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Category: Publications
Parent category to all problems relating to the physical aspect of the body
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Common Disorders of the Ear, Nose, and Throat: A Clinical Update
By Joan Lewis, MD
OtorhinolaryngologistIntroduction
Disorders of the ear, nose, and throat (ENT) are the cause of many patient visits to a primary care physician. Some of the common ENT disorders include acute and recurrent otitis media (OM); acute, chronic, and recurrent tonsillitis; and allergic and recurrent rhinitis and chronic rhinosinusitis (CRS). However, the common cold remains one of the most frequent upper respiratory tract infections (URIs). Approximately half of the cases of colds in children can be attributed to a wide variety of up to 200 different viruses that are seasonally active, such as rhinoviruses in the early fall, spring, and summer. Other viruses that might cause URIs include coronavirus, parainfluenza virus, adenovirus, enterovirus, and respiratory syncytial virus.¹
The subsequent development of recurrent sinusitis²–³ and OM⁴ commonly has been related to viral URIs that last longer than a week. A child can be expected to have 6 to 10 colds annually, whereas adolescents may have only 2 to 4 colds per year. In developing countries, URIs tend to be more severe, such as pneumonia and influenza, with a higher risk of complications. Therefore, URIs can be a leading cause of death for children younger than 5 years.⁵
An increased understanding of the pharmacoeconomic incidence, relevance of antibiotic resistance, physician involvement, and anatomical and physiological features of each of the common ENT disorders will improve clinical outcomes. An integrative medical approach that uses complementary and alternative therapies, such as antihomotoxic medications, in addition to mainstream medical therapies is a therapeutic strategy that shows much promise in reducing the current disease burden and preventing further recurrences.
Pharmacoeconomic Incidence
The annual cost of time lost from school for adolescents and from work for adults because of URIs is substantial and is estimated to be as high as $15 billion in direct treatment costs by practitioners, with more than half of that amount being for ambulatory care centers in hospitals. The indirect cost of wages from URIs is estimated at $9 billion.⁶
The over‑the‑counter cough and cold remedy market was identified as being the “most competitive category in North America,” with sinusitis showing the most potential growth. Figures extrapolated from a survey of 4,000 US residents suggested that a total economic burden of $40 billion, including income lost from time off for these occurrences, was related to noninfluenza viral URIs alone.
Antibiotic Resistance
In 2007, prudent antibiotic use was not correlated with appropriate knowledge of microbial resistance;⁷ thus, the reduction of unnecessary antibiotics as treatment options for the virally associated common cold was identified in 2008 as a public health priority.⁸
Recent public opinion polls show an increased understanding of the relationship between the development of resistant bacterial strains and inappropriate antibiotic use and also report a significantly higher level of trust in physicians who did not prescribe antibiotics for the common cold.⁹ However, 45% of respondents in the United States in 2008 and 41% of a population in Belgium in 2001 still did not understand the lack of efficacy of antibiotics in treating viral illnesses.¹⁰ These data suggest that there is still a considerable opportunity to better educate patients and health care providers.
Environmental Impact
In the pediatric population, the close proximity of children in day‑care centers contributes to the transmission of respiratory tract disease.¹¹ Childhood exposure to common environmental pollutants, such as firsthand or secondhand smoke, and common household allergens, such as aerosolized cleaning products, in persons with a genetic predisposition might be associated with later development of asthma and allergic conditions through inappropriate sensitization.¹² Furthermore, asthmatic children have URIs more frequently than their nonasthmatic classmates. The polycyclic aromatic hydrocarbons present in diesel exhaust particles have recently been shown to stimulate the release of interleukin (IL)‑4, IL‑8, and histamine from basophil cells,¹³ suggesting that other common environmental pollutants also can play a role in the development of asthma and allergic rhinitis.
Physician Involvement
Most persons with ENT disorders visit their health care practitioners early in the disease process because the associated signs and symptoms are readily apparent to both the patient and practitioner and frequently affect activities of daily living. The mechanical and physical appearances of structures (e.g., teeth, palate, gingiva, and tongue) indicate a variety of physiological states and can be used diagnostically with a minimal investment of time. For example, fasciculations of the tongue might indicate neural disorders; a glossy tongue is associated with nutritional deficiencies, such as a deficiency in vitamin B12. Dental caries or loss correlates with impaired immune systems, smoking or tobacco use or exposure,¹⁴ and poor nutritional status. Xerostomias are linked to poor hygiene, and temporomandibular joint disorders can be attributed to trauma or articular disorders.¹⁵
Relevant Anatomical and Physiological Features
Lymphatic tissue in the Waldeyer ring is designed to protect the body from pathogens and toxins encountered in this vulnerable area; therefore, it is strategically placed to protect critical respiratory and digestive functions. It is the first protective barrier encountered by orally ingested and inhaled toxins, viruses, and bacteria. An interaction with the body’s lymphatic tissues provokes a reaction that includes copious nasal discharge, sneezing, coughing, and mucosal engorgement as a mechanism to remove the offending substance. The resultant reaction, with its associated signs and symptoms, is diagnosed as the common cold or rhinitis. Further progression to include fever and exhaustion, and the presence of clusters of similar infections in the community and a documented influenza virus infection, would lead to a diagnosis of the flu.
Treatment for these uncomfortable reactions is largely symptomatic.
Pathological Conditions
A short review of the relevant pathological features of each of the common ENT disorders is included to provide further insight into potential therapeutic strategies.
Otitis Media
Acute OM
Acute OM is the most frequent ailment encountered by pediatricians. Persistent middle ear effusion from a failure of the mucus and microbial and immune system debris in the middle ear to drain via the Eustachian tube to the pharynx is associated with recurrent OM.¹⁶ Implicated factors include functional obstruction of the Eustachian tube, anatomical differences in the infant’s Eustachian tube, and a more horizontal position when bottle feeding an infant in a supine position, favoring a retrograde flow of milk. Furthermore, passive smoke environments impair normal ciliary movement that sweeps away debris, and immune system disorders are associated with increased mucus production.Recurrent OM
Preexisting antibiotic treatment is associated with an increased rate of recurrent OM in young children, supporting the hygiene hypothesis, in which interruption of a normal inflammatory response during childhood leads to an imbalance in Th1/Th2 cell regulation, predisposing a child toward allergy.¹⁷ Novel otopathogens can be cultured in those with recurrent OM after a month‑long course of antibiotics for acute OM.¹⁸ Long‑term morbidity, with recurrent OM occurring before the age of 3 years, might affect the child’s subsequent decreased comprehension when reading.¹⁹Bioregulatory Treatment
For acute OM, use the basic/symptomatic approach as follows: prescribe Belladonna-Homaccord (8–10 drops twice daily) and Traumeel (8–10 drops or 1 ampoule warmed and instilled into the affected ear twice daily). If resolution does not occur within a reasonable time, individualize therapy:- With confirmed bacterial etiology and significant inflammation, prescribe Echinacea compositum: 1 tablet every 30–60 minutes up to 12 tablets per day for acute conditions; for chronic conditions, 1 tablet dissolved in the mouth three times daily. Injectable route (IM, SC, ID, or IV) 1–3 times per week may be used if within regulatory framework.†
- With confirmed viral etiology, prescribe Engystol: 1 tablet three times daily or 1 ampoule daily (injectable routes as above for acute situations).
- For marked restlessness, fever, and agitation, prescribe Viburcol suppositories: adults, 1 suppository 2–3 times daily; infants under 6 months, half a suppository up to one per day.
If signs and symptoms persist, consider the 3‑pillar regulation approach (detoxification and drainage; immunomodulation; cell and organ support).† During latent phases, Mucosa compositum (± Coenzyme compositum, Ubichinon compositum) supports cells and organs; Traumeel for immunomodulation; and the Detox‑Kit (comprising Lymphomyosot, Nux vomica-Homaccord, and Berberis-Homaccord) for detoxification and drainage. Persistent effusion may require referral for myringotomy.
Tonsillitis
Acute Tonsillitis
Tonsils are antigen‑presenting lymphatic tissue in the Waldeyer ring, mounting an appropriate B‑cell response. Acute tonsillitis presents as erythematous, swollen tonsils with stertorous breathing. Hypertrophied tonsils can cause sleep disorders and daytime inattentiveness in children. Microbiological evaluation (culture or rapid antigen tests) is required to exclude streptococcal pharyngitis, which necessitates antibiotics to prevent cardiovascular or renal complications.²⁰Chronic Tonsillitis
Generally bacterial in etiology and more prevalent in adults. Crypts containing pus can form; surgical excision is controversial due to postoperative pharyngitis despite no visible recurrent infection. Post‑tonsillectomy changes in oral flora suggest the chronically infected tonsil may harbor anaerobic bacteria, and removal may restore normal flora.²¹Recurrent Tonsillitis
In children, recurrent tonsillitis differs from adult chronic forms by higher antigen presence in acute stages. If peritonsillar abscess occurs, immediate tonsillectomy may be first‑line.²² Antigen presentation and B‑cell function remain intact; if possible, avoid tonsillectomy to preserve natural killer cell maturation.Bioregulatory Treatment
For acute tonsillitis: prescribe Angin-Heel (initial: 1 tablet every 15 minutes for 2 hours; then 1 tablet three times daily), Vinceel spray (once daily), and Mercurius-Heel (1 tablet three times daily). If unresponsive:- Bacterial etiology: Echinacea compositum as above.
- †Regulation approach: use detoxification, immunomodulation, and organ support as outlined for OM.
References
- Common cold viruses and URIs; rate in children and adults.
- Recurrent sinusitis etiology overview.
- Recurrent sinusitis pathophysiology.
- Otitis media linkage to viral URI.
- URI mortality in children <5 years.
- Dixon RE. Economic costs of respiratory tract infections in the United States. Am J Med. 1985;78(6B):45‑51.
- McNulty CA, et al. Public’s knowledge and attitudes to antibiotic use. J Antimicrob Chemother. 2007;59(4):727‑738.
- Earnshaw S, et al. European Antibiotic Awareness Day survey. Euro Surveill. 2009;14(30):19280.
- Andre M, et al. Public knowledge of antibiotic use in Sweden. J Antimicrob Chemother. 2010;65(6):1292‑1296.
- Edgar T, Boyd SD, Palame MJ. Sustainability for behaviour change against antibiotic resistance. J Antimicrob Chemother. 2009;63(2):230‑237.
- Fleming DW, et al. Day‑care attendance and pediatric URIs. Pediatrics. 1987;79(1):55‑60.
- Arshad SH. Indoor allergen exposure and allergy development. Curr Allergy Asthma Rep. 2010;10(1):49‑55.
- Lubitz S, et al. Diesel exhaust proallergic effects. Environ Toxicol. 2010;25(2):188‑197.
- Tanaka K, et al. Smoking and tooth loss in Japanese women. Ann Epidemiol. 2005;15(5):358‑364.
- McNeill RA. Bacteria in ear and nasopharynx in acute OM. J Laryngol Otol. 1962;76:617‑622.
- Emerick KS, Cunningham MJ. Tubal tonsil hypertrophy after adenoidectomy. Arch Otolaryngol Head Neck Surg. 2006;132(2):153‑156.
- Mattila PS. Amoxicillin and recurrent OM in young children. J Pediatr. 2010;156(1):163.
- Kerschner JE, et al. Otitis media risk factor knowledge. Int J Pediatr Otorhinolaryngol. 2005;69(1):49‑56.
- Luotonen M, et al. Recurrent OM and linguistic skills. Pediatr Infect Dis J. 1996;15(10):854‑858.
- Bonsignori F, et al. Upper respiratory tract infections in children. Int J Immunopathol Pharmacol. 2010;23(suppl 1):16‑19.
- Burton MJ, Glasziou PP. Tonsillectomy vs non‑surgical for chronic/recurrent tonsillitis. Cochrane Database Syst Rev. 2009;(1):CD001802.
- Page C, et al. Immediate tonsillectomy for peritonsillar abscess. J Laryngol Otol. 2010:1‑6.
†The 3‑pillar regulation approach comprises detoxification and drainage; immunomodulation; and cell and organ support.
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Prevention of cadmium-induced toxicity in liver-derived cells by the combination preparation Hepeel®
Rolf Gebhardt*
Institute of Biochemistry, Medical Faculty, University of Leipzig, Johannisallee 30, 04103 Leipzig, Germany
ARTICLE INFO
Article history:
- Received 21 May 2008
- Received in revised form 11 December 2008
- Accepted 18 January 2009
- Available online 31 January 2009
Keywords:
- Antioxidants
- Apoptosis
- Cadmium
- Cytochrome C
- Hepatoprotection
- Plant tinctures
ABSTRACT
Cadmium is a heavy metal of considerable environmental concern that causes liver damage. This study examined the possible prevention of cadmium toxicity in human HepG2 cells and primary rat hepatocytes by Hepeel®, a combination preparation of tinctures from seven different plants. Hepeel® prevented cadmium chloride (CdCl₂)-induced cell death in both HepG2 cells and hepatocytes, and also reduced the loss of glutathione, lipid peroxidation, nuclear fragmentation, caspase activation and release of mitochondrial cytochrome C. To compare their relative efficacy, the seven constituent plant tinctures of Hepeel® were also separately tested. The tinctures China and Nux moschata, which exert solely anti‑oxidative effects, failed to reduce cytotoxicity, and only protected against loss of glutathione and lipid peroxidation. In contrast, the tinctures Carduus marianus and Chelidonium, demonstrated anti‑apoptotic effects, and protected HepG2 cells and primary hepatocytes against CdCl₂-induced cell death. These results demonstrate how the effectiveness of Hepeel® is determined by the synergistic features of its constituent tinctures. Furthermore, we conclude that cadmium toxicity in the liver is mainly due to stimulation of the intrinsic apoptotic pathway, but may be intensified by increased oxidative stress.
© 2009 Elsevier B.V. All rights reserved.
1. Introduction
Environmental exposure to fluctuating concentrations of heavy metals poses an enormous challenge for biological organisms. Toxic metals cause a vast array of adverse effects, including neurotoxicity, hepatotoxicity and carcinogenicity (Waalkes et al., 2000; Godt et al., 2006). Due to the global dispersion of heavy metals and their extensive use in modern society, some human exposure to toxic metals is inevitable. This ongoing prevalence of metal exposure necessitates protective measures at the environmental, social and individual level.
Cadmium is one of the most common toxic heavy metals, due to its primary accumulation in the liver and kidney (Godt et al., 2006). Cadmium causes hepatic, renal, skeletal, respiratory, and vascular disorders in humans (Nordberg, 1992; Waalkes et al., 2000), and it may also affect Leydig cells of the testes and hepatocytes and stellate cells of the liver (Koizumi et al., 1992; Dudley and Klaassen, 1984; Fariss, 1991; Souza et al., 2004a,b). Furthermore, cadmium is a potent carcinogen (Godt et al., 2006).
There is growing evidence that the oxidative stress (Sarkar et al., 1995) via reactive oxygen species (ROS) generation and mitochondrial damage are among the basic mechanisms of cadmium toxicity (Sarkar et al., 1995).
The combination preparation Hepeel® is frequently used to stimulate liver function and improve antioxidant function in acute and chronic diseases, such as cholangitis and cholecystitis (Gebhardt, 2003). Hepeel® also demonstrates several other protective features, such as induction of glutathione-S-transferase activity (Gebhardt, 2003). These findings prompted the present investigation of the hepatoprotective potential of Hepeel®, and its seven constituent plant tinctures, against cadmium-induced hepatocellular damage. To thoroughly examine this, and to provide comparative experimental data for two different cell types, we used the human hepatoblastoma cell line HepG2 and primary rat hepatocytes. Exposure to Hepeel® largely prevented cell death, and oxidative and apoptotic pathomechanisms were differentially affected by the constituent tinctures. The combined anti-oxidative and anti-apoptotic properties of Hepeel® and its constituent tinctures support its overall protective effect against cadmium-induced toxicity in liver cells.
