What is Homotoxicology?

by Urenus .

Classical homeopathy according to Hahnemann (1811) orients itself based on the so-called ‘drug picture’ to determine the appropriate remedy. It claims that symptoms of disease behave reciprocally towards those symptoms which the healthy test person develops after  the intake of a mother tincture or a diluted substance (potency.) The principle of action which can be derived thereof is known as the Simile Principle (Similia similibus curentur = Likes may be cured by likes.) The clinical syndrome occurring in a patient can be overcome by an artificially induced, similar disease. The Aequalia Principle (Isopathy = the condition may be healed by the causative substance) can also be applied with potentised allopathic substances or partly with nosode preparations in anti-homotoxic medicine and/or with vaccines in conventional medicine.

Classical homoeopathy works with single remedies which are only partly truly single- constituent remedies, (e.g., sulphur, mercury, arsenic, etc.), or which are otherwise botanical extractions containing a highly complex mixture of numerous constituents. Repertories (lists of symptoms produced by drugs) facilitate the selection of the most appropriate remedy in homoeopathy.

Anti-homotoxic medicine usually pursues an indication-oriented approach. The anti- homotoxic remedies predominantly represent mixtures of substances of low to middle potencies. Through practical application in homoeopathy it became obvious that the use of concentrated or poisonous tinctures could damage the patient and that, therefore, they could only be used in homoeopathic dilutions, i.e., potencies. This practice was scientifically supported by Rudolf Arndt (psychiatrist, 1835-1900) and Hugo Schulz (pharmacologist, 1853- 1932) through a quantitative differentiation of the medicinal effect on bio-systems and still applies as the Arndt-Schulz Principle. It states:

  • weak stimuli stimulate the life functions (retro-action of homoeopathic preparations)
  • moderately strong stimuli accelerate them
  • strong stimuli act as inhibitors
  • the strongest stimuli suspend the life functions

Since several tissue-incompatible substances are usually involved during the development of a disease, the simultaneous use of several potentised ”antitoxins“, as present in the anti- homotoxic preparations, is justified.

Against the background of the conflicting medicinal and therapeutic concepts promulgated in humoral pathology, cellular pathology, molecular pathology, and related fields including modern cybernetics, the German physician Dr. Hans-Heinrich Reckeweg formulated Homotoxicology in 1952. This conception was developed from homoeopathy for the purpose of providing a holistic perspective on the synthesis of medical science.

Reckeweg formulated an essential tenet of Homotoxicology, as follows:

”According to Homotoxicology all of those processes, syndromes, and manifestations, which we designate as diseases, are the expression thereof that the body is combating poisons and that it wants to neutralize and excrete these poisons. The body either wins or loses the fight thereby. Those processes, which we designate as diseases, are always biological, that is natural teleological processes, which serve poison defence and detoxification.“

Referring to conventional medical indications connects anti-homotoxic medicine with allopathy, while therapy with potentised substances unites it to homoeopathy. Anti-homotoxic medicine is the connecting link between allopathic medicine and homoeopathy.

Fig. 1

 

Conventional medicine:

The higher the concentration, the stronger the effect (dose-effect relation; increase of side effects).

 

Homoeopathy:

Increase of the effect with decreasing concentration (effect optimum not definable). Anti-homotoxic medicine:

Connecting link between conventional medicine and homoeopathy.

 

  1. Fundamental principles of Homotoxicology

1.1.1 Homotoxins

Homotoxins are all of those substances (chemical/ biochemical) and non-material influences (physical, psychical), which can cause ill health in humans. Their appearance results in regulation disorders in the organism. Every illness is due therefore to the effects of homotoxins. Homotoxins can be introduced from the exterior (exogenic homotoxins) or originate in the body itself (endogenic homotoxins).

1.1.2 Homotoxons

These are understood as chemical reaction products from compounds of homotoxins with each other or with other substances (e.g., products of metabolism) which neutralize the poisonous property of the homotoxins. The best example thereof is the liver, in whose cells homotoxins and metabolic products are united to detoxify the organism.

