Allergic disorders

Chapter 1

Allergic disorders Introduction The immune system is key to the survival of the organism. It is responsible for recognizing self vs nonself. Vigilance and defense are preferred to attack (The Theory of Endobiogeny, Volume 2, Chapter 3). When the immune system is hyperfunctioning, it is at risk of favoring attack over other roles. Allergies and autoimmune diseases are both disorders of immune hyperfunctioning. Because of the rising prevalence of these disorders around the world, understanding the underlying Endobiogenic terrain allows for the approach to therapy to be restorative and even curative, rather than merely suppressive. The immune system is engaged in a triadic relationship with the autonomic nervous system and endocrine system. The corticotropic and thyrotropic axes are most implicated. The less competent one aspect of the triad is that the greater the other branches will be in compensation. In allergic disorders, the adrenal cortex is incompetent in its response to aggression, producing more anabolic steroids related to cortisol, and creating a more permissive terrain related to an adaptive one. To compensate, the ANS, thyrotropic axis and immune system become more active, leading to hyperimmunity. Therefore, most simply, allergies are a hyperimmune response to an agent that has contacted the body. Allergies pose a particular challenge for the physician. The incidence of allergic disorders has increased considerably.1 In a 10-year period, food allergies in children increased fivefold. Skin allergies have increased 2.5-fold. The approach of preventative medicine and social work has been to reduce exposure to allergens. The assumption is that allergens are bad and must be reduced or eliminated. An allergen is like the color red. Red is neither intrinsically good nor bad. It simply is. Proteinaceous moieties simply are. They serve an intrinsic function for living systems. What makes them an allergen is not their existence but how the other reacts to it. This approach by reducing the allergen burden is wise because it reduces the further degradation of the terrain but does not offer a way to strengthen the buffering capacity nor address the ­elements of terrain. It mistakes

The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816964-3.00001-8 © 2019 Elsevier Inc. All rights reserved.

the aggressor for the cause of allergies, which according to the Theory of Endobiogeny is a hyperimmune terrain. The approach of biomedicine and pharmacology has been primarily to suppress the mechanisms of response to allergens and allergic symptoms. Over the last four decades, the number of oral and intravenous therapies of escalating potency and side effects has only increased, ever on the “hunt” for new approaches to suppression.2 Over this same time, the total failure to reverse or even diminish the incidence of allergic disease should serve as sufficient witness to the scientific bankruptcy of this approach except in the reversal of anaphylactic shock. According to the Theory of Endobiogeny, the precritical and critical terrain implicates mental, emotional, neurotransmitter, autonomic, endocrine, digestive, immune, and emunctory activity. The Endobiogenic approach reintegrates the allergen, allergic mechanism, allergic terrain, and external environment in order to personalize treatment to the individual.

Classification of allergic disorders Classically, allergic disorders are classified by the branch of the immune system that is most implicated in the allergic response. Recall that there are two types of immune response. The first is nonspecific or innate. The response is repetitive and general, and not specific to any particular type of allergen. The second type is specific or adaptive immunity (The Theory of Endobiogeny, Volume 2, Chapter 3). This response is highly choreographed and specific to particular allergens. There are also two forms of immune actors: cellular and humoral. Cellular elements are cells (Table 1.1). Humoral elements are protein-based products, typically released from cells, which travel through the blood (viz., humor). Allergic disorders are classified classically into four groups based on the elements of immunity involved (Table  1.2).3 This chapter will focus on type 1 allergies with a specific emphasis on eczema. Therefore, we will be discussing adaptive and humoral allergic disorders involving IgE.

1

2  The Theory of Endobiogeny

TABLE 1.1  Cellular and humoral elements of immunity Nonspecific: innate

Specific: adaptive

Cellular

Humoral

Cellular

Humoral

Neutrophils

Complement

T-lymphocytes

Immunoglobulins

B-lymphocytes

Cytokines

Natural killer Monocytes

Interleukins

Basophils Eosinophils NK lymphocytes NK, natural killer.

TABLE 1.2  Classification of immune disorders Disorder

Adaptive

Type 1 IgE mediated

Innate

Aspect

Example(s)

•

IgE from B-lymphocytes

Eczema, allergies, asthma (extrinsic), anaphylaxis, angioedema, urticaria, food and drug allergies

Type 2 IgG mediated

•

IgG from B-lymphocytes

Blood transfusion reactions, autoimmune hemolytic anemia

Type 3 Immune complex-mediated

•

Compliment-antibodyantigen complexes deposited in tissues and organs

Glomerulonephritis, rheumatoid arthritis, lupus

Type 4 Cell-mediated

•

T-lymphocytes

Infections: syphilis, TB, leprosy, viruses, parasites, contact dermatitis, autoimmune disease

•

Type 1 IgE mediated hypersensitivity: Summary of terrain The primary focus of the classical biomedical approach has been to focus exclusively on suppressing the mechanisms of allergy symptoms, histamine being the most well-known amongst them. The Endobiogenic approach establishes the proper place of histamine within the larger context of the global terrain and Endobiogenic equilibrium of each patient. 1. Cause: Hyperimmune precritical terrain 2. Agent: Allergen exposure 3. Response: Hyperimmune activity 4. Mechanism: Immune mediators (i.e., histamines, leukotrienes, etc.) 5. Effect: Allergic symptoms: pruritis, inflammation, heat, swelling, etc.

Cause: Precritical terrain: Hyperimmunity The precritical hyperimmunity terrain has three aspects: overfabrication of immune elements, spasmophilia, and permissive adrenal cortex activity. Overproduction (The Theory of Endobiogeny, Volume 2, Chapter  3) is initiated by excessive estrogens activity, due to its role in protein metabolism. The exocrine pancreas is solicited to increase the uptake of protein elements from the diet. The liver as a metabolic organic also contributes to the fabrication of immune elements (Fig. 1.1). Implicated in this fabrication is prominent parasympathetic tone and serum TSH. There is a latent hepatic insufficiency as an emunctory which plays a role in the critical terrain. The second aspect is the latent spasmophilia. There is elevated parasympathetic and alpha-sympathetic activity (The Theory of Endobiogeny, Volume 2, Chapter 11).

Allergic disorders Chapter | 1  3

Agent: Allergen exposure In most disorders, a single exposure to the agent or aggressor is sufficient to install the critical terrain. In the case of Type 1 allergies, mediated by immunoglobulin E (IgE), repeated exposure is required (Fig. 1.2).4

Response: Allergic terrain

FIG.  1.1  Endobiogenic terrain favoring overfabrication of immune elements. See text for details. (Images by PandaVector and EgudinKa/ Shutterstock.com © 2015 Systems Biology Research Group.)

The third aspect is the permissive adrenal cortex activity (The Theory of Endobiogeny, Volume 1, Chapter 6). The permissive activity of the adrenal cortex refers to the way in which its hormones create an environment favorable to actions of other hormones, physiologic and metabolic functions (Table 1.3). The more the adrenal cortex is dedicated to the production of adrenal androgens and estrogens, the greater its permissive function, and the lesser its adaptive capabilities. Based on the genetic inheritance, patients with an allergic terrain have a predominance of adrenal estrogens. The less efficient the gonads are in producing estrogens and androgens, the greater the appeal to the adrenal cortex. This tends to occur at the expense of metabolic activity dedicated to the production of glucocorticoids. These adrenal estrogens are not responsive to diminished feed-forward activity of FSH. Therefore, they serve as an unregulated source of estrogen for oversolicitation of proteins in the production of immune elements.

