Clinical Essentials of the Thyrotropic Axis

Clinical Essentials of the Thyrotropic Axis

Chapter 10 Clinical Essentials of the Thyrotropic Axis Introduction The Thyrotropic axis is the second of the two catabolic axes, the other being the...

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Chapter 10

Clinical Essentials of the Thyrotropic Axis Introduction The Thyrotropic axis is the second of the two catabolic axes, the other being the corticotropic. This axis assists in adaptation, growth, and creation of cell energy (The Theory of Endobiogeny, volume 1, Chapter 8). These actions occur both centrally and peripherally and this observation is key to understanding the types of disorders related to this axis. In general, we can say that this axis is responsible for: 1. Acute change (αΣ + TRH): adaptive or adaptative activity, strongly influenced by perceptions, reactions, and prior experiences. Example: Acute adaptive: situational anxiety with racing mind and tachycardia, acute adaptative: acute on chronic aggravation of Grave’s disease 2. Disorders of adaptation (αΣ + TRH + various hormones): Examples: chronobiologic: spring cancer metastasis, spring allergies, structural adaptation: Crohn’s disease, psoriasis, structural spasmophilia, functional adaptation: Grave’s disease, Hashimoto’s thyroiditis, functional spasmophilia. 3. Disorders of growth (αΣ + TRH vs TSH): quality of growth: hyperplastic vs hypertrophic vs cystic. Examples: tonsil hypertrophy, prostate adenoma, ovarian cyst, cystic acne. 4. Affective states (αΣ + thyrotropic axis): psychophysiologic insomnia, anxiety, fugue psychosis, etc. Example: Insomnia in a 42-year-old divorced, working mother with 2 children: Cortisol 10 in structure (S), 7 in function (F) (normal: 3–7), Global adrenal cortex 1 (S), 2.5 (F) (normal: 2.7–3.3), Cortisol/adrenal cortex ratio 10 (S), 2.8 (F) (normal: 2–3). Treatment approach is to reduce alpha-sympathetic and cortisol, and increase adrenal androgen production: e.g., Passiflora incarnata MT + Eleutherococcus senticosus MT.

A brief review of key hormones Essence: Management of adaptability and growth. Key: relative balance of thyrotropin-releasing hormone (TRH) The Theory of Endobiogeny. https://doi.org/10.1016/B978-0-12-816965-0.00010-X © 2020 Elsevier Inc. All rights reserved.

to thyroid-stimulating hormone (TSH): imagination vs ideation, potential vs achievement, glucose vs proteins, adenosis vs amylosis, etc. Embryology: Ectoderm: nervous system, pituitary, adrenal medulla (βΣ), immunity, etc. The corticotropic and thyrotropic axes are linked together to disorders of adaptation and adaptability, both are relaunched by αΣ, a process called yoking (cf. The Theory of Endobiogeny, volume 1, Chapter  10, section Yoking). These two axes are particularly linked to conscious, subconscious, and physiologic perceptions of and response to aggression (cf. The Theory of Endobiogeny, volume 1, Chapter 12, Adaptation syndromes). Metabolism: Catabolism (TRH, T4, PTH) > anabolism (TSH, T3, calcitonin). Metabolite(s) and minerals: The catabolic hormones mobilize, the anabolic ones utilize. Its primary metabolite is lipids, used as a source of durable energy. However, all metabolites are mobilized or utilized by the thyrotropic axis (Table  10.1). Its primary mineral is calcium, used to adapt the rate of function of calcium-dependent processes, from clotting to enzymatic function to muscle contraction. This complements the role of the axis in ATP production.

Pathophysiology The four key hormones thyrotropic hormones for which the greatest number of symptoms, signs, and Biology of Function indexes are available are TRH, TSH, thyroxine (T4), and tri-iodothyronine (T3). TRH has wide-ranging effects centrally and peripherally (Table  10.2), as does TSH (Table  10.3) on comportment and metabolism. With respect to peripheral thyroid dysfunction, many of the symptoms attributed to T4 and T3 arise from central dysfunction. The Endobiogenic assessment clarifies this, which allows for a more targeted and rational approach to treatment (Tables 10.4 and 10.5). 87

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TABLE 10.1  Mobilization and utilization of metabolites by the thyrotropic hormones. Mobilization Metabolite

TRH

Glucose



Amino acids



T4

Utilization PTH/D3



Lipids



Calcium



TSH

T3









D3

Calcitonin





• •



D3, Vitamin D3; PTH, parathyroid hormone.

