Guest guest Posted December 28, 2007 Report Share Posted December 28, 2007 THANK YOU DOUG HANEY. > > Happru/All: > > There is only one disturbing thing that I am reading with your comment. An IgE reaction is not an " inflammatory stage. " Medically termed, it is the " allergen " stage or an " allergenic response " as the Merck Manual indicates on Page 1015, Para. 7, 17th Ed. Please, I am not mentioning this to demean your contributions to this Board in any manner, and forgive me should I make you feel as such. However, I am attempting to incorporate/contribute a bit more accuracy. > > I wrote a paper in 2003 which I would like to share with you and others: > > > IMMUNOGLOBULIN TESTING > By R. Haney > Copyright © November 2003 > > > It seems, there is a great deal of confusion and misunderstanding being dispensed throughout the medical community concerning immunoglobulin testing and its specific value and reliability. Recently I received a message from a friend back east who was informed by a well respected Neurotoxicologist that this form of testing, " only determines that a person was once exposed to a particular allergen, and does not determine how current an exposure an allergen exposure is, or when the person was first exposed. " Part of this statement is true, medical science has very little to go on in determining when an initial exposure to a particular allergen occurred, and so medical science must rely upon first-hand accounts of patient histological reporting in order to guess, if need. > > Currently, blood-serum tests of immunoglobulin cells serve as a primary tool for the detection of microfungi activity in the human body. Antibody proteins are referred to medically as " immunoglobulins, " or " Ig. " All immunoglobulins have many common structural features. The antibodies are made of protein " chains " linked together by chemical bonds. These protein chains are termed as " heavy " and " light " chains. There are five different classes of " heavy " immunoglobulin molecule chains referred to collectively in classes as, IgA, IgD, IgE, IgM, and IgG, respectively depending upon their specific functions and activities. > > The class referred to as IgA, is a type of antibody that protects against infections of mucous membranes lining the mouth (sputum), and is observed in the airways, tears, nasal fluids, sweat, genito- urinary and gastro-intestinal tracts, and lung secretions. This is the most common type of immunoglobulin deficiency occurring in approximately 1 of every 400 humans. It protects against bacterial and viral infections. (Primary Source: Mosby's Medical Dictionary, 6th Edition, 2002) > > Very little is known about the specific purpose of the class referred to as IgD. It is found in small amounts of serum tissue. However, IgD is mainly found on the surface of B-lymphocytes (B- cells) developed though bone marrow and are thought regulate B-cell function or development activity. IgD increases in quantity during allergic reactions to milk, insulin, penicillin, and various toxins. (Primary Source: Mosby's Medical Dictionary) > > The most studied class of immunoglobulin antibody is IgE, however its protective role in humans is unclear. IgE is frequently increased in parasitic infestations and atopic individuals (those with a hereditary predisposition to immediately react hyper-allergically to the presence of a specific allergen). It is concentrated in the lungs, skin, and mucous membranes. > > > > The IgE antibody provides the primary defense mechanism against environmental antigens and is believed to be responsive to IgA. IgE reacts with certain antigens to trigger the release of chemical mediators that cause anaphylactic hypersensitivity reactions characterized by wheal and flare. (Primary Source: Mosby's Medical Dictionary) > > The class, IgG is the major antibody found in the blood that is able to penetrate into human tissues. In tracking down antigens, it coats the germs in its ability to attract and assist other immune defense cells seek and destroy them. This protein molecule also maintains the longest attraction mechanisms of the immune process, lasting up to 30 days in duration, and currently is the most persuasive indicator in detecting invasive diseases, e.g., aspergillosis, cancers, etc. It is synthesized in response to " invasions " by bacteria, microfungi, and viruses. IgG crosses the placenta and protects the fetus against red cell antigens and white cell antigens. (Primary Source: Mosby's Medical Dictionary) > The class, IgM is an antibody that remains in the bloodstream where it can kill bacteria that enter the blood stream. Elevated levels of IgM are associated with Waldenstrom's Macrobulinemia, a cancer of mature plasma cells, B-lymphocytes, that causes overproduction of monoclonal macroglobulin (IgM antibody). It is sometimes called a lymphoplasmacytic disorder. It is the largest antibody in molecular structure, is observed in circulating fluids, and is the first immunoglobulin molecule produced, when the biological system of a human is antigenically challenged. IgM triggers the increased production of immunoglobulin G, and the complement fixation required for effective immune response. It is the dominant antibody in the " ABO " blood group incompatibilities. (Primary Source: Mosby's Medical Dictionary) > Immunology is the branch of biomedical science concerned with the body's response and protection against environmental agents that are foreign to the organism; it is also concerned with the body's recognition of self and not self. Immunology encompasses the study and function of the immune system, immunization, organ transplantation, blood banking and immunopathology (diseases of the immune system). > A foreign molecule (i.e. pollen) or molecule(s) on the surface of an infectious agent (i.e. bacteria, fungus, virus, etc.) that elicits an immune response is called an " immunogen. " These are also referred to as antigens. Antibodies are one of nature's most brilliant solutions to the problem of antigens or " foreign " material. Acquired immunity (relatively new in evolutionary terms - present only in vertebrates) is initiated, as the name implies, by initial contact with the foreign agent (immunization). The initial contact triggers a chain of events that leads to the activation of certain cells (lymphocytes) and the production of proteins (antibodies) with specificity against the foreign agent. Antibodies attach themselves to antigens and start the immune response cascade that leads ultimately to the neutralization of