TABLE 1.3  Permissive activity of adrenal cortex Function Adrenal metabolic

Cellular nutrition

Comment Androgens

Favors production of adrenal androgens

Estrogens

Favors production of adrenal estrogens

Active membrane permeability

Favors the dynamic flux of nutrients into the cell for structural purposes relative to functional ones

Active intracellular osmolar gradient

Favors the dynamic flux of electrolytes and water into the cell for structural purposes relative to functional ones

Upon reexposure to an allergen, the organism, as noted above, engages in a nearly immediate response. The role of the neuroendocrine system is to manage this response. A response must be made, histamines must be expressed to allow immune cells (monocytes, neutrophils, etc.) to migrate from their hematogenous circuit of surveillance to the localized area of aggression. The problem is not that there is a response or that histamine is released. It is the quantity, quality, chronology and duration of the response that is responsible for the allergic disorder. The factors implicated, in order of importance, are Alpha, Corticotropic, Thyrotropic, Gonadotropic, and Somatotropic axes. Recall the general relationship of the catabolic axes to histamine and other mediators of inflammation (Table 1.4)

ANS Part of the spasmophilic nature of allergies is that the alphasympathetic activity is prolonged and the beta is delayed or insufficient. The intensity of the alpha has a number of direct effects: 1. Increased ACTH → increased histamine receptors 2. Increased TRH → increased histamine release 3. Increased histamine as an autacoid for Alpha Congestion of emunctories is another expression of the spasmophilia.

Corticotropic There is a hyperfunctioning ACTH (Fig. 1.3) for at least two reasons: hyperfunctioning Alpha, and insufficiency of the adrenal cortex response. The three results of this are: 1. Eosinophilia and basophilia, both of which play a role in the release of inflammatory mediators. It is compensatory for the insufficiency of cortisol response to the aggression and reflective of the intensity of the ACTH response.5, 6 Fundamentally, the role of the eosinophils are as an indirect method of adaptation and congestion when the adrenal cortical response is not sufficiently adapted to the needs of the organism. 2. T-lymphocyte maturation7, 8 (which adapts production of IgE) 3. Upregulation of histamine receptors on mast cells and other immune cells. The logic of this is that histamines stimulate ACTH.9 Histamines are in turn regulated by endorphins, which they directly stimulate and cortisol is relaunched by ACTH.10

4  The Theory of Endobiogeny

FIG.  1.2  Sensitization to allergens and manifestation of allergies. (A) Primary sensitization involves local macrophages (dendritic cell), which forms an epitope with a native T cell. Memory T-cells are formed and B cells activated to develop IgE receptors. (B) Shows that in the initial exposure, there is a rise in the number of IgE and T cells. Because IgE has not been released to circulating, symptoms are latent. On second exposure ((A) lower half), there is a proliferation of memory T-cells. Based on the balance of T regulatory cells to other lymphocytes, the response can be regulated or amplified ((B) middle and lower graphs). With subsequent exposure (C) in susceptible individuals, an immediate, then late phase reaction can develop. There is an IgE mediated response, with degranulation of mast cells and activation of basophils. Antigen presenting cells (APC’s) stimulate non-IgE dependent mechanisms of response including pro-inflammatory and immune activating interleukins and eosinophils. Various sites can be the scene of allergic manifestation (lower right corner). MHC, major histocompatibility complex; SIgA, secretory mucosal immunoglobulin A; T-reg, T-lymphocyte regulator cell; TCR, T-lymphocyte cell receptor. (Reproduced from Valenta R, Hochwallner H, Linhart B, Pahr S. Food allergies: the basics. Gastroenterology 2015;148(6):1120-1131 e1124. https://doi.org/10.1053/j. gastro.2015.02.006.)

TABLE 1.4  ANS-endocrine mediators of histamine activity Origin

Factor

↑ Demand

↑ Receptors

↑ Release

↓ Activity

Brain stem: ANS

αΣ

•

Pituitary: corticotropic

ACTH

Hypothalamus: thyrotropic

TRH

Peripheral: corticotropic

Cortisol

•

Variable: corticotropic

Endorphins

•

• •

Allergic disorders Chapter | 1  5

Thyrotropic TRH, stimulated by alpha (Fig. 1.3), augments the general rate of function of immune activity and impacts the mechanisms of allergies as follows: 1. Histamine release by immune cells (primed by ACTH) 2. TSH relaunching → T-lymphocyte release from thymus → IgE production 3. TRH mediated T4 → T3 conversion with heightened oxidative burst and inflammation

Gonadotropic Gonadotropic activity tends to be hyperfunctioning both at the central and peripheral levels within the follicular line of activity. FSH can be oversolicited from ACTH or TRH or both. The results of this hyper-FSH are:

1. Horizontal TSH relaunching → Lymphocyte excretion 2. Vertical estrogen relaunching → further hyperfabrication of immune elements 3. Congestion of mucosal lining → prolonged local inflammation and hyperpara response The further increase of estrogens has four effects: 1. Amplification of the hyperfabrication of additional immune productions 2. Thyroid relaunching11 3. Growth hormone (GH) relaunching12, 13 4. Extravasation of immune cells into tissues14

Somatotropic Once again both central and peripheral somatotropic hormones are implicated in allergic responses, especially when they evolve into a chronic state. The details of this will be

aS

TRH

ACTH

Histamine Re le

as

Cortisol

e

Histamine receptors

Ma

tura

tion

TSH

Interleukins Thymus gland

T3

Inflammation Eosinophil

Basophil

Extravasation

Oxidative burst

lgE

VL

VH

lgE

VL

CH1

VH

lgE

VL

CH1

Lympho T cell Lymphocyte T cell Lymphocyte T cell

VH

CH1

CL CH3 CH2

CH4 CH3 CH4 CH3

Lymphocyte

CH4

B cell

FIG. 1.3  Alpha stimulates ACTH and TRH. There is an insufficient cortisol response to ACTH. As ACTH continues its stimulation to readapt cortisol to the Endobiogenic requirements of the organism, it upregulates histamine receptors in anticipation of TRH’s actions. It mobilizes eosinophils and basophils to act in the time with insufficient cortisol. Finally, it stimulates the release of T-lymphocytes from the thymus. TRH stimulates the release of histamines, which prolong the time of alpha and play an important role in allergy symptoms. It also stimulates TSH, which in the long term stimulates the maturation of T-lymphocytes released by the thymus. TRH stimulates the conversion of T4 to T3, which increases the rate of oxidative burst, participating in the general inflammatory milieu. The release of interleukins, from T-cells, from Alpha, etc. creates an inflammatory environment that allows for the extravasation of T-cells. T-cells stimulate B cells that release IgE, which further stimulates basophils and other inflammatory mediators. (© 2015 Systems Biology Research Group.)

6  The Theory of Endobiogeny

discussed later. GH, insulin resistance, and hyperinsulinism are capital with respect to inflammation and restoration of tissue. Prolactin can play the following roles: 1. ACTH relaunching → increased histamine receptors and increased lymphocyte maturation 2. Insulin excretion, inflammation, and extravasation of immune cells15, 16 3. Sensibilization to estrogens

Emunctory Liver congestion as an emunctory: In the precritical terrain, liver is oversolicited as a metabolic organ and in a latent state of congestion as an emunctory.

Whenever possible, especially with children, determining the precise allergens is the easiest on the family dynamics and child’s compliance with a restrictive diet.

Nosology of type 1 allergic disorders by location Allergic disorders can be typed by their localization. This is a 19th-century nosologic system that persists and perpetuates the illusion that these disorders and their treatments are unrelated.