1.1.3 Retoxins

Deposits of homotoxins with endogenic substances, which cannot be eliminated via excretion or irritation, are designated as ”residual poisons“ (retoxins). The most important example thereof is the non-enzymatic glucosilisation of tissues and cell surfaces in case of glucose excess, as with, among others, latent diabetes mellitus.

1.1.4 Homotoxicosis - The Concept of Disease in Homotoxicology

Homotoxicosis is a non-physiological condition which arises after reaction of a homotoxin on cells and tissues. A homotoxicosis occurs as a humoral or cellular appearance and can be followed by morphological changes on tissues. The homotoxicosis is named after the homotoxin which triggers it. The homotoxicosis leads to defensive measures of the organism whose goal is to eliminate the homotoxins and to restore the physiological conditions when possible.

1.1.5 The Ground Regulation

This refers to the local regulation possibilities of the ground system along with its superimposed nervous, hormonal, and humoral regulation systems. The ground system is composed of the ground substance plus cellular, humoral, and nervous components. The ground substance (extracellular matrix) is formed of highly polymerised sugars  (proteoglycans and glycosaminoglycans) plus structural and meshing glycoproteins.

1.1.6 The Phase theory

The Six-Phase-Table illustrates the chronological courses of various symptoms of a disease within the framework of the ground regulation. The single phases are transient into each  other and demonstrate typical phasal indicating signs. The Six- Phase-Table is subdivided into three sections (humoral phases, matrix phases, cellular phases), each of which is subdivided into 2 phases. Two phases are allocated to the excretion principle (phases 1 + 2), the deposition principle (phases 3 + 4), and the degeneration and/or deterioration principle (phases 5 + 6). The Biological Division runs within the matrix phases.

Fig. 2: The Six-Phase-Table

  1. The humoral phases

In the humoral phases the intracellular systems are not disturbed. The defence system is intact and can excrete the homotoxins via various paths.

  1. Excretion This phase contains manifestations of increased physiolo- phase gical excretion mechanisms.

  • Reaction Illnesses of this phase are marked by an exudative inflam- phase mation, which enables an accelerated excretion of toxins

from the body.

B) The matrix phases

In these phases the homotoxins are deposited at first in the mesh of the extracellular matrix. During the further course its structural components as well as functions are al-tered. In case of continuing illness increasing stress and damage of the intracellular structures result.

  • Deposition In this phase the excretion mechanisms of the body are phase overworked and toxins are deposited in the matrix.

This phase often progresses with few symptoms.

  • Impregnation Diseases in this phase are characterized by the presence phase         of toxins which become a part of the connective tissue

and the matrix, along with changes in the structural com- ponents as well as their functions. The typically increasingly severe symptoms and signs of this phase demonstrate damage of the organ cells.

C) The cellular phases

During the cellular phases of a disease, cell systems are increasingly destroyed. The defence system is no longer able to excrete the toxins out of the cells or out of the matrix by virtue of its own strength. Typical for these phases is the so-called regulation rigidity.

  • Degeneration During this phase, courses of disease cause serious dam- phase age, and destruction of larger cell groups of an organ

takes place.

  • Dedifferentiation Diseases of this phase are characterized by the devel- (neoplasm)      opment of undifferentiated, non-specialized cell forms. phase Malignant diseases stand at the end of this phase.

1.1.7 Biological Division

The Biological Division refers to the imaginary boundary between the deposition and impregnation phases. It demarcates the pure deposition in the matrix from the integration of toxins into its structural components. Whereas a simple excretion of the toxins is possible during the deposition phase, structural and functional changes are found in the impregnation phase. Thus the spontaneous endogenic excretion of the homotoxins is impeded.

1.1.8 Vicariation

The term ”vicariation“ refers to the transition of the indicating signs of an illness within one phase to another organ system, or the change of the fundamental symptoms and signs into another phase, with or without a change of the organ system.