TABLE 10.2  Summary of central and peripheral TRH physiology and pathophysiology. Location

Physiology

Pathophysiology

Central

Neuromodulation

Fugue states, tremors, anxiety, negative imagination, OCD

Chronobiology, pacemakers

Seasonal and circadian disadaptation: insomnia, seasonal depression, spring allergies, seasonal cancer growth, etc.

Rational adaptation: dopamine-induced analytical function

Psychiatric disorders of excess: anxiety, panic attacks, schizophrenia

Contextual adaptation via limbic area

Consumption of buffering capacity: traumatic rumination, harmful adaptation responses, seasonal depression, winter bronchitis, etc.

Qualification of global adaptation response: αΣ, TRH, DA, limbic system

Adaptability: states of adaptability, esp. thyrotropic axis, autoimmunity, seasonal depression, winter bronchitis, etc.

Vigilance, creativity, neuroplasticity

Overstimulation: diurnal hypervigilance, nocturnal nightmares, night terrors, etc.

Serotonin-dopamine-TRH: Intensification of arousal, pain, pleasure, reward, movement, sleep, cardiopulmonary rhythms, gastric secretions

Prolonged adaptative states: migraines, depression, suicide, narcolepsy, pain processing, dysrhythmias, gastric hyperacidity

Muscle tone, posture

Peripheral Neuromuscular disorders: clonus, tremors, fasciculation, hypertonicity, Parkinson’s disease. Insufficiency of TRH: ataxia

Thyrotropic stimulation: TSH, T4 → T3, Calcitonin

Thyrotropic disorders: hyperthyroidism, adenosis (tonsils, prostate, breasts), amylosis (Alzheimer’s, diabetes, atherosclerosis), cysts, thyroid cancer, etc.

Somatotropic stimulation: prolactin

Hyperprolactinosis: implosive adaptation, infertility, schizophrenia, menstrual disorders, pancreatic cancer, metastasis of solid tumors, acceleration of aberrant growths

Thyro-pancreatic stimulation: glucagon, insulin

Disorders of adaptative TRH with hyperglycemia: depression with traumatic rumination, ADHD, autoimmune flare ups; disorders of hyperplasia: growth of aberrant tissues by cell multiplication

Cell: DNA transcription

Oncogenesis: DNA fracture, biologic toxin accumulation

Tissue: myolysis, adenosis (cell hyperplasia), dromotropy

Adenoidal disorders: tonsils, prostate, breasts (adenofibroids), muscle-wasting disorders, arrhythmias

Peripheral

AA, amino acids; ADHD, attention deficit hyperactivity disorder; OCD, obsessive-compulsive disorder; SCN, suprachiasmatic nucleus.

Clinical Essentials of the Thyrotropic Axis Chapter | 10  89

TABLE 10.3  TSH physiology and pathophysiology. Physiology

Pathophysiology

Estrogen sensitivity

High serum TSH: increased estrogen sensitivity, favors hyperestrogenism: adenoidal growth, menorrhagia, atopic disease, etc.

High insulin resistance

High serum TSH: diabetes mellitus type 2

Apoptosis

High serum TSH: mucosal congestion, i.e., appendicitis

Necrosis

Low serum TSH: amyloidosis: Alzheimer’s, Parkinson’s, Huntington’s diseases, atherosclerosis, rheumatoid arthritis

Low insulin resistance

Low serum TSH: chronic fatigue, fibromyalgia, hypoglycemia

Oxidation, harmful free radicals

Low serum TSH: chronic inflammation: demyelination, chronic fatigue syndrome, fibromyalgia, brain fog, etc.