Airway 1. Allergic rhinitis 2. Asthma

Common allergens Any substance potentially can become an allergen. However, when you hear the sound of hoof beats, think of horses, not zebras. The more common allergens are listed below.

Gastrointestinal 1. Eosinophilic esophagitis 2. Food allergies

Airborne If it is not practical or when it is too costly to determine the precise environmental allergens, avoid what is commonly responsible for allergies. Avoidance implies efforts to meticulously clean not only the house of the patient but also sheets and stuffed animals, evaluating hidden and open leaks in bathrooms, basements, etc.

TABLE 1.5  BoF values of the general atopic terrain Axis

Index

Value/comment

Corticotropic

ACTH

↑

1. Dust mites 2. Pets (dander) 3. Pollen 4. Molds 5. Roaches

Adaptation

↑

Cortisol

↓/normal

Adrenal cortex

↑/normal

Cortisol/adrenal cortexa

<2

Dietary

Aromatization of adrenal hormones

↑

Permissivity of the adrenal cortex

↑

Adaptationpermissivity of the adrenal cortex

↓ or negative (regardless of absolute value)

Evoked histamines

↑

Gonadotropic

FSH

↑

Thyrotropic

Genito-thyroid

↓

Thyroid relaunching corrected

↑/normal

Somatotropic

Somatostatin

↑/normal

Carcinogenesis

Interleukin-1

↑/normal

There are controversy and confusion regarding the immunologic nature of the reaction to specific foods. That is to say, there are those who associated certain symptoms with the presence of IgG and IgA antibodies to foods. These types of responses, if true, would fall under different categories of immune response. What we refer to below is with respect to IgE antibodies in type 1 immune responses. The following foods are so commonly implicated that some academic centers in the United States forgo testing and empirically remove the most common foods. The following is an example for Eosinophilic esophagitis, an atopic disorder as determined by case review17: 1. Dairy (72% of cases) 2. Wheat (26%) 3. Eggs (17%) 4. Soy (10%) 5. Peanuts (6%)

a

Not an index; the individual indexes are divided to obtain the value.

Allergic disorders Chapter | 1  7

Cutaneous 1. Eczema 2. Urticaria

Systemic 1. Anaphylaxis

Biology of functions indices of the critical allergic terrain The general hyperimmune allergic terrain has general commonality in the biology of function (BoF) findings (Table 1.5). With particular disorders, specific axes and related indexes will also be outside the normal range. What is presented below is the common BoF indices related to the atopic terrain, be it for eczema, allergies, or allergic rhinitis.

Nosology of type 1 allergic disorders by metabolite and physiologic process Atopy: A brief discussion The term atopy is coined from the Greek a- (without) topos (place) to indicate allergic disorders where the site of pathology was not local to the site of exposure. This definition is outmoded and not accurate for a number of reasons. This definition may apply to eczema, but not to other atopic disorders, such as allergies and asthma. This terminology denies a true physiologic approach to the disorder, which is based on understanding the differentiating factor in each type of atopic disorder. In this way, an Endobiogenic assessment of terrain can be applied to the disorder and personalized treatment. According to the Theory of Endobiogeny, atopy is a hyperimmune allergic disorder affecting epithelial tissue. Recall that there are four types of tissue: connective (including blood), muscle, nervous, and epithelial. Epithelial tissue lines cavities and envelopes the exterior of structures. Epithelial tissue is avascular and receives nutrients by passive­diffusion. It cannot regulate the precise quantity

or quality of nutrients received. Epithelial structures are the site of disease expression but the pathophysiologic response may originate from the adjacent connective tissue or from regional or global dysregulation. Table 1.6 briefly summarizes atopic disorders by the metabolite and endocrine axis most implicated. The order of the listing is significant. It is what is referred to as the “atopic march,” the progression of allergic disorders in children over time: eczema, food allergies, asthma, then rhinopharyngitis (The Theory of Endobiogeny, Volume 2, Chapter  9). The logic of the unfolding of the various “atopic” disorders follows the logic of the chronobiologic development of the endocrine system (The Theory of Endobiogeny, Volume 1, Chapter 13: Art of the history). The disorders arise when there is a disadapted state in regards to the recalibration of endocrine function. At 2  months of age, the infant experiences adrenal relaunching after a period of decline relative to fetal life (Table  1.7). In infants with atopic disease one finds that the adrenal cortex expresses a high rate of aromatization of adrenal androgens to estrogens at the expense of cortisol, thus the origin of the estrogen excess-hyperimmunity is established. If the dysregulation is latent, the patient does not develop eczema or eczema may be of a transient infantile variety. At 4–6 months during a time of thyroid tissular and metabolic activity, the diet is expanded beyond human breast milk and thus one observes the onset of food allergies. If the central response is greater than the peripheral thyroid activity, it favors increased histamine expression (cf. above). A second time for onset of food allergies is around 9 months of age with the relaunching of peripheral somatotropic metabolic management. Asthma typically occurs for the first time between 1 and 7 years of age, the time of thyroid metabolic and thyroid tissular phases of growth (Table 1.8). During this time, TRH sensitizes the organism to estrogens (The Theory of Endobiogeny, Volume 2, Chapter 11, cf. structuro-­functional spasmophilia). This increases the rate of metabolism and thus oxygen demand. In this time the organism should have an augmentation of peripheral thyroid activity to satisfy this requirement for oxygen uptake and utilization. It is this core

TABLE 1.6  Atopic disorders by metabolite and endocrine axis implicated Disorder

Epithelium

Origin of pathology

Endocrine

Metabolite

Eczema

Epidermis

Mesoderm: dermis

Gonadotropic

Proteins: over solicited

Food allergies

Small intestines

Mesoderm: subcutaneous tissue

Gonadotropic

Asthma

Bronchi

Oxidative metabolism

Gonadotropic

Oxygen: insufficient supply

Rhinopharyngitis

Respiratory

Endoderm: respiratory epithelium

Somatotropic

Glucose: excess presentation

8  The Theory of Endobiogeny

TABLE 1.7  Chronobiology of endocrine activity of infancy

TABLE 1.8  Chronobiology of endocrine activity of early childhood

dynamic which favors the expression of asthma as the liminal expression of atopy (cf. Chapter 2). The remainder of this discussion applies the general Endobiogenic concept of allergies to the specific condition of eczema.

Cutaneous allergic disorders: Eczema Definition A pruritic hyperimmune dermatitis.

Precritical Terrain In vagotonic patients, there is gonadotropic overactivity that is expressed at the level of the dermis and hepatobiliaryintestinal congestion.

Genetic studies suggest a relationship in defective epidermal integrity with water loss. However, the eczematous lesions on the epidermis are rich in keratin, a proteinaceous structure originating from the dermis. The dermis is a connective tissue of mesodermal origin, implicating the gonadotropic axis as the endocrine axis most implicated in the precritical terrain. Hepatobiliary-intestinal congestion is capital in the precritical terrain. It obligates the skin to act as an emunctory beyond its capacity, resulting in congestion and stagnation. In contrast, the vagotonia and estrogenism oversolicits the skin as a metabolic organ in its management of proteins.

Agent The agent or aggressor is some type of allergen, typically food-based.

Presentation The localization of the pruritic eczematous lesions evolves as the chronobiologic unfolding of endocrine function marches on in childhood (Tables 1.7 and 1.8). The general localization witnesses the compensatory adaptative response of the organism to aggression by an allergen (Table  1.9). The topology or semiology of eczema has a certain logic to its evolution (Table 1.10). It is based on the development of truncal stability and movement in infants and correlating endocrine development. It explains why infants at a certain age develop or evolve the presentation of their eczema.

