophilia.

Osteocalcin Osteocalcin is a bone matrix protein. It plays a role in the restoration of calcium into bone. However, because the bone plays a role in global metabolism, osteocalcin is solicited to help regulate nonbone metabolism. Thus, the serum level of osteocalcin is inversely related to the endocrinometabolic activity of estrogens, to insulin, bone calcium restoration, and mitochondrial efficiency.50, 51, 53

Phosphorous

Signs supportive of a dysendocrinism

Typically, within normal limits or slightly elevated relative to serum magnesium.

When evaluating for signs of dysendocrinism, remember to evaluate both comportment and morphology.

Magnesium

Autonomic

Typically, within normal limits, though RBC levels may be diminished.

Evaluate for signs of para and alpha functioning evaluating both global function and targeted areas related to symptoms (Chapter  1). They are both often elevated. In adults, beta is typically blocked or delayed. In children, beta is often elevated, but can be blocked or delayed with or without an exaggerated response (i.e., an intense and long-lasting tantrum, tossing, and turning in bed).

Calcium

Adrenal hyperfunctioning

One may find elevated urine calcium levels. Evaluate phosphorus and PTH activity.

Evaluate for central (ACTH) and peripheral signs of hyperfunctioning or oversolicitation (Chapter 2).

Hyperthyroidism Evaluate for central and peripheral signs of hyperfunctioning or oversolicitation (Chapter 10).

Hyperestrogenism Evaluate for central and peripheral signs of hyperfunctioning or oversolicitation (The Theory of Endobiogeny, Volume 3, Chapter 3).

Both serum and ionized calcium levels are typically normal, even during a spasmophilic crisis.

Diagnostic studies: Urine Calciuria

Diagnostic studies: Electrophysiological Calcium is a key element in the regulation of the electrical activity of the organism. Thus, various electrophysiological measures of activity offer quantitative and qualitative assessments of global and regional electrophysiological function. The following findings can support a diagnosis of spasmophilia.

Electromyogram On electromyogram (EMG) one may find repetitive muscular activity that resolves with hyperventilation.

Spasmophilia Chapter | 11  181

Quantitative electroencephalogram Quantitative electroencephalogram (QEEG) is a form of EEG that uses sophisticated algorithms to analyze quantitative and qualitative evaluation of brain activity. It also evaluates the coherence and integration of various types of complex cognitive functions and personality across different areas of the brain. Findings of diminished coherence can be consistent with central spasmophilia.54

Electrocardiogram On electrocardiogram (ECG), one typically finds U waves and prolonged QT intervals.

Differential diagnosis Quantitative organic pathologies—especially life-threatening ones such as long QT syndrome—should be ruled out before arriving at a diagnosis such as spasmophilia. Due to the variable symptoms, the possible disorders in the differential diagnosis are large. What is listed below is not exhaustive but indicative of commonly diagnosed disorders. 1. Metabolic: quantitative deficiencies of calcium and related minerals and metabolites a. Electrolytes i. Calcium ii. Sodium iii. Potassium iv. Phosphorous v. Magnesium b. Metabolites i. Glucose ii. Oxygen 2. Endocrine a. Pineal adenoma b. Hypothalamic adenoma c. Pituitary adenoma d. Hypoparathyroidism e. Hypothyroidism f. Hyperthyroidism g. Adrenal insufficiency h. Hypogonadism i. Pancreatic disorders 3. Cardiac a. Wolf-Parkinson-White b. Prolonged QT syndrome c. Syncope 4. Neurologic a. Seizure disorders b. Demyelinating disorders c. Amyloid disorders d. Spinal cord disorders 5. Muscular a. Degenerative muscular disorders

6. Cancer a. CNS b. Spine c. Thyroid d. Parathyroid e. Metastasis to liver, pancreas, lungs, spine, CNS, etc.

Evolution of untreated Spasmophilia Spasmophilia is a state that degrades the endobiogenic terrain. This degradation impairs the buffering capacity of the organism and brings out a susceptibility to the great degenerative disorders of our time that cause a slow, whispering extinction of life: 1. Pulmonary a. Asthma b. Chronic obstructive lung disease 2. Cardiovascular a. Myocardial infarction b. Stroke c. Rhythm disorders 3. Rheumatologic a. Arthrosis b. Rheumatoid arthritis 4. Neurologic a. Multiple sclerosis b. Epilepsy c. Migraines 5. Oncologic a. Cerebral tumors (TRH) b. Breast cancer (gonadotropic + TRH)

Principles of treatment The endobiogenic approach to treatment is divided three stages: acute, subacute and chronic. The immediate aim is symptom relief. This is the cessation of the spasmodic state, be it mental, neuromuscular, digestive, etc. It can be symptomatic (e.g., analgesic), substitute (e.g., GABA-ergic) or para-sympatholytic/alpha-sympatholytic. The subacute goal is restoration of adaptability and buffering capacity. In this way, latency period is prolonged and the threshold to return to the critical state of spasmophilia is raised. Finally, the chronic goal is to treat the elements of the precritical terrain related to the patient’s spasmophilia. NB: Do not forgo the treatment of comorbid conditions as they can degrade the terrain and keep the patient permanently in a spasmophilic state. For example, a 42-year-old woman has a 6-year history of recurrent sinusitis (Chapter 9) that occurs in the spring and autumn when her environmental allergies flare up. She presents to your office 16 h into a new infection with complaint of intense sinus pressure, headache, green nasal discharge, and mild fever. The spasmophilic aspect of her disease is the blocked sinus passage and sinus headache. The acute endobiogenic treatment is the topical essential oil blend discussed

182  The Theory of Endobiogeny

in Chapter 9, which breaks the spasmophilia and is analgesic (it is antiinfectious as well). The subacute treatment is aggressive biliary drainage, especially with plants containing sulfur. The chronic treatment is goal is treating the allergic terrain, especially ENT and liver drainage.

Acute treatment of spasmophilia The general approach to acute treatment is to restore the endobiogenic equilibrium of the ANS relationship. This may be the actual nervous system, or whatever sequential function that has been disturbed (Table  11.7). Typically, this involves reducing alpha or para and alpha. The factors that drive this disturbance (i.e., mental, emotional) can also be treated. This can be accomplished in two ways. The first is pharmaceutical. The second is nonpharmaceutical.

Pharmaceutical treatments Pharmaceutical treatments are favored when 1 or more of the following are present: (1) decompensation, be it mental, emotional, or physical, e.g., hysteria, intractable pain, etc., (2) symptoms lasting >8–12 h, and (3) frequent recurrence. For example, a 38-year-old woman with three school-aged children who presents with 16 h of migraine rated 10/10 and muscular spasms of the neck that prevents her from turning her head is a good candidate for pharmaceutical treatment. A 38-year-old woman with three school-aged children who

presents with 6 h of migraine rated 6/10 and muscular spasms of the neck that are uncomfortable can be treated with a pharmaceutical product if that is her preference. Otherwise, she is a good candidate for the use of medicinal plants in acute phase treatment. Pharmaceutical treatments can be used at various doses during a spasmophilic crisis as well as for prophylaxis (Table  11.22). They can be selected based on the clinical presentation and biology of function indexes. In all cases, pharmaceuticals should be used for as short a period of time as possible at the lowest effective dose and with the aim of correcting the imbalances within the terrain.

Magnesium Magnesium is antispasmodic and relaxant. Its areas of activity include CNS, neurologic, neuromuscular, and muscular (Table 11.4). The endobiogenist must select the proper galenical form and dose of magnesium based on the requirements of the patient and advantages of each galenical form (Table 11.23). With respect to chelates, glycinate and citrate are more bioavailable than oxide and can be used at lower doses. Oral magnesium can cause bowel laxity. Dosing in Table 11.23 is for adults, listed per dose and can be repeated up to every 3 h with bowel tolerance.

Medical plants There is a class of medicinal plants that are spasmolytic because of their actions on the ANS or ANS-like ­sequences.