TABLE 10.4  Role of various aspects of the thyrotropic axis in hyperthyroidism. Thyrotropic factor Factor

↑TRH

↓TSH, serum

Endocrine Symptom

Tremors Muscle wasting Insomnia

Exam

↑Deep tendon reflex Eyelid flutter Clonus

Inflammation Hair loss Brain fog

↑T4

↑T3

Overproduced from overstimulation

Overproduction, Overconversion

Heat intolerance (if insufficient conversion to T3)

Cold sensitivity

Skin temperature elevated

↑Osteoclasty

Structural Types of hyperthyroidism Reactive

Hypercatabolic, reactive thyroid state: asthma, Spring arthritis

Fundamental

Low TSH relaunching; peripheral hyperthyroidism: hyper-estrogenic (thus hyper T4), hyper beta, risk of breast cancer; psoriasis Treatment: Lycopus europaeus, Borago officinalis; if DHEA, ACTH implicated in the estrogenism: Fragaria vesca

TABLE 10.5  Role of various aspects of the thyrotropic axis in hypothyroidism. Thyrotropic factor Factor

TRH insufficient

↑TSH, serum

↓T4

↓T3

Endocrine

Insufficient conversion of T4 to T3

Insufficient production of T4

Anabolic predominance

Mitochondrial strain

Symptom

Repetitive dreams

Weight gain

Hair loss Thinning eyebrows Alteration in timber of voice: low, weak, and/or hoarse

Fatigability

Exam

Hyperestrogenism

Types of hypothyroidism Latent

Lymphocytosis; cardiac vegetations; tonsil hypertrophy; appendix hypertrophy

Entrained

Elevated TRH or PL or DA (dopamine); If there is elevated GH → appeal to glucose with diminished effect of GH (from strong insulin response)

Reactive TSH compensation

Fat pad above ankles (like Kurdish pants); cobble stoning of posterior pharynx; Treatment: Avena sativa, Verbascum thapsus

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Clinical pearl Along with the ANS (Chapter  7), regulation of central thyrotropic activity (TRH, TSH) offers the most rapid and effective method of symptomatic relief of psychological and physiological disorders. It involves a three-step process: (1) determine role of αΣ-TRH vs αΣ-TSH vs both, (2) determine level: central, peripheral, or both, (3) select therapies to address all levels of dysfunction simultaneously. 1. Example 1: insomnia with racing thoughts, tachycardia, eye twitching a. Terrain: αΣ, hyper TRH: central and peripheral + Spasmophilia b. Treatment: Lavandula angustifolia (alpha) + Leonurus cardiaca (TRH) + Valeriana officinalis (psychoneuromuscular spasmolytic) 2. Example 2: acute sinusitis with thick, green mucous a. Terrain: αΣ, insufficient TSH and thymus: peripheral + insufficient cortisol: peripheral b. Treatment: Lavandula angustifolia (alpha) + Avena sativa (readapt gonado-TSH-thyroid) + Rhodiola rosea (readapt cortico-thyro-thymic activity) 3. Example 3: Hashimoto’s thyroiditis a. Terrain: αΣ + hyper TRH, TSH: peripheral > central + insufficient thyrotropic: peripheral b. Treatment: Scutellaria lateriflora (alpha), Fabiana imbricata (TRH, TSH), Lithospermum officinale (TSH, Thyroid), Avena sativa (readapt gonado-TSH-thyroid)

TABLE 10.6  Symptoms related to the thyrotropic axis. Category

Finding

Level

Brain

General mental fatigue

Thyroid insufficient or excessive

Dermatologic

Pruritis

Thyroid elevated

Psoriasis

T4 elevated

General physical fatigue

Thyroid insufficient

Chronic fatigue

TSH low serum

Energy, lack of

Thyroid insufficient

Ear, nose, throat

Enlarged tonsils

Thyroid insufficient, serum TSH elevated

Genito-urinary

Reduction in the duration on menstruation

Thyroid excessive

Reduction in the volume of menstrual flow

Thyroid insufficient

PMS with great irritability

Thyroid increased

Menstrual flow heavy

Thyroid insufficient

Heat intolerance

T4 hyperfunctioning

Cold sensitivity

T3 hyperfunctioning

Constantly cold

Thyroid deficient in response

Weight loss despite a good appetite

Thyroid excessive

Weight gain

Thyroid insufficient, especially with elevated TSH serum and relative to global adrenal cortex activity

Insomnia with great agitation

TRH hyperfunctioning

Dreams animated, vivid

TRH predominant

Dreams in black and white

TRH insufficient

Repetitive dreams

TRH insufficient

Energy

Metabolic

In conclusion, when evaluating thyrotropic function, each hormone must be evaluated for signs of hyper- or ­hypofunctioning: TRH, TSH, T4, and T3, in order to determine the most appropriate type of treatment.