Allergic disorders Chapter | 1  9

TABLE 1.9  Topology of allergic disorders Neuroendocrine Anatomy

Alpha + ↑ Para

Alpha + ↓ Betaa

ACTH

Forehead

•

Retroauricular

•

Visage

•

Cheek bones

•

Cheeks

•

Sinuses

•

Upper thorax

•

Upper arms

FSH: ACTH > 1

FSH: E2 > 1

Pit. + thyroid

GH > ACTH

•

•

Buttocks

•

•

Back

•

•

Flexural folds

•

Flexor surfaces

•

Extensor surfaces

•

Trunk

•

Peri-articular

•

Distal extrem.

•

a

Beta: beta insufficiency without prejudice to quantitative value. Pit.: Pituitary. ACTH, adrenocorticotropin hormone; E2, estrogens; Extrem., extremity; FSH, follicle simulating hormone; GH, growth hormone.

TABLE 1.10  Logic of the topological evolution of eczema Age

Mobility

Location

Endocrine adaptative role

2–6 months

Stationary Sitting

Face and scalp

Alpha > Beta ↑ ACTH for adrenal cortex relaunching

6–12 months

Crawling

Extensor surfaces

FSH > ACTH by vertical stimulation as ACTH continues to attempt to relaunch the adrenal cortex

Trunk

FSH > estrogens

Flexor folds: antecubital, popliteal

Alpha + Para: to relaunch metabolism, relaunch catabolic activity for movement

Flexor surfaces

ACTH: cortico-thyrotropic harmonization for gross motor activity with ambulation

Peri-articular: wrists, ankles

General pituitary over solicitation with peripheral thyroid > adrenal cortex or estrogen response with hypermetabolism focused on the joints, which are active with increased gross motor movements

Distal extremities: hands, feet

GH > ACTH due to lifestyle and excessive eating, alpha relaunching for somato-corticotropic harmonization

≥1 year

Adults

Ambulatory

10  The Theory of Endobiogeny

Physical exam: Neuroendocrine topology of allergic reactions According to the Theory of Endobiogeny, because of the role of the endocrine system in morphology and tissue development, the relative predominance of various ANS and endocrine responses to the allergen will localize the allergic response with respect to the exterior of the organism. Topical allergic disorders, such as eczema and hives, offer a direct ability to determine the neuroendocrine influence on the specific localization of lesions (Table 1.9).

Phase 3: Oozing There is a hyper ANS activity with conflicting para and alpha during the attempt to regulate wound healing after phase 2. There is central hyperfunctioning of the somatotropic axis with GH > PL. This period favors the risk of superinfections.

Phase 4: Desquamation

The eczematous lesions have four possible phases of evolution of their pathophysiology beyond excess deposition of keratin (Table 1.11). The advancement depends on the evolution of the Endobiogenic response to eczema. The common ANS preponderance is a hyperalpha in response to hyperpara. The common emunctory congestion is ­hepatobiliary (primary), intestines (secondary), and skin (tertiary)

Eczema concludes its evolution, either by restitutio ad integrum or transition to chronicity with lichenification. If the insulin response is well-calibrated in quantity, quality, and chronology, the skin will heal. If GH > insulin, lichenification will result. In all cases of eczema, ACTH is the primary factor of terrain implicated in the critical terrain. Alpha sympathetic is second as a factor solicited to prolong and calibrate the activity of ACTH. Hyperpara follows the alpha response. With respect to emunctories, the hepatobiliary unit is the primary emunctory evolved, followed by the intestines and then the skin.

Phase 1: Pruritic erythema

Biology of functions of eczema

A hyperfunctioning alpha induces a histamine response and pruritis. The specific area is determined by the factors noted above. The pruritis will continue to be present during the evolution.

The general observations of the allergic terrain are the same as noted earlier. As we have characterized the evolution of the autonomic nervous system and somatotropic system in the four phases of eczema, the specific indices will once again vary, by phase and by age. Table 1.12 mentions specific changes in the somatotropic terrain most commonly associated with phase 1 eczema, the most common variety seen in general practice.

Evolution

Phase 2: Vesicular The vesicular lesions (vesicle or bullae) form under the influence of a hyper GH and hyper insulin environment. If thyroid activity is also hyperfunctioning, a cyst can form.

TABLE 1.11  Terrain of the phases of eczema

+, Proportionality or degree of hyper functioning; ++, very hyper functioning; 1°, primary; 2°, secondary; 3°, tertiary; GH, growth hormone.

Allergic disorders Chapter | 1  11

TABLE 1.12  BoF values in the somatotropic axis in phase 1 eczema Index

Value/comment

Pro-amyloid

↑

GH growth score

↑

Insulin

↓ for age

Somatostatin

↑/normal

Redox

↓

Fibrosis

↑/normal

o­ften short-term relief. The second is to use medicinal plants with antihistaminic and antiallergic properties, internally, or externally.

Antipruritic An antipruritic neutralizes expressed histamine and other immune mediators. It is the most downstream approach of what is discussed here. A poultice applied to the skin is quite efficient and effective as an antipruritic. Clay functions as both an absorbent and adsorbent. Sodium bicarbonate (baking soda) is an alkalizing agent that neutralizes histamines. Any cooling or astringent plant can also be used when preparing a poultice for the skin (cf. Viola tricolor below). ●

Treatment: Symptomatic The treatment of pruritis serves two purposes. First, it offers relief to the patient. Second, it reduces the risk of aggravation of the disorder such as superinfections and chronic evolution of the disease.

Pharmaceutical Antihistamines offer rapid relief from pruritis, especially when associated with insomnia. The acute use of antihistaminics should not be forgone, especially in children, those with an increased risk of superinfections or those who suffer from mental or emotional disturbance from their pruritis. The Endobiogenic approach is to use them at the lowest dose possible for the shortest period of time while the Endobiogenic terrain is being corrected. 1. Nonsedating: best choice when pruritis-induced insomnia is not an issue a. Cetirizine b. Loratadine 2. Sedating (least to most sedating) a. Chlorpheniramine b. Diphenhydramine c. Promethazine d. Hydroxyzine: Helpful short-term for insomnia secondary to pruritis, especially in patients with a comorbidity of anxiety 3. Broad acting agents with antihistaminic properties a. Cyproheptadine: reserve for short duration at low doses for patients with advanced psychological disturbances related to pruritis and/or insomnia or with comorbidities such as anxiety, abdominal migraines, etc. Risk of side effects is elevated.

Nonpharmaceutical There are two Endobiogenic approaches to symptomatic treatment. The first is antipruritic. This offers rapid but

●

●

Clay, 1 tbsp or Baking soda 1 tsp. or both Optional, Essential oils (1–2 drops total): ● Lavandula officinalis (Lavender) Antihistaminic ● Anthemis nobilis (Roman chamomile) Avoid if patient has ragweed (Ambrosia ssp.) allergy ● Matricaria recutita (German chamomile) Carrier fluid (choose 1), 1 tbsp ● Water ● Hydrolat: Rose (all ages) or peppermint (3 and older, for the intense feeling of heat) ● Chamomile tea (cooled)

Instructions 1. Mix dry ingredients 2. Add essential oil(s) if desired and mix well 3. Add carrier fluid and mix into a smooth paste 4. Apply to affected area. a. If the area is too sensitive to apply paste, apply the paste to cheesecloth and lightly apply to the affected area. In this case, add more fluid to soak the cloth.