TABLE 11.22  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)55 CBD oil56, 57

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 4–6 months without a break) or prolonged high-dose consumption (>10,000 IU/day >3 weeks) inhibits intestinal calcium absorption and inhibits endogenous vitamin D activity. Low serum vitamin D has been ­erroneously cited as a causative factor of a host of disorders. Chronic vitamin D supplementation has not been proven to reverse most disorders associated with it64–69 and may be harmful

in certain clinical conditions.70, 71 The indications for use of vitamin D are: 1. Moderate dose in times of weakness (400–2000 IU/day) 2. States of hyperconsumption of calcium 3. According to the endobiogenic assessment of terrain considering (400–10,000 IU: the higher the dose, the shorter the period of use) a. Adaptation b. Immunity c. Thyrotropic integration d. Growth e. Antigrowth f. Bone turnover Endogenous production of vitamin D is best supported in the following ways: 1. Drainage: recall that vitamin D is metabolizes in three places: skin, liver, and kidney a. Hepato-reno-dermal: Ulmus campestre (English elm) GM b. Hepato-renal i. Betula ssp. (birch bud) GM, decoction, sap ii. Juniperus communis (juniper bud) GM iii. Zea mais (corn silk) MT, GM iv. Bitter foods v. Diuretic foods 2. Diet a. Mushrooms b. Cold water fish 3. Lifestyle a. Daily sun exposure b. Stress reduction

Regulating exogenous calcium uptake Organic silica improves absorption of calcium in a fashion that the organism can regulate according to its endobiogenic needs. It is the preferred method of improving calcium absorption according to the theory of endobiogeny. 1. Clay: bioavailable silica with trace amounts of lithium and other minerals 2. Equisetum arvense (horsetail): a. Galenic: DE, MT, BH b. Summary: a broad-acting plant with pituitary and thyro-somatotropic regulation; use for 3–6 months then take a break c. Actions: Metabolic: remineralizer (Si, CaCO3, CaPO4, KCl, KSO4, Mg, Na, S), antisclerotic, hypolipemant; endocrine: pituitary regulator, augments peripheral GH receptors (esp. bone), diminishes PTH; immune: antiinflammatory d. Precautions: can augment the effect of CNS stimulants and diuretics. AVOID: active cancer, edema due to renal or cardiac insufficiency

186  The Theory of Endobiogeny

Nonspecific: Oligoelements The following are listed in order of therapeutic importance and order of administration: 1. Magnesium (cf. above) 2. Silica (cf. above) 3. Potassium (adrenal overstimulation, muscle cramps) 4. Phosphorous (cellular necrosis, insufficient apoptosis, delayed wound healing) 5. Lithium (mental and neuromuscular spasmophilia, especially with low serum TSH and elevated cortisol activity) 6. Ionic preparations of trace minerals: quinton water, blue-green algae, etc. Certain oligoelements are complementary to calcium regulation at the level of the intestines or kidneys, or in its utilization (Table 11.6).

Nutrition

milk for infants, the animal milks from easiest to most difficult to digest and easiest to obtain are: (1) sheep, (2) water buffalo, (3) goat, and (4) cow. Raw milk in those who are not immune compromised is easier to digestion. Otherwise, fermentation and aging allow for the partial or complete breakdown of casein and lactose to offer the most bioavailable and easy-to-digest sources of calcium. Thus, we can conclude that the following guidelines can be followed with respect to consumption of dairy products: (1) full fat, (2) raw, fermented, or aged hard cheeses, and (3) easier to digest milks. Practically speaking with respect to dairy products, we can suggest the following foods, whose digestive and therapeutic values increase as they meet 1, 2, or all 3 of the guidelines, noted above, such as aged Parmesan cheese or cottage cheese. Table 11.24 lists the most efficient foods for calcium per realistic serving size as well as their calories TABLE 11.24  Foods rich in calcium

Calcium-rich foods

Food

Serving size

Calcium (mg)

Calories

The sum result of calcium metabolism as regulated by the thyrotropic axis is net loss. The greater or more prolonged the solicitation of the axis, the greater the loss of calcium. A regular consumption of calcium-rich foods offers a valuable resource for the organism. The majority of calciumrich foods are not dairy products. In fact, most of them are vegan. However, dairy products are perhaps the most consumed calcium-rich products in the industrially developed countries of North, Central and South America, Europe, Russia, and the Middle East. Therefore, dairy products offer a natural and facile source of calcium for the majority of the population in countries. Unfortunately, there are numerous challenge with contemporary dairy production. They are fed genetically modified grain and soy instead of pastured on grass. They are administered recombinant GH, steroids, and antibiotics as needed for poor sanitary conditions. The fat is removed. The milk is homogenized and pasteurized, destroying enzymes key to digestion and bioavailability of nutrients. Finally, the milk protein casein is relatively difficult to digest compared to other proteins, and the milk sugar lactose is not universally digestible by humans. The fat in dairy improves the health value of dairy products and reduces their potential impact on cardiovascular disease and metabolic syndrome.72–74 Milk from pastured animals living a rhythmic life coherent with their evolutionary development produces the most healthful milk.74 It is not clear if these same observations can be extended to contemporary practices of milk production. Finally, the composition of animal milk varies and some types of animal milk are easier to digest than others. Excluding human breast

Tofu

4 oz

775

164.4

Sesame seeds

0.25 cup

351

206.3

Buttermilk

1 cup

350

137

Sardines

3.20 oz

347

188.7

Parmesan reggiano, aged >17 months

1 oz

311

121

Yogurt, kefir

1 cup

296

149.4

Collard greens

1 cup

268

62.7

Spinach

1 cup

245

41.4

Turnip greens

1 cup

197

28.8

Cottage cheese

1 cup

174

206

Mustard greens

1 cup

165

36.4

Beet greens

1 cup

164

38.9

Bok choy

1 cup

158

20.4

Cow’s milk

4 oz

138

74.4

Swiss chard

1 cup

102

35

Kale

1 cup

94

36.4

Cabbage

1 cup

63

43.5

Broccoli

1 cup

62

54.6

Brussels sprouts

1 cup

56

56.2

Green beans

1 cup

55

43.8

Summer squash

1 cup

49

36

Parsley

0.50 cup

42

10.9

Spasmophilia Chapter | 11  187

per serving. Dairy products are listed in bold. One will note that the top two foods are vegan.

Magnesium- and potassium-rich foods The following foods offer an excellent combination of magnesium and potassium to compliment calcium intake (Table 11.25). Most can be eaten raw or lightly cooked except where indicated. All are easily digestible.

TABLE 11.25  Foods rich in magnesium and potassium Magnesium (mg)

Therapy for the terrain: Functional spasmophilia Recall that functional spasmophilia is a disadaptation to an aggression. Generally, one finds a hyperfunctioning of para and alpha with a delay or blocked beta. The two catabolic axes are implicated typically with hyperfunctioning central activity > peripheral activity (Table 11.26). Do not forget to address catabolic emunctories and the splanchnic bed.

Autonomic nervous system The plants listed can all be used as essential oils by various routes of application (in tinctures, inhaled, diffused, sublingual, rectal, topical). They can also be prepared as a tisane (listed as bulk herb: BH).

Food

Serving size

Potassium (mg)

Beet leaves

1 cup

1300

100

Swiss chard

1 cup

960

150

Lima bean

1 cup

955

Sweet potato

1 cup

950

Spinach

1 cup

840

Lentils

1 cup

730

Avocado

1 cup

730

Bok choy

1 cup

630

Beets

1 cup

520

Papaya

1 med.

500

Brussels sprouts

1 cup

500

30

Broccoli

1 cup

450

30

TABLE 11.26  Summary of treatment goals

Cantaloupe

1 cup

425

20

Factor

Subfactor

Action

Tomato

1 cup

425

ANS

Para

↓

Asparagus

1 cup

400

Alpha

↓

Barley

1 cup

240

Beta

↑

Pumpkin seed

¼ cup

190

ACTH

Regulate

Quinoa

1 cup

145

Adrenal cortex

Regulate

Sesame seed

¼ cup

125

TRH

↓

Black bean

1 cup

120

TSH

Regulate

Cashew

¼ cup

117

T4, T3, PTH

Regulate

Sunflower seeds

¼ cup

114

Splanchnic bed

Unblock

Liver

Drain

Buckwheat

1 cup

85

Kidney

Brown rice

1 cup

84

Lung

Millet

1 cup

77

Intestines

Flax seed

2 tbsp

55

Skin

155

40

Parasympatholytic and alphasympatholytic 1. Lavandula angustafolia EO best overall plant by all routes of administration 2. Anthemis nobilis EO: avoid internal use in children due to the taste 3. Matricaria recutita EO: use with chronic anger or inflammation; avoid internal use in children due to the taste

Corticotropic

Thyrotropic

Emunctories

188  The Theory of Endobiogeny

Beta acting Beta-mimetic

Cortisol/adrenal cortex ratio: >4 Treatment ● Reduce overstimulation of corticotropic axis ●

●

1. Cinnamoma zeylanicum EO: best general purpose for change of seasons, states of asthenia, digestive, infectious, and asthmatic spasmophilia 2. Satureja montana EO: excellent for change of seasons, digestive and infectious spasmophilia with androgen insufficiency 3. Thymus vulgaris EO: excellent for total adrenal support (cortex and medulla) and in vagolytics 4. Abies balsamea EO: excellent for autumn and winter spasmophilia related to the respiratory tract, especially with delayed recovery and asthenia

- Passiflora incarnata, Lavandula angustafolia, Lithium oligoelement

Support metabolic shift from glucocorticoids to adrenal androgens

●

- Sequoia gigantea GM (sequoia bud) - Rosa canina GM (dog rose bud)

Support adrenal cortex

●

- - - - - -

Beta re-launcher

Diminish prolactin if indicated

●

- Mercurialis annua (annual mercury: stronger than salad burnette in its inhibition of prolactin) - Poterrium sanguisorba (salad burnette)

