allergy indications - Heel BHI

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inTroducTion Allergies pose major health problems. Not only does disease-like allergic rhinitis affect 20 to 40 million people annually, it also results in an accumulative 3.8 million lost work and school days. The wide coverage of anti- allergic medicine in the media and on supermarket shelves also alludes to the widespread impact of this condition. The allergic response Allergy represents an inappropriate reaction of an organism to a mostly innocuous substance. Allergens could be seasonal, such as mold, grasses, trees and pollens, as well as perennial (through the year), such as dust mites and animal dander. Irritants, like cigarette smoke and diesel exhaust fumes may promote the allergic response, but are not allergens in themselves. It is important to note that for the immune system to develop an allergic response, the substance needs to possess a peptide sequence or an amino acid sequence. Why is the immune system so vulnerable today? As with the development of all diseases, the development of allergies depends on three factors: genetic predisposition, environmental influences and a trigger. The genetic predisposition has been well studied in patients with allergies. Experiments conducted in the 1920’s already showed that if two parents were allergic, 50% of their offspring would be allergic, and even if one parent was allergic, 30% of thier offspring stood a chance to be allergic. The effects of environmental toxins have been mentioned, but it is also important to note that allergic mediators, such as histamine, are internal toxins and are cleared from the system through liver detoxification. If the liver is overloaded, or missing certain important co-factors, the patient will not be able to remove the histamine from the system, and will have more symptoms of allergy. If certain immunotoxic chemicals are not cleared from the body, and are stored in the matrix, they can contribute to an abnormal immune response. Detoxification and support of the detoxifying organs is an integral part of the homotoxicological approach to allergy. The cytokine environment in the tissues is also of special importance. It is well recognized now that patients with allergies have an immune response which, on a cellular level, is skewed towards a certain reaction, namely a TH2 response. Normally, T-helper cells circulate as T-0 cells, and depending on which antigen it is presented with (via the antigen presenting cells such as macrophages and dendritic cells) it will develop into a TH1 cell, TH2 or a TH3 cell (Figure 2). Fig. 1: The allergic response. Dust Mite The incidence of allergy is increasing and numerous factors have been postulated for this. People living in urban areas are more prone to allergic disease. Environmental factors, such as diesel exhaust fumes, and especially sulfur dioxide, as well as ozone and overcrowding have all been implicated in allergic disease. Environmental toxins like sulfur dioxide not only predispose the immune system to allergy, but also change the quality of the nasal mucosa so that it has a hyper-responsiveness towards allergens. It may also change the structure of an antigen-like pollen so that it becomes more allergenic. These cells secrete different messengers called cytokines, which will then generate the appropriate immune response. In the case of a virus or fungal infection, a TH1 response is preferred. TH1 will generate a cellular immune response via the secretion of the cytokines IFN gamma, Tumor Necrosis Factor IL-2 IFN gamma TNF Inflammation DHEA TGF-ß Inhibition Cortisol IL-4, 13 IL-5 IL-10 Allergy (TNF), and IL-1 to kill these invaders. Antibodies are made when TH2 cells are stimulated, as TH2 cells will activate plasma cells. The TH2 cells secrete other cytokins Interleukin 4, 5, 10, and 13, apart from other cytokins. These cytokines are closely involved in the allergic response, as Interleukin 4 and 13 induce IgE formation, Interleukin 5 enhances the growth of eosinophils and Interleukin 10 promotes mast cell growth (See also the Immunology of Allergy). TH3 helper cells are regulatory T-cells and secrete mainly a cytokine called Transforming Growth Factor beta (TGF-ß), which is an anti-inflammatory that facilitates tissue repair, and may be able to restore the balance between TH1 and TH2. In healthy individuals there is a small daily oscillation between TH1 and TH2 cells, so that the body is always ready to respond in a certain fashion. It is a well known fact that allergic patients are slanted towards a TH2 response. Some patients are born with this skewed response, especially if they are allergic from birth. This means that the immune system will easily go down the TH2 pathway in response to antigens, and cause allergic reactions more easily. Fig. 2: TH1/TH2 balance. In Homotoxicology, we call this skewed response “regulation rigidity” and we should endeavor to restore the normal physiological oscillations between TH1 and TH2 cells. Traumeel has been shown to down regulate the pro-inflammatory cytokines, and to increase TGF-ß, and it is postulated to induce TH3 cells.