2. Materials and methods
2.1 Materials
Hepeel® tinctures were prepared from seven different plants, according to procedures 3 and 4 of the German Homeopathic Pharmacopoeia (HAB, 2000), and were provided by the Biologische Heilmittel Heel GmbH (Baden-Baden, Germany). The following seven constituent tinctures were used: (1) Chelidonium majus, prepared from Chelidonium majus L. (Ch-B 007009, 10⁻² dilution), (2) Carduus marianus, prepared from Silybum marianum L. (Ch-B 007034, 10⁻² dilution), (3) Verratrum album L. (Ch-B 007050, 10⁻³ dilution), (4) Colocynthis, prepared from Citrullus colocynthis L. (Ch-B 007058, 10⁻³ dilution), (5) Lycopodium, prepared from Lycopodium clavatum L. (Ch-B 007001, 10⁻³ dilution), (6) Nux moschata, prepared from Myristica fragrans Houtt (Ch-B 007026, 10⁻³ dilution), and (7) China, prepared from Cinchona pubescens, Vahl (Ch-B 007018, 10⁻³ dilution). Hepeel® is a combination of all tinctures at the dilutions given above, with the addition of Phosphorus, a 10⁻³ dilution of yellow phosphorus. Hepeel® was supplied in sterile ampoules by Biologische Heilmittel Heel GmbH. The relative volume composition of 1:1 mL Hepeel® injection solution is: Chelidonium majus, 10⁻³ dilution) 1.1 μL; Carduus marianus (Silybum marianum, 10⁻³ dilution) 0.55 μL; Verratrum album, 10⁻² dilution) 2.2 μL; Colocynthis (Citrullus colocynthis, 10⁻³ dilution) 3.3 μL; Lycopodium clavatum, 10⁻² dilution) 1.1 μL; Nux moschata (Myristica fragrans, 10⁻³ dilution) 1.1 μL; China (Cinchona pubescens, 10⁻³ dilution) 1.1 μL and Phosphorus (white phosphorus 0515.41).
Dichlorodiphenyltrichloroethane (DDT) was purchased from Sigma (Daisenhofen, Germany). All other chemicals were from Roche Diagnostics (Mannheim, Germany), Merck (Darmstadt, Germany), Roth (Karlsruhe, Germany) or Sigma (Daisenhofen, Germany). Cell culture plates with tissue culture filter inserts were from Techno Plastic Products AG (Trasadingen, Switzerland).
2.2 Culture of HepG2 cells
HepG2 hepatoblastoma cells were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) (Gibco, Eggenstein, Germany) supplemented with 2 mM glutamine, 10% fetal calf serum, 40 U/mL streptomycin and 50 U/mL penicillin, as previously described (Gebhardt, 1997). Cells were passed weekly, when confluent. Cell stocks (passage ≤31 till 40) were kept frozen in liquid nitrogen. Frozen cells were thawed, cultured for one week, and passed at least once before use. Confluent HepG2 cell cultures were used for all experiments.
2.3 Preparation and culture of rat hepatocytes
Sprague-Dawley rats were bred and maintained at the Medizinisch-Experimentelles Zentrum at the University of Leipzig, according to local ethical rules for animal care. They were kept on normal maintenance diet V1534 (Sniff, Soest, Germany) and tap water, ad libitum. Primary hepatocyte cultures were prepared by the livers of male rats (200–310 g) with collagenase perfusion, as previously described (Gebhardt, 1997). Cells were cultivated in Williams medium E (Lonza, Verviers, Belgium) on collagen-coated plastic plates, at a uniform cell density of 125,000 cells/cm². During the first 2 h, culture medium was supplemented with 10% fetal calf serum, and culture medium was used thereafter. The medium volume was maintained at 100 μL/cm² of plating area. Additional details of cell culture have been reported elsewhere (Gebhardt, 1997; Gebhardt et al., 1994). For toxicity experiments, incubation in various agents usually started 2 h after plating.
2.4 Induced toxicity with cadmium chloride
The nominal concentration of CdCl₂-induced cytotoxic effects was different for each cell type. For HepG2 cells, culture medium was supplemented with concentrations ranging from 3 to 8 μM. For primary rat hepatocytes, concentrations ranged from 2 to 6 μM. The highest CdCl₂ concentrations caused the greatest cell death in each cell type. In HepG2 cells, 8 μM CdCl₂ caused about 52% cell death, within 30 h of incubation, in hepatocytes, 6 μM CdCl₂ caused 72% cell death within 24 h of cultivation.
2.5 Preparation of Hepeel® tinctures
To prepare a working dilution of each tested compound, one part Hepeel® or tincture was mixed with 5 parts v/v of serum-free Williams Medium E, and gently shaken for 20 min at room temperature. This working solution of effective 0.1 dilution was used for further dilutions with Williams Medium E as specified in figure legends. Appropriate controls replaced each tincture or Hepeel® with equal volumes of ethanol.
2.6 Determination of cytotoxicity
Cytotoxicity of the tested compounds was determined using the colorimetric MTT-assay (MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), as previously described (Gebhardt, 1997).
2.7 Determination of lipid peroxidation and ROS production
Malondialdehyde (MDA) measurements were used to quantify lipid peroxidation (Gebhardt, 1997). HepG2 cells or rat hepatocytes seeded on 60 mm petri dishes were incubated with or without CdCl₂ (3 or 4 μM) for 60 min after 30 h and 24 h of cultivation, respectively. In order to enhance oxidative stress, some plates were simultaneously exposed to t‑butyl hydroperoxide (t‑BHP; final concentration 1.5 mM). Thereafter, cells were washed with 0.9% NaCl, resuspended, and scraped into 1 mL of 50 mM potassium phosphate buffer (pH 7.4), then homogenised by sonication for 10 s (15 μs maximal sonpower, Sonipuls HD 2200, Bandelin electronic, Berlin, Germany). MDA was determined by thiobarbituric acid (TBA) assay (Esterbauer and Cheeseman, 1990; Gebhardt, 1997). The protein content of homogenates was measured following the procedure of Lowry et al. (1951).
Measurement of intracellular ROS was accomplished by using the DCFH assay (Wang and Joseph, 1999). HepG2 cells or rat hepatocytes cultivated on collagen-coated 95-well black flat bottom plates were washed 3 times with Krebs‑Ringer‑HEPES (KRH) solution pH 7.2 (Pavlica and Gebhardt, 2005). Cells were preloaded with 0.1 mM DCFH in either DMEM (HepG2 cells) or Williams Medium E (rat hepatocytes) for 30 min, then washed 3 times with KRH buffer. Cells were then treated simultaneously with CdCl₂ (3 μM) and the test compound diluted 1:10 with different starting dilutions (indicated in Table 1) for an additional 30 min. Fluorescence (485/520 nm, excitation 485/emission 520 nm, microplate reader, TECAN) was recorded for up to 30 min, while temperature was maintained at 37 °C. Percentage increase in fluorescence units/well was calculated by the formula: F₃₀/F₀ × 100, where F₃₀ = fluorescence at time 30 min, and F₀ = fluorescence at time 0 min (Pavlica and Gebhardt, 2005).
2.8 Determination of cellular glutathione content
To measure cellular glutathione (GSH) content, cells were cultured in 6-well plates for 30 h (HepG2 cells) or 24 h (primary rat hepatocytes). Test compounds were added 2 h after plating, along with the first change of medium. At the end of the incubation period, cells were washed and scraped into HEPES buffered isotonic medium as previously described (Pavlica and Gebhardt, 2005). Determination of GSH content was performed according to the method of Gebhardt and Faustel (1997).
2.9 Detection of apoptotic nuclei with DAPI
The blue nuclear dye DAPI (4′,6-Diamidino-2-phenylindole) was dissolved in methanol at 5 μg/mL and stored as stock solution. Cells were washed twice in potassium phosphate buffer (PBS) and fixed with ice-cold methanol. Thereafter, a working solution of DAPI (1 μg/mL) in methanol was added, and cell nuclei were stained for 15 min at 37 °C. Destaining was achieved by replacing methanol with pure methanol, followed by two rounds of washing with PBS.
2.10 Determination of caspase activity
Measurement of caspase-3 activity was based on the cleavage of a colorimetric substrate determined by the increase in absorbance at 405 nm. The assay was performed according to the instructions of the manufacturer (caspase-3 activity assay kit; Oncogene, Bad Soden, Germany) and adapted for HepG2 cells as described by Ochiai et al. (2004). Recombinant caspase-3 was used for assay calibration.
2.11 Preparation of cellular fractions and Western blot analysis
To measure cytochrome C release, cellular extracts were prepared by lysing cells in 10 mM Tris-buffer (pH 7.4) containing 2 mM EDTA, 1 μM pepstatin, 1 mM PMSF, leupeptin, 100 μM PMSF (phenylmethylsulfonyl fluoride), and 250 mM sucrose. Cells were homogenized by repeated passage through a 26-gauge needle, and were centrifuged at 14,000 × g for 10 min at 4 °C. Cytosolic supernatants and pellets containing mitochondria were collected and analyzed for spectral concentrations of mitochondrial protein, then used for Western blot analysis as previously described (Haupt et al., 2000). Cytochrome C was detected using a cytochrome C (Ab-8) antibody (sc-13156, Santa Cruz Biotechnology Inc., Heidelberg, Germany) followed by alkaline phosphatase-conjugated secondary antibody.
2.12 Statistical evaluation
Data were analysed for significance with a Student’s t-test for comparisons between two groups. Data are presented as mean ± standard deviation (SD) of three to four measures, except when stated otherwise.
3. Results
3.1 Cytotoxicity of cadmium chloride on hepatocellular populations
The cytotoxic effect of CdCl₂ on HepG2 cells was concentration- and time-dependent. Within the first 24 h of exposure, HepG2 cells tolerated up to 5 μM CdCl₂, but quickly died at higher concentrations (Fig. 1). At 7 μM CdCl₂, almost all cells were dead or had detached from the substrate. At 5 μM CdCl₂ or below, no visible alterations in cell morphology and nuclei were detectable after 24 h (data not shown). However, deterioration was seen at 5 μM CdCl₂ when cultivation was continued for another 6 h (Fig. 1). At that time, cadmium-induced cytotoxicity was already apparent at lower concentrations. The first signs of cytotoxic influence were detected above 2 μM, and almost all cells died at a concentration of 5 μM, as determined by MTT reduction to less than 10% of controls. The EC₅₀-value for CdCl₂-induced cytotoxicity in HepG2 cells was determined to be 5.9 μM after 24 h, and 2.8 μM after 30 h of cultivation.
Rat hepatocytes were even more sensitive to cadmium, and cytotoxicity was more prominent than in HepG2 cells, at all culture times. At 24 h after addition of CdCl₂, MTT reduction was already decreased in a concentration-dependent manner, above 2 μM doses (Fig. 2). At 6 μM, absorbance was reduced by approximately 70%. The EC₅₀-value for CdCl₂-induced toxicity was 3.7 μM. After 30 h, cell detachment in the MTT assay had further dropped, and were lower than those of HepG2 cells at all concentrations of cadmium (data not shown). Therefore, all subsequent measurements of cell viability were performed in HepG2 cells at 30 h of cultivation, and in rat hepatocytes at 24 h of cultivation.
3.2 Protection against cadmium cytotoxicity by Hepeel® and constituent tinctures
In the presence of Hepeel®, cadmium cytotoxicity was reduced in both cell types. In HepG2 cells at 30 h of culture, Hepeel® application resulted in the gradual increase of viability from 32% (control) to 53%, as dilutions changed from 10⁻³ to 10⁻¹ (Fig. 3A). At the 10⁻² dilution, there was significant enhancement of viability (P < 0.01).
Among the constituent tinctures, only Carduus marianus and Chelidonium, were effective in reducing cadmium cytotoxicity (Table 1). Within the range of 10⁻⁵ to 10⁻³ dilutions, Carduus marianus caused increased cell viability in a concentration-dependent manner, to values between 60 and 70% (Fig. 3B). Chelidonium application resulted in maximal values slightly above 60% (Fig. 3C). Also, the cell sensitivity was slightly higher with Carduus marianus, and significant differences were seen starting at the 2.5 × 10⁻⁴ dilution, whereas with Chelidonium significant differences were not apparent until the more concentrated dilutions of 10⁻⁴ and lower.
Similar results were obtained with rat hepatocytes after 24 h of cultivation. The 10⁻³ dilution of Hepeel® increased viability from 68% to almost 88%. At the same 10⁻³ dilution, Carduus marianus reached 95% and Chelidonium increased 87% viability (Table 1). As for HepG2 cells, the other constituents of Hepeel® did not reduce cytotoxicity (Table 1).
3.3 Cadmium-induced lipid peroxidation and ROS production
Exposure of HepG2 cells to CdCl₂ for 24 h did not change the rate of lipid peroxidation, as evidenced by the unchanged cellular production of malondialdehyde (MDA) compared to control measures (Table 2). However, when challenged with 1.5 mM t‑BHP, HepG2 cells exposed to 3 μM CdCl₂ responded with a 2.1-fold increase, and those exposed to 4 μM responded with a 2.3-fold increase of MDA, compared to control cells not exposed to cadmium.
Likewise, ROS production of HepG2 cells detected by DCFH fluorescence was stimulated by CdCl₂ only in the presence of t‑BHP (Table 2). The relative increase in ROS production was comparable to that for lipid peroxidation.
As shown in Table 3, Hepeel® significantly reduced t‑BHP-induced MDA production in both untreated HepG2 (control) cells and HepG2 cells exposed to CdCl₂ for 24 h. Among all tinctures, Carduus marianus was the most effective (Table 3). Dilutions were almost as broad.
Likewise, ROS production of HepG2 cells was reduced in a pattern similar to that of MDA measures: Hepeel® (31%), Carduus marianus (36%), China (18%), and Nux moschata (16%). All other tinctures were ineffective at reducing the CdCl₂-induced MDA production (data not shown).
The results for rat hepatocytes were different. In these cells, CdCl₂ led to an increase of MDA production of 55%, and an increase in ROS production of 32%, compared to control hepatocytes exposed to cadmium. However, as in HepG2 cells, the sensitivity to t-BHP in the presence of cadmium was also increased approximately 2-fold, from 155% to 302% for MDA, and from 132% to 273% for ROS. The following agents significantly counteracted the impact of CdCl₂, as apparent via the following reduction in MDA measures: Hepeel® (31%), Carduus marianus (36%), China (18%), and Nux moschata (16%). All other tinctures were ineffective at reducing the CdCl₂-induced MDA production (data not shown).
3.4 Cadmium-induced loss of GSH
A moderate drop in cellular GSH (19 ± 5%) was observed in HepG2 cells in response to exposure to CdCl₂ at a concentration of 3 μM (Table 4). This value is in accordance with an EC₅₀-value of approximately 4.5 μM. This loss was considerably enhanced (55 ± 4%) when cells were additionally exposed to t‑BHP. Only Hepeel® and the tinctures Carduus marianus, China and Nux moschata were able to significantly counteract the influence of CdCl₂, with or without additional t‑BHP (Table 4). When used alone, Hepeel® and Carduus marianus were able to completely restore cellular GSH content.
3.5 Cadmium-induced apoptosis
Cadmium toxicity via apoptosis was measured by DAPI-staining in two different ways; counting of fragmented nuclei and monitoring of cell death. Within 30 h of 3 or 4 μM CdCl₂ exposure, apoptotic fragmentation in HepG2 cell nuclei was apparent after DAPI staining, and total cell numbers were decreased (Fig. 4). Specifically, the percentage of apoptotic nuclei increased from less than 0.1% (controls) to about 8% in the presence of 3 μM CdCl₂ (Table 5). At earlier time points, such as 24 h, the proportion of fragmented nuclei was lower than at 30 h.