1. Menyanthes trifoliata (bogbean): Exercise fatigue, asthma, inflammatory conditions that degrade the terrain

Beta producer 1. S-adenosyl methionine (SAMe): Depressive tendencies, asthenia

Case 3: Excessive global adrenal function relative to cortisol ●

Corticotropic Corticotropic disadaptation can have several variations. Three are presented below:

Case 1: Low global adrenal function ●

●

BoF ● Adrenal cortex index: low ● Cortisol index: low, normal, or slightly elevated ● Cortisol/adrenal cortex ratio: vagolytic; Endo: ● Cortico: reduces adrenal cortex activity;

1. Projet Vitadil urticaire Londres 2.doc.

Appendix A 207

●

● ● ● ●

● ● ●

● ●

Neuro: central nervous system sedative, GABAergic, can accentuate the effects of central nervous system sedatives, urinary antispasmodic, antimyalgic, antineuralgic; Immune: antiallergic; Pulm: respiratory antiinflammatory, expectorant; GI: choleretic, hepatobiliary, and renal drainer; GU: pelvic decongestant (venous activity), uterotonic; CV: arterial dilatator, venotonic, hypotensive; Heme: anticoagulant (vitamin K antagonist); ID: antibacterial (streptococcus, staphylococcus), antiinfectious (biliary, cutaneous, genital, urinary, intestinal ENT and pulmonary), antiparasitic scabicide), antiinflammatory, antioxidant; Derm: antibacterial, scabicidal, cicatrizing; Renal: volumetric diuretic;

●

●

● ● ●

Use: ● ● ●

Use: ●

●

●

Hyperalpha states: immune suppression; hyperimmunity, hypertension, tachycardia, arythmias, migraines, asthma, spasmophilia, anxiety, insomnia, ulcers, gastritis, colitis, constipation; congestion: pelvic, bronchial, venous; Infections: esp. aggravated by spasms or congestion: sinusitis, otitis media, bronchitis, infleunza, cystitis, vaginitis, prostatitis, dysbiosis; Derm (pruritic, erythematous): eczema, psoriasis, acne;

Method: MT: 1–3 mL BID-TID, EO: 2–3 drops BIDTID, tisane: 1.5 g (2 tsp) steeped 3–5 min, BID-TID, Bath: 15 min infusion of tisane or 5–10 drops EO mixed with salt, EO topical: 3%–10%; dilution, friction rub, EO neat: on upper lip, in antihelical fold.

Matricaria recutita (German chamomile) Essence: #1 nonsedating plant for treatment of anger and its physiologic consequences, excellent antiinflammatory and antimicrobial. Part used: flower and leaf Galenic: EO, MT Actions1, 2:

Leonurus cardiaca (motherwort)

Actions1, 2: ●

●

●

Endo: thyroid: TRH antagonist, thyroid-stimulating hormone (TSH) antagonist, cortico: inhibits cortisol, reduces fixation of cortisol to its receptors; gonado: slightly estrogenic, emmenagogue, uterotonic—­improves uterine contractions; Neuro: central nervous system sedative (lowers alpha, TRH),17 neurotropic antispasmodic; ANS: alpha-sympatholytic, beta-blocker (by regulating adrenal cortex activity), mild para-sympatholytic;

CV: hypertension, anxiety-induced dysrhythmias, Endo: thyro: Grave’s induced tachycardia, Neuro: all neurologic conditions rooted in hyperfunctioning of TRH especially if exacerbated with elevated cortisol: neurosis, psychiatric disorders (esp. with excessive, bizarre, or uncontrollable thoughts), poor sleep due to intense dreams, brain fog with central hyperthyroidism (+ Sambucus nigra MT, Arnica montana MT, R. nigrum GM),

Contraindications: Hypotension, bradycardia, pregnancy, esp. first trimester, lactation (may reduce the production of milk through inhibition of prolactin). NOTE: reinforces effects of beta-blockers, CNS sedatives and antiepileptics.

●

Essence: #1 plant of thyrotropin-releasing hormone (TRH) disorders related to anxiety and thyro-cardiac manifestations. Parts used: whole plant Galenic forms: BH, MT, DE

CV: cardiosedative, antiarrhythmic, hypotensive, bradycardic, hypotensive, inotrope positive, chronotrope negative, bathmotrope negative; MS: reduces muscular hyperexcitability (slightly vagolytic); Pulm: expectorant, Renal: diuretic; Cancer: antineoplastic (lymphoma, breast, colon, prostate);

●

●

● ● ●

●

●

● ●

GI: increases secretions: salivary, gastric, biliary; choleretic, aperitif, eupeptic, antigastralgic, antigastritic, antiulcerous, antacid, musculotropic digestive antispasmodic; Immune: antiinflammatory (uterine, digestive), febrifuge, sudorific, antihistaminic; ID: antibacterial (EO: gram +; tisane: gram +, gram −), antifungal, antiparasitic; Derm/mucosal: cicatrisant of digestive mucosa; ANS: sympatholytic, vagolytic; Endo: • Cortico: reduces adrenocorticotropic hormone (ACTH); Neuro: antalgic, sedative, neurotropic antispasmodic (arteries); Osteoarticular (EO, topical): antiinflammatory, antalgic, muscle relaxant; CV: hypotensive; Drainage: decongestant: hepatic, splanchnic, pelvic;

208  Appendix A

●

●

Heme: leukocytogenic (increases leukocytes), mitostatic, chemoprotective, anticoagulant (platelet antiaggregant): can potentiate the effect of anticoagulants; Cancer: antimitotic, antiproliferative;

Use: ●

● ●

●

●

● ● ●

ID: all noninfectious pathologies requiring a general inhibition of secretory and congestive phenomena Wound: cicatrization ANS: inhibition of alpha-sympathetic and para-­ sympathetic activity GI: indigestion, gastric ulcer, duodenal ulcer, ulcerative colitis, Crohn’s ilitis, GI infections, inflammation, spasmodic colitis Neuro/Psych: anger, nervous conditions, insomnia, depression (overstimulated), abdominal migraines, neuralgia Allergies: allergies, allergic asthma, infected eczema GU: herpetic vaginitis. Menstral spasms Metab: cachexia, loss of appetite

Method: Tisane (GI, infections, gargle, compress): 2–3 tsp. in ¾ c. water; infuse 5–10 min, 3–4 cups per day; gastric ulcer: tisane: 1 tsp. leaf +1 tsp. Fragaria vesca, steep 15 min in 1 cup water + ¼ tsp. colloidal silver; drink TID for 1–2 weeks; colitis: Hamamelis virginiana MT + essential oils of M. recutita, Boswellia carterii, and Lavandula officinalis, in a base of olive oil and PEG-20: instill 5 mL of mixture over 5 min per rectum; repeat 4 times per day until resolution of colitis.

Melissa officinalis (Melissa, lemon balm) Essence: #1 neuro-thyroid adaptogen in Hashimoto’s thyroiditis and spasmophilics. Parts: stem with leaves Galenic: MS, BH, DE, EO

Use: ●

●

● ● ●

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/L 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; Contraindications: central hypothyroidism; severe bradycardia.

Mentha piperita (peppermint) Essence: excellent digestive tonic, antiinfectious and antalgic for superficial neuromuscular and dermatologic disorders. Parts used: leaf and flower Galenic forms: EO, BH Actions1, 2: ●

● ●

●

Actions1, 2: ●

●

●

● ●

● ●

GI: eupeptic, digestive, antinausea, antispasmodic, antigastralgic, choleretic, hepatoprotective; CNS: anxiolytic (GABA-ergic, prolongs GABA activity), neurocalmative, cognitive enhancer (muscarinic and nicotinic receptors), enhances attention and memory; CV: antiarrhythmic, bathmotrope negative, vascular antispasmodic; Metabolic: hypocholesterolemant; Immune: antiviral (aqueous extract), bacteriostatic, fungistatic, antiparasitic (Leishmania), antioxidant, antiinflammatory, antineoplastic (minor effect); ANS: alpha-sympatholytic; Endo: central: antioxytocic, adaptogenic (nervous system, thyroid18), inhibits FSH, LH (lithospermic acid), inhibits TSH.

Spasmophilia: spasmodic digestive disorders: gastric ulcers, duodenal ulcers, dyspepsia, colic GI/ID: dysbiosis, nausea, spasmodic cardiac disorders: arrhythmias, arterial hypertension; Neuro/Psych: dyskinesia, insomnia, nervousness Endo: thyro: central hyperthyroidism GYN: uterine spasms of third trimester, morning sickness, pelvic spasms,

●

● ●

GI: antiflatulent, digestive, eupeptic, cholagogue, choleretic, exocrine pancreatic stimulant (lipase, amylase), antinausea, balances enteric flora19; Neuro: antalgic, analgesic; Spasmophilia: antispasmodic (biliary, intestinal, bronchial); Pulm: pulmonary antispasmodic, expectorant, antiinfectious; ID: antiinfectious (antibacterial, antiviral) tropism: ENT, pulmonary; ANS: mild: sympatholytic, para-sympathomimetic; Endo: gonado: mild antigonadotrope;

Use: ●

●

● ● ●

GI: bloating, borborygmus, irritable bowel, colitis, spasmophilia, biliary spasm, constipation ID: dysbiosis, pharyngitis, bronchitis, sinusitis, otitis, asthma, insect bites Allergies: pruritis Neuro: migraines ANS: sympatholytic

Method: EO: depends on variety used, in general: 0.1%–1% analgesic, 25%–1% nasal, buccal, 1%–5% anatalgique; hydrolat: PO: 1–3 tsp. bid, diffusion, compress;

Appendix A 209

tisane: 1 tsp. dry leaves in ¾ c. water, 10 min infusion (keep covered!), before meals. Note: Menthones in high doses can be neurotoxic, and, can cause glottic closure in infants with inhalation.