Infections with parasites and fungi can also promote the TH2 response. These organisms are mostly eliminated via a TH1 response, but they have developed a mechanism to escape this by pushing the immune system into the TH2 state via some of the surface proteins, like mannan, in the case of fungi. Allergy is often a concomitant finding in these diseases. The hygiene hypothesis is of particular interest, where it is postulated that the modern use of vaccines and antibiotics to ban banal disease (which mostly will mount a TH1 response), results in a skewed immune response towards the allergic (TH2) side. In Homotoxicology, we recognize both the effects of toxins on the organism (in this case the immune system), as well as the dangers of suppressing banal disease in the development of chronic disease and regulation rigidity. The Homotoxicological approach to allergy will focus on three points: • Drainage and detoxification • Treatment of the regulation rigidity of the immune system • Treatment of the symptoms of allergic disease. These three points cause the most distress in patients. The allergic response itself is depicted in the diagram below (Figure 1), and consists of three phases: Phase I: sensitization or priming, Phase II: the Early Allergic Response (EAR), and Phase III: the Late Allergic Response (LAR). Allergy is never seen on the first exposure to an antigen, because the allergic response is a type-I (anaphylactic) response which is mediated by IgE antibodies, and cells such as macrophages, mast cells, T-helper cells (especially TH2 cells), and eosinophils. The first sensitization occur and that the mast cell gets primed with IgE, which is specific for that allergen. The immunology of The allergic response 1. sensitization: It may take up to 4 years for the primed mast cells to reach a critical mass for a specific antigen in a region in order to illicit an allergic response to that antigen. It is important to note that an allergic response may also occur without apparent previous exposure to an antigen, such as penicillin. This is due to cross allergies. The priming or sensitization of the immune system may have taken place via mold in the environment, which has an antigenic similarity to penicillin, and upon exposure to penicillin (a mold) for the first time, the patient may then get an allergic reaction. Cross allergies also exist between food and environmental allergens. For instance, grass pollens cross-react with tomatoes, and seeds of legumes such as peas and beans, and grains while natural latex cross reacts with bananas, avocados and grains. Therefore, a patient eating a lot of bananas may suddenly develop an allergy to latex gloves. 2. The early allergic response (ear) This takes place in the first 2-20 minutes after re-exposure to the antigen and in the presence of enough mast cells primed with IgE to react to that specific antigen. The mediators, such as histamine, increase vascular permeability and an influx of fluid. Leukotrines and prostaglandins cause inflammation. Chemo attractants are responsible for the recruitment of other immune cells, like basophils. The clinical result is itching, sneezing and bronchospasm. 3. The late allergic response (lar) The Late Allergic Response is mediated via the cytokines from the products of the mast cells and TH2 cells, this develops in 4-10 hours after re-exposure. LAR involves the attraction of immune cells and also the maturation of the aforementioned cells. IL5 (from the mast cell and TH2 cell) can induce the growth of eosinophils, which are the main cells associated with the Late Allergic Response. The eosinophils de-granulate and secrete a number of substances, notably major basic protein and other substances like eosinophil derived neurotoxin, and peroxides. This will cause tremendous inflammation, which is the key characteristic of chronic allergy. The Late Allergic Response is responsible for the severity of asthma and is the component that is treated by corticosteroids. It is also the hallmark of diseases such as Chronic Eosinophilic Allergic Sinusitis where the response to a fungus is that of an eosinophilic infiltration, which eventually will give rise to destruction of the mucosa via the major basic protein (Figure 1). homoToxicology and allergy According to the theory of Homotoxicology, disease follows the body’s inability to maintain homeostasis by regulation in the face of a toxin or other aggressor. In this case, the internal toxin is histamine and the dysregulation is the skewed immune response. The actions of histamine upon various tissues can be followed quite well in the body, and offer one of the best examples of a phenomenon called vicariation. Histamine in its different isoforms is active in various tissues like the skin, the mucosal membranes of the nose and lung, as well as in the gastric mucosa, the brain, and even the heart. It is involved in allergic rhinitis in the nose, asthma in the lung, eczema on the skin, ulceration in the gastric mucosa and also plays a part in myocardial infarction. Reckeweg postulated from the work of Constantine Hering and others, that if the normal regulatory mechanisms are suppressed or not successful, toxins such as histamine will cause disease in the body from the outside, inward, or from superficial embryological tissues to deeper ones. This is depicted on the Six-Phase Table of Homotocicology and is called progressive vicariation if it goes deeper and to the right on the table, and regressive vicariation if it moves toward more superficial tissues and the left of the table.
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allergy indications - Heel BHI

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