Antihistaminics, antiallergics Antihistaminics prevent further expression of histamine by stabilizing mast cells (Table 1.13). They are midstream agents. Antiallergics function by various upstream neuroendocrine and some downstream neutralizing effects of mechanisms of allergies (Table 1.14). Some common medicinal plants have dual action (Table  1.15). The most efficient plants are Lavandula angustifolia, Agrimonia eupatoria, and Viola tricolor.18, 19

Etiologic treatment of eczema: Restoring adaptability to the global terrain Restoring adaptability to the global terrain has three general aspects: autonomic, endocrine, and drainage of inflammatory products. The general goals are summarized below, then matched to treatments in Table 1.16.18, 19

12  The Theory of Endobiogeny

TABLE 1.13  Antihistaminic medicinal plants Indication/ comment

Medicinal plant

Galenical

Arnica montana

BH, MT

Alpha > para and/ or low insulin resistance

Artemisia dracunculus

EO, BH

Mental spasmophilia: anxiety, depression, etc.

Hamamelis virginiana

BH, DE, MT

Constipation, pelvic congestion

Eucalyptus globulus

EO

Asthma comorbidity

Matricaria recutita

BH, EO, DE, MT

Anger exacerbates eczema, strong inflammatory component Safe on open wounds

BH, bulk herb; DE, dry extract; EO, essential oil; MT, mother tincture.

1. Autonomic: Relieve spasmophilia a. Para-Alpha: Reduce global hyperfunctioning b. Beta: Restore chronologic integration 2. Endocrine: Support Somato-Corticotropic integration a. First loop: i. Adrenal cortex response to adaptation demands

ii. Somatotropic installation of insulin resistance b. First-to-Second loop i. Somatotropic relaunching of second loop corticotropic activity for the second peak of cortisol > DHEA 3. Drainage: Hepatobiliary-Intestinal drainage a. Reestablish primary drainage mechanisms b. Relieve congestion of the skin as an emunctory

Etiologic treatment of the local terrain: Drainage and skin healing Drainage Drainage of the skin and regulation of local expressions of histamine activity are important intermediate steps in reducing symptoms and reversing the degradation of the terrain. They need to be used along with a treatment of the global factors of terrain discussed above. Both Burdock and Wild Pansy offer local and global drainage support, making them highly efficient and effective in all stages of eczema. NB: aggressive or rapid skin drainage can aggravate eczema if hepatobiliary-intestinal drainage has not been instituted at a prior time or simultaneously with regulated skin drainage. Arctium lappa (Burdock)18–20 Galenic: MT, DE, BH Summary: A polyvalent drainer and depurative ideal for immunodermatologic disorders.

TABLE 1.14  Antiallergic medicinal plants Medicinal plant

Galenical

Indication/comment

Arctium lappa

BH, MT

Polyvalent pancreatic-skin drainer, advanced inflammatory state

Borago officinalis

BH, MT

Regulation of edema and estrogenism

Cichorium intybus

BH, HL

Dysbiosis prominent in immune dysregulation

Citrus limon

EO

Congestion around wound

Cnicus benedictus

BH, MT

Difficulty initiating liver drainage, secondary fungal infection

Glycyrrhiza glabra

BH, MT

Asthma comorbidity Food allergy comorbidity Intestinal permeability

Ribes nigrum

GM

Adrenal insufficiency, tissue drainage required

Rosmarinus officinalis

BH, DE, EO, GM

Adrenal insufficiency, delayed wound healing

Rubus idaeus

GM

Asthma comorbidity and menstrual cycle dysregulation

Sambucus nigra

MT, leaf

Brain fog, viral implication

Taraxacum officinale

BH, DE, MT

Auto-toxicity, low insulin resistance, elevated CRH, strong hepatic implication

Urtica dioica

BH, DE, MT, Leaf

Skin drainage where hyperglycemia and elevated insulin resistance play an important role

BH, bulk herb; DE, dry extract; EO, essential oil; GM, gemmomacerate; HL, hydrolat; MT, mother tincture.

Allergic disorders Chapter | 1  13

TABLE 1.15  Dual antihistaminic, antiallergic plants Medicinal plant

Galenical

Indication/comment

Agrimonia eupatoria

BH, MT

Indirect antiallergic through drainage of pancreas

Fagus sylvatica

GM

Hypogammaglobulinemia

Fumaria officinalis

BH, HL

Strong implication of biliary congestion

Inula helenium

BH, MT

Asthma comorbidity Recurrent ENT infections Peripheral cortico-gonadotropic insufficiency

Lavandula angustifolia

BH, DE, EO, MT

Prominent spasmophilia, anxiety

Plantago major

BH, MT

Hepato-pancreatic implication Asthma comorbidity

Syzygium aromaticum

EO

Recidivistic infections; avoid in open wounds

Viola tricolor

BH, MT

Indirect antiallergic through drainage of pancreas hyperhistaminemia and multiemunctory congestion

BH, bulk herb; DE, dry extract; EO, essential oil; GM, gemmomacerate; MT, mother tincture.

TABLE 1.16  Summary of treatment of global terrain of eczema Category

Goal

Medicinal plant

Autonomic

↓ Para-alpha

Lavandula angustifolia (lavender) EO, BH, HL, MT Anthemis nobilis (Roman chamomile) EO, BH, HL, MT Matricaria recutita (German chamomile) EO, MS, BH, HL, MT

↑ Beta

Cinnamomum zeylanicum (cinnamon) EO, BH, HL Citrus paradisi (grapefruit) EO Crataegus oxyacantha (hawthorne): MT, GM, DE

↑ Cortisol

Ribes nigrum (cassis) GM, MT, Fruit Abies pectinata (balsam fir) GM Quercus pedunculata (oak) GM Thymus vulgaris (thyme) EO, BH Satureja ssp. (savory) EO, BH

↓ Aroma-tization

Achillea millefolium (yarrow) EO, BH, MT

Regulate GH-PL

GH low, cortisol low: Lamium album (white deadnettle) MT, BH GH elevated, cortisol low: Fragaria vesca (strawberry leaf) MT, BH

↓ Insulin resistance

Arctium lappa (burdock): MT, BH Agrimonia eupatoria (agrimony): MT, BH Juglans regia (walnut): MT, GM

Hepatobiliary

Arctium lappa (burdock): MT, BH Agrimonia eupatoria (agrimony): MT, BH

Intestinal

Viola tricolor (wild pansy): MT, BH Agrimonia eupatoria (agrimony): MT, BH Lamium album (white deadnettle) MT, BH

Corticotropic

Somatotropic

Drainage

BH, bulk herb; DE, dry extract; EO, essential oil; GM, gemmomacerate; HL, hydrolat; MT, mother tincture.