Passiflora incarnata (passionflower)

●

Essence: #1 sympatho-corticotropic regulator with anxiety and disorders of elevated cortisol. Part used: flower Galenic forms: MT, BH, DE

● ●

●

● ●

●

Actions1, 2: ●

●

●

Neuro: musculotropic and neurotropic antispasmodic (digestive and cardiovascular), sympatholytic, ­sedative20–26 without somnolence or reduction of vigilance, improves sleep latency and quality, GABA-ergic, antiepileptic; ANS: alpha-sympatholytic; CV: hypotensor, (−) chronotrope, (−) dromotrope, improves peripheral circulation, circulatory drainer; Pulm: oxygenator, pulmonary antispasmodic,

●

●

● ● ● ●

Use: ● ●

●

●

●

ANS: all hyperalpha states Neuro/Psych: epilepsy, migraines, anxiety, hysteria, anguish, depression Spasmophilia: spasmolytic states that affect mind-gut activity: nervous diarrhea, colic, abdominal migraines, cephalgic migraines Endo: cortico: all disorders rooted in hyperalpha with elevated cortisol: depression (peripheral), posttraumatic stress disorder, chronic fatigue syndrome, fibromyalgia, migraines, etc., CV: supraventricular tachycardia (SVT), hypertension, pulmonary hypoxia (+ Vinca minor + Crocus sativa)

Method: Tisane: 2 g (1 tsp)/150 mL water, steep 10– 15 min, drink 2–3 times per day. Precautions: excessive doses can cause headaches and altered vision; can augment the effect of hypnotics.

Use: ●

●

●

● ● ●

● ●

Plantago major (plantain) Essence: #1 polyvalent drainer for disorders of ear, nose, throat, upper and lower airways, and GI. Part used: leaf Galenic forms: MS, MT, DE, BH Actions1, 2: ●

●

Pulm: antitussive, mucolytic, antispasmodic, ENT: ENT drainer and antiinfectious,

Immune: immunostimulant: interferon, lymphocytes, digestive antiinflammatory, antiallergic (antihistaminic, reduces leukotrienes): “by reducing excess histamine, plantain participates in the diminution of pathologic urticarial manifestations as well as all cutaneous disorders of a dermatologic nature,2” GI: antigastritic, antacid, astringent, digestive antispasmotic antiulcer: gastric and duodenal, Hepato-renal: hepatorenal drainer, hepato-protector, Pancreas: hypoglycemiant by its invertase and other diastase activity, CV: venotonic, venoconstrictor, mild antihypertensive, Heme: hematopoetic—bone marrow and spleen, antihemorrhagic, Metabolic: hypolipemiant by hepatorenal drainage and enzymatic activity, ID: antiinfectious (ENT, pulmonary: staph, beta-­ hemolytic strep, antiviral: herpes, adenovirus, antiparasitic: helminths), Renal: diuretic (volumetric, urcosuric, azoturic), Neuro: antispasmodic, Cancer: antitumoral, Drainage: GI: hepatic: enzyme inducer, intestinal: astringent, pancreatic: increased activity of digestive enzymes; respiratory: expectorant; urinary: volumetric diuretic, uricosuric,

General: all disorders rooted in hepato-pancreatic dysfunction of a digestive or infectious nature, particularly ear, nose, throat, bronchus and lungs, and inflammatory conditions rooted in hepatobiliary dysfunction Drainage: liver, kidney, exocrine pancreas ear, nose and throat, airways GI: gastritis, hyperacidity, nausea, vomiting, diarrhea, liver disease ID: tonsillitis, otitis, cystitis Pulm: bronchitis, asthma, chronic cough Allergies/Immune: asthma, allergic reactions, psoriasis, hives, urticaria (+ J. regia + Zn, vitamin E) Metab: hypercholesterolemia, edema, gout Wound: wound healing in eczema, psoriasis, conjunctivitis, ulceration of skin, contusions, anal fissures, hemorrhoids, venous congestion, insect bites

Method: Tisane: 2–3 tsp./1 cup water, steeped 5 min, 3–4×/day; compress for eye disorders: infuse 2 tbsp in ¾ cup water for 15 min. Contraindications none.

expectorant, 2. Projet Vitadil urticaire Londres 2.doc.

210  Appendix A

Raphanus niger (black radish) Essence: #1 pre-spring adaptation and detoxifier, disorders of digestive-pulmonary stasis. Part used: root Galenic forms: MS, MT, DE Actions1, 2: Rich in sulfur, sulfurated compounds, vitamin C, Mg, K, Na, Ca, P, Fe; ●

●

●

● ●

● ●

GI: cholagogue, choleretic (volume and fluidity), hepatobiliary drainer, hepatic detoxifier (inhibits phase 1, activates phase 2 enzymes, i.e., GSH peroxidase, augments excretion of xenobiotics) digestive antispasmodic, mild laxative (via biliary flow); Pulm: mucolytic, fluidifies mucous, augments bronchial excretions, bronchial antiseptic; ID: antibacterial; tropism against Helicobacter pylori, Staphylococcus aureus, antifungal; Immune: immune stimulant, antioxidant; Derm: antiinflammatory (topical application), cicatrizing, vulnerary; Renal: diuretic, antilithic; Endo: thyro: may reduce production of T4 and increase TRH, TSH;

Use: ●

●

●

● ● ● ●

Best used for short periods of time, i.e., change of seasons; disorders of a hepatobiliary nature: cirrhosis, hepatitis, sclerosing cholangitis (+ C. marianus ± Acer campestre GM), cholecystitis, adjuvant for ­chemotherapy toxicity (+ Juniperus GM) siderosis, hepatoprotection (alcohol, drugs, xenobiotics), food poisoning, gastritis with delayed gastric emptying from biliary dyskinesia, gastric ulcers; Disorders requiring good sulfur activity and hepatobiliary drainage: ● Pulm: acute sinusitis, acute bronchitis, ● MS: rheumatoid arthritis (inflammatory phase), arthrosis, ● Derm: psoriasis, urticaria, eczema, acne, furuncles, anthrax; Disorders benefitting from reduction of peripheral thyroid activity: ● Grave’s disease, functional hyperthyroidism; ID: whooping cough; Neuro: abdominal migraine; Metab: obesity with oxidative insufficiency; Vitiligo (as simple syrup or juice);

Method: Mother tincture: 2 mL TID; juice (fresh): 1–2 oz. before the 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.

Contraindications: biliary obstruction; relative: latent or frank hypothyroidism. Precautions: gastritis.

Rosmarinus officinalis (rosemary) Essence: polyvalent plant for all allergic and autoimmune disorders with inflammation rooted in adrenal cortex insufficiency. Parts used: flower, young shoots Galenic forms: EO, GM, MT, DE Actions1, 2: EO, tisane, decoction, GM: ●

● ● ● ● ●

● ●

● ● ●

GI: eupeptic, hepatoprotector, intestinal antispasmodic, antiulcer, choleretic > cholagogue; CV: inotrope +, chronotrope + (weak), dromotrope −; Immune: antiallergic; ID: bacteriostatic, fungostatic, antiviral; ONC: antitumoral, antimutagenic; Pulm: antitussive, mucolytic, antispasmodic, decongestant; Endo: cortico: adrenal cortex stimulant; Neuro: spasmolytic (bronchial, digestive), cerebral stimulant (short-term memory, spatial memory), cholinergic; OSTEO: antalgic, antiinflammatory; Derm: antiseptic, cicatrisant, epitheliogenic; Renal: diuretic: volumetric, uricosuric;

GM Only: ● ● ●

ID: antiinfectious: biliary, pulmonary, urinary tropism, Heme: increases leukocytes, increases erythrocytes, Neuro: mild euphoric,

Use: ●

●

●

● ●

●

Internal: GI: digestive troubles due to hepato-biliary insufficiency: loss of appetite, abdominal cramps, intestinal colic, dyspepsia, burping, flatulence, constipation (+ Q. pedunculata GM), GU/GI: infectious and inflammatory maladies: intestinal inflammation (+ Vitis vinifera GM, Vaccinium vitis idaea GM), cholecystitis, hepatitis, colitis, cystitis, acute bronchitis, acute sinusitis; chronic allergies, rheumatoid arthritis, rheumatic affectations, Neuro: memory disturbance with adrenal insufficiency, certain neuro-degenerative disorders, Heme: bone marrow insufficiency, anemia, leukopenia, Neuro: certain types of depression (+ Ribes GM), frigid infertility, Topical: joint pain, myositis, muscle spasms, alopecia, fungal skin disease,

Method: EO, internal (ct. 1,8 cineole or verbenone): do nt exceed 300 mg/day, hydrolat: 1–3 tsp. BID to TID; EO external (ct. camphor): musculo-articular 2%–10%;

Appendix A 211

EO external (ct. 1,8 cineol): pulmonary: 2%–10%; tisane: 5–10 g/1 L water, 15 min steep, 1–3 cups/day; bath: EO: 10–20 drops in excipient, bath decoction: 50 g/1 L, decoct 10 min, add to bath water (avoid before bed). Contraindications (EO primarily): Ct. verbenone, Ct. camphor: pregnancy, small children, epileptics; general: adrenal-overstimulation; Precautions (EO): GI irritation, nephritis, dermatitis, allergic reactions.