Progressive vicariation: Progressive vicariation refers to an aggravation of the total  symptoms and signs of illness.

Regressive vicariation: Regressive vicariation refers to an improvement of the total symptoms and signs of an illness.

1.2   The principles of action of anti-homotoxic medicine

The different components of the anti-homotoxic preparations activate the defence system of the body:

Fig. 3: Functional circle of the anti-homotoxic therapy

The immune system with its memory and regulation systems can be compared to the spiritual-mental self, the ego. The deposition phase, and more frequently the impregnation phase, is characterized by immunological processes such as chronic inflammations and auto- aggression. The humoral area (via immunoglobulins from B-lymphocytes) and the cellular area (T-cells, granulocytes, macrophages) still counterbal-ance each other in this case. A regressive vicariation is still possible in these matrix phases.

Herein lies a great opportunity for anti-homotoxic medicine. The immunological bystander reaction represents a theory of anti-homotoxic therapy for inflammatory illnesses. It is based on low dose antigen reactions particularly of substance combinations in the range of D1 to D12, with D4 to D8 appearing to be the most favourable (Heine, 1997b). The bystander effect cannot be triggered at higher potencies, however experience shows that higher potencies as well as trace elements and intermediary catalysts are able to stimulate the ground regulation. (Functional circle of the anti-homotoxic therapy; Fig. 3; Heine, 1997a.) It is significant that, for the potency ranges D3 to D12, a considerable difference exists in the activation of specific enzyme systems compared to substances conventionally diluted in the same concentration. The dose-action relationship of potentised substances compared to diluted substances demonstrates thereby a non-linear relationship (Hoariest and Dittmann, 1997).

Ground regulation system

Every organism requires energy to maintain its vital functions which must be continuously provided by the metabolism. Therefore, disorders of the energy metabolism impair  the energy supply which is controlled by the endogenic regulation. The organism is an energetically open system for which suitable energy (in the form of food) must be supplied, and unsuitable energy must be evacuated. In this manner an unstable state of order can be maintained, far from a thermodynamic balance, for a longer period of time (”life-span“). All reactions of the organism proceed at relatively low temperatures in the aqueous milieu, therefore they must be accelerated, i.e., catalysed. The prerequisite for an effective catalysis is suitable substrates between and in the cells. Be-cause the extracellular space is located in front of the cells, the cells can only react as they have been informed via the extracellular space. The dynamic structure of the extracellular space and its regulation (”Ground regulation“) have therefore a decisive impact on the effectiveness of extracellular and intracellular catalysts. This depends on the structure of the ground substance (extracellular matrix and/or matrix). It forms in all cells and cell groups a molecular sieve of matrix components such as highly polymerised sugar protein complexes and sugar complexes (proteoglycans-glycosaminoglycans, PG/GAGs), structural proteins (collagen, elastin) and meshing glycoproteins (e.g., fibronectin) (see Figure 4). The PG/GAGs are electro-negatively charged and are therefore able to bind water and exchange ions as well. They are therefore the guarantors for isoiony, isoosmy, and isotony in the matrix.

Fig. 4: Diagram of the ground regulation

Reciprocal relationships (arrows) between capillary system (capillaries, lymph vessels), ground substance, terminal autonomic axons, connective tissue cells (mast cells, defence cells, fibroblasts etc.) and parenchyma cells. Epithelial and endothelial cell groups rest on a basal membrane which mediates to the ground substance. Every cell surface carries a glycoprotein and glycolipid film connected to the ground substance (dotted line), to which the histocompatibility complexes (MHC) also belong. The ground substance is connected to the endocrine system via the capillary system and via the axons to the central nervous system. The fibroblast is the metabolically active centre. (Heine 1997b)8)