Addition of Hepeel® to the culture medium considerably reduced the apoptotic response at all concentrations of CdCl₂ in HepG2 cells and hepatocytes (Table 5). This influence was particularly pronounced in hepatocytes exposed to 4 μM CdCl₂, wherein the proportion of apoptotic nuclei was diminished from 42% to 4% (Table 5). A similar but less pronounced effect of Hepeel® could be observed in the presence of 5 μM CdCl₂ (cf. Fig. 5D).
Similar to the results seen in the MTT assays, the co-application of either Carduus marianus or Chelidonium with CdCl₂ effectively reduced the number of apoptotic nuclei, and enhanced cell survival (Fig. 4C and D). In the presence of 4 μM CdCl₂ and 10⁻⁴ final tincture dilutions, the proportion of fragmented nuclei in hepatocytes was 7% for Carduus marianus and 11% for Chelidonium (Table 5).
3.6 Cadmium-induced activation of caspases
Results for caspase-3 activity measurements were similar to those for apoptosis. In HepG2 cells, 3 μM CdCl₂ induced a significant increase in caspase-3 activity within 24 h (Table 6), with a 1.8-fold increase in caspase-3 and a 2.5-fold increase of caspase activity as measured by caspase-3/7 assay. Simultaneous addition of Carduus marianus at a 10⁻⁴ dilution to the culture medium resulted in a decrease of caspase-3 activity to about 1.3-fold, and the 10⁻³ dilution decreased caspase-3 activity to about 1.2-fold, relative to the vehicle-treated controls. Chelidonium was slightly less effective, but still reduced caspase-3 activity significantly in both assays (Table 6). A similar result was obtained for the Hepeel® 10⁻⁴ dilution, which reduced CdCl₂-induced caspase activity in both assays by approximately 40% (Table 6). Aside from Carduus marianus and Chelidonium, none of the other constituent tinctures was effective (not shown), since many HepG2 cells detached or decomposed completely within 30 h of CdCl₂ exposure.
3.7 Cadmium-induced release of cytochrome C
The release of cytochrome C from mitochondria of HepG2 cells was significantly higher in the presence of 3 μM CdCl₂ than in unexposed cells, which showed almost no release (Fig. 6). Densitometric analysis revealed a 27-fold increase in cytochrome C in CdCl₂-treated versus vehicle control cells. Hepeel® (10⁻¹) reduced the release of cytochrome C by about 5-fold, and Carduus marianus (10⁻³) reduced it by 7-fold (Fig. 6). Chelidonium was almost as effective as Carduus marianus, while treatment with China showed no effect (data not shown).
4. Discussion
Our results demonstrate a strong protective effect of the combination preparation Hepeel® and several of its constituent plant tinctures against cadmium-induced hepatocellular damage in both human hepatoblastoma cell line HepG2 and primary rat hepatocytes. We showed that cadmium-induced hepatocellular damage is effectively counteracted by these agents, thus gaining insight into potential mechanisms of this protective effect, which focus on two aspects: oxidative stress, and occurrence of apoptosis.
There are conflicting reports in the literature about oxidative stress during cadmium cytotoxicity. While some authors report that cadmium toxicity is due to, or at least associated with, increased oxidative stress and lipid peroxidation (Dudley and Klaassen, 1984; Fariss, 1991; RIkans and Yamano, 2000; Souza et al., 2004a,b; Koizumi et al., 2006), other authors could not detect enhanced lipid peroxidation in response to cadmium exposure in vivo and in vitro (Harvey and Klaassen, 1983; Aydin et al., 2003).
Concerning the occurrence of apoptosis in response to cadmium exposure our results are consistent with findings in mouse and rat liver (Habeebu et al., 1998; Pourahmad et al., 2001; Li and Lim, 2007) as well as human hepatocytes (Lasfer et al., 2008), and corroborates similar conclusions based on the observation of DNA laddering and other markers of apoptosis in response to cadmium exposure in HepG2 cells (Aydin et al., 2003; Oh and Lim, 2006).
Our results with DAPI staining also showed that treatment with Hepeel® and the single plant tinctures, which protected against cadmium toxicity, reduced the number of apoptotic nuclei. Furthermore, these agents also inhibited the activation of pre-apoptotic caspases and the release of mitochondrial cytochrome C. Therefore, these results strongly suggest that the most effective single tinctures, Carduus marianus and Chelidonium, are able to counteract intracellular processes other than oxidative stress, such as events leading to caspase activation and subsequent apoptosis, in response to cadmium. Silybin is an active substance in the Carduus marianus tincture, and is known to exert an anti-apoptotic influence in other systems (Singh and Agarwal, 2004; Pock et al., 2006). Thus, silybin may contribute to the protective effects of the tincture. However, direct anti-apoptotic properties of Chelidonium have not yet been described. Interestingly, alkaloids derived from Chelidonium such as chelerythrine and sanguinarine interact with the cytoskeleton (Slaninova et al., 2001), and of these, the alkaloid chelerythrine is an inhibitor of protein kinase C (Herbert et al., 1999). In addition, chelerythrine recently described as an inhibitor of BclXL function, which may help explain the pro-apoptotic effect observed with Chelidonium (Chan et al., 2003). In fact, detailed studies on the molecular interactions of chelerythrine revealed binding sites distinct for the Bcl3 (Bcl-2 homology 3) binding cleft (Zhang et al., 2006). This finding raises the possibility of alternate mechanisms favouring interactions of pro-survival members of the Bcl-2 family. In light of these findings, the concentrations of chelerythrine in our experiments is much lower than the EC₅₀ value for its pro-apoptotic effect (Chan et al., 2003; Maliková et al., 2006). Thus, at low concentrations anti-apoptotic influences of chelerythrine and sanguinarine seem to predominate.
Therefore, our results strongly suggest that the protective function of Hepeel® against cadmium-induced cytotoxicity results from the synergistic actions of its composite tinctures. The decisive anti-apoptotic influence of Hepeel® may be supported by its antioxidative features that help stabilize cellular GSH content, and consequently the sulfhydryl status of cellular proteins. Further studies are needed to discern whether this protective effect is specific to cadmium toxicity in hepatocytes, or can be generalised to other toxins and cell populations.
In conclusion, Hepeel® efficiently antagonised cytotoxic and apoptotic effects of the heavy metal cadmium in hepatocyte cell populations. This protective function is likely based on anti-apoptotic influence distinct from anti-oxidative function, but may be rendered more efficient by the synergistic effects of both. These observations add to the list of beneficial effects recently reported with this preparation (Gebhardt, 2003), and support the possible therapeutic use of Hepeel®, particularly for cases of heavy metal poisoning.
Conflict of interest
None.
Acknowledgement
This work was supported in part by the University of Leipzig (KST 764100100); and Biologische Heilmittel Heel GmbH, Baden-Baden, Germany (97000-050). The author would like to thank Mrs. D. Keller, Mr. F. Struck and Mrs. B. Woite for excellent technical assistance and Dr. A. Gerasimova for valuable comments and editing.
References
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- Pavlica S, Gebhardt R. Induction of glutathione-S-transferase by Hepeel and single plant tinctures in HepG2 cells. Phytother Res. 2005;19(2):139–2.
- Gebhardt R, Faustel H. Determination of GSH content in hepatocytes: methodological improvements. Toxicol Appl Pharmacol. 1997;146(2):179–88.
- Gebhardt R, Hope J, Louw L. Cadmium toxicity in primary rat hepatocytes: morphologic alterations and induction of apoptosis. Toxicol Appl Pharmacol. 2000;162(1):32–40.
- Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951;193(1):265–75.
- Esterbauer H, Cheeseman KH. Determination of aldehydic lipid peroxidation products: malondialdehyde and 4-hydroxynonenal. Methods Enzymol. 1990;186:407–21.
- Wang H, Joseph JA. Quantifying cellular oxidative stress by dichlorofluorescein assay using microplate reader. Free Radic Biol Med. 1999;27(5-6):612–6.
- Aydin HH, Devaki R, Karacaali S, Mete N, Alarco U, Batur Y. Oxidative stress and mitochondrial damage in cadmium-treated HepG2 human hepatoma cells. Biol Trace Elem Res. 2003;92(1):43–50.
- Ochiai T, Okamoto K, Akihane K, Higure A, Todoroki H, Abe Y, Kikuchi K. Mitochondrial signaling in cadmium-induced apoptosis through down-regulation of caspase-3 activity. Cancer Lett. 2004;203(1):43–50.
- Lasfer M, Vidal JD, Biondi L, Bruguière JF, Feldmann C, Reyl-Desmars F. Cadmium induces mitochondria-dependent apoptosis of normal human hepatocytes. Toxicol. 2008;241(1-2):121–26.
- Li Y, Lim L. Cadmium-induced apoptosis of hepatocytes is not associated with death receptor-related caspase-dependent pathways in rat. Environ Toxicol Pharmacol. 2006;24(1):231–8.
- Habeebu SS, Beltz WF, Shelton J, House DE, Barnett JB. Cadmium-induced apoptosis in mouse liver. Toxicol Lett. 1998;102-103:319–29.
- Pourahmad J, Hosseini MJ, Eskandari MR, Eghlidoura S. Role of mitochondrial permeability transition in cadmium-induced apoptosis of rat hepatocytes. Toxicol Appl Pharmacol. 2001;174(2):120–9.
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- Slaninova I, Smejkal J, Modrianský M, Hrkal Z. Interaction of chelerythrine with animal and yeast caspases. Toxicol Vitr. 2001;15(3):425–30.
- Herbert JM, Augereau JM, Gleye J, Hammanip JP. Chelerythrine is a potent and specific inhibitor of protein kinase C. Biochem Biophys Res Commun. 1992;99(3):399–903.
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Homotoxicology can play an important role in cancer management
HOMOTOXICOLOGY AND CANCER
Homotoxicology can offer an alternative approach to cancer. Recent research in cytology confirms that oncogenesis starts at the cellular level, and progresses over decades before any symptoms or biochemical parameters can be detected. This long process gives the general practitioner a window of opportunity to discuss complementary prevention programs with his or her patients, particularly those with a family history of cancer.
The extracellular matrix in which cells bathe provides information to the cells, directing their function and activity in the global scheme of things. When this “environment” is contaminated by toxins it passes along faulty information sequences and results in cellular dysfunction. Tasks such as cell division are corrupted. This insidious process is often the conception of oncogenosis. Unless the misinformation leaking from the extracellular matrix is corrected, the misguided processes can continue for decades eventually bearing a tumor. The benefit the practitioner can derive from the slow course of oncogenosis is an opportunity to mediate the process in an attempt to arrest progression. Homotoxicology offers great potential as it works gently to remove underlying toxins that, if accumulated, could, depending on the patient’s constitution, cause cellular chaos and possible neoplasia.
The latest in cancer research has contributed new evidence about oncogenosis which reveals processes that can possibly be manipulated over time in the hope of intervening the pathogenesis of neoplasia. One such discovery is the theory of maturational arrest compared to dedifferentiation. It has been assumed that tumors arise from dedifferentiation of mature cells. The latest research now reveals that tumors form from partial or complete arrest in differentiation. In their book, “Mechanisms of Disease”, Slauson and Cooper purport that neoplasia is born from cells involved in tissue renewal; they clearly state that: “tumors are composed of neoplasic stem cells and their well differentiated progeny, which form a “caricature” of their tissue of origin.”
Because homotoxicology’s underlying purpose is to detoxify the body and can be targeted to different systems to detoxify the patient’s affected terrain and redirect healthy tissue renewal, the application of drainage methods with antihomotoxic remedies can be useful in the complementary approach to cancer. Further evidence from research points to the role of certain viruses in the formation of tumors, another avenue for the complementary intervention with antihomotoxic remedies.
With this new evidence, we see how homotoxicology can play an important role in cancer management.
Homotoxic physicians use Galium aparine extensively in their approach to cancer. According to German researcher Boericke, Galium aparine as a homeopathic composite, can halt the process of oncogenesis. It favors healthy granulation tissue of ulcers. Leading expert in, and professor of clinical homotoxicolgy, Dr. Ivo Bianchi considers Galium aparine to be highly cleansing and draining of toxins, not only those at the cellular phase of oncogenesis, but in secondary phases of neoplasia. Dr. Bianchi purports that Galium-Heel is highly anti-inflammatory and anti-degenerative. Keeping in mind that the inflammatory process is at the origin of all disease processes and the arrest of maturation seen at the onset of oncogenesis, the remedy Galium-Heel matches the disease process.
PROTOCOL:
DR. BIANCHI recommends 20 drops of Galium-Heel morning and night for a minimum of 2 months, to be repeated 3-4 times a year.
DR. BIANCHI emphasizes the importance of Galium-Heel for people over 40. He recommends that this age group take Galium-Heel for long periods of time: 20 drops morning and night taken daily for several months; repeat 2-3 times a yearThe treatment of cancer is more complicated, but no less conducive to the use of anti-homotoxic remedies. As a general rule, treatment starts with the administration of drainage remedies: Galium-Heel, Lymphomyosot and Glyoxal-comp. are staples.
Glyoxal-comp. unblocks damaged respiratory processes, mainly by catalyzing enzymes associated with cellular respiration while it is highly neutralizing to toxins released by damaged cellular processes. Unlike Galium-Heel, Glyoxalcomp. should not be given frequently, and it must be allowed time to work. Glyoxal-comp. works slowly but very effectively.
The type of cancer will define the remedies to use. In general, protocols for draining and eliminating can be initiated for 2-5 weeks before the specific treatment protocol. The draining/detoxifying protocol for neoplasia applies especially well after tumor removal and /or chemotherapy.
Unlike prevention, the treatment protocol should use the drinkable ampules and be formulated for each patient according to the type of cancer, its affected tissues or organs, and the stage of malignancy.
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Anti-Viral Remedies for Protection against Viral Diseases, Flu, Communicative Diseases and Prophylactics

Engystol® is an effective medicine that has been shown to have a dual mode of action that boosts your immune system and together with its antiviral activity fights off flu-like infections and colds:
Studies have shown that Engystol® does the following in your body:
- Increases the number and activity of scavenger cells, called phagocytes that remove the virus from your respiratory tract.
- Reduces the inflammation caused by the infection.
- Stimulates your immune system to produce antiviral compounds, known as interferons that weaken the virus. Interferons also play a significant role in regulating immune responses.
- Provides antiviral activity against viruses such as the Rhinovirus type 14, the Adenovirus type 5, and the Respiratory Syncytial Virus or RSV.
Natural at its core
Engystol stimulates the body’s initial defense mechanisms and in this way helps to overcome the cold at an early stage. This is ensured among other things by the natural ingredients Swallowwort and Sulfur. Swallowwort, also called Vincetoxicum hirundinaria, has an anti-inflammatory and supporting effect on the immune system. Sulfur acts against the inflammation of the mucous membranes, mainly found in the throat at the beginning of a cold.
When should I take Engystol®?
When you are experiencing an onset of cold or flu-like symptoms, you may take Engystol® more often to combat the virus:
- Adults and children over 12: In case of acute complaints, dissolve 1 tablet in your mouth every 30 to 60 minutes, no more than 6 times a day.
- Children 6-11: In case of acute complaints, take 2/3 of a tablet every 30 to 60 minutes, no more than 6 times a day. Dissolve 1 tablet in approx. 150 ml of water. Give your child 2/3 of the amount and discard the rest.
- Children 1-5: In case of acute complaints, take 1/2 of a tablet every 30 to 60 minutes, no more than 6 times a day. Dissolve 1 tablet in approx. 150 ml of water. Give your child 1/2 of the amount and discard the rest.
To continue stimulating your immune system after initial symptoms of cold and flu-like infections have been reduced, the following dosage is recommended:
- Adults and children over 12: Dissolve 1 tablet 3X daily in your mouth.