Thymus vulgaris (thyme) Essence: #1 immuno-adrenal support for vagotonics with atopia, infectious or digestive complications. Parts used: stem and flowers Galenic forms: EO, BH, MT Actions1, 2: ●

● ●

● ●

● ● ●

Immune: antiinfectious (ENT, pulmonary, intestinal, pharyngeal, urinary, genital, cutaneous), antifungal, antibacterial (gram +, gram −), antiviral, antiherpetic, anthelminthic, vermifuge; immune stimulant; antioxidant, antiinflammatory; febrifuge; Pulmonary: mucolytic, expectorant; Digestive: neurotropic digestive carminative, eupeptic, choleretic, antigastritic; ANS: para-sympatholytic (strong vagolytic); Endo: cortico: adrenal cortex stimulant, gonado: emmenagogue, binds to estrogen, progesterone receptors; Neuro: analgesic; Neuromuscular: spasmolytic; Renal: volumetric diuretic;

●

●

Methods: EO: topical, internal (PO) acute: 2 gtt 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 T. 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. Contraindications: Pregnancy, hypertension, glaucoma, hypersecretory states

Valeriana officinalis (valerian) Essence: #1 plant for acute spasmophilia and chronic regulation of spasmophilic terrain. Parts used: rhizome, roots, stolons Galenic forms: BH, EO, DE, MT Actions1, 2: ●

● ● ●

●

●

● ● ● ●

General: all disorders in vagotonic individuals, ­hyperpara-sympathetic states, adrenal insufficiency or infections Spasmophilia: All chronobiologic spasmophilias, structuro-functional spasmophilias where improvement of cortisol activity regulates estrogens, of childhood; All spasmophilic disorders of vagotonics: depression, asthma, migraines (certain types), etc. ID: all infectious disorders due to regulation of ANScorticotropic function; sinusitis, pharyngitis, tonsillitis, otitis media, parotitis, bronchitis (wet), nephritis, cystitis, infected dermatitis, especially weeping or wet, gingivitis, dental carries GU: dysmenorrhea, amenorrhea (certain types) Psych: paralytic fear, anticipatory anxiety, depression CV: hypotension GI: digestive disorders: gastroesophageal reflux rooted in compensatory alpha from hypervagal states, dysbiosis, infectious colitis, etc.

Neuro: GABA-ergic, serotonergic, melatonergic, sedative hypnotic, anxiolytic, antiepileptic soporific, dual spasmolytic: neurotropic and musculotropic, ANS: sympatholytic, vagolytic, CV: hypotensor, (−) bathmotrope, GI: digestive antispasmodic,

Use: ●

●

Use: ●

Rhume: rheumatic disorders, especially topical application of essential oil Heme: neutropenia

● ●

●

Spasmophilia: all spasmophilic states, structuro-­ functional or adaptive, all areas and systems Neuro: insomnia (+ P. incarnata MT, L. cardiaca MT, L. angustifolia EO), hysteria (+ Eschscholzia ­californica), hyperesthesia (+ E. californica + Cannabis sativa (CBD oil)), somnambulism (sleep walking) CV: tachycardic hypertension, palpitations GI: abdominal spasms, abdominal colic esp. with great discomfort and emotional reactivity, spasmodic colitis GU/women: hot flashes (+ Eleutherococcus senticosus MT, Medicago sativa MT), menstrual cramps

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. 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 (the 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.

212  Appendix A

Vitex agnus-castus (chaste tree) Essence: #1 plant for regulation of neuro-gonadotropic excess: diminishes peripheral and central gonadotropic activity but favors catabolic thyroid activity to support peripheral gonadotropic factors. Parts used: berry, flowering tops Galenic forms: MT, FE, MS, bulk herb Actions1, 2: ●

● ●

● ● ●

Neuro: sedative, dopamine agonist (inhibiting Prolactin)27, 28 ANS: alpha-sympatholytic Endo: central: inhibits the general relaunching of hypothalamic and pituitary hormones;27, 28 gonado: follicular: inhibits FSH (risk relaunching ACTH by blocking FSH), inhibits estrogen uptake at peripheral receptors (ERα ERβ27, 28), luteal: diminishes serum testosterone, (favors progesterone through altering LH activity28–47); thyro: increases T4/T3 ratio, somato: low doses: relaunches prolactin; higher doses: reduces prolactin by stimulation of D2 dopaminergic receptors, reduces prolactin sensitivity to TRH stimulation28, 48 GU: uterine antispasmodic, regulator of menstrual cycle Derm: antiseptic, vulnary ONC: antitumoral

Homeopathic: ● ●

1DH: central oxytocic (caution: may relaunch prolactin) 3DH: peripheral oxytocic, antivasopressin

Use: ●

●

● ● ●

GU: PMS (esp. lasting into luteal phase), mastodynia, fibromas, PCOS, polycystic ovaries, endometrial hyperplasia, menorrhagia, uteritis (+ Alchemilla vulgaris MT 30 mL, A. millefolium MT 30 mL, A. millefolium macerate oil 30 mL + Cinnamomum zeylanicum EO 2 mL, Syzygium aromaticum EO 2 mL, L. angustifolia EO 2 mL: vaginal infusion OR topical friction rub, improve lactation (low dose: 1 capsule/day); Neuro: insomnia (esp. in hyperluteal women with elevated alpha) Derm: acne ONC: breast cancer Psych: frigidity, low libido (3DH to 30CH)

Contraindications (standard and high dose): pregnancy, nursing, conditions in which relaunching of ACTH is undesirable.

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21.

Sampath C, Holbik M, Krenn L, Butterweck V. Anxiolytic effects of fractions obtained from Passiflora incarnata L. in the elevated plus maze in mice. Phytother Res. 2010;25(6):789–795. 22. Grundmann O, Wahling C, Staiger C, Butterweck V. Anxiolytic effects of a passion flower (Passiflora incarnata L.) extract in the elevated plus maze in mice. Pharmazie. 2009;64(1):63–64. 23. 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. 2 4. Dhawan  K, Dhawan  S, Chhabra  S. Attenuation of benzodiazepine dependence in mice by a tri-substituted benzoflavone moiety of Passiflora incarnata linneaus: a non-habit forming anxiolytic. J Pharm Pharm Sci. 2003;6(2):215–222. 2 5. 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. 2 6. Dhawan  K, Kumar  S, Sharma  A. Anxiolytic activity of aerial and underground parts of Passiflora incarnata. Fitoterapia. 2001;72(8):922–926. 2 7. Carmichael A. Can vitex agnus castus be used for the treatment of mastalgia?What is the current evidence? Evid Based Complement Altern Med. 2007;5:247–250. 2 8. Wuttke W, Jarry H, Christoffel B, Spengler B, Seidlova-Wuttke D. Chaste tree (Vitex agnus-castus)-pharmacology and clinical indications. Phytomedicine. 2003;10:348–357. 2 9. Dante G, Facchinetti F. Herbal treatments for alleviating premenstrual symptoms: a systematic review. J Psychosom Obstet Gynaecol. 2010;32(1):42–51. 3 0. Mazaro-Costa R, Andersen ML, Hachul H, Tufik S. Medicinal plants as alternative treatments for female sexual dysfunction: ­ utopian vision or possible treatment in climacteric women? J Sex Med. 2010;7(11):3695–3714. 3 1. Freeman EW. Therapeutic management of premenstrual syndrome. Expert Opin Pharmacother. 2010;11(17):2879–2889. 32. van Die MD, Bone KM, Burger HG, Reece JE, Teede HJ. Effects of a combination of Hypericum perforatum and Vitex agnus-­castus on PMSlike symptoms in late-perimenopausal women: findings from a subpopulation analysis. J Altern Complement Med. 2009;15(9):1045–1048. 3 3. 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. 3 4. Doll  M. The premenstrual syndrome: effectiveness of Vitex agnus castus. Med Monatsschr Pharm. 2009;32(5):186–191. 3 5. He Z, Chen R, Zhou Y, et al. Treatment for premenstrual syndrome with Vitex agnus castus: a prospective, randomized, multi-center placebo controlled study in China. Maturitas. 2009;63(1):99–103.