The connection to the central nervous system is conducted via the autonomic nerve fibres blindly ending in the matrix. The connection to the system of endocrine glands (pituitary gland, thyroid gland, suprarenal gland, etc.) is conducted via the capillary system which permeates the matrix. Both systems are connected to each other in the brainstem and to superimposed centres of the brain (Fig. 4). In this manner the matrix is regulated not only on site but also under the influence of superimposed control areas. The regulation centre in the matrix is the fibroblast (corresponding to the glia cell in the central nervous system). It reacts immediately to all incoming information (hormones, neural substances, metabolites, catabolites, pH-value changes etc.) with a synthesis of matrix components suited to the situation. It does not differentiate thereby between ”good“ or ”bad“ information.  In  this manner every surplus or deficit can lead in certain circumstances to detrimental consequences for the total system depending individually on a circulus vitiosus (vicious circle).

It is important to note that due to the sieve-like as well as connective properties of the PG/GAGs, the danger of slagging of the matrix also exists through the development of a latent tissue acidity, increase of free radicals, and the activation of the proteolytic system turning into a pro-inflammatory situation. Ultimately, damage of all humoral and cellular elements may arise progressing at first from persistent feelings of ill health to chronic diseases and malignant processes. (See 1.1.6, page 11; summary in Heine 1997a.)7)

Immunological Bystander Reaction

Whether administered orally, as aerosol, nasally, i.v., s.c. or i.m., the anti-homotoxic preparations are either directly confronted non-specifically with the macrophages/monocytes or the substances are offered to them by lymphocytes patrolling the mucosa epithelia after superficial contact. After phagocytosis the macrophages return an amino acid motive (9 to 15 amino acids) of the substances to its surface. There they are bound to the MHCI complex (histocompatibility antigens) (Fig. 4). Thus the motives for yet undetermined (”naive“) lymphocytes (Th0) become recognizable. They accept the motives and convert themselves thereby into regulatory Th3-cells. Afterwards they wander via the lymph vessels into the nearest lymphatic node and form _motivated“ cell clones which enter the bloodstream via the post-capillary venulae and are distributed throughout the whole organism via the circulation. In dysregulatory areas, in particular inflammatory regions, the Th3-cells are chemotactically attracted (complement factors, chemokines etc.). According to their motives they can recognize inflammatory lymphocytes (T4-cells and their subpopulations T-Helper1- and T- Helper2 lymphocytes). A similarity of the motives (the Simile Principle of anti-homotoxic medicine!) suffices thereby to stimulate Th3-cells to secrete the anti-inflammatory cytokines TGF-b (tissue growth factor-beta) and to a slight degree interleukin-4 and -10. TGF-b is the most potent anti-inflammatory cytokine in the body. It suppresses the T4- and its helper cells. The Th2-cells support thereby their own inactivation through the release of IL-4 and IL-10

through which TGF-b is considerably strengthened in its anti-inflammatory function (Fig. 4). Simultaneously the B-lymphocytes are stimulated to synthesize immunoglobulins.

It remains to be noted that the immunological bystander reaction can only proceed in the low dose antigen range (ca. 1 µg to maximally 1 g per day and body weight).

[An excellent overview of the literature on the phenomenon of the low dose antigen reactions (”Bystander Suppression“) can be found in Weiner L, Meyer F. Oral tolerance: Mechanisms and Applications. Ann New York Acad Sci 1996; 778: 1-418.]

As demonstrated by Carvalho and Vaz (Scand. Journal Immunology 1996; 6: 13-18) in  animal experiments, the injection of a tolerated antigen, e.g., endogenic fibrinogens is not immunologically neutral: A previously stimulated bystander reaction is possibly amplified thereby! The authors also explain this with the action of suppressive cyto kines from lymphocytes. These findings fit with the progressive auto-sanguis therapy according to Reckeweg.