- Children 6-11: In case of chronic forms, take 2/3 of a tablet 1 to 3 times a day. Dissolve 1 tablet in approx. 150 ml of water. Give your child 2/3 of the amount and discard the rest.
- Children 1-5: In case of chronic forms, take 1/2 of a tablet 1 to 3 times a day. Dissolve 1 tablet in approx. 150 ml of water. Give your child 1/2 of the amount and discard the rest.
Is Engystol® safe?
Yes. Engystol® is a natural medicine without the side-effect profile of many synthetic cold medications. This makes Engystol® even suitable for children* and elderly as well as at-risk groups such as asthmatic patients.
Will Engystol® help me get over flu-like infections and colds more quickly?
Yes. In fact, over 88% of people suffering from a flu or cold found that Engystol® improved their symptoms within the first week of treatment.
How does Engystol increases body defences?
Dual Action in prevention of Viral infections How is Engystol® different from other medications?
Most synthetic cold medications focus on treating symptoms as rapidly as possible, by suppressing key immune system components. However, these medications can prolong the recovery process. Engystol® tackles flu-like infections and colds at the root.
Can I take Engystol® with other medications?
Yes. Engystol® can be taken with other medication.
In one study with people with colds and flu-like infections, 77,1% of them using Engystol in combination with other medications (inhalations, analgesics, vitamins and decongestants) reported significant relief in their symptoms within 3 days, compared to 61.7% of people only using synthetic cold medications.
Other Viral Remedies

How does Traumeel work? 





The natural approach to regulating inflammation and supporting recovery
Non-steroidalanti-inflammatory drugs (NSAIDs) are among the most commonly used pain relievers worldwide. NSAIDs are unspecific COX enzyme inhibitors that reduce the formation of prostaglandins, which are triggers of inflammation. NSAIDs include medicines like diclofenac, ibuprofen, ketoprofen and naproxen. In contrast to NSAIDs, the natural multi-component medicine Traumeel® provides both pain relief and support of tissue repair and results in an accelerated healing process. See the difference between NSAIDs and Traumeel®.
How Traumeel can help?
- Inflammation is a complex, multifactorial process, which is essential to tissue repair, e.g. after muscle or joint injury. However, excessive inflammation can cause pain and be detrimental to recovery.
- Cytokines serving as messenger signals within the immune system of the body can either increase (pro-inflammatory cytokines) or reduce (anti-inflammatory cytokines) inflammation.
- Imbalance of pro-inflammatory and anti-inflammatory cytokines can lead to excessive and prolonged inflammation and pain.
- Traumeel® restores the balance of pro- and anti-inflammatory cytokine activity.
Traumeel® has proven ability to relieve pain and inflammation
According to controlled clinical trials, Traumeel® can reduce pain and inflammation of different causes and at different sites in the body, for instance:
Treatment of symptoms such as pain and inflammation caused by injuries of various types (sporting, accidents) such as sprains, strains, bruising, haematomas, bone fractures, etc., degenerative processes that progress with inflammation and suppuration of different organs and tissues (for example parodontitis, gingivitis, parodontosis) and of the musculoskeletal apparatus and ligaments (tendovaginitis, bursitis, tennis elbow), osteoarthritis of the hip, knee and small joints
Acute ankle sprain
A recent large-scale study has shown that Traumeel® cream & gel was as effective as diclofenac in pain reduction and functional improvement in the treatment of acute ankle sprains. Compared with a placebo, Traumeel® cream was an effective treatment for activity-related ankle sprains, significantly improving mobility and reducing pain.
Acute musculoskeletal injury
Compared with a placebo, Traumeel® cream was significantly more effective in restoring muscle function and reducing pain from musculoskeletal injuries.
Tendon pain
Compared with diclofenac (an NSAID), Traumeel® cream reduced pain and achieved a significantly faster return to normal activities.
Enriching the body with the nutrients that it needs:

Find out which are of your specific interest.
gastrointestinal health.
digestive and draining functions.
liver function support
balanced solution against iron deficiency.
specific amino acid composition for the human body in dietology and clinical
nutritional support for athletes
normal blood cholesterol levels.
respiratory system support
physical and mental well-being in menopause
your natural boost of energy
vitamin C supports absorbtion of minerals
reduce tiredness and fatigue support healthy muscles keep healthy skin
supports the body’s natural defenses and the respiratory tract.
acid-base metabolism balance body detoxifying functions mental well-being.
the synergy of 6 active ingredients for a better mental
protects and detoxifies the gastrointestinal system
physical and mental fatigue immune system support
innovative and unique association of 6 exclusive probiotic strains with
synergistic innovative prebiotic and nutraceutical food supplement for the wellness
Minor health problems may be caused by poor or unbalanced diet. It is well known that industrial food processing does not often guarantee an adequate intake of nutrients essential to maintain our health and wellbeing.
Guna Laboratories have developed “physiological nutraceuticals”, a unique line of innovative and specific nutritional supplements that allow to maintain the normal physiological functions by providing a well-balanced intake of carefully selected nutrients.
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Percentage of People using Alternative and Homeopathic Medicines
Sometimes shortened to CAM – is a system of healing which encompasses variety of practices, theories, beliefs and modalities. These methods can often be used by themselves or along with orthodox medicine in treatment or in prevention of a disease in Human and Veterinary patients.
% of population using: Complementary medicine Acupuncture Homeopathy Osteopathy chiropractic Herbal medicine Belgium 31 19 56 19 31 Denmark 23 12 28 23 No info France 49 21 32 7 12 Germany 46 No info No info No info No info Netherlands 20 16 31 No info No info Spain 25 12 15 48 No info UK 26 16 16 36 24 USA 34 3 3 30 9 Comparative usage of complementary medicine (Fisher and Ward, 1994) Homeopathy is a system which can be used inline with other forms of treatments. Everything that can be known about the patient can be used to consider the remedy. It is referred to as holistic therapy because of its approach to heal the patient and not the disease.
Popularity of Homeopathy is increasing significantly due to a lot of push factors such as delayed appointments with GPs, lack of time spent with the doctors assessing patient, diagnostical delays in hospital settings, disenchantment using antibiotics, ever increasing side effects and antibiotic resistance. -
THE COLLAGEN MEDICAL DEVICES IN THE LOCAL TREATMENT OF THE ALGIC ARTHRO-RHEUMOPATHIES
REVIEW OF THE CLINICAL STUDIES AND CLINICAL ASSESSMENTS 2010-2012
INTRODUCTION
Reliable epidemiologic data recorded in Italy (Mannaioni et Al., 2003) and in Europe [Jordan et Al., 2003-European League Against Rheumatism (EULAR)] show that 15-20% of the general population suffers from pathologies involving the osteo-arthro-myo-fascial Apparatus (better defined as arthro-rheumopathies), representing 70% of the patients with chronic pain.
– In the near future, these data will probably undergo an increase, especially due to increased life expectancy, overall average increase in body weight, greater propensity to inactivity amid people above 50, higher incidence of amateur sports activity and consequent traumas (mostly among people aged between 20 and 45), overuse of NSAIDs and unhealthy diet, basically high in proteins. The arthro-rheumopathies (connective tissue inflammatory and/or degenerative diseases) are all characterized by collagen disorders.
Collagen’s physiological tissue organization and quantitative and qualitative composition – which dramatically decrease from = 60 years of age (Heine, 2009) – determines the organoleptic characteristics of connective tissues. – Collagens are merged into a vast family of structural proteins of the extra-cellular matrix having unique and peculiar characteristics, also from the phylogenetic point of view (in Milani, 2010).
Up to the present more than 30 genetically
distinct varieties (Types) of collagen have been identified.Genetic alterations of some Types of
collagen determine complex and paradigmatic phenotypes (alterations in the collagen Type I: e.g. osteogenesis imperfecta; Type I, III, V: e.g. Ehlers-
Danlos syndrome; Type IV: e.g. Alport syndrome; Type II, XI: e.g. cartilage genetic diseases). The fibrillar collagen Type I (COL1A1 and COL1A2 coding genes) is the most abundant ubiquitous protein in adult humans, accounting for 90%of the total collagen: it is involved in the
A A – Continuity of collagen fibers in the ligament of adult rats.
Electron Microscope images from Provenzano P.P. and Vanderby R. Jr. – Collagen fibril morphology
and organization: Implication for force transmission in ligament and tendon. Matrix
Biology 25(2006) 71-84.composition of the main connective tissues and represents the bulk of certain structures such as skin, dentine, cornea, joint capsules, ligaments, tendons, aponeurotic layers and fibrous membranes. – In the tendons, for example, collagen Type I = 97%; elastin = 2%; proteoglycans = 1-5%; inorganic components (Cu, Mn, Ca) = 0.2% (Jozsa and Kannaus, 1997; Lin et Al., 2004); in ligaments, collagen Type I = 85% (Frank, 2004; Vereeke et Al., 2005). The in vivo fibrillogenesis is a multi-step process involving both the intracellular compartment and the extracellular one, defined by tenocyte (a very specialized fibrocyte) (FIG. 1). – The tenocyte, in addition to collagen Type I, also synthesizes the matrix proteoglycans (PGs) and the metalloproteinase (MMP) 1-interstitial which is involved, together with the MMP8-neutrophil, in the degradation of the fibrils, either because old or damaged by the inflammatory/traumatic process (Birk et Al., 1995; Canty, 2004). The MMP1 is primarily involved in the processes of fibrillo- (collagen)-lysis: the study of Maeda et Al. (1995) highlights a very high concentration of MMP1 in the synovial fluid of patients with rheumatoid arthritis, which is related to the degree of inflammation (reliable marker of the disease status). Provenzano andVanderby Jr. (2006) ), using the electron microscope, exhibit a wide range of very impressive photographs proving that healthy adults collagen fibrils (FIG. 2A) are very precise, parallel to each other, continuous and laid longitudinally along the main axes of the anatomical structures to which they belong and which characterize, transmitting the force directly and not through the PGs bridges.
– The collagen turnover is very slow. The mechanical failure and the presence of free radicals can increase the degenerative process, causing a spontaneous, slow and imperfect neofibrillogenesis: the process of spontaneous repair leads to the neoformation of disordered, twisted, juxtaposed, discontinuous fibers, (FIG. 2B), morphologically much more similar to the fetal ones rather than the adult ones (Provenzano et Al., 2001). It also leads to increased vascularization and increased deposits and clusters of inflammatory cells. These phenomena all contribute to the further weakening of collagen Type I (Shrive et Al., 1995; Frank et Al., 1999) and to the increased synthesis of collagen Type III (Liu et Al., 1995; Hsu et Al., 2010), which is functionally much less suitable.

B B – Post-traumatic repair of the collagen texture.
Electron Microscope images from Provenzano P.P., Hurschler C., Vanderby R. Jr. – Connect.
Tiss. Res. 42:123-133, 2001.During the fibrillogenesis process, the PGs play a crucial role in guiding and stabilizing neofibrils, assisted by the SLPR (Small Leucine Rich Proteoglycans) (Jepsen et Al., 2002), represented above all by decorin, lumican, and fibromodulin. The rare overt genetic alterations of these 3 small PGs affect distinct phenotypes, clinically severe. – Minor alterations with variable penetrance and expressivity are probably not diagnosed and are the primary cause of highly pathologically susceptible conditions: collagen fibrils altered in shape and diameter which affect the joints and posture long before the physiological decay. – I conclude these brief topics on collagen, which supplement and detail what presented in a previous publication (Milani, 2010) to which I refer, indicating that collagen is also a template for bone mineralization, which promises new and revolutionary solutions in Orthopedics and Traumatology.
The anatomical structures composing the extra-articular environment of the joints – with containing and stabilizing functions – are represented by:
- joint capsule, ligaments and fibrous membranes (“direct hold”);
- tendons and muscles (“indirect hold”).
These elements – which unite and wrap the distal end of a bone and the proximal end of the adjacent bone (superoinferior) (bone segments in connection) – are the actors of the containment-stabilization and of the joint mobility.
– Although anatomically distinct and functionally different, these structures are in close continuity (contiguous or overlapping anatomical planes; some collagen fibers of each structure merge with the neighboring ones) to form an elastic-stretch sleeve performing primarily two functions:- Articular establishment in static / dynamic physiological position;
- Articular mobility with maximum range.
FIGURE 3 shows as exemplification the fibrous structures of the extra-articular environment of the elbow.
– In addition to the extra-articular structures, few joints also have intra-articular intrinsic ligaments that connect two skeletal segments inside the joint capsule (e.g. cruciate ligaments of the knee joint, coxofemoral round ligament).
– The extra-articular structures (primarily: joint capsule, ligaments and tendons) are constituted by collagen Type I: the quality and the quantity of this protein ensure a physiological joint movement, repeated over time and optimal movement.Progressive depletion and / or damage to organoleptically suitable collagen Type I is produced by aging (discrepancy between neofibrillogenesis and fibrillo-lysis), misuse or disuse of the joints, traumas aggravated by the coexistence of internal diseases and – in some age groups – even by vitamin deficiencies (vitamin C, but also vitamin A and E), copper
deficiency, noble proteins deficiency, and the use / abuse of drugs (particularly corticosteroids).
– In particular, Elder et Al. (2001), Warden (2005), and Warden et Al. (2006) show that NSAIDs COX-2 inhibitors inhibit the healing of injured ligaments, leading to the lack of mechanical strength (imbalance between joint stability and mobility) and causing extra- and intra-articular damages. The trial of these drugs demonstrates unequivocally that the anti-inflammatory benefit in the short term is converted into serious harm in the medium and long term.
– Fournier et Al. (2008), and Ziltener et Al. (2010) maintain that the use of NSAIDs in the treatment of periarticular soft tissues (ligaments, capsule) should be very limited in time, or absent.
A – Left elbow joint, front.
B – Right elbow joint, front.
The containing and stabilizing
structures of the elbow joint are
represented by extra-articular
connective-collagen Type 1 structures.
They are represented by:
– ulnar collateral ligament (A, B);
– radial collateral ligament (A, B);
– anular radial ligament (A, B);
– sacciform recess (A);
– joint capsule (lifted in A; B);
– brachial biceps tendon (B).
All these structures allow the
large variations in flexion, extension
and torsion of the forearm on
the arm.
– Images translated and elaborated by the
author from W. Spalteholz – R. Spanner,
Atlante di Anatomia Umana. Società
Editrice Libraria (Vallardi) – Milano, 5th Italian
edition (1962) in the 16th German edition
(1959-61); 1st Vol.; pp. 232-3.Barton and Bird (1996) indicate the laxity or hyperlaxity of anatomical structures as the most important cause of pain of one or more joints. The quoted authors’ studies follow those by:
- Rotes-Querol (1957), which identified joint laxity as the main factor of altered posture;
- Teneff (1960), indicating the clinical significance of congenital
joint laxity; - Donayre and Huanaco (1966), which show that the orthopedic
joint laxity is the cause of many diseases (defined
by the authors as “arthrocalasis”).
Recently: - Philippon and Schenker (2005) show high incidence of
coxofemoral traumas in athletes with femoral laxity; - Paschkewitz et Al. (2006) describe the generalized ligament
laxity associated with proximal dislocation of the tibio-
peroneal joint; - Hauser and Dolan (2011), indicate in joint instability and
unhealed ligament injuries the primary cause of osteoarthritis.
These are just some historical data and the most recent ones among those that can be extrapolated from the available literature on the topic which indicate that the joint hypermobility due to deficiency of joint containment (ultimately: deficiency of collagen Type I in the extra-articular environment) is the primary cause of the arthropatic etiology.