14  The Theory of Endobiogeny

Actions: Immune: immunomodulating (reduces TNFα, increases macrophage activity), antiallergic (leukotriene inhibitor), regulates abscess formation and regulation, helps eliminate pus. ID: antiinfectious (cutaneous and urinary): antibacterial (staphylococcus, streptococcus, gonococcus, and pneumococcus) antifungal: candida. Derm: cutaneous drainer. Onc: antitumoral. GI: choleretic, pancreatic stimulant (exocrine and endocrine) prebiotic (inulin), ­hepato-protectant, mild laxative through choleretic activity. Metabolic: antihyperglycemic, normalize blood sugar by increases hepatic storage of glycogen. Renal: diuretic (volumetric and azoturic). Use: All disorders requiring hepatopancreatic, renal, and/or cutaneous drainage, pulmonary disorders; DERM: wet, oozing eczema, psoriasis, cutaneous infections, cystitis, diabetics with cutaneous manifestations, and cradle cap. Method: Decoction of root: 2–3 g, minced, in 5 oz water: boil for 1 h, filter, and drink TID; Poultice: Infuse 20 g leaves in 8 oz water 15 min. Note: synergistic with hypoglycemants and diuretics can augment the activity of vagolytics such as Thyme. Viola tricolor (Wild pansy)18, 19, 21–25 Galenic: MT, BH Summary: The most broad-acting antiallergic, antiatopic plant. Actions: Immune: antiinflammatory (salicylates), skin, bronchopulmonary, genitourinary. Drainage: general depurative, Skin: #1 cutaneous drainer; hepatic drainer, intestines, Kidneys: volumetric diuretic. Dermatologic: keratolytic, cicatrisant. Infectious: antiinfectious. Pulm: antiinflammatory, expectorant. CV: veinotrope, anticoagulant, inhibits platelet aggregation. GI: mild laxative (mucilage). Use: inflammatory and infected dermatoses: eczema, psoriasis, urticaria, acne; varicose ulcers, venous insufficiency with pruritis of lower extremities; allergic asthma; Method: Tisane or Compress: Infuse 1 tsp. in 8 oz water 10 min, drink TID before meals or apply to affected area;

Wound healing: Oligoelements 1. Manganese (Mn) series: a. Manganese (Mn): i. Primary support for healing of the connective tissue (i.e., the dermis) ii. Clearing toxic material including microbial fragments b. Manganese-copper (Mn-Cu): When superinfections persist due to poor oxidation (evaluate oxidation and oxidoreduction indices in BoF) c. Manganese-copper-cobalt (Mn-Cu-Co): i. Chronic, degenerative eczema ii. Strong emotional disturbance or stress related to aggravation of disease

2. Sulfur (S): use for poor quality of skin repair. Cf. Asthma: Nutrition for a discussion 3. Zinc (Zn): use with recurrent skin superinfections

Alimentation Dietary interventions should start with the elimination of known or common food and environmental allergens, followed by a high fiber diet with bitter and sour foods to help drain the intestines and liver, respectively. Cruciferous vegetables (rich in sulfur—cf. Chapter  2) and foods rich in magnesium (cf. The Theory of Endobiogeny, Volume 2, Chapter 11) and those that support the liver (i.e., beets) are encouraged.

Conclusions Allergic disorders are hyperimmune disorders arising from a spasmophilia with overfabrication and overmobilization of immune elements relative to the downregulation of immune activity. This chapter addresses type 1 allergic disorders, which are IgE mediated with a particular emphasis on eczema. These disorders require an initial exposure to an allergen, which primes the system followed by a subsequent exposure, which initiates the hyperimmune response and inflammation. The general approach to treatment involves both reduction of exposure to known allergens and regulation of the terrain. The latter involves resolving ANS spasmophilia, supporting peripheral catabolic activity, reducing anabolic activity, and instituting appropriate drainage of the liver, gallbladder, intestines, and skin.

Case study #1: Chronic, recurrent worsening eczema in a child Chief complaint A 4-month-old infant was brought to the clinic with a complaint of itchy rash and constipation. The patient typically has 6–8 soft stools per day. Every 10–12 days, he will not stool for 2–3 days. The infant is exclusively breastfed and the mother is on a restrictive diet, avoiding dairy products and gluten-containing grains (Table 1.17).

Past medical history He was a product of natural spontaneous conception and delivered by assisted home birth with prolonged labor. The mother reported feeling traumatized emotionally by the difficulty of the labor. The infant has mild jaundice that resolved by the third day of life without phototherapy. The infant had a poor latch for breastfeeding and underwent frenectomy for sublingual ankyloglossia (Table 1.17).

Allergic disorders Chapter | 1  15

TABLE 1.17  Interpretation of history and examination Sign/symptom

ANS

Prolonged labor

↑ Alpha

Endocrine

Neonatal jaundice

Hepatobiliary insufficiency

Early feeding trouble

↑ Alpha (response)

Constipation

↑ Alpha > ↑ para

Eczema: general

↑ Alpha > beta

Eczema: pruritis

↑ Para ↑ Histamine

Physical examination It confirmed pruritic eczematous lesions on the cheeks with scratch marks in the area. The skin is intact with no signs of pus or infection (Table 1.17).

Treatment The patient was started on a topical treatment and given a decoction of Arctium lappa (Burdock). Topical solution, applied 4 times daily to cheeks: ● ● ●

● ●

●

Hepato-biliary-intestinal congestion Skin congestion ↑ ACTH > cortisol response

TABLE 1.18  Relationship of treatment to the signs, symptoms, and terrain Sign/symptom

ANS

Treatment

Constipation

↑ Alpha > ↑ para

Matricaria recutita

Eczema: general

↑ Alpha > beta

Matricaria recutita

Eczema: pruritis

↑ Para ↑ Histamine

Agrimonia eupatoria Arctium lappa Lavandula angustifolia (Topical) Baking soda

Baking soda 1 tbsp Lavandula officinalis (Lavender) EO 1 drop Eczema tisane (cf. below) 2 tbsp Internal: A tisane was made of the following:

●

Emunctory

Equal parts Arctium lappa (Burdock), Agrimonia eupatoria (Agrimony), and Matricaria recutita (German chamomile) ½ tsp. was steeped for 6 min in 200 mL of water, then cooled 4 times per day in between nursing ● The boy received 15 mL (1 tbsp) by a bottle with a nipple. The remainder was refrigerated for 48 h. Whatever was not consumed by that time was discarded and a fresh tisane made every second day.

Eczema resolved in 14 days. The patient continued the treatment for 3 months in total then discontinued it. The following table places the medicinal plants at the level of each symptom or sign (Table 1.18). The boy was presented again at 3-years for further treatment of chronic, intermittent eczema. From 4 months on he was maintained on a restrictive diet (Weston Price—cf. end of the chapter for details), fermented cod liver oil, exocrine pancreatic support, and Rosa canina (Dog rose) bud gemmotherapy DH1; despite this, eczema presented with greater severity with each recurrence. The patient was then started on a tincture of Avena sativa MT, Rosa canina GM D1, Ribes nigrum GM D1

Hepato-biliaryintestinal congestion Skin congestion

Matricaria recutita Agrimonia eupatoria Arctium lappa

at a dose of 1.5 mL twice per day. He was continued on exocrine pancreatic support, fermented cod liver oil, and the Weston Price diet. Eczema resolved within 6 months. The Avena sativa offered two key actions. The first was ­regulation of the gonado-thyrotropic relationship, critical for the precritical terrain. The second was exocrine pancreatic substitutive support, allowing for downregulation of the gonado-­thyrotropic solicitation of the organ. The Ribes nigrum offered a more general corticotropic support, general drainage, and correction of the allergic terrain.