Because the number of antigens is not known during inflammatory processes, it is very advantageous to offer a greater number of motives, as is customary in anti-homotoxic medicine, to approach an inflammatory process immunologically from several sides. (Fig. 5). The bystander reaction can be supported thereby by the auto-sanguis therapy according to Reckeweg. Thus, anti-homotoxic medicine offers great advantages because:

  • it is not necessary to know the specific antigen in order to treat an illness of a specific organ, as similarity is sufficient (see Brandtzaeg, 1996),

  • an adequate combination of low dose antigens must exist (D1 to approximately D14) to attain a corresponding bystander reaction,

  • a circulating antigen blood level need not be provable (Weiner et al., 1994),

  • individual differences occur in the reaction to various epitopes of the regulatory lymphocytes (Friedman and Weiner, 1994; Weiner et al., 1994),

  • the bystander reaction can obviously also be triggered regardless of the method of application (oral, nasal, s.c., i.m.)

(Al-Sabbagh et al., 1996; Carvalho and Vaz, 1996, Chen et al., 1996),

  • the bystander reaction regulates dysfunctions and does not block them,

  • a function cycle of anti-homotoxic therapy exists, which acts in a regulatory manner in the ground system.

Fig. 5: The immunological bystander reaction as a principle of action of anti-homotoxic medicine

 

A D1-D14 potency of an anti-homotoxic preparation contains sufficient substance quantities to stimulate macrophages to form antigen motives after application (top). This is the prerequisite for the formation of regulatory lymphocytes (th3) (middle row). Th3 cells find chemotactically phlogogenic lymphocytes (t4, Th1, Th2) with similar antigen motives and suppress these by releasing TGF-b (bottem). (Heine 1997)8)

  1. 1.3   References

  1. Al-Sabbagh A et al. Antigen-driven peripheral immune tolerance: suppression of experimental autoimmune encephalomyelitis and collagen-induced arthritis by aerosol administration of myelin basic protein or type II collagen. Cellular Immunology, 1996; 171: 111-9
  2. Brandtzaeg P. History of oral tolerance and mucosal immunity. In: Weiner HW, Mayer LF (Eds.): Oral Tolerance: Mechanisms and Applications. Ann New York Acad Sci 1996; 778: 1-27
  3. Carvalho CR, Vaz NN. Indirect effects are independent of the way of tolerance induction. Scand Journal Immunology 1996; 6: 613-18
  4. Friedmann A, Weiner HL. Induction of energy or active suppression following oral tolerance is determined by antigen dosage. Proc Natl. Acad Sci USA 1994; 91: 6688-92
  5. Hahnemann S. Reine Arzneimittellehre. Dresden, 1811; ders.: Kleine med. Schriften, published by D. Ernst Stapf, Dresden and Leipzig, 1829; ders.: Unterricht für Wundärzte. Leipzig, 1789; ders.: Die chronischen Krankheiten. Dresden and Leipzig, 1835; ders.: Organon der Heilkunst. Dresden and Leipzig, 1829.
  6. Harisch H, Dittmann J. Untersuchungen zur Wirkung von Ubichinon Injeel and Injeel forte mit zellfreien Systemen. Biol Med 1997; 26(3):99-104
  7. Heine H. Lehrbuch der biologischen Medizin. 2. Auflage Stuttgart: Hippokrates 1997a
  8. Heine H. Neurogene Entzündung als Basis chronischer Schmerzen. Beziehun- gen zur antihomotoxischen Therapie. Vortrag 31. Med. Woche Baden-Baden, 01.11.97b (Biol. Medizin, in Druck)
  9. Reckeweg H-H. Homotoxikologie. Ganzheitsschau einer Synthese der Medizin. Baden-Baden: Aurelia, 1976
  10. Reckeweg H-H. Materia Medica Homoeopathia Anti-homotoxica. 3rd rev. English ed. Baden-Baden: Aurelia-Verlag, 1996.
  11. Weiner L, Mayer L. Oral Tolerance: Mechanisms and Applications. Ann New York Acad Sci 1996; 78: 1-418
  12. Weiner HL et al. Oral Tolerance: Immunologic mechanisms and treatment of animal and human organ specific autoimmune diseases by oral administration of autoantigens. Ann. Rev. Immunol. 1994; 12: 809-37


Share this


Explore more


Popular posts