It is necessary to distinguish between joint hypermobility due to impaired containment from the one due to paraphysiological laxity, such as:- in childhood (Cheng et Al., 1993; Bird, 2005; Simpson, 2006);
- in females, especially during the menstrual cycle (Schultz, 2005);
- In individuals belonging to African (Beighton et Al., 1973) and eastern (Walker, 1975) anthropological varieties,
and the one due to joint instability of various pathological degree, which starts when the contiguous bone segments forming a joint do not respect the optimal axes and – consequently the angles among them. Paradigmatic examples – not the only ones, though – of such situations are:
- valgus/varus tibio-femoral joint (FIG. 4) and valgus/varus coxofemoral joint,
- the extra/internal rotation of the head of the femur in the acetabulum,
- the lordosis/kyphosis of the rachis segments,
- cavus/flat foot.

Situations that can worsen joint hypermobility are paraphysiological variations and real alterations of the diaphyseal shape, the alteration of the muscle tone and abnormal proprioception.
All the above conditions necessarily lead to pathological osteo-cartilaginous hyperload which cause the overuse processes. The bone reacts with the production of marginal osteophytes, subchondral bone cysts, subcortical hardenings or deformities and/or epiphyseal osteopenia.
These extra-physiological forces cause, especially in the load joints, slippage of the adjacent bone heads, which are anteroposterior, medium-lateral and rotational of greater or lesser severity.
– In such situations the loose structures of the extra-articular environment are exposed to mechanical stress: the pain due to extra-articular cause is added to the one due to intra-articular cause (which is frequently inflammatory), thus aggravating the status and prognosis of the disease.
The organism performs mechanisms of local and remote compensation by establishing the activation (hyperactivation) of ascendants and descendants muscle-proprioceptive chains which only rarely get the desirable effect: the control of the vascular tone is unintentional and self-organizing, at central and peripheral level.
– Currently, the treatment of arthro-reumopaties offers different options; it includes different, unique treatments or – more frequently – a combination of:
- non-pharmacological treatments (e.g. ultrasound therapy, magnetic therapy, laser therapy, TENS, acupuncture, moxibustion, etc.);
- conventional pharmacological treatments [e.g. COXIB, NSAIDs, paracetamol, corticocosteroids (the latter also intra- articularly injected)];
- unconventional pharmacological treatments [e.g. specific medicines formulated by Homeopathy, Homotoxicology (the latter also via intra-articular injection, periarticular injection, mesotherapy, homosiniatry treatment), Physiological Regulating Medicine, Herbal Medicine];
- physical-rehabilitation treatments (see review by Di Domenica et Al., 2004);
- surgical treatment: mobile (prosthesis, especially hip, knee, shoulder) or fixed (arthrodesis).
Symptomatic slow-acting treatments include viscosupplementation with hyaluronic acid (see review by Bellamy et Al., 2008) or with hylan G-F 20 (derived from the hyaluronic acid) (see review by Conrozier and Chevalier, 2008), administered mainly via injection into the knee, hip and shoulder. They are viscous lubricants whose prevailing action is supplementary and cushioning.
The viscosupplementation replaces the (usually degraded) hyaluronic acid of the synovial fluid of the joints of the pa- tients affected by osteoarthritis.
The hyaluronic acid is mostly used to inject the knee in or- der to treat gonarthrosis.
Nevertheless, the members of the EULAR (European League Against Rheumatism) Committee for clinical trials on osteoarthritis of the knee met in 1998 and came to the con- clusions that the hyaluronic acid and symptomatic slow-ac- ting antiarthritic drugs have modest efficacy in gonarthro- sis. Moreover, they stated that the patients who may benefit from this therapy are hardly identifiable and that pharma- coeconomic data are uncertain. The opinion of 21 experts has placed the use of the hyaluronic acid for the treatment of gonarthrosis in 13th place out of 23 entries (Pendleton et Al., 2000).
- Since 2010, also the treatment of algic/degenerative dis- eases of the musculoskeletal system takes advantage of the
use of the injectable Collagen* Medical Devices (MDs) (Gu- na Laboratories, Milan – Italy).
The Collagen MDs can be used alone (e.g. MD-Lumbar: low back pain with high arthritic imprint), or – more frequently variously mixed according to the patient’s clinical and func- tional needs (e.g. MD-Lumbar + MD-Neural: low back pain with algic nerve imprint; MD-Lumbar + MD-Muscle: low back pain with prevailing myo-fascial imprint).
The Collagen MDs are applied locally through:
- periarticular injections
- intra-articular injections (obviously in the joints allo- wing a clear intra-articular approach: knee, hip, shoul- der)
- subcutaneous and/or intradermal injections (in trig- ger points, in spontaneously painful points, in points whe- re average digitopressure causes pain, in local acupunc- ture points, etc.).
or systemically:
– intramuscular injections (into muscle trigger points), and in supportive treatment (mainly at home).
The 13 Collagen Medical Devices are produced from der- mal tissue of swine origin (trophism) + ancillary excipients of natural origin allowing an efficient and specific positio- ning on site (tropism).


The ancillaries were selected according to different criteria such as: traditional use, dedicated literature, clinical eviden- ce, quality profiles, etc.
The swine’s dermal tissue contains » 50% of collagen Type I (Gly = 22.8%; Pro = 13.8%; OH-Pro = 13%).
- The purpose of the in situ injections of the Collagen MDs is essentially structural.
From 2010 to 2012 10 clinical trials on humans were car- ried out, involving most of the treatable anatomical districts with Collagen MDs: 3 gonarthrosis, 1 patello-femoral arth- ropathy, 2 coxarthrosis, 2 shoulder pain, 1 PMID (Painful Mi- nor Intervertebral Dysfunctions) of cervical rachis, 1 acute lumbar back pain.
- In the following pages it is presented the synopsis of the experiments; the Authors’ conclusions of the 10 trials are faithfully reported.
► EFFICACY AND SAFETY OF THE GUNA MDs INJEC- TIONS IN THE TREATMENT OF OSTEOARTHRITIS OF THE KNEE
Authors: Rashkov R., Nestorova R., Reshkova V.
- Clinical Assessment presented at the Bulgarian National Congress of Rheumatology – Pravets (October 2011), at the European Congress on Osteoporosis and Osteoarthritis – Bor- deaux (F) (March 2012), and at the 3rd Bulgarian National Congress on Osteoporosis and Osteoarthritis – Sandanski (No- vember 2012).
Experimental sites: Rheumatology Clinic of the Medical University of Sofia, Rheumatology Center St. Irina (Sofia – Bul- garia).
Pathologies considered: symptomatic gonarthrosis (Kellgren- Lawrence* Rx grade II-III) without aftereffects of the periar- ticular soft tissues.
Outcomes
- assessment of pain at rest and during movement before and after treatment;
- assessment of the Lesquesne Algofunctional Index** be- fore and after treatment;
- effectiveness of the MDs used (evaluation by the patient and by the physician).
Inclusion/exclusion criteria: stated.
Patients enrolled: 28 (12 M, 16 F, aged 55-70).
Treatment: MD-Knee, 1 ampoule + MD-Muscle, 1 ampou- le: 2 intra-articular injections/week for 2 consecutive weeks
+ 1 intra-articular injection/week for the next 6 weeks (total: 10 injections in 2 months).
Results
Statistically significant reduction of pain (VAS *** = 0-10) at rest (maintained even 30 days after the end of the therapy) and during movement (VAS = 0-10) (maintained even after the end of the therapy) (TABLES. 1, 2). Statistically significant improvement of the indicators of the Lesquesne Algofunctional Index (TABLES 3, 4).
Authors’ conclusions:
- Intra-articular administration of MD-Knee + MD-Muscle in gonarthrosis Kellgren-Lawrence Rx grade II-IIII reduces si- gnificantly pain at rest and during movement and improves the functional activity of patients, who assessed excellent + good in 65% of cases.
- The effect persists even after treatment.
There were no adverse effects in any case.
► EFFECTIVENESS OF THE GUNA COLLAGEN MDs INJECTIONS IN PATIENTS WITH GONARTHROSIS, ANALYSED CLINICALLY AND WITH ECOGRAPHY
Authors: Nestorova R., Rashkov R., Reshkova V., Kapandjieva N.
- Clinical Assessment presented at the 9th Central Congress of Rheumatology (CECR 2012) 3rd Annual Meeting of the Polish Rheumatologists – Krakow (Poland) (September 2012), and at the European Congress on Osteoporosis and Osteoarthritis – Bordeaux (F) (March 2012).
Article published in Rp./Orthopedic 2011/3, Medicine and Sport 2011/4 and PRM 2012; 37-39.
Experimental sites: Rheumatology Center St. Irina (Sofia); Rheumatology Clinic MBAL “St. Ivan
Experimental sites: Rheumatology Center St. Irina (Sofia);
Rheumatology Clinic MBAL “St. Ivan Rilski” (Sofia); Rheu- matology Center MBAL – Rousse (Bulgaria).
Pathologies considered: symptomatic gonarthrosis (Kellgren-Lawrence* Rx grade III-IV) with aftereffects of the periarti- cular soft tissues.
Outcomes
- assessment of pain at rest and during movement (VAS = 0-10; Lesquesne Algofunctional Index**);
- ecographic evaluation before treatment, after 30 days and at the end of the treatment;
- evaluation of effectiveness of the MDs used.
Inclusion / exclusion criteria: stated.
Patients enrolled: 35 (aged 62-79).
Treatment: MD-Knee, 1 ampoule + MD-Matrix, 1 ampou- le: peri-articular injections / week for 2 consecutive weeks
+ 1 peri-articular injection /week for 6 more weeks (total: 10 injections in 2 months).
Results
- Statistically significant reduction of pain (VAS*** = 0-10) at rest (maintained even after the end of treatment) and du- ring movement (maintained even 30 days after the end of treatment) (TABB. 5, 6).
- Statistically significant improvement of all indicators of the Lequesne Algofunctional Index (examples in TABB. 7, 8).
- 60% of patients do not have any edema; 30% achieved a reduction of edema
– Authors’ conclusions:
- ) Intra-articular administration of MD-Knee + MD-Matrix in gonarthrosis Kellgren-Lawrence Rx grade II-IIII reduces si- gnificantly pain at rest and during movement and improves the functional activity of patients.
- The effectiveness of treatment was evaluated as excellent
+ good in 68% of patients and 72% of physicians.
- Periarticular edema improves in 90% of cases as proven by ecography.
- The effect is maintained even after treatment.
The analysed MDs have a very high safety profile.



► APPLICATION AND ASSESSMENT OF EFFICACY OF COLLAGEN INJECTIONS GUNA MDs IN GONARTHRO-SIS
Author: Boshnakov D.
– Clinical Assessment presented at the XIX Days of Bulga- rian Orthopedics and Traumatology, Tryavna, (September 2012).
Experimental sites: Saint Anne University Hospital, Varna(Bulgaria).
Pathologies considered: gonarthrosis.
Outcomes
- assessment of pain at rest and during movement (VAS = 0-10);
- assessment of Lequesne Algofunctional Index for:
a.pain when walking; b.maximum walking distance (in me- ters); c.daily activities;
3. assessment of efficacy of treatment from the patient’s view- point.
Inclusion/exclusion criteria: unstated.
Patients enrolled: 14 (8 M; 6 F; aged 51-72).
Treatment: MD-Knee, 1 ampoule + MD-Muscle, 1 ampou- le: 2 intra-articular and peri-articular injections/week for 2 consecutive weeks + 1 intra-articular and peri-articular in- jection/week for the following 6 weeks (total: 10 treatments in 2 months).


Results
- Pain at rest: VAS from 2.85 at treatment start (moderate pain) to 0.95 at the end of treatment (no pain) (TAB. 9).
- Pain when moving: VAS from 7.3 at treatment start (un- bearable pain) to 3.5 at the end of treatment (moderate/se- vere pain) (TAB. 10).
- Lequesne Algofunctional Index: from 1.6 at treatment start to 1.1 at the end of treatment (TAB. 11); maximum walking dis- tance from 100-300 meters before treatment (5.2 score) to 400-700 meters after treatment (3.6 score) (TAB. 12).
Author’s conclusions:
- Intra-articular injections of Collagen MDs improve: a) lo- calized pain; b) pain at movement; c) joint mobility.
- Intra- and peri-articular injections improve the patients’ functional activity and quality of life.
- The injections of Collagen MDs are a new and effective method to treat gonarthrosis.
► PATELLO-FEMORAL CHONDROPATHY TREATED WITH MD-KNEE + ZEEL® T TRANSMITTED WITH O2 VERSUS
NIMESULIDE + CHONDROITIN SULPHATE
Author: Posabella G.
- Clinical trial presented at the Meeting Sport Medicine, the challenge for Global Health – Rome (September 2012).
Article published in La Med. Biol., 2011/3; 3-11, and in PRM 2012/1; 3-10.
Pathologies considered: patella-femoral chondropathy stage I-II-III according to Kellgren-Lawrence.
Outcomes
assessment of clinical response (analytical WOMAC****; Le- quesne Index) after administering MD-Knee + Zeel® T trans- mitted with hyperbaric O2 (Group A) versus nimesulide + chondroitin sulphate (Group B).
Inclusion/exclusion criteria: unstated; randomization.
Patients enrolled: Group A, 20 [15 M, 5 F; average age 46.4 years (31-66)]; Group B, 20 [15 M, 5 F; average age 46.9 years (28-65)].
Treatment: Group A – MD-Knee, 1 ampoule + Zeel® T, 1 ampoule, both applied onto the knee skin and transmitted with hyperbaric O2, 1 application/week.
Group B – nimesulide in 100 mg sachets + Condral (galaco- tosaminoglucuronoglycan sulphate sodium salt) 400 mg, 1/die per os.
Results
- After the first week of treatment the patients of both groups (A; B) showed a reduction of the total WOMAC score com- pared to baseline, even if not statistically significant.
WOMAC Group A = 50 points – Lequesne Index = 17.05 WOMAC Group B = 54 points – Lequesne Index = 17.9
-Second week
WOMAC Group A = 47 points WOMAC Group B = 53 points
-Third week
WOMAC Group A = 44 points WOMAC Group B = 51 points
-Sixth week (1st follow-up) WOMAC Group A = 41 points WOMAC Group B = 50 points
-Twelfth week (2nd follow-up)
WOMAC Group A = 39 points – Lequesne Index = 10.4 WOMAC Group B = 47 points – Lequesne Index = 15.3
Author’s conclusions:
- Both Groups of patients (A; B) showed a considerable im- provement of pain and functional limitation.
- The data show a more rapid clinical and functional im- provement in the patients of Group A compared to the pa- tients of Group B.
- No side effects in the patients of Group A.
– For comparative analysis of the 4 clinical trials on the osteoarthritis of the knee see TAB.13.
► INTRA-ARTICULAR ADMINISTRATION OF MD-HIP IN 7 PATIENTS AFFECTED BY HIP OSTEOARTHRITIS UNRE-
SPONSIVE TO VISCOSUPPLEMENTATION.
-SIX MONTH MULTICENTER TRIAL
Authors: Migliore A., Massafra U., Bizzi E., Vacca F., Tormenta S.
– Clinical trial presented at the International Symposium Intra Articular Treatment; Rome (October 2011).
Experimental sites: UOS (Simple Operating Unit) of Rheu-
matology – San Pietro Fatebenefratelli Hospital, Rome. Pathologies considered: osteoarthritis X-Ray I-III stage ac- cording to Kellgren-Lawrence affecting the hip joint unre- sponsive to viscosupplementation with hyaluronic acid (6 pa- tients) or hylan (1 patient) (2 ultrasound guided injections at least).
Outcomes
- assessment of efficacy using VAS scale and Lequesne al- gofunctional Index;
- NSAIDs consumption before treatment and during follow- up;
- safety profile of MD-Hip.
Patients enrolled: 7
Treatment: MD-Hip (2 ampoules = 4 ml), 1 ultrasound gui- ded intra-articular injection.
Results
- VAS of osteoarthritis pain = from 6.15 (before treatment) to 4.23 (after 3 months), to 4.23 (after 6 months).