Symptoms related to the Thyrotropic axis There are a number of symptoms related to the thyrotropic axis (Table 10.6). Some are chronic, some acute.

Evaluation of the Thyrotropic axis The signs of the thyrotropic axis can be observed in the temperament and by inviting a discussion of the patient’s inner life (Table  10.7). Neurologic signs are particularly linked to the axis (Table  10.8). There are signs related to the head, ear, eyes, nose, and throat (Table  10.9), thyroid gland and chest (Table 10.10), and miscellaneous findings (Table 10.11).

Sleep

Clinical Essentials of the Thyrotropic Axis Chapter | 10  91

TABLE 10.7  Temperament and internal mental life. Finding

Level

Great vivacity

Thyroid dynamically efficient

Goal oriented

TRH predominant

Process-oriented

TSH predominant

Soft, easily gives in

Thyroid insufficient, especially during adaptation

Fearfulness

Thyroid insufficient

Anxiety and nervousness

TRH hyperfunctioning

Expansive creativity

TRH predominant

Juxtapositional creativity

TSH predominant

Depressive tendency

Thyrotropic dysfunctional

TABLE 10.9  Signs related to head, ears, eye, nose, and throat. Part

Quality

Finding

Level

Body

Build

Sharp features

TSH predominant

Voice

Quality

Weak and hoarse

Thyroid insufficient

Skin

Temperature and moisture

Cold and dry

Thyroid insufficient

Nail

Thickness

Fine and breakable

Thyroid insufficient

Hair

Quality

Thick

Favorably adapted

Curly hair

TRH predominant

Fragile

Thyroid insufficient

Thin

Thyroid not predominant

Falls out easily

Thyroid insufficient

Alopecia

Thyroid insufficient

Arch

Convex

TRH predominant

Pilosity

Fine

Thyroid strong

Thinning from hair loss at the ends

Thyroid diminished

Length

Long

Thyroid wellfunctioning

Curvature

Curled at ends

Thyroid insufficient to demand

Size

Large

TRH, alpha, central strong

Small

Thyroid insufficient

TABLE 10.8  Neurologic signs. Part

Quality

Finding

Level

General

Startle response

Startles easily to the lightest touch or sound

TRH reactive

Eyelids

Flutter

Spontaneous at rest

TRH hyperfunctioning

Eyelids

Flutter

Spontaneous interacting

TRH hyperfunctioning

Glabellar tap

Postglabella tap movement

Eyelid rapid flutter

TRH reactive

Eye

Pupillary light reflex

Exaggerated constriction to light

TRH reactive

Clonus

Foot

Brisk, diffuse

TRH elevated

DTR

Tendons

Brisk, diffuse

TRH elevated

Extremities

Arms, hands, legs

Tremors

TRH excessive

Biology of Function indices related to the Thyrotropic axis A complete assessment of the thyrotropic axis involves (1) serum endocrine evaluation: TSH, free T4, free T3, thyroid antibodies, etc. and (2) Biology of Functions indexes. Quantitative measurement informs you of the output of the pituitary and thyroid, or, amount of circulating hormones

Eyebrow

Eyelashes

Eye

Tonsils

Size

Hypertrophy

Thyroid insufficient responsiveness to TSH

Pharynx

Deformity

Cobble stoning

Thyroid insufficient responsiveness to TSH

from replacement therapy. BoF indexes ­evaluate notions related to systems thinking according to the theory of Endobiogeny. There are central indexes evaluating the αΣTRH relationship in adaptation (Table 10.12), radial gonadothyrotropic calibration (Table 10.13), the thyroid gland and efficacy of peripheral thyroid hormones (Table 10.14), and parathyroid and bone metabolism ­activity (Table 10.15).