36.

Imai  M, Kikuchi  H, Denda  T, Ohyama  K, Hirobe  C, Toyoda  H. Cytotoxic effects of flavonoids against a human colon cancer derived cell line, COLO 201: a potential natural anti-cancer substance. Cancer Lett. 2009;276(1):74–80. 37. Daniele  C, Thompson Coon  J, Pittler  MH, Ernst  E. Vitex agnus castus: a systematic review of adverse events. Drug Saf. ­ 2005;28(4):319–332. 38. Halaska  M, Beles  P, Gorkow  C, Sieder  C. Treatment of cyclical mastalgia with a solution containing a Vitex agnus castus ­extract: results of a placebo-controlled double-blind study. Breast. 1999;8(4):175–181. 3 9. 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. 4 0. Atmaca M, Kumru S, Tezcan E. Fluoxetine versus Vitex agnus castus extract in the treatment of premenstrual dysphoric disorder. Hum Psychopharmacol. 2003;18(3):191–195. 4 1. 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. 4 2. Gorkow C, Wuttke W, Marz RW. Effectiveness of Vitex agnus-castus preparations. Wien Med Wochenschr. 2002;152(15–16):364–372. 4 3. Schellenberg R. Treatment for the premenstrual syndrome with agnus castus fruit extract: prospective, randomised, placebo controlled study. BMJ. 2001;322(7279):134–137. 4 4. Berger D, Schaffner W, Schrader E, Meier B, Brattstrom A. Efficacy of Vitex agnus castus L. extract Ze 440 in patients with pre-menstrual syndrome (PMS). Arch Gynecol Obstet. 2000;264(3):150–153. 4 5. Bergmann  J, Luft  B, Boehmann  S, Runnebaum  B, Gerhard  I. The efficacy of the complex medication phyto-hypophyson L in female, hormone-related sterility. A randomized, placebo-controlled clinical double-blind study. Forsch Komplementarmed Klass Naturheilkd. 2000;7(4):190–199. 4 6. 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. 4 7. Halaska  M, Raus  K, Beles  P, Martan  A, Paithner  KG. Treatment of cyclical mastodynia using an extract of Vitex agnus castus: results of a double-blind comparison with a placebo. Ceska Gynekol. 1998;63(5):388–392. 4 8. 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;n43(7):752–756.

Index Note: Page numbers followed by f indicate figures and t indicate tables.

A

Achillea millefolium (yarrow), 112, 201–202 Acute bronchitis, 138 anatomy, 138, 139f cause, 138 induction of, 139, 140f precritical terrain, 138 review of general function, 138 symptomatic treatment of, 139–142, 141t Adaptive immunity therapeutics, 53–54 Adaptogens, 50, 98 Adenosine triphosphate (ATP), 25 Adenylyl cyclase (AC), 160f Adrenal cortex index, 22–23 Adrenal hyperfunctioning, 180 Adrenaline, 163–164 glucagon vs., 11, 110 Adrenal steroids, 22f Adrenocorticotropic hormone (ACTH), 13, 15t, 20, 56, 58, 162 Agrimonia eupatoria (agrimony), 54, 113, 202–203 Alkaline phosphatase bone isoenzyme, 180 Alnus glutinosa, 52, 113 Alpha-melanocyte stimulating hormone (αMSH) index, 15t, 20 Amino acids, 36 Androgenic women, 171–172, 172t, 190 Androgens, 163 Angelica archangelica (angelica), 203 Annexin, 158, 158f ANS. See Autonomic nervous system (ANS) Anthemis nobilis (Roman chamomile), 12, 203–204 Arctium lappa (burdock root), 54 Artemisia dracunculus (tarragon), 204 Asthenia, 176 Autoimmunity, 44–45, 88–89 drainage for, 60 neuroendocrine terrain, 59–60 oligoelements, 60 vitamins, 60 Autonomic hyperfunctioning, 108 Autonomic nervous system (ANS), 1, 4t, 55–56, 96–98 abdomen, 8t activity by area of terrain, 163–164, 163t, 164f biology of functions, 9, 10t branch, 2 calcium regulation

direct, beta, 164 indirect, para-alpha, 164 cardiopulmonary systems, 8t chest, 7t exocrine pancreas, 117 hands, 9t head, 6–7t historical findings, 1 hyperimmunity, 57 muscle, 9t nervous system, 9t observation, 5t physical examination findings, 2 secretions, 9t skin, 6t in spasmophilia, 164–165, 166f, 166t sweating, 9t system of body, 1, 3t thyroid relaunching corrected indexes, 9 Autonomic spasmophilia, 165 Autumn dysthymia, 189 Autumn spasmophilia, 169–170 Avena sativa, 124

B

Bacterial overgrowth, 79 Beta-melanocyte stimulating hormone (βMSH) index, 15t, 20 Beta-sympathetic activity, 55–56 Betula pubescens, 52, 52f, 113 Bile acid, 79 Biliary stasis, 80t Biology of function (BoF), 54–55 autonomic nervous system, 9, 10t corticotropic axis, 20–23, 21t dysbiosis, 91 exocrine pancreas, 121–122, 127t hepatobiliary insufficiency, 109–111 immune system, 42–43, 54–55 recurrent streptococcal pharyngitis infection, 198–199, 199t shock, 168, 168–169t thyrotropic indexes, 151 Biomarkers, serum, 180 Blood immune system, 33 tissues vs., 30 B-Lymphocytes, 54 Bone isoenzyme, 180 Bone marrow, 32–33, 42–43, 54 Brain, exocrine pancreas and, 124

C

Calcium, 180 dialectic of, 155–156 free vs. bound, 156–157 metabolism, 155, 185–186 functional, 159 structural, 157–158, 157f structuro-functional, 158 minerals role in regulation of serum, 159, 159t, 160f regulating exogenous calcium uptake, 185 regulation of, 161t roles in organism, 155–156, 156t and terrain, 159–164 autonomic nervous system, 163–164, 163t endocrine system, 160–163 magnesium role, 159, 160t minerals, 159, 159t, 160f organs and pH buffering, 160, 161t and vitamin D, 185 Calcium-rich foods, 186–187, 186t Calciuria, 180 Calmodulin, 157 Carbohydrates, 70, 107 Carduus marianus (milk thistle), 111, 204–205 Catabolic axes, 145t Central nervous system, 116 Chemical herbalism, 49–50 Chicory (Cichorium intybus), 93 Choleresis, 80t Cholestasis signs of, 108 symptoms of, 108 Chronobiologic hypoandrogenism in adolescents, 174, 174t in adults, 174, 174t Chronobiologic impositions age, 84 seasons, 84–86 Chronobiologic spasmophilia, 155 Cichorium intybus (chicory), 205 Cinnamoma zeylanicum, 12, 56 Commensal organisms, immune system, 35 Complement system, 30–31, 31f Congestion, immune system, 40 Constitutional hypoandrogenism, men, 172 Constitutional vagotonia, 190 Cornus sanguinea (blood twig bud), 52, 52f, 54, 113 Corticotropic axis, 145 adrenal cortex index, 22–23 biology of functions indices, 20–23, 21t

215

216  Index

Corticotropic axis (Continued) βMSH/αMSH index, 15t, 20 cortisol indices, 22–23 disadaptation, 163 excessive global adrenal function relative to cortisol, 188 low global adrenal function, 188 evaluation of, 13 historical findings abdomen, 19t adrenal androgens, 16t back, 19t cardiovascular systems, 18t chest, 18t cortisol, 16t extremities, 20t fat distribution, 19t head and neck, 18t by hormone, 13 observational findings, 17t skin, 17t by system, 13, 14–15t Corticotropic plants, 56–58 Cortisol, 26–27, 40f, 44, 118 antiinflammatory response of, 158 indices, 22–23 Cough, spasmodic, 142 Crataegus oxyacantha (hawthorn), 205–206 Cynara scolymus (artichoke), 111, 206

D

Dehydroepiandrosterone (DHEA), 39–40 Depression, 176 Diet alimentary patterns, 83 initial diet, 81 regional nutrient predominance, 81–83 Dry bronchitis, 142 Dysbiosis, 63, 201 accumulation, diseases of, 89 alimentation, 91–93 and asthenia, 96–97 autoimmunity diseases, 88–89 bacterial overgrowth, 79 bile acid, 79 biology of functions indexes, 91 chronobiologic impositions, 84–86 diet, 81–83 digestive tropism, 98–99 and dyspepsia, 97 elimination, diseases of, 89 endogenous and exogenous elements, 77–79 enteric flora, 79 environment, 86 exocrine pancreas, 79 exogenous factors, 79–87 fermented foods, 91–92 food hygiene, 92 gut microbiome, 87f hepatobiliary function, 79 historical findings, 89–90 iatrogenic interventions, 86 implications, 87–89 large intestines, 90

liver, 77–79 nature of, 87 with nervous disposition, 97–98 noncommensal organisms, 83–84 physical examination, 90–91 prebiotics, 92 small intestines, 89 splanchnic system, 79 systemic factors, 79 treatment, 91–93, 95–98 Dysendocrinism, 180 Dysregulated immunity, 45 Dysthymia, 189