- Lequesne Index = from 1.94 (before treatment) to 5.9 (af- ter 3 months), to 5.83 (after 6 months).
- NSAIDs consumption = from 7.57 (before treatment) to 4.25 (after 3 months), to 5.78 (after 6 months).
– Author’s conclusions:
- MD-Hip showed to be effective (all the average values of the results at 3 and at 6 months after the last treatment have been statistically significant) and safe in patients affected by hip osteoarthritis unresponsive to viscosupplementation.
- The data suggest that the results can be evident from the very first injection and are stable for 6 months.
- The preliminary data offer new research opportunities in the field of intra-articular therapy.
► EFFICACY OF INJECTIONS MD-HIP AND MD-MATRIX IN TREATMENT OF COXARTHROSIS.
- CLINICAL AND ULTRASONOGRAPHIC EVALUATION
Author: Tivchev P.
Article published in Bulgarian Journal of Orthopaedics and Traumatology. Vol 49/2012; 123-8
Experimental sites: Serdika Hospital (Sofia); Deva Maria Hospital (Bourgas – Bulgaria)
Pathologies considered: x-Ray stage I-II-III hip osteoarthritis according to Kellgren-Lawrence.
-
Progressive Auto-Sanguis Therapy according to Reckeweg
Introduction and remarks on theoretic aspects
Medical history indicates autohemotherapy’s effects to have first been recognized as a result of the following observation: in persons having sustained blunt traumata with haematoma formation, other affections were also discovered to vanish during the course of haematoma absorbtion. Consequently, therapy with the patient‘s own blood (autohaemotherapy) initially consisted of withdrawing a small quantity of blood from the patient and immediately re-introducing it through intramuscular, hypodermic injection. In this manner, an artificial hematoma was created. The conjecture then was that the injection of one’s own blood would activate defensive powers which, in turn, would combat the ”forces of illness within the blood.” Since then, autohemotherapy has been modified and perfected in multifarious ways, yet in actual practice, the original form of autohaemotherapeutic treatment – as irritation therapy, reversal therapy, non-specific excitation, or stimulation therapy – still finds application in numerous individual cases (e.g., in treatment of acne) with highly successful results.
Progressive auto-sanguis therapy according to Reckeweg is autohaemotherapy in a specialized form. Developed from the fundamentals of homoeopathy in conjunction with Reckeweg’s homotoxicological principles, this technique has proven in practical experience to be reliable and exceptionally effective in treating an extremely wide variety of chronic and degenerative diseases including bronchial asthma, eczema, hepatic damage and numerous other disorders (see also ”Empirically-Proven Indications”).
According to the teachings of Reckeweg’s Homotoxicology, virtually every illness may be defined as either a defensive reaction by the organism against toxins or as the expression of toxic damage. It follows, therefore, that the blood of each patient contains those pathogenic poisons (homotoxins) typical for the disease from which that patient suffers. Through withdrawing a patient’s blood, homoeopathically potentizing it over several levels and subsequently re-introducing it by means of hypodermic injection, Reckeweg holds that precisely these pathogenic poisons undergo modification to yield a homoeopathically active therapeutic agent ideal for application in stimulation therapy. In keeping with the Arndt-Schulz Law in the sense of the inverse effect, this agent stimulates the bodily defense systems, thus increasing detoxification and promoting the healing process.
In accordance with Bürgi’s Principle, the addition of appropriate homoeopathic injection preparations intensifies efficacy of the potentized auto-sanguis blood to an even higher degree. When potentizing the patient’s blood during administration of progressive auto-sanguis therapy, therefore, it has proven expedient to employ the homoeopathic preparation which is therapeutically indicated in each individual patient’s case. In summary, progressive auto-sanguis therapy is treatment designed to exert a counteractive effect against exogenic and endogenic homotoxins (including toxic deterioration products from the body’s own cells), thus promoting the healing of chronic disease in a manner harmonious with the laws of nature.
Also discussed in Homotoxicology are further mechanisms of action which play a role in auto-sanguis therapy, the homoeopathic inverse-effect exerted against both auto- antibodies and antigen-antibody reactions in particular. This effect is due to a complement factor which, as a component of the patient’s own blood, is automatically injected in increasing degrees of attenuation during the course of treatment (the so- called complement-inverse-effect; at the 4th level, potentizing of the blood reaches a degree which approximately corresponds to that of C4!).
This would also explain the positive effects in the area of desensitization/hyposensitization which progressive auto-sanguis therapy is frequently observed to achieve in cases of auto-aggressive disease. One must add, however, that no major scientific studies exist on the subject at this time. Presented here, rather, are the results of hypothetical deliberation based on the positive observations made during the course of daily medical practice.
-
Suis-organ preparations
What are suis-organ preparations?
An important component of anti-homotoxic therapy is the suis-organ preparation. These are preferably employed for chronic courses of diseases in the cellular phases. Subsequently, they offer an excellent possibility for the reactivation of organ functions, particularly of elderly patients. The preparations are employed according to the simile principle, that is, the respective preparation of the organ to be treated is applied. Suis- organ preparations contain organic tissues which have been homoeopathically processed, i.e., attenuated and potentized in accordance with Specification 42 of the official German Homoeopathic Pharmacopoeia 1978 (HAB 1) whose primary materials originate from healthy swine. In accordance with their action, the suis-organ preparations can be characterized as organ-specific medications with stimulative properties. The mechanism through which the suis-organ preparations function is based on the organotropic effects of the substances and/or stimulants contained therein.
Keeping of the donor animals and organ acquisition
The following provides detailed information on the rearing and keeping of swine for the purpose of gaining suis-organ preparations: All swine designated for utilization in gaining organ extracts are descendants from the same breeding line, bred in an operation certified for keeping SPF (”specifically pathogen free”) livestock. This operation is monitored at six- week intervals by the governmental veterinary health service having jurisdiction. At a suitable age, the piglets are transferred and raised in a different agricultural facility. On delivery to this rearing operation, an initial examination is performed by the livestock veterinarian, ensuing passage of which the animals are kept separate from other animals, under veterinary surveillance. Animals requiring medicinal treatment due to any affection are excluded from organ extraction. The animals are given vegetable feed produced on the operation’s own premises. Both operational proprietors have agreed by contract to utilize neither animal meals from mammals, nor waste materials as feed. Upon attaining slaughtering weight and passing release-control by the jurisdictional public veterinarian, the swine are transported to the nearest abattoir, which must possess E.E.C. status. In accordance with regulations for meat hygiene, a live examination of the donor animals is then carried out, as well as meat inspection ensuing slaughter. In all meats attaining the rating ”suitable for human consumption,” samples are drawn for the following additional tests: bacteriological inspection, a test for inhibitory substances, as well as serological analysis for brucellosis, leptospirosis, and yersiniosis in accordance with the Zoonosis Recommendations (July 8, 1991) of the German Federal Ministry of Health.
Removal of the required organs is subsequently performed in an area entirely separate from the remainder of the abattoir, which is utilized exclusively for this purpose. The organs obtained in this manner remain under quarantine until all examination findings have been determined. Only then are the extracted organs released for further processing by the quality control department of the Heel company. The organ preparations are first processed by means of potentization, after which sterilization is then carried out. In this manner, the material preserves the character of the living tissue during potentization; also the preparations thus maintain a direct protein correlation with the affected organ. The measures presented here, all of which are additionally documented by means of official veterinary reports, serve to fulfill one objective: to ensure the highest feasible standard of medicinal safety (zoonosis) for the suis-organ preparations.
The swine as a donor animal
The human organism and that of swine demonstrate numerous similarities in the aspects of chemical and biological constitution, thus a situation of homoeopathic similitude exists. The morphological and other biological similarities between the organisms of man and pig have been the topic of repeated reports during the past several decades. An overview of the factors which man and pig have in common as compiled by Kirkman is provided below (Kirkman, R. L. (1989): ”Of Swine and Man: Organ Physiology in Different Species” In: Hardy, M.A. (ed.): Xenograft 25. Elsevier, Amsterdam and others).
Similar characteristics of man and swine (according to Kirkman, 1989):
- Size
- Dietary habits: omnivorous
- Digestive physiology
- Nephritic structure and function
- Rate and volume of respiration
- Location of the coronary arteries
- Hemodynamics
- Tendency to create fat deposits
- Highly susceptible to disease
- Social behaviour
From the homoeopathic point of view, therefore, despite the difference in species, an organ preparation acquired from swine and subsequently processed in accordance with homoeopathic techniques may be deemed a simile to the homologous human organs due to the numerous existing functional and structural similarities. As Reckeweg observed, it is on the grounds of these similarities that organ remedies obtained from swine possess greater efficacy than such derived from cattle or sheep.
Suis-organ preparations: fields of application
The suis-organ preparations are employed in treatment of the homologous human organs. The Commission D, the committee in the German Federal Ministry of Health concerned with medicinal processing with jurisdiction over homoeopathy, included the following excerpt in their definition of characteristics for organ preparations manufactured in accordance with the German Homoeopathic Pharmacopoeia, HAB 1: ”Homoeopathically- processed organ preparations are applied on the concept that insufficiency or disturbance of the homologous target-organ in humans shall receive succor through the corresponding organ-medication.” Further, the applicational fields are designated by this commission as ”supportive therapy in cases of insufficiency or disturbance of the homologous human organ.”
The suis-organ preparations are indicated particularly, and primarily, in treatment of cellular phases, especially for chronic affections (i.e., the phases of impregnation, degeneration, and dedifferentiation). Yet these remedies may certainly also find application in phases located to the left of the biological division, e.g., in therapy of pathologically disturbed excretion phases (hyperhidrosis, dysmenorrhea, constipation, eliminatory weakness of the kidneys, etc.) One should also bear in mind that therapy with suis-organ preparations is indicated in treatment of numerous deposition phases as well, such as rheumatic diseases, myomas, adiposis, calculi, and the like.
Dosage and modes of administration
The following table presents a general therapeutic plan for the application of suis-organ preparations in treatment of chronic and/or degenerative organic damage.
Fig. 9
Approximate Periods Approx. Periodes 3-4 weeks Preliminary treatment with detoxification agents, i.e. Hepeel, Lymphomyosot, Galium-Heel, Engystol N, Psorinoheel, Ubichinon compositum, Coenzyme compositum etc. 4-5 weeks Suis-organ preparations administered 1-2 x weekly 8i.m.; s.c., i.d., at acupuncture points, orally or as progressive auto-sanguis therapy; initially in injeel form,
after 6-8 injections in injeel-forte form) conjointly with the individually appropriate antihomotoxic remedies.3-4 weeks Suis-organ preparations discontinued. adjuvant anti- homotoxic medication continued alone. Second injection-series with suis-organ preparations as required.
Upon achieving clinical cure, possible reapplication of organ preparations every 2-3 weeks.As indicated in the above table, after four to five weeks’ administration of the suis organ preparations in Injeel form, the Injeel forte form is applied i.m. or s.c. on a trial basis, as a type of test ampoule in order to determine the degree in which the affected organ’s functional regeneration has progressed; i.e., whether the healing process has become largely established at that point in therapy or not. In treating severe degenerative phases as well as in therapeutic attempts for dedifferentiation phases more frequent injections may be required (every 2 – 3 days) in addition to the support of agents which foster and promote regressive vicariation (Galium-Heel, Engystol N, Traumeel S). This is performed most conveniently by means of combination injections. Also frequently expedient are such combination injections utilizing the organotherapeutically-indicated biotherapeutic remedy appropriate in each case (e.g., in conjunction with Hepeel). It often occurs that several suis-organ preparations are indicated in a single patient. This is best performed by syringe, either simultaneously by means of a combination injection, or injected periodically in alternation.
Application of suis-organ preparations through i.v. injection should be initially exercised with restraint. This mode of administration is to be employed only ensuing comparatively lengthy i.m., s.c. or i.d. injection (see above!).
Prior to using the organotherapeutically indicated suis-organ preparation, it is advisable in many cases to apply the corresponding, functionally underlying suis-organ preparation with toxic cleansing (=channeling) action for a period of 2 to 3 weeks, i.e., for the treatment of hepatic disorders, Vesica fellea suis prior to Hepar suis, of the renal disorders Vesica urinaria suis and Ureter suis, as well as Pyelon suis prior to Ren suis etc. In case of severe toxic affliction, the most expedient procedure is to precede usage of the specially indicated suis-organ preparation with application of the organ preparation Colon suis D10, D30, D200 (1-2x weekly i.m. or s.c. for 2 to 3 weeks). Colon suis is beneficial here as it supports and normalizes the eliminatory function of the intestine.
Employment of suis-organ preparations in progressive auto-sanguis therapy
This is appropriate, for example, in treating iatrogenic damage, toxic hepatic damage, migraine, chronic eczema, bronchial asthma, duodenal and ventricular ulcers, arthrosis, as well as lymphatism. See also the related data on hyperimmunization-therapy employing suis-organ preparations (page 44).
Applicational restrictions
Since immunological mechanisms are stimulated through the suis-organ preparations, a stimulative action of the suis-organ preparations is frequently no longer expected in cases of pronounced cachexia and/or marasmus. On the other hand, a possibly occurring focal reaction during the degradation of damaged cells can endanger cachectic and marantic patients in certain circumstances.
Forms in which suis-organ preparations are supplied
For parenteral (and possibly oral; see point 4!) organotherapy, the suis-organ preparations are available in ampoules of 1.1 ml as potency chords in two degrees of strength: as the potency chord D10, D30, and D200, and as the forte form with potency chords D8, D12, D30, and D200. A number of suis-organ preparations are available as single potencies D6 and D200; these are also supplied in ampoules of 1,1 ml. each.
Constituents
In order to conserve space, the entries below have been presented in condensed form. Both degrees of strength – identified in each case through the corresponding addendum ”Injeel” or ”Injeel forte” – contain potency chords and volumes as indicated above.
Example:
Aorta suis-Injeel 1,1 ml injection solution cont.: 0,367 ml each of Aorta suis D10, Aorta suis D30, Aorta suis D200 Aorta suis-Injeel forte 1,1 ml. injection solution cont.: 0,275 ml each of
Aorta suis D8, Aorta suis D12, Aorta suis D30, Aorta suis D200. 1,1 ml. injection solution cont.: 0,275 ml each of Aorta suis D8, Aorta suis D12, Aorta suis D30, Aorta suis D200.Arteria suis-Injeel 1,1 ml injection solution cont.: 0,367 ml each of Arteria suis D10, Arteria suis D30,
Arteria suis D200Arteria suis-Injeel forte 1,1 ml injection solution cont.: 0,275 ml each of
Arteria suis D8, Arteria suis D10, Arteria suis D30, Arteris suis D200.All the suis-organ preparations are formulated in the same general pattern as illustrated here. Prescriptions should always bear the precise designation ”Injeel” or ”Injeel forte” in order to facilitate acquisition of the proper medication through the chemist and wholesaler.
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Catalysts
The use of catalysts of the intermediary metabolism is a specialty of the anti-homotoxic therapy. The substances designated as intermediary catalysts are physiological constituents of cellular respiration and energy production (citric acid cycle, redox systems). In part these are also substances which are formed during other enzymatic conver-sions and/or are catalytically effective in these processes. Damage to enzyme systems is frequently of iatrogenic nature because many conventional pharmaceutical medications are based on the inhibition of enzymes as the active principle. Enzymes especially are impeded in their activity by increasing environmental stress (e.g., by heavy metals or pesticides). Due to the deficiency of enzyme function a backup of metabolites present before the respective enzymatic reaction occurs as well as a lack of substrates to be metabolized after this reaction.
The administration of the corresponding catalysts in homoeopathic preparations is based upon the concept that the metabolic process is activated and that blocked cell or enzyme functions are reactivated. Since enzyme damage expresses itself as chronic and/or degenerative diseases, the application of catalysts is therefore primarily indicated for such diseases.