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TABLE 10.10  Signs related to the thyroid gland and chest. Part

Quality

Finding

Level

Thyroid

Volume

Increased

Thyroid augmented

Consistency

Nodules

Thyroid oversolicited

Consistency

Goiter

Thyroid insufficient

Clavicle, bilateral

Proximal

Pain on palpation

Sternum

Orientation

Convex sternum

PTH elevated

Breasts

Asymmetry

Left > right

TSH predominant

Heart

Rate

Heart rate rapid

Thyroid augmented

TABLE 10.11  Others signs by region. Part

Quality

Finding

Level

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

Transverse, distal, left

Pain on palpation

TSH strong

Colon

Transverse, distal, right

Pain on palpation

TRH predominance

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

Para spinal, 2.5 cm lateral

Pain on palpation

TRH oversolicitation of exocrine pancreas

Scapula, right

Inferior-medial, T7–T8

Pain on palpation

FSH, TRH

Scapula, left

Inferior-medial, T7–T8

Pain on palpation

TSH, PL

General

Extremities

Lymphatic congestion

Thyroid latent hypothyroidism

Palm

Central

Erythematous

Thyroid strong

Leg

Medial to ankle, bilateral

Adiposity

TSH elevated

Leg

Proximal tibia, most medial aspect

Pain on palpation

T4 diminished efficiency

Leg

Proximal tibia, most medial aspect

Pain on palpation

TSH strong

Ankle

Superior to ankle

Fat pad

TSH reactive

TABLE 10.12  Central thyrotropic indexes with peripheral impact. Index

Definition

Import

Thyroid relaunching

TRH reactivation by Alpha in response to exogenous adaptation

High: TRH and/or thyrotropic axis relaunched due to a perception of exogenous aggression by alpha. Reduce TRH: Fabiana imbricata, Leonurus cardiaca, Vibernum lantana; Reduce Alpha: higher the index, more sedating the sympatholytic (most to least sedating): Valeriana officinalis, Scutellaria lateriflora, Passiflora incarnata, Lavandula angustifolia

Thyroid relaunching corrected

TRH reactivation by Alpha in response to endogenous adaptation

High: As above, except due to endogenous aggression; emotional perception of threat may also be playing a role. Treatment is the same, but may also require counseling intervention

TRH/TSH

Relative tissular activity of TRH vs TSH

High: TRH > TSH: congestion > hyperplasia, nutrition > metabolic production, neuroendocrine > organo-metabolic adaptation, tangential thinking > concrete thinking Low: Opposite interpretation

Clinical Essentials of the Thyrotropic Axis Chapter | 10  93

TABLE 10.13  Radial gonado-thyrotropic index. Index

Definition

Import

Genito-thyroid

General role of estrogens in relaunching the thyroid vs the responsiveness of TSH in adapting the thyroid

High: Favors inflammation and autoimmunity: TSH responds too quickly to estrogen demand Low: Favors hyperimmunity, atopy: TSH does not respond quickly enough to estrogen demand

TABLE 10.14  Indexes evaluating the thyroid gland and its activity. Index

Definition

Import

Thyroid index

Effective cellular metabolic activity of T4, T3

High: Cellular thyroid metabolic activity elevated, regardless of serum levels of TSH, T4, or T3 Low: Cellular thyroid metabolic activity diminished, regardless of serum levels of TSH, T4, or T3

Thyroid yield

How quickly thyroid is adapted by TSH when its activity declines

High: Thyroid adapted too quickly, risk of mucosal inflammation: sinusitis, urinary cystitis, colitis, etc. Low: Thyroid adaptation delayed, risk of tissular hypertrophy: tonsils, breast mass, prostate adenoma, etc.

TABLE 10.15  Parathyroid and bone indexes. Index

Definition

Import

Parathyroid hormone index (PTH)

PTH endocrinometabolic activity

High: Thyroid inefficient, PTH used to liberate calcium from bone to compensate, risk of mitochondrial strain Treatment: support thyroid activity, e.g., Avena sativa, Zingiber officinale, iodine, selenium, tyrosine, creatine, etc. Low: Opposite; Treatment: diminish thyroid activity if indicated, e.g., Lithospermum officinale, Lycopus europaeus, Cornus sanguinea, etc.

Bone remodeling

Extent of bone turnover to adapt peripheral metabolism through activity of osteocalcin

High: Bone is oversolicited to adapt peripheral metabolism. Treatment: Adapt adrenal cortex: Quercus pedunculata GM, Adapt gonadothyrotropic: Salvia officinalis, Avena sativa

Conclusions The thyrotropic axis is implicated in psychiatric, neurologic, dermatologic, and osseous disorders, as well as in adaptation, gonadotropic, and somatotropic disorders. Thus,

one finds a rich array of signs and symptoms implicated well beyond thyroid disease. The theory of Endobiogeny offers a systematic approach to evaluating central and peripheral thyrotropic function: TRH, TSH as well as peripheral hormones.