E

Electrocardiogram (ECG), 181 Electromyogram (EMG), 180 Emunctories, 54, 98 Endocrine, 54, 98 augmentation of serum calcium levels, 160–161 corticotropic axis, 162 gonado-somatotropic, 163 gonado-thyrotropic, 162, 162–163f gonadotropic axis, peripheral, 162 immune system, 35–36 management, 41–42t, 42–43 pancreas, 117–118 regulation of adaptive serum calcium availability, 162 solicitation of calcium utilization, 162 thyro-somatotropic, 163 thyrotropic axis, peripheral, 160–161, 161f, 161t turnover and regulation of calcium, 162–163 Energy calibration, 11–12, 110–111 Enteric flora, 79 Estrogenism, 190 Estrogens, 118, 163 Eupeptic plants, 122–123 Exocrine, 54 Exocrine pancreas alimentation, 124–125 allergies, 119 autonomic nervous system, 117 biology of functions, 121–122, 127t case study, 125–127 childhood development of function, 116 dysbiosis, 79, 90 embryology, 115 endocrine pancreas, 117 energy and metabolism, 119 functional anatomy, 115–119 gastro-duodenal, 117 hepatobiliary and, 117, 123 historical findings, 119 immune system, 36, 117, 119 infections, 119 intestinal and, 123 joints and, 117, 123 lungs and, 117, 123 medicinal plants, 122 and parotids, 119–120 physical examination, 119–120

skin and, 117, 123 stool, 119 structural anatomy, 115 therapeutics, 122

F

Fagus sylvatica (beech tree bud), 54 Fasciculation of skeletal fibers, 180 of skeletal muscles, 180 tongue, 179–180 Fatty skin, exocrine pancreas, 120–121 Fermented foods, 91–92 Ficus carica (fig bud), 54 Follicle-stimulating hormone (FSH), 146 Folliculinic hysteroids, 172t Folliculinic with hyperthyroidism, 189–190 Food hygiene caloric intake, 92 culture of eating, 92 FSH. See Follicle-stimulating hormone (FSH) Functional spasmophilia, 155, 165–170, 167f, 170t cosmobiologic, 169–170 lifestyle, 169, 170f shock, 167–169 therapy for terrain, 187–189, 187t autonomic nervous system, 187 beta acting, 188 corticotropic disadaptation, 188 para-sympatholytic and alphasympatholytic system, 187

G

Gallbladder, dysbiosis, 90 Gamma-aminobutyric acid (GABA), 116 Gammaglobulins, 54 Gastro-duodenal, 117 Gastrointestinal tract, 108–109 Genito-thyroid index (GTi), 42–43 Glabella tap, 179, 179t Glucagon, 117 vs. adrenaline, 11, 110 Gonadotropic axis, 35–36, 56, 58–59 Grape cure, 92–93 Group A streptococcus (GAS), 49 Gut-associated lymphoid tissue (GALT), 65

H

Hepatobiliary, 54, 117 exocrine pancreas, 123 function, 79 Hepatobiliary insufficiency ANS and, 106–107 biology of functions, 109–111 embryology, 101 emunctory-emunctory, 105 endocrine gland-emunctory, 105 functional anatomy, 102 general endocrine-liver, 105 hepatic circulation, 102–103 hepatobiliary unit, 106 historical findings, 107–108 immunity and, 105, 107

Index  217

intestinal and, 104 Kupffer cell activity, 113 by level of demand and response, 102t metabolism and adaptation, 106 pancreatic and, 104 physical exam findings, 108 portal decongestant, 113 postprandial warmth, 107 splanchnic congestion, 105–106 splanchnic decongestant, 113 starter index, 109–111 structural anatomy, 101 therapeutic approach, 111–113 Hepato-pancreatic fullness, 108 Hepatorenal drainers, 54 Hippus, 177–179, 178f, 178t Histamine alpha-cortico-thyrotropic activity in, 40f neuroendocrine regulation of, 39, 39t Humoral immunity complement system, 30–31 lymphocytes, 31–32 phagocytes, 31 Hygiene theory, 67 Hyperemotional states, 176 Hyperestrogenism, 173–174, 180 Hyperfolliculinic hyperthyroid hysteroid women, 171 Hyperfolliculinic hysteroid women, 171, 171f Hyperimmunity, 43–44, 55t, 57–59 drainage for, 59 indexes favoring, 81t neuroendocrine terrain, 59 oligoelements, 59 therapeutics, 57–59 vitamins, 59 Hyperparotidism, 120 Hyperthyroidism, 180 folliculinic with, 189–190 thyrotropic axis in, 147t Hypoandrogenic men, 190 Hypoandrogenism, 180 of adolescence, 190 of adulthood, 191 chronobiologic in adolescents, 174, 174t in adults, 174, 174t constitutional, 172 Hypoimmunity, 43, 55–57, 55t indexes favoring, 81t states, 57 Hypothyroidism, 147t Hysteria, 155, 182 Hysteroid, 171 folliculinic, 172t personality, 189

I

Ileocecal zone, 74 Immune system adaptive immunity therapeutics, 53–54 adaptogens, 50 alimentation and, 60–61 attack, 26

biology of functions, 42–43, 54–55 bone marrow, 42–43, 54 cellular vs. humoral components, 29 complement system, 30–31, 31f congestion, 40 corticotropic, 56 defense, 26 definition, 25–26 development, disruption in, 67 elements, 29–32, 35–37 emunctories, 54 endobiogenic consideration, 26t endocrine, 42–43, 54 exocrine, 54 exocrine pancreas, 117 foods with nutrients favorable, 60, 60t function, 25–26, 37–42 gammaglobulins, 54 global system, 26–29 gonadotropic, 58 hepatobiliary, 54 hepatorenal drainers, 54 hyperimmunity therapeutics, 57–59 hypoimmunity therapeutics, 55–57 imbalance, 43–45 liver, 52 lymphatics, 53–54 lymphocytes, 31–32 lymphoid tissues, 53–54 mononuclear phagocytosis system, 50–53 MPS drainage, 52 needs, 25 neuroendocrine terrain, 59–60 pancreas, 54 phagocytes, 31 phagocytosis, 52 specific vs. nonspecific responses, 29 splanchnic system, 53 thyro-somatotropic, 56 thyrotropic, 59 tissues and organs, 32–35 tissues vs. blood, 30 tolerance, 26 vigilance, 25–26 Immunoglobulin A (IgA), 67 Infectious disease, 129 Inflammation alpha sympathetic, 39 corticotropic, 39 immune system, 39–40 rate of function, 39–40 thyro-somatotropic, 39 thyrotropic, 39 Innate immunity complement system, 30–31 lymphocytes, 31–32 phagocytes, 31 Innate immunity tissue, 50–53 Inositol tri-phosphate (IP3) production, 157 Intestinal flora equilibration of, 93–94 exocrine pancreas, 123 iatrogenic interventions, 86 restoration, 95 Intestinal signs

downstream, 121 upstream, 120 Ischemia, neuromuscular response to, 177 Isoenzyme, 180

J

Joints, exocrine pancreas, 117, 123 Juglans regia (black walnut), 54, 206

K

Kupffer cells, 30, 52, 113

L

Large intestines, 74, 90–91 Latent spasmophilia, 164, 165t Lavandula angustifolia (lavender), 1, 206–207 Leonurus cardiaca (motherwort), 207 Leukocytes function of, 41t mobilization index, 9–11, 10t structure and function of, 42, 42t Lipid metabolism, 108 Lipothymia, 175 Liver, 52 adaptation, 78–79 congestion, 77–78 dysbiosis, 90 immune system, 36, 78 metabolism and nutrition, 77 vs. spleen, 11, 109 Lungs, exocrine pancreas, 117, 123 Lymphatics, 53–54 Lymphocytes, 31–32, 42–43 Lymphoid tissues, 31–35, 53–54

M

Magnesium, 159, 160t, 180, 182, 183t Magnesium-rich foods, 187, 187t Materia medica, 201 Matricaria recutita, 12, 58, 207–208 Maxillary sinus, 133f Medicinal clay adverse reactions, 94 benefits, 94 constipation, 94 effectiveness, 94 equilibration of intestinal flora, 94 food poisoning, 95 preparing, 94 Medicinal plants, 54, 182–185, 201 exocrine pancreas, 122 hepatobiliary insufficiency, 111–112 thyro-somatotropic axis, 59 Melanocyte stimulating hormone (MSH), 20 Melatonin, 41 Melissa officinalis (Melissa, lemon balm), 208 Mental spasmophilia, 177–179, 178t Mentha piperita (peppermint), 208–209 Menyanthes trifoliata (Bogbean), 12