Case study #2: Chronic, recurrent eczema with biology of functions The patient was presented at 10.5 years of age with a history of precocious puberty, moodiness with dark, brooding thoughts and irritability, and difficulty concentrating. All

16  The Theory of Endobiogeny

symptoms were worse when she consumed gluten and/or sweets. Past medical history was significant for eczema as a child. She had been asymptomatic for over 6 years. She was treated solely based on history and physical examination (Table 1.19). Within 6 months of treatment (Table 1.20) (including avoidance of aggravating foods), her temperament was bright and happy. Her concentration had improved and she was sleeping better and waking with more energy. On her 11th birthday, she had a BoF performed. The indexes of the corticotropic axis can be divided into structural and functional values (Table  1.21). The function values represent the global adaptive response to aggression. Here, we see the Adaptation index is elevated, indicating that in the adaptation response, ACTH is more predominant relative to FSH because the peripheral response is less efficient within the corticotropic axis in relationship to the gonadotropic (The Theory of Endobiogeny, Volume 1, Chapter 15). Cortisol activity is insufficient, as is the global adrenal cortex response,

with a Cortisol/Adrenal cortex ratio of 0.33. This indicates that the absolute output of both is low and that the relative ratio is also low, relatively favoring adrenal anabolic activity. The relationship imposes two outcomes. The first is a relative predominance of anabolism related to catabolism (Catabolism/ Anabolism index, low). The second is an extremely elevated expression of histamines. The elevated interleukin-1 index serves as a proxy for the general rate of function of the immune system. The index, 31 times above the upper limit of the normal range is indicative of hyperimmunity. The net allergic tendency was elevated (allergy index). Once the risk was adjusted for the role of the exocrine pancreas (cf. Table 1.24) one sees the true expressed allergic tendency (Allergy index adjusted). The structure values represent the structuro-functional activity of the organism that results in the formation of eczematous plaques. The relative predominance of anabolism in relationship to catabolism (catabolism/anabolism index, low) is once again repeated to evaluate the imposition of

TABLE 1.19  Physical exam findings and their correlation with the terrain Region

Finding

Terrain

Head, ears, nose, throat

Lips full

Pancreatic congestion

Lips dry with vertical lines

Dehydration, elevated alpha and angiotensin

Lips red

Mitochondrial insufficiency

Low hairline

Adrenal androgens

Cheeks red

Elevated beta bursting

Tongue: tip erythematous

Small bowel inflammation

Unremarkable: tonsils, sublingual veins Chest

Breasts: Tanner stage 3

Precocious puberty with increased estrogens, growth factors, insulin

Extremities

Hands warm and sweaty

Elevated beta, parasympathetic

Dark hair on lower legs

Adrenal androgens

Dermatographism: 2 s blanching, then prolonged and deep erythematous response Abdomen

Neurologic

Doughy, dense tissue

Hyperinsulinism

Liver: tender on palpation, superior-medial

Hepatic vascular congestion

Liver: tender on palpation, inferior-lateral

Hepatic metabolic congestion

Pancreas: tender above umbilicus

General pancreatic congestion

Pancreas: tender right of umbilicus

Exocrine pancreatic oversolicitation

Pancreas: tender left of umbilicus

Endocrine pancreatic oversolicitation

Colon: all points tender

Hypothalamic-pituitary oversolicitation

Glabella tap: brisk, upper and lower, no flutter

Elevated alpha and dopamine

Clonus, L > R, 3–4 beat

General peripheral neurologic incoherence from elevated TRH

Allergic disorders Chapter | 1  17

TABLE 1.20  Empirical treatment and its effects by axis and actions on the terrain Treatment

Ingredients

Axes

Actions

Atomidine

Trichloro-iodine

Thyrotropic

Improves efficiency of production and action of thyroid hormones

Vitamin D 1000 IU/ drops: 5 drops qAM

Vitamin D

Thyrotropic

Regulates duration of thyrotropic participation in adaptation, regulates immunity

Pituitary blend #1: 3 mL BID with meals

Rhodiola rosea

Adaptogenic

Regulates responsiveness of corticotropic axis in adaptation, regulates pituitary and immune function

Inula helenium

Pituitary

Regulates pituitary efficiency in stimulation of peripheral endocrine glands, antiallergic, antihistaminic

Ribes nigrum GM

Corticotropic Immunity

Supports peripheral corticotropic function, immunity, antiallergic

Quercus pedunculata GM

Corticotropic Pituitary

Supports peripheral corticotropic function, Endocrine redistributor

Melissa officinalis MT

Central nervous system thyrotropic digestion

Regulates thyrotropic, neurologic function and digestion

Vaccinium myrtillus MT

Somatotropic

Regulates peripheral insulin sensitivity, circulation

Arctium lappa MT

Drainage

Skin, hepatobiliary, pancreas, depurative, blood purifier, pancreatic stimulant, immune modifier, antiallergic

Digestion blend #1: 3 mL BID with meals

BID, twice per day; GM, gemmomacerate; MT, mother tincture; qAM, every morning.

TABLE 1.21  Indexes of the corticotropic axis at pretreatment

a Not an index but a ratio of two indexes. (F), function value; (S), structure value. High low values presented in red/blue respectively.

a metabolic program at the structuro-functional level. The ACTH index is evaluating the general organometabolic activity of the pituitary tropin on the adrenal cortex. By extension, it is evaluating the relative predominance of DHEA in relation to that of cortisol. By extension it is evaluating the role of ACTH in preparing the cell for metabolism through hydroelectric fluctuations that precede aldosterone and the implications of what aldosterone shall bring. Thus, in eczema, we evaluate the ACTH index in structure. The adaption-permissivity is presented in structure, again, related to the adaptive activity of the adrenal cortex in relation to its permissive in structuro-functional adaptation. It is ­quantitatively elevated, slightly favoring adaptation, but negative. The negative sign indicates that the actual achievement is not occurring as anticipated by the absolute value. The permissive actions of the adrenal cortex predominate, distorting the orderly process of anabolism, participating in the irregular, disorderly arrangement of the proteinaceous plaques in eczema. Finally, the rate of aromatization of adrenal androgens to adrenal estrogens is elevated, indicating there is a source of estrogens to drive hyperimmunity and plaque formation on the skin that is not regulated by FSH. The genito-thyroid index was quite low, typical in atopic disease, and indicative of a lymphocytic predominance. The gonado-thyrotropic index was quite elevated. It indicates that the solicitation of the thyrotropic axis by e­ strogens is

18  The Theory of Endobiogeny

r­esponsible for dysfunctional structuro-functional adaptation. Serum TSH was elevated. Serum TSH was quite elevated. Regardless of the free levels of T4 and T3 (not measured), the functional effects of peripheral thyroid hormones were in the upper limits of the normal. Thus, the patient was not effectively hypothyroid, but had a latent hypothyroid, as concluded by the low genito-thyroid and thyroid yield. The importance of the TSH is that it created profound imbalances within the somatotropic axis (Table 1.22). In the gonadotropic axis, we mention three indexes (Table  1.23). The FSH index is elevated, which indicates a congesting role of mucosal tissue. This is occurring because the organotissular estrogen yield is low. The conclusion is that relative to the intensity and duration of FSH activity, the ­organotissular activity of estrogens is insufficient. The tissular endocrinometabolic activity of estrogens is also insufficient (corrected estrogen index). It is now clear why the adrenal cortex has become the second gonad in producing estrogens. Finally, in the somatotropic axis, one notes two key groups of findings. The first group is factors related to overproduction and growth related to the adaptation response. These indexes are listed in their function values. First amongst them is the role of the pancreas, noted by the elevated somatotropic index (cf. The Theory of Endobiogeny, Volume 2, Chapter 8). It indicates that the exocrine pancreas is oversolicited and somatostatin has not been successful in ending this process (Table  1.24), nor has cortisol in suppressing it (Table  1.21), in this case.1 Insulin resistance

TABLE 1.22  Indexes of the thyrotropic axis at pretreatment

a Not an index. (F), function value. High low values presented in red/blue respectively.

TABLE 1.23  Indexes of the gonadotropic axis at pretreatment

(F), function value; (S), structure value. High low values presented in red/blue respectively.

