The Theory of Endobiogeny: Volume 3: Advanced Concepts for the Treatment of Complex Clinical Conditions

By Kamyar M. Hedayat and Jean-Claude Lapraz

Theory of Endobiogeny, Volume 3: Advanced Concepts for Treatment of Complex Clinical Conditions explains complex and multi-factorial disorders and diseases using the theory of endobiogeny. It provides detailed applications of biological modeling, in-depth assessment into common disorders, an endobiogenic analysis, guidance on using biological modeling tools, and suggestions for treatment using standard of care treatments that also take into account diet, lifestyle and medicinal plants. This approach is an evolution in thinking from reductionism to holism, offering advice for symptomatic treatments that can be used in conjunction with a new way of thinking about diseases and disease management.

• Covers complex and multi-factorial disorders and diseases using the theory of endobiogeny
• Provides detailed applications of biological modeling that can be used within current clinical practice
• Extends systems biology from the cell level to the physiology level using pattern recognition

• Language: English
• Publisher: Academic Press
• Release date: Sep 10, 2019
• ISBN: 9780128173329

Kamyar M. Hedayat

Kamyar M Hedayat is a global leader in research and training in Endobiogeny and protégé of Dr. Lapraz. A Stanford-trained critical care physician, he has been practicing endobiogenic medicine since 2008. Drs. Hedayat and Lapraz are cofounders of the American Society of Endobiogenic Medicine and Integrative Physiology and copresidents of the Systems Biology Research Group.

Book preview

Endobiogeny.

Chapter 1

Allergic disorders

Abstract

There are two types of disorders related to hyperfunctioning of the immune system: allergic and autoimmune. They can be divided into four types based on the elements of adaptive and/or innate immunity involved. This chapter presents a general overview of allergic disorders. The expression of allergies in certain parts of the body depends on two factors. The first is the autopathogenic endocrine axis. For example, if it is the gonadotropic axis, there is a risk of dermal atopy. The second is the organ or tissues with the greatest metabolic activity. This can be structural, such as a joint, into which immune complexes can deposit, or it can be metabolic or emunctory, such as the lungs. The remainder of the chapter focuses on eczema as an exemplary expression of type 1, IgE mediated allergy. The precritical terrain of eczema is (1) hyperimmunity, (2) spasmophilia, (3) adrenal cortex tendency toward permissive and anabolic activity, and (4) hepatobiliary-intestinal congestion. The critical terrain involves insufficient cortisol and overfunctioning of the thyrotropic axis. The terrain of the four stages of eczema evolution is discussed, along with the neuroendocrine origin of the topology of eczema. The chapter concludes with two case studies illustrating the evaluation and treatment of eczema in an infant and adolescent.

Keywords

Adaptive immunity; Adrenocorticotropic hormone (ACTH); Allergic disorder; Antihistamine therapy; Eczema; Endobiogeny; Endocrinology; Endoderm; Food allergies; Histamine; Immunoglobulin E (IgE); Innate immunity; Thyrotropin-releasing hormone (TRH)

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 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).

Table 1.1

NK, natural killer.

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.

Table 1.2

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.

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 second aspect is the latent spasmophilia. There is elevated parasympathetic and alpha-sympathetic activity (The Theory of Endobiogeny, Volume 2, Chapter 11).

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

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

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.)

Response: Allergic terrain

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)

Table 1.4

ANS

Part of the spasmophilic nature of allergies is that the alpha-sympathetic 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

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.)

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 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.

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.

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.

1.Dust mites

2.Pets (dander)

3.Pollen

4.Molds

5.Roaches

Dietary

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%)

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

Gastrointestinal

1.Eosinophilic esophagitis

2.Food allergies

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.

Table 1.5

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

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 passive diffusion. 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.

Table 1.6

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.

Table 1.7

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 dynamic which favors the expression of asthma as the liminal expression of atopy (cf. Chapter 2).

Table 1.8

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 hepatobiliary-intestinal 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.

Table 1.9

Pit.: Pituitary. ACTH, adrenocorticotropin hormone; E2, estrogens; Extrem., extremity; FSH, follicle simulating hormone; GH, growth hormone.

a Beta: beta insufficiency without prejudice to quantitative value.

Table 1.10

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).

Evolution

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)

Table 1.11

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

Phase 1: Pruritic erythema

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.

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.

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

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.

Biology of functions of eczema

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.

Table 1.12

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 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).

●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

Table 1.13

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

Table 1.14

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

Table 1.15

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

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

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

Table 1.16

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

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.

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).

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