218  Index

Metabolite, of thyrotropic axis, 145 Microbiome correlation, 72f factors impacting, 70f function, 67–69 structural activity, 65–66, 66f Minerals, in serum calcium regulation, 159, 159t, 160f Mononuclear phagocytosis system (MPS), 33–35, 50–52 Mucosa, 130 Mycophenolic acid (MPA), 33

N

Nasal airway, 130 Nasal cavity, 129–130 Nasal mucosa, 129 Neuroendocrine regulation, 37–42 calibration, 37, 39 diminution, 37, 41 inflammation, 39–40 localization, 41 mobilization, 37, 40 rate of extravasation, 39 rate of production, 39 Neuroendocrine terrain, 57 Neutrophil-to-lymphocyte ratio (NLR). See Genito-thyroid index (GTi)

O

Olea europaea (olive leaf, bud), 54 Oligoelements, 54, 57, 59, 112, 186 Organic silica, 185 Oronasal tonsils, 134f Osteocalcin, 180 Otitis media (OM), 136 agents of aggression, 137 anatomical and functional review, 136, 136f autonomic nervous system, 137 cause, 137 critical terrain, 137 emunctory, 137 endocrine, 137 immunity, 137 precritical terrain, 137 treatment guidelines, 137 Otitis media with effusion (OME), 137

P

Palpation, 108 Pancreas, 54. See also Exocrine pancreas Pancreatic drainage, 123 Parasympathetic activity, 108 Parasympathetic nervous system, 158 Passiflora incarnata (passionflower), 209 Pathogens, 129 Peppermint (Mentha piperita), 93–94 Peripheral thyroid function, 169 Phagocytes, 31 Phagocytosis, 33–35, 52, 98–99 Pharyngeal mucosa, 129 Phosphorous, 180

Phytotherapy, 201 Plantago major (plantain), 209 Plantain leaf (Plantago major), 113 Platelet mobilization index, 11 Portal decongestant, 98, 113 Postprandial pain, 109 Postprandial warmth, 107 Potassium-rich foods, 187, 187t Poterrium sanguisorba (salad burnet), 1 Prebiotics, 92 Probiotics, 95 Protein metabolism exocrine pancreas, 120 symptoms concerning, 108 Prothrombin, 158 Psycho-neuro-endocrino-immunologic (PNEI) supersystem, 28, 28f Pupillary light reflex, 177

Q

Quantitative electroencephalogram (QEEG), 181 Quercus pedunculata, 50

R

Radial gonado-thyrotropic index, 152t Raphanus niger (black radish), 210 Rational clinical phytotherapy, 201 Recurrent streptococcal pharyngitis infection biology of functions, 198–199, 199t childhood, 195 chronobiological disadaptation, 199 gastrointestinal system, 195 history, 195, 196t lifestyle and dietary recommendations, 197, 198t peripartum, 195 physical examination, 196–197, 197t review of systems, 195, 196t temperament and personality, 195 treatment, 197–198, 198t Reticular activating system, 179–180 Rhinopharyngitis, 129 anatomy review, 129, 130f autonomic nervous system, 130 cause, 130 critical terrain, 131 endocrine, 131–132 etiology, 131 functional review, 129–130 inducers of pathology, 131 induction of, 130 precritical terrain, 130 terrain, 131t treatment guidelines, 131–132 Rhodiola (Rhodiola rosea), 50, 51f Ribes nigrum, 50 Rosmarinus officinalis (rosemary), 210–211

S

Salvia officinalis (Dalmatian sage), 113 Salvia sclarea (clary sage), 54, 122 Saprophyte, 63

Satureja montana, 56 Seasonal chronobiologic adaptation syndrome, 170f Seasonal diet, 92–93 Serum biomarkers, 180 Sex hormone-binding globulin (SHBG), 171 Shock associations, 168–169 biology of functions, 168, 168–169t defined, 167 pathophysiology, 167–168, 167f Short-chain fatty acids (SCFAs), 70, 72t Sinusitis, 132–133 anatomy review, 132, 132f autonomic nervous system, 133–134 cause, 132 critical terrain, 133 functional review, 132 induction of disease, 133, 133–134f precritical terrain, 132 treatment guidelines, 133–134 Skeletal fibers, 180 Skeletal muscles, 180 Skin, exocrine pancreas, 117, 123 Small intestines dysbiosis, 89–91 symbiosis, 74 Somatostatin, 117, 121–122 elevated, 121–122 low, 122 Spasmodic cough, 142 Spasmophilia, 155 autonomic nervous system role in, 164–165, 166f, 166t autumn, 169–170 chronobiologic, 155 comportment asthenia, 176 depressive tendency, 176 hyperemotional states, 176 diagnostic studies serum biomarkers, 180 urine, 180–181 differential diagnosis, 181 evolution of untreated, 181 functional, 155, 165–170, 167f, 170t iatrogenic causes of fragilization of terrain, 174–175, 174t latent, 164, 165t mental, 177–179, 178t observation posture, 176 respiration, 176 sequence of events, 156 signs diagnostic of, 176–180 Chvostek’s sign, 176–177, 177f hippus, mental spasmophilia, 177–179, 178f, 178t Trousseau’s sign, 177, 177–178f spring-induced, 169 structuro-functional, 155, 170–174, 171f symptoms, 175–176, 175t cardiovascular, 176 gastrointestinal, 176

Index  219

genital, 176 lipothymia, 175 musculoskeletal, 175–176 neurologic, 175 urinary, 176 terrain management, 159t treatment, 181–182 acute, 182–185 antispasmodic sedatives, 183 cardiopulmonary, 184 cardiovascular, 184 dual neuro-musculotropic antispasmodics, 183–184 genital, 185 hepatobiliary, 184 intestinal, 184–185 magnesium, 182 medical plants, 182–185 muscular antispasmodic, 183 pharmaceutical, 182, 182t Spasms, 109 Sphincter of Oddi, 108–109 Splanchnic system, 79 congestion, 105–106, 108 decongestant, 53, 98, 113 indexes, 55t Spleen immune system, 35 liver vs., 11, 109 Spring allergies, 189 Spring-induced spasmophilia, 169 Starter index, 11–12 Structuro-functional spasmophilia, 155, 170–174, 171f, 189–191 androgenic women, 171–172, 172t chronobiologic hypoandrogenism in adolescents, 174, 174t in adults, 174, 174t constitutional hypoandrogenism, men, 172 hyperestrogenism, thyrotropic disequilibrium (emancipation), 173–174 hyperfolliculinic hyperthyroid hysteroid women, 171 pituitary-parathyroid, 174 pure hyperfolliculinic hysteroid women, 171, 171f

vagotonia of childhood: 1.5–6 years, 172–173, 173t Submaxillary glands hypertrophy, 120 Sulfur, 54 Symbiosis, 63 commensal flora categorization, 64–65 endobiogenic cartography, 73–74 endo-enteric relationships, 73f, 73–74t ontology of, 64–65 teleology of, 65–73 correlation, 72f development and adaptation, 63–64 hygiene theory, 67 metabolism, 70, 71f microbiome, 65–66 structuro-functional benefit, 69 teleology, 70–73 Sympathetic nervous system, 167–168

T

Taraxacum dens leonis (dandelion), 111–112 T cells, 53 Temperament, and internal mental life, 148t Terrain, dysbiosis, 95–98 Thickened skin, exocrine pancreas, 120 Thymus, 32–33, 53 Thymus vulgaris, 56, 211 Thyroid, 124 Thyroid relaunching corrected indexes, 9, 10t Thyroid-stimulating hormone (TSH) exocrine pancreas, 117 immune system, 36–37 implication of, 135 Thyro-somatotropic axis, 56–57, 59 Thyrotropic axis, 56, 59 anatomy, pathophysiology, 146 clinical approach to, 145 clinical significance of, 146 in hyperthyroidism, 147t in hypothyroidism, 147t metabolite of, 145 signs, 146, 150–151t head, ears, eye, nose, and throat3, 149–150t neurologic, 149t

thyroid gland and chest, 150t symptoms related to, 148t Thyrotropic function, 188–189 Thyrotropic hormones, 146t Thyrotropic indexes biology of functions, 151 parathyroid and bone indexes, 153t with peripheral impact, 151t radial gonado-thyrotropic index, 152t thyroid gland and activity, 152t thyroid relaunching corrected indexes, 152f Thyrotropic regulation, 189 Thyrotropin-releasing hormone (TRH), 1, 2f, 117, 146, 188 Tongue exocrine pancreas, 120 fasciculation, 179–180 Tonsil hypertrophy, 120 Tonsillitis, 134–135 anatomy review, 134 autonomic nervous system, 135 cause, 134–135 critical terrain, 135 emunctory, 135 endocrine imbalances, 135 functional review, 134 precritical terrain, 134–135 treatment guidelines, 135–136 TRH. See Thyrotropin-releasing hormone (TRH)

U

Urine, 180–181

V

Vagomimetics, 122 Vagotonia of childhood (1.5–6 years), 172–173, 173t Valerian (Valeriana officianalis), 183, 211 Vitamin D, 185 Vitex agnus-castus (chaste tree), 212

W

Wet bronchitis, 142