TABLE 1.24  Indexes of the somatotropic axis at pretreatment

(F), function value; (S), structure value. High low values presented in red/blue respectively.

is also elevated, favoring hyperglycemia that exacerbates overgrowth of structures. The third is the growth hormone (GH) growth score, which is elevated, even adjusted for age. The second is cellular metabolism, whose values are presented in structure to evaluate their role in the production of the eczematous lesions. They are also elevated in function (not shown), which relate to the production of immune factors. First amongst them is the rate of metabolism. We reproduce the relative anabolic predominance (Catabolism/Anabolism index) noted in Table 1.21. The rate of metabolism is also elevated, concluding that the organism is in an absolutely hypermetabolic, hyperanabolic state with an anabolic predominance over catabolism. At the interface of global function and the cell is the insulin index. The low value, adjusted for age, indicates insufficient insulin sensitivity, which feeds into the profound oxidative insufficiency that is relative (redox) and absolute (oxidation index). The result is an important functional mitochondrial insufficiency often seen in atopic patients. Finally, the autophagy 2 index is elevated. Autophagy is the process of cellular destruction of biologically derived waste products. The index evaluates the relative risk of insufficient cellular autophagy in the face of oversolicited organotissular metabolism imposed by global metabolic demands. By extension it favors ­autotoxicity of the interstitial space, in this case, localized to the skin. By extension, it favors an interstitiallymphatic drainage regiment. One efficient prescription is Alnus glutinosa GM + Ribes nigrum GM (interstitial drainage) + Juniperus communis GM (hepatorenal drainage for autotoxicity) + Sorbus domestica GM (lympho-venous-hepatic drainage). Based on her birthday BoF and her adrenal androgen tissular phase of growth, she was started on the treatments listed in Table 1.25. The patient was requested to avoid high glycemic foods and gluten. She was encouraged to explore her artistic side

Allergic disorders Chapter | 1  19

TABLE 1.25  Rational treatment and its effects by axis and actions on the terrain Treatment

Ingredients

Axes

Actions

Atomidine

Trichloro-iodine

Thyrotropic

Improves efficiency of production and action of thyroid hormones

Oligoelements

Zinc-nickel-cobalt oligoelement

Pituitary-thyro-somatotropic

Pituitary regulation (zinc fingers: DNA transcription), insulin production, food sensitivity, methylcobalamin (B12) production, stress management

Pituitary blend #2: 3 mL BID with meals

Salvia sclarea MT

ANS-endocrine harmonization Cortico-gonado-thyrosomatotropic harmonization Dermatologic

Regulates hypothalamic TRH relaunching by alpha, supports adrenal cortex, estrogens, thyroid, digestion, pancreatic drainer, supports exocrine pancreatic excretions; cutaneous antiinflammatory and astringent

Avena sativa MT

Gonado-thyrotropic

Gonado-thyrotropic harmonization of estrogen responsiveness to FSH and thyroid responsiveness to estrogens, pancreatic function

Ribes nigrum GM

Corticotropic Immunity

Supports peripheral corticotropic function, immunity, antiallergic

Plantago major MT

Drainage

Hepato-biliary-pancreatic drainage, antiallergic, antihistaminic, immune regulator

BID, twice per day; GM, gemmotherapy; MT, mother tincture.

(aunt is a professional artist). She was compliant with the treatment for 9 months until summer time. She stopped the treatment before leaving for summer camp in Europe. While away at camp, she had a dysregulated sleep schedule and ate all her aggravating foods (high-glycemic and gluten-containing foods). She returned from camp with a resurgence of eczema that had not been present since her early childhood. The distribution of the eczema was the scalp, left ear, and left antecubital fossa (Table 1.26). In addition, she had 3 episodes of otitis media over the summer. Her fits of crying, dark mood, and irritability returned. She also complained of feeling fatigued. The patient had a number of significant improvements in her findings in her current BoF and comparison to the prior year’s BoF. Based on these changes, her treatment was revised to increase the quality of dermatologic and hepatobiliary drainage and antihistamine therapy (Table 1.27). TABLE 1.26  Topology of eczema and its correlates in the terrain Neuroendocrine hyperfunctioning Anatomy

Alpha + Para

Retro-auricular Flexural folds Distal extremities

ACTH

GH > ACTH

• • •

Her BoF was subsequently repeated 8 months after the second evaluation. The arc of evolution of the indexes is presented in Tables 1.28–1.31. Clinically, her eczema progressively improved and she began losing weight.

Discussion At 11 years of age, her precritical terrain for eczema was more severe than at 12 years. However, she did not manifest eczema at that time. The reason for this was that hepatobiliary and exocrine pancreatic function was sufficiently regulated that proteins were not overabsorbed, immune factors not overproduced and catabolic waste products insufficiently drained. The stress of going away to summer camp in another country and the consumption of a­ggravating foods brought out the ­necessary changes in her atopic terrain to manifest eczema, which had been latent for years. As the patient continued with her treatment over the following 8 months, she continued to have improvements in her eczema terrain and a reduction of the clinical expression of eczema. The duration of treatment and the lack of quick resolution is because of two reasons. First, the genetic ­nature of the disorder and the ease at which the phenotypic ­expression is maintained. This is due to the second reason: the patient was not compliant with the recommended dietary changes. Thus, there were constant solicitations on the exocrine pancreas, adaptative congestion of her liver and skin, and adaptative neuroendocrine changes. Despite this, the treatments were able to ameliorate the terrain. This witness the importance of a multifactorial approach to the treatment of eczema: terrain, alimentation, and lifestyle.

TABLE 1.27  Rational treatment and its effects by axis and actions on the terrain Treatment

Ingredients

Axes

Actions

Atomidine

Trichloro-iodine

Thyrotropic

Improves efficiency of production and action of thyroid hormones

Topical

1 tsp. coconut oil + lavender EO 1 drop to scalp BID

Dermatologic Corticotropic

Reduce inflammation, histamine expression

Drainage #1

Arctium lappa MT Raphanus niger MT Achillea millefolium MT

Drainage

Supports digestion, drainage

Pituitary blend #3: 3 mL BID with meals

Salvia sclarea MT

ANS-endocrine harmonization Cortico-gonado-thyrotrosomatotropic harmonization Dermatologic

Regulates hypothalamic TRH relaunching by alpha, supports adrenal cortex, estrogens, thyroid, digestion, pancreatic drainer, supports exocrine pancreatic excretions; cutaneous antiinflammatory and astringent

Viburnum lantana GM

Central nervous system Thyrotropic

Regulates TRH expression within the hypothalamus and its responsiveness to alpha relaunching

Arctium lappa MT

Drainage

Skin, hepatobiliary, pancreas, depurative, blood purifier, pancreatic stimulant, immune modifier, antiallergic

Plantago major MT

Drainage

Hepato-biliary-pancreatic drainage, antiallergic, antihistaminic, immune regulator

BID, twice per day; GM, gemmotherapy; MT, mother tincture.

TABLE 1.28  Evolution of corticotropic indexes

a Not an index but a ratio of two indexes. (F), function value; (S), structure value. High low values presented in red/blue respectively.

Allergic disorders Chapter | 1  21

TABLE 1.29  Evolution of thyrotropic indexes

a Not an index. (F), function value. High low values presented in red/blue respectively.

TABLE 1.30  Evolution of gonadotropic indexes

(F), function value; (S), structure value. High low values presented in red/blue respectively.

TABLE 1.31  Evolution of somatotropic indexes

(F), function value; (S), structure value. High low values presented in red/blue respectively.

References 1. Sampson  HA. Food allergy: past, present and future. Allergol Int. 2016;65(4):363–369. 2. Thangam  EB, Jemima  EA, Singh  H, et  al. The role of histamine and histamine receptors in mast cell-mediated allergy and inflammation: the hunt for new therapeutic targets. Front Immunol. 2018;9:1873.

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22  The Theory of Endobiogeny

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