Catalysts are substances which accelerate the equilibration of chemical reactions without disturbing the balance of the process themselves. The extent to which a catalyst is able to accelerate a reaction is impressive. An increase of the reaction speed by six decimal powers is not uncommon, since one single enzyme molecule is often capable of converting more than 10,000 substrate molecules per second. At the end of a reaction the catalyst remains unchanged and is again available to immediately catalyse the same reaction on the next molecule. The described process is designated as catalysis. When the reactions occur in bio-systems, they are referred to as ”bio-catalysts.“
The catalysis may be additionally increased by activators, but it also may be reduced or blocked by ”poisons“ (homotoxins). The citric acid cycle is the ”turntable of metabolism,“ which represents the principal path of the catabolic metabolism of the pyruvate and/or the acetyl co-enzyme A. It is a basic, closed, reaction path present in humans, animals, and plants; the cleavage products of the carbohydrate metabolism, the oxidative carbohydrate metabolism, the oxidative decomposition of fatty acids and – after transamination – the cleavage products from the protein metabolism as well all end in it. Furthermore, it supplies important elements for synthesis of the organism. In conjunction with the respiratory chain the citric acid cycle is simultaneously the most significant source of energy for the metabolic process. It supplies the hydrogen for the biological oxidation and is thus closely linked to the energy metabolism of the cells.
The elements of the citric acid cycle are Acidum citricum (citric acid), Acidum cis- aconiticum (cis-aconitic acid), Axidum oxalsuccinicum (oxalosuccinic acid), Acidum a- ketoglutaricum (a-ketoglutaric acid), Acidum succinicum (succinic acid), Acidum fumaricum (fumaric acid), Acidum DL-malicum (malic acid) and the salt Natrium oxalaceticum (oxalo-acetic sodium).
The transformation of one carboxylic acid into the next within the citric acid cycle is mediated by enzymes. The involved enzymes may be inhibited conditionally by noxae (e. g., competitive inhibition, final product inhibition, substrate inhibition), which can lead to concentration variations of single acids of the citric acid cycle. This can in turn trigger reactions or blockades with consecutive symptoms or disease manifestations in various tissues.
It must be taken into consideration that catalysts can only act when the milieu is correct. In control systems and metabolic chains not only the hydrogen ion concentration (pH-value) is involved, but the corresponding substrates and ”co-factors“ must also be available. The co-factors include vitamins and trace elements, including certain metal ions. Some catalysts have to be activated first by these co-factors to render them functionable. Metal enzyme complexes are frequently referred to as metallo-enzymes. Some of these metal ions are ”two-faced“ and while enabling the catalysis in small doses, in larger doses they may inhibit or block functions.
For therapeutic application, the term ”catalyst“ is more broadly defined than in physiological contexts; it includes catalysts in a strict sense (enzymes) as well as the respective substrates, intermediary products, and co-factors.
The available preparations may be classified into three groups:
Group A: Acids of the citric-acid cycle and their salts.
Group B: Quinones and their derivatives as well as other intermediary respiratory catalysts.
Group C: Compounds which effect stimulation: biogenic amines, hormones, elements (cerium), botanical extracts (anthocyanins).
General Recommendations
The implementation of bio-catalysts has a strong stimulative effect on patients (e. g., severe tiredness after administration of the remedy). It is recommended to drink at least 2 to 3 liters during the first three days of treatment and to extense refrain from physical activities as well. In addition a low toxin diet is desirable. Signs of a regressive vicariation should not be suppressed but rather excreted through the assistance of biological therapeutic remedies.
Exact timing is of the greatest importance for the implementation of catalysts. False timing may trigger progressive vicariations in some cases. This phenomenon occurs when the body is in an extremely unstable condition or is too weak to be subjected to a stimulation therapy. It must be particularly ensured with patients in a weakened condition that the treatment is very slowly commenced and is not applied with massive doses of remedies.
Example: Begin with 1/2 ampoule orally 2x weekly or 2x weekly dissolve 1 ampoule in 1 1/2 liters of water and drink this solution in small sips throughout the day. The bio- catalysts frequently achieve the desired effect without the occurrence of severe healing crises.
For all catalyst preparations of Group B, a repetition of injections should only be conducted after subsidence of the possible occurrence of initial aggravation and always when complaints recur. Furthermore, a proper drainage is important, that is, for patients with severe toxic affliction, the endogenic defence system should be mobilized before the therapy with catalysts.
Three phases of the bio-regulation therapy can generally be distinguished:
- Stabilization of the disease process, that is, treatment of possible inflammatory processes, whereby, in certain cases, the conventional therapy may not be dis- continued immediately. A stabilization can be achieved through a diet, sensible life style, sufficient exercise, support of the endogenic defence system, etc.
- Supplementation of deficient substances, including vitamins and trace elements, as well as the treatment of present dysbiosis. A weakened organism with severe deficiencies and dysbiosis must be treated first with parenteral vitamin pre- parations. With regard to mineral and trace elements, particularly zinc, calcium, potassium, and magnesium are important.
- Surgical treatment; removal of inflammation centres: e.g., tooth extraction, sanitation of the paranal sinus, removal of amalgam, etc.
Group A catalysts
Acids of the citric acid cycle and/or their salts
General Information
Control systems and metabolic chains can only fulfil their function when all links of the chain are intact; this means for physiological processes that the initial substrate, enzymes, and intermediary products must be adjusted to each other for the individual metabolic process steps (e.g., citric acid cycle). Functional disorders can be generated in the material or dynamic area; the consequences are always reciprocal. The following constellations result there from:
- The initial substrate is quantitatively insufficient or qualitatively altered. Based on the Michaelis Menten relation of the dependency of the catalytic reaction on the available substrate, a dysregulation is given at the initial step.
- An insufficient quantity of the enzyme is available or it is completely lacking. The metabolic process is impeded or obstructed at this point. The product to be catalysed is either insufficiently or not formed at all – the metabolic process chain is weakened or interrupted.
These basic processes occur at many points in metabolic process chains. The cited performance of the chain is always determined by the weakest link – substrate, enzyme, or intermediary product. Due to the situation that, after every enzymatic dysfunction, the subsequent product to be catalysed is no longer sufficiently formed, the intermediary products play an essential role in the further course of the chain reaction. Therefore, during therapy, enzymatic defects should not only be affected with the lacking or deficient enzyme – when at all possible – but should also be specifically treated with the intermediary products behind the enzyme obstruction.
Several enzyme reactions require magnesium or manganese ions as additional activators. Thus, all kinase reactions require magnesium ions for the phosphate transfer, whereas alkaline phosphatases are activated by magnesium and manganese ions and peptidases by manganese. In many cases the magnesium ions can be replaced by manganese ions when necessary. Thus, it makes sense and is understandable that specific therapy with the intermediary catalysts of the citric acid cycle is initiated or combined with an injection of magnesium and manganese ions as phosphate compounds due to the significance of the anorganic phosphate.
Fields of application
All diseases classified as cellular phases (degeneration phases, dedifferentiation phases) and which are consequently characterized by defective enzymatic control, blockages and/or defective cellular oxidation, e.g.:
- Paresis, neuralgia, toxic neuritis, vegetative dystonia, migraine
- Dermatosis, neurodermitis, pruritus (including pruritus vulvae), psoriasis, vitiligo, pemphigus, sclerodermia
- Bronchial asthma
- Gastric and duodenal ulcer, hepatosis, cirrhosis of the liver and injurious hepatic disorders, pancreopathy
- Nephropathy, e.g., nephrosis and chronic nephritis
- Myocardial impairment, angina pectoris, treatment subsequent to myocardial infarction, arteriosclerosis, cerebral sclerosis
- Dysfunction and dysregulation of endocrine glands, e.g., diabetes mellitus, dysthyroidism
- Precancerous and dedifferentiation phases (previously: neoplasm phases) within any tissue whatsoever
- During and ensuing X-ray and radioactive exposure (several enzymes, e.g. the maleate dehydrogenase, are sensitive to radiation)
- Thrombocytopenia, leucopenia
Dosage
Most expedient is the injection of the individual acids of the citric acid cycle and/or their salts in the sequence in which they are generated within the cell during the course of metabolism to reach all possibly existing defects, obstructions, and instances of faulty regulation. It is advisable in such therapy to inject two to three acids (and/or their salts) simultaneously in the form of a combination injection. For reasons of practicality, these injections are best applied either s.c. or i.m.
As magnesium and manganese ions activate a number of enzymatic processes – the kinase reactions in particular, during which phosphate transfer occurs (see subsection
General Information) – the Magnesium-Manganum-phosphoricum-Injeel included in the combination pack is to be administered with the initial (combined) injection.
The injections are generally applied 1-2x weekly. Upon completion of a series – i.e., after 4 combination injections (see below) – catalyst therapy may possibly require interpolation by a treatment-free interval of 2 to 4 weeks until the injections’ effects have subsided. During this period, however, the indicated anti-homotoxic preparations (Injeels, Homaccords, and other Heel combination preparations, as well as suis-organ preparations and nosodes) are to be applied. Indeed these may also be employed in conjunction with the acids/salts of the citric acid cycle even during the injection period.
During the intake of a homoeopathic remedy present symptoms may be temporarily aggravated (initial aggravation). The patient is advised to consult his/her therapist.
Plan of subcutaneous injections
After an application-free interval of 2 to 4 weeks, repetition of this series of injections. Each acid and/or its salt may be injected separately and repetitively in the Injeel-forte form as well. This is indicated primarily when a particularly effective action during one of the combined injections listed above (1 to 4) was achieved. The ampoules contained in this combination should subsequently be applied individually.
The diet should include ample fresh fruit, grape juice, bilberries, and beet root. The latter are rich in anthocyanins (activators of cellular respiration, hydrogen acceptors); also refer to intermediary catalysts, Group C: Myrtillus, Beta vulgaris rubra!
Package sizes
Packages containing 5, 10, 50 and 100 ampoules of 1,1 ml each.
Citric-Acid-Cycle combination pack (contains 9 ampoules of single constituent Injeels + 1 ampoule Magnesium Manganum-phosphoricum-Injeel).
List of group A catalysts
The Injeel preparations contain the following potency chord in all preparations: D10, D30, D200 0,367 ml each. Exception: Magnesium-Manganum-phosphoricum-Injeel D12, D30, D200.
The Injeel forte preparations contain the following potency chord in all preparations D6, D12, D30, D200 0,275 ml each.
Acidum cis-aconiticum-Injeel forte
Acidum succinicum-Injeel forte
Acidum succinicum D4
Acidum citricum-Injeel
Baryum oxalsuccinicum-Injeel forte
Magnesium-Manganum-phosphoricum-Injeel
Acidum fumaricum D6
Magnesium-Manganum-phosphoricum-Injeel forte
Acidum a-ketoglutaricum-Injeel
Natrium oxalaceticum-Injeel
Acidum a-ketoglutaricum-Injeel forte
Natrium oxalaceticum-Injeel forte
Acidum DL-malicum-Injeel forte
Natrium pyruvicum-Injeel forte
Group B catalysts
Quinones as well as other intermediary respiratory catalysts
General information
Organic compounds which contain one or several carbonyl groups (> C=O) play an important role in electron transfer processes such as cellular respiration and redox reactions without direct O2-involvement. These compounds include quinones, hydroquinones, aldehydes, ketones, and carboxylic acids.
Electron transfers which involve oxygen contain radical intermediates. Radicals can counteract condensation processes as they occur in the impregnation, degeneration, and dedifferentiation (neoplasm) phases in particular. Free radicals are short-lived, highly reactive products of metabolism which contain one or more unpaired electrons (molecules, atoms, and ions). In the 1930s William Koch introduced free radicals and the catalytic effects into medicinal research and employed them successfully for the healing of diverse diseases. At that time, the knowledge of the existence of free radicals was developed based on his research.
The quinones possess the special ability to neutralize oxygen radicals. A quinone therapy improves the cellular respiration (biological oxidation).
Toxins which must be removed during the course of a lifetime can be decomposed by oxidation as well. Oxidation signifies the consumption of oxygen and subsequently, the existence of risk of an inefficient metabolism. It is possible to treat the consequences of a faulty regulation with quinones. Quinone therapy sets high standards on the toxic defence system of the organism. The support of the toxin defence system and a deliberate excretion therapy are important. Bonded amino groups can be transferred to carbonyl groups by transamination and are thus mobilized.
The quinones and methylene blue have certain characteristics in common. For example, both possess the capability of representing the enzyme succino-dehydrogenase (dehydrogenation of succinic acid into fumaric acid) under anaerobic conditions. Without oxygen, methylene blue can serve in place of this enzyme as an electron acceptor.
Fields of application
The preparations within Group B are to be applied preferably for clinical syndromes and/or cellular phases to the right of the Biological Division, i.e., for impregnation, degeneration, and dedifferentiation phases (previously: neoplasm phases).
Dosage
Dosage must always be determined on an individual basis, depending on each patient’s findings, state of health, and individual response to these preparations, which can vary considerably from case to case – even in instances of identical diagnosis! It is generally advisable to apply the catalyst preparations of Group B once, perhaps twice, weekly (i.m., s.c., i.c.; when required also in the corresponding acupuncture points and possibly i.v.).
We wish to point out that, as with the nosodes, catalyst preparations from Group B may also be advantageously employed in the therapy of cellular phases by administering them in conjunction with those preparations required otherwise.
Special therapeutic stipulations
- As a rule, Glyoxal and Methylglyoxal should be applied relatively seldom. For this reason, these two preparations should always be allotted an extensive period of time in which to expend their after-effects.
- In cases requiring the use of para-benzoquinone, it is advisable to precede such treatment with approximately 3 applications of hydroquinone
- Quinhydrone should be coupled with a homoeopathic metal preparation, e.g., with Aurum-Injeel, Argentum-Injeel, or Ferrum metallicum-Injeel.
Package sizes
Packages containing 5, 10, 50 and 100 ampoules 1.1 ml each.
List of group B catalysts
The Injeel preparations contain the following potency chord in all preparations: D12, D30, D200 0.367 ml each.
The Injeel-forte preparations contain the following potency chord in all preparations D8, D12, D30, D200 0,275 ml each.
Anthrachinon-Injeel
Naphthochinon-Injeel
Anthrachinon-Injeel forte
Naphthochinon-Injeel forte
Chinhydron-Injeel
Para-Benzochinon-Injeel
Chinhydron-Injeel forte
Para-Benzochinon-Injeel forte
Glyoxal-Injeel
Trichinoyl-Injeel
Hydrochinon-Injeel
Trichinoyl-Injeel forte
Hydrochinon-Injeel forte
Ubichinon-Injeel
Methylenblau-Injeel
Ubichinon-Injeel forte
Methylenblau-Injeel forte
Ubichinon D6; D30
Methylglyoxal-Injeel
Group C catalysts
Other compounds with stimulative action
General Information
Other compounds with stimulative action and catalytic effects on metabolic and respiratory functions include:
Homoeopathically prepared vitamins of the vitamin B-group as well as of vitamin A and vitamin C (in lowest potency D6, respectively) – as co-factors and/or co-enzymes; compounds with other stimulative and catalytic effects, e.g., biogenic amines such as adrenaline, serotonine (5-hydroxi-tryptamine) and histamine (4-(2’-aminoethyl)-imidazol) and/or their precursors such as the amino acids tryptophane (b-indolalanine = precursor of serotonine) and histidine (b-imidazolalanine and/or b-imidazolylalanine = precursor of histamine) as well as the amino acids cysteine (contains sulphur), Acidum L(+) asparagicum and Acidum glutaminicum, further the degradation products of tryptophane indole and scatole (b-methylindole) and the amino acid derivatives guanidine (Imino-urea) and methylguanidine as well as anthozyanins (activators of cell respiration; hydrogen acceptors) and elements (trace element factors), e.g., cesium and cerium (redox catalytic action).
Dosage
Generally, injections are administered 1-2x weekly. The injection of one or several catalysts is only repeated after the effect of the previous injection has subsided. As the healing consolidates injections are generally more seldom required.
Package sizes
Packages containing 5, 10, 50 and 100 ampoules 1,1 ml each. List of group C catalysts
Nosode preparations
Definition of nosode preparations
Nosodes are disease triggering agents whose virulence or toxicity was eliminated through homoeopathic processing, but whose information fully attains the recognition mechanisms and enables corresponding stimulation which promotes healing. We differentiate between auto-nosode preparations and hetero-nosode preparations.
Auto-nosode preparations
These are substances gained from the patient’s own organism such as blood, urine, lachrymal fluid, sputum, pus, stools, or diseased tissue. The initial substances are homoeopathically adjusted and applied to the same patient.
Hetero-nosode preparations
These are substances which do not originate from the own organism. There are:
Viral nosode preparations e.g. e.g.
Herpes zoster-Nosode
Coxsackie A9 and/or Coxsackie B4Bacterial nosode preparations e.g. Tuberculinum
Staphylococcinum StreptococcinumVaccine-nosode preparations
(from microorganisms or vaccines)e.g. Influenza nosode Rabies vaccine Rubeola vaccine Tissue nosodes (from pathologically altered organs and/or tissues and products of metabolism including body secretions) e.g.
Gastritis-Nosode Tonsillitis-Nosode Sinusitis-Nosode
Mastopathia cystica-NosodeSource material
Nosodes are preparations produced according to a homoeopathic processing technique from pathologically altered organs or organic constituents of human or animal origin, further, from non-living cultures of micro-organisms, decomposition products of animal origin, or from bodily fluids containing pathogens or pathological products, e.g., liquor, or puncture liquid. The identity of the source material is verified by a protocol of the specialist’s findings of the operation material or laboratory results and, when required, by certificates of the suppliers of the bacteria and viruses. The HAB (German Homoeopathic Pharmacopoeia) stipulates that the base material for nosode preparations is first sterilized and that it afterwards complies with the sterility control pursuant to the German Pharmacopoeia (DAB 10). The homoeopathic processing is only conducted upon completion of these prerequisites. Nosode preparations are, therefore, neither vaccines, nor sera, nor other such agents; they are remedies exclusively and purely of a homoeopathic nature. Mother tinctures are manufactured from this source material according to regulations 43 or 44.
The definition of the nosode preparations conforms to the definition of material stipulated in § 3 of the German Drug Law, particularly in items 3 and 4. Thus substances within the meaning of the law are:
- Chemical elements
- Plants and botanical components
- Bodies of animals, including those of living animals as well as body parts, com- ponents thereof and metabolic products of human or animal origin in a proces- sed state
- Microorganisms including viruses as well as their components or metabolic products
There are two different directives for the production of nosode preparations, namely the HAB 1 (German Homoeopathic Pharmacopoeia) specification 43 for mother tinctures from pathologically altered organs or organic components of human or animal origin and specification 44 for mother tinctures from non-living cultures of microorganisms or from decomposition products of animal organs or from bodily fluids containing pathogens or pathological products.
The following examples illustrate the production of nosode preparations:
Viral nosode preparations
Coxsackie-Virus-B4-Nosode This is produced from dead Coxsackie-B4 viruses adjusted to 109 plaque-forming units per milliliter. Herpes Zoster-Nosode This is produced from dead Herpes-Zoster viruses adjusted to 106 plaque-forming units per milliliter Bacterial nosode preparations
Bacterium coli-Nosode This is a preparation produced from Escherichia-coli bacteria cultures adjusted to a specific titer (107 KBE/g). Bacterium lactis aerogenes-Nosode This is a nosode preparation produced
from an Enterobacter-aerogenes bacteria culture (107 KBE/g).Tissue nosodes
Tonsillitis-Nosode This is produced from surgically removed inflamed tonsils (Tonsilla palatina). Gastritis-Nosode This is produced from gastric mucous removed surgically from a gastritis patient Sinusitis-Nosode This is a mucous mass gained from inflamed sinuses. Otitis media-Nosode The source material is pus from patients suffering from a middle ear infection General application information
Nosode preparations are applied according to the
- symptomatic/anamnestic similarity (simile principle) and
- applied at the end and/or after a previously overcome acute illness.
The following remarks refer to the above items:
To a.
The application of the nosode preparations should be administered according to the symptomatic similarity, that on the basis of the fundamental homoeopathic rules of similitude and/or according to the anamnestic etiological similarity to a past illness which has apparently since been cured. The preparation Diphtheria-Nosode (Diphtherinum-Injeel and forte), for example, is not employed primo loco in treatment of acute diphtheria – which would correspond to a similarity to a developing acute infection – but rather for the treatment of cardiac diseases displaying similar symptoms as are present in a heart damaged by diphtheria (= symptomatic similarity) and/or for the treatment of heart-disease patients whose case history includes diphtheria (= anamnestic etiological similarity).
The following is important when employing nosode preparations under the aspect of current etiological similarities:
All nosodes may be used specifically, i.e., as isotherapeutic agents of the corresponding affections from which they were developed. Generally, they are administered in this case as an intermediary remedy in addition to the indicated homoeopathic remedies, whereby particularly excretive, matrix-channeling anti-homotoxic remedies, (e.g. Lymphomyosot, Galium-Heel), play an important role.
To b.
After the disease has been overcome, nosodes are excellent to induce the toxins deposited in the matrix to be excreted more rapidly. Quite frequently, the toxins removed through this technique are not the sole causative agents but also remnant deposits of contagion with latent pathogenic foci as well as colonies of agents which are no longer pathogenic (sources of continuous exudation). This applies particularly with regards to the infectious diseases such as measles, rubella, varicella, influenza, erysipelas, scarlet fever, typhoid fever, diphtheria etc. It can also be assumed that the specific defence processes against the pathogens are reinduced by the nosode preparations. The clinical confirmation of this immuno-modulative effect is found in the regression of currently forced antibody formations as the expression of the incomplete toxin release of the pathogens. Thus the normalization of a pathologically increased antistreptolysin titer is frequently observed after the application of the streptococcus nosode.
Indications for a nosode therapy
- Chronically exudative diseases
- Chronically proliferative diseases
- Degenerative diseases
- Auto-aggression diseases (Caution!)
- Iatrogenic damages
Nosodes may be designated as terrain remedies. Therefore, they are particularly indicated for the treatment of dyscrasia, i.e., constitutional diseases and/or summation states of integrating and/or integrated dispositions. In terms of Homotoxicology, they are useful for cellular phases, especially for re-toxically inhibited phases, for the treatment of auto- aggression diseases (Caution!), of psoric diseases according to Hahnemann, as well as allergies. Auto-aggression diseases should only be treated after corresponding pre- treatment, such as excretion therapies with matrix-channeling anti-homotoxic remedies. Nosodes are not only indicated however for cellular phases but also frequently for humoral phases, particularly when a dyscrasic component is involved or complications threaten to arise or in case of reduced immunopotency.
The effect of nosodes results in terms of a positive vicariation in detoxification and excretion of homotoxins. This signifies simultaneously an increase of the self-healing processes controlled by the defence system. In most cases a summation of known and possibly unknown poisonous substances (homotoxins) is to be assumed, and based on this knowledge is also the necessity and justification of a simultaneous application of a series of nosodes (e.g., Diphtherinum + Psorinum + Medorrhinum), which are to be applied possibly in conjunction with other single-constituent Injeels, combination preparations etc. as a broad spectrum anti-homotoxic remedy in order to cleanse the cited terrain.
Psorinoheel N (drops, ampoules) is, for example, such a broad spectrum nosode preparation which also contains, aside from the two Psora-nosode preparations (Psorinum and Medorrhinum), vaccininum and bacillinum, furthermore two constitution remedies (sulphur and thuja) and a series of additional homoeopathic remedies. This combination preparation is primarily indicated for the phases of the constitution, i.e., for the cellular phases, as well as for the disposition phases or humoral phases. In case of unclear clinical syndromes and/or clinical syndromes which cannot be immediately clarified, with regard to the anamnestic etiological similarity as well as with regard to the symptomatic similarity, it is frequently advisable to include such a combination preparation based on nosodes in the therapy plan particularly for the cellular phases.
Nosodes exercise a profound constitutional effect. Virtually every type of therapy can be effectively reinforced with nosode preparations. They frequently fulfil the role of a missing link in a chain of therapeutic reactions, whereby cure without nosodes is inconclusive or can only be achieved with extreme difficulty. The effect occurs thereby via subliminal antigen-antibody-reactions as well as via the homoeopathic counteracting mechanism of co-repressors.
Dosage
As a matter of principle, dosage is always to be determined strictly on an individual basis, depending upon each patient’s findings, state of health and particular response to each of the nosode preparations, all of which can vary considerably from case to case. In general, dosage consists of 1 ampoule, administered 1 to a maximum of 3x weekly. The duration of therapy with nosode preparations is also to be determined individually, and is to be adjusted in keeping with each given case. A brief interval of treatment (approximately 2 – 4 weeks) is recommended when applied in the aftermath of an acute affection, whereas chronic disorders should receive therapy over a relatively extensive period (approximately 6 months) depending upon the individual reactive condition of each patient.
It is recommended to begin nosode therapy with the normal Injeel form, later adopting application of the forte form, particularly when the corresponding reactions or improvements should fail to materialize as anticipated. In the event the Injeel-forte form should also fall short of achieving the desired therapeutic success, low single potencies are then to be applied.
For example, Anthracinum-Injeel in single potency D10 is several potencies lower than Anthracinum-Injeel forte, which contains the potency chord D15, D20, D30, D200. Bacterium coli in single potency D5 is one potency lower than Bacterium coli-Injeel forte, which applies for several other ”bacterial“ nosode preparations, e.g., also for Bacterium lactis aerogenes, Bacterium proteus, Bacterium pyocyaneus, and Brucella abortus Bang.
Higher potencies (single higher potencies) should only be employed when excessive reactions occur to the normal Injeel form of the corresponding nosode preparations. Thus, Variolinum in single potency D200 and/or D1000 and/or Vaccininum in single potency
D200 will be employed when excessive reactions to Variolinum-Injeel (D20, D30, D200) and/or to Vaccininum-Injeel (D20, D30, D200) occur once.
The following rule for treatment in general is particularly true in regard to nosode therapy: The higher potencies (D12, D30, etc.) are indicated for treating:
- increased irritability (Arsenic, Phosphate, Iodine or Chamomile Type)
- diathesis
- allergy and
- chronic disorders
The lower potencies (approximately D6/D8 and lower) are indicated in treatment of affections which are more or less acute:
- slow-reacting types of individuals (Sepia, Nux-vomica, Graphites, Silicea types)
- when organotropic action on a specific organ is desired (e.g., the tonsils: Tonsillarpfröpfe-Injeel forte and/or Tonsillitis Nosode-Injeel forte, each in potency chords D6, D10, D30 and D200).
Indications for higher potencies generally require relatively lengthy intervals of up to several weeks’ duration between applications.
Conversely, indications for lower potencies usually require only brief periods between applications, approximately 3 doses per week.
The recommended procedure is to commence administration by means of i.m., s.c. or i.d. injection (neural and/or acupuncture points); only in the event that this mode of application fails to evoke response may the corresponding nosode be administered i.v. in appropriate cases.
The application of the nosode Injeels during a progressive auto-sanguis therapy is advantageous. The nosodes should however always be applied during the last stage.
Note on dosage and potentization of nosodes in therapy of children
No essential difference exists between the dosage of nosode preparations and that of other homoeopathic agents in treating young patients, i.e., children receive a (somewhat) smaller dose than the adult patients.
Dosage (per application) for children:
0– 1 years of age approximately 0,3 ml 1– 6 years of age approximately 0,5 ml 6–12 years of age approximately 0,6 ml > 12 adult dosage For children, the lower potencies of D4 – D8 are administered at the beginning of therapy as well as in treatment of affections which are more or less acute; thus the same procedures are followed as for adults. Likewise, the higher potencies (approximately D12– D30) are used in both child and adult patients ensuing initial treatment with lower potencies (D4 – D8) and/or for therapy of chronic affections. Thus the same particulars apply for children in regard to potentization as they do in treatment of adults.
General
In their capacity as ”terrain remedies,” nosodes provide effective reinforcement for virtually every type of therapy. Nosodes frequently fulfil the role of a missing link in a series or chain of therapeutic reactions, whereby cure without the nosode is inconclusive or can be attained only under extreme difficulty. From a homotoxicological aspect, nosodes are chiefly applied in order to transform cellular phases into humoral phases, i.e., in order to achieve regressive vicariation. Nosodes are indicated in treatment of humoral phases as well, especially in cases which are in jeopardy of lapsing into a chronic condition such as in which there is impending danger of progressive vicariation.
Therapists working in the field of electro-acupuncture find the use of nosodes especially interesting due to the capabilities of such specialists to precisely determine the corresponding nosodes through the technique of medicinal testing. Thus therapy with nosodes is exceptionally effective in combining ”apparatus medicine” by means of the above-mentioned medicinal testing (bioelectric technique of drug determination), where appropriate, with the therapist’s ”eye for clinical diagnosis” or ”visual diagnosis.” Here, as always, the nosodes are to be administered according to symptomatic similarity, i.e., on the basis of the fundamental homoeopathic rules of similitude and employing the ”diagnostic aid” provided by the anamnesis, whereby any anamnestic, etiological similarity to a past, apparently cured illness is also taken into consideration. One should bear in mind in this respect that the extraordinarily good diagnostician and the excellent therapist is often recognizable by his or her ability to compile a skilful and accurate anamnesis.
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Single Constituent Preparations and Classical Homeopathic Remedies
Single-constituent homoeopathic preparations
Available both in Injeel (Injection-remedy Heel) and in single-potency form, these homoeopathic single-remedy agents may be subcutaneously injected, i.m., s.c., i.d. (segment therapy) or i.v. All single-constituent preparations and Injeels may also be administered orally in water or tea (see chapter C, section 2, page 439), an attribute particularly suitable for treatment of infants and small children. Each ampoule of an Injeel comprises several potencies of the same basic remedy in parallel existence to one another within a potency chord.
The basic potency of an Injeel is generally D10 or D12, with equal parts of D30 and D200 as additional components. As a rule, Injeels of the ”forte” type contain equal parts of (D4), D6, D12, D30, D200 and possibly D1000. With the administration of a potency chord the organism is addressed on several hierarchical levels, namely on the organotropic level by the low potency, on the functiotropic level by the medium potency, and on the ”informative“ or ”mental“ level with the assistance of the higher potency.
Since, particularly during the course of regressive vicariations of chronic or severe illnesses of phases 4, 5 or even 6, considerable functional and informative errors occur in addition to the macroscopically detectable organic-structural errors, such potency chord preparations are also suited for the excretion of cellular illnesses due to the high potencies contained therein.
The principle of the potency chord is that any adverse reaction which may occur upon application of lower potencies of a medicinal agent can be mitigated and reduced through the simultaneous administration of higher potencies of the same medication (high-potency inverse effect). As a rule, treatment should always commence with simultaneous application of single-remedy Injeels, catalysts, and specialized preparations. The forte forms are to be administered in treatment of acute disease and illnesses which have become organically detectable.
Classical homoeopathic remedies
Anti-homotoxic medicine seldom requires – especially when the indication is obvious – homoeopathic single constituent remedies in single potencies. These single remedies are administered in terms of classical homoeopathy according to the simile principle. In anti- homotoxic medicine these single remedies are available as ampoules. Figure 7 shows an overview of the single remedies in single-potencies (ampoule form), which are available in addition to the single remedies in potency chords, nosodes, suis-organ preparations, etc.
D = X