the foreign agent. > > > The IgG antibody is the predominant immunoglobulin of internal components such as blood, cerebrospinal fluid and peritoneal fluid (fluid present in the abdominal cavity). IgG is the only class of immunoglobulin that crosses the placenta, conferring the mother's immunity on the fetus. IgG makes up 80% of the total immunoglobulins. It is the smallest immunoglobulin, with a molecular weight of 150 000 Daltons. Thus, it can readily diffuse out of the body's circulation into the tissues. The synthesis of IgG is largely governed by antigen stimulation, so that in germ free animals, IgG levels are very low but rise rapidly on transfer to a normal environment. > IgG, IgM, IgA, IgE, and IgD can be subdivided into subclasses as well. They can differ from one another in that portion of the molecule that binds specifically to the respective antigen type- IgG for instance, that bind only to a " specific " microfungi species, and an IgG type that bind to " another " specific type of microfungi antigen. This of course can also apply to the IgM, IgA, IgE immunoglobulin classes as well. (Primary Source: " Immunoglobulin Explanation " Guy Sherwood, 2001) > The purpose in explaining the Ig testing process involving immunoglobulin classifications is that many people observed as part of our microfungi health-related research consistently demonstrate ELISA Ig testing which tends to increase with each testing, if proper medical treatment is not sought, when a person is adversely affected with a health conditions such as aspergillosis, histoplasmosis, Coccidioidomycosis, etc. > Many medical professionals indicate that the symptoms of microfungi invasion in humans subside as a person moves away from an infested environment into a healthy environment. This is true to an extent as far as symptoms go, but nothing has effectively stopped the invading microbes from continuing to formulate into colonization. Thus, eventually as the human body weakens symptoms tend to reappear later in life (e.g., respiratory problems and sometimes more serious problems as acid reflux disease or pneumonia). This tells me that pathogenic microfungi do not leave the human body willingly and instead continue to grow subtly toward their eventual ability to cause human disease development. > One problem is that colonized microfungi are rarely specifically tested for and do not show up readily in normal blood tests. This is perhaps due to a phenomenon referred to as " molecular mimicry. " Microfungi infestation in humans is often overlooked in the medical profession because few physicians have the time to actively monitor their patient's complete medical history, and many patients fear discussing fungal exposures with their doctor. A person is medically observed, and his/her history reviewed in the doctor's office for perhaps 15 minutes or so, and then their file is usually " shelved " until the doctor reads the patient chart again on their next visit- unless special testing indicates a specific health issue exists. > > > In medical school, future physicians are rarely adequately trained to rule out microfungi as a " causation " factor in the health symptoms of their patients- specifically, they are not taught in-depth, the ecological methods microbes and plant life use to negotiate and perpetuate their own survival. Current medical dogma supports the theory that only seriously ill or immunocompromised patients are subject to major health complications due to mold infestations. This view is seriously flawed in its scope! > One person B.H., living in Arizona and monitored since 1999, with a high IgG count for 9 microfungi species (previously on a medically- supervised treatment program where antifungal drugs " were not prescribed, " and proper nutrient intake and detoxification methods were the focus), clearly demonstrated increasing IgG blood serum microfungi level reactions over several interval IgG antibody tests, even though these same test also showed a dramatic lowering of mycotoxin reactivity as the body was detoxified. > If microfungi are being extracted in the human immune process, under highly controlled medical intervention, as they have been in this patient (i.e., his removal from all microfungi infested environments, elimination of infested food products with a medically monitored and restricted dieting regiment, and an ongoing medically- controlled mycotoxin detoxification and nutritional infusion process), we as observers, might expect a major decrease in the Ig levels of this person as microfungi " die-off. " In this case, the exact opposite was observed as IgG (whose cell life is approximately 30 days) levels for the 9-microfungi species actually increased to exceedingly high concentrations. > This poses a serious question. If IgG individual cell life expectancy is only 30 days, and repeatedly demonstrates a progressive decrease over the course of proper medical treatment, how can doctors continue to believe that once exposed, a patient's immunoglobulin antibody levels will continue indicate exposure to the antigen that was responsible. In other words, if all of the cytotoxic/pathogenic microfungi were killed and a patient became completely recovered how is it possible for the immune system to continue to produce IgG antibody for the antigen? The answer of course is that it would not continue to be produced. The flaw comes in the fact that once a person has been exposed to a specific antigen the immune system now has the immune cell chemistry stored to readily create more IgG antibody in response to the microbial invader, if the IgE antibody fails success in its initial insurgence. The patient B.H., whom I feared for the worse three years ago is now on proper antifungal medication, and is demonstrating marked improvement to both his physical stamina and lowered microfungi species Ig levels. > The Ig testing process confirms two major aspects of contention relating to indoor microfungi exposures. First, those who are demonstrating long term symptoms of cytotoxic and/or pathogenic microfungi exposures, once exposed, are constantly incubating microfungi colonization. > > > Why? It due to the fact that body immunity is constantly being antigenically-challenged by microfungi. Environmentally, microfungi survive and grow unobstructed by a weakened biological biosphere that climatically is controlled by an average 98.6oF degree temperature (actually demonstrates " low-grade " reduction to 97-97.8oF degrees in long term exposed people), and anywhere from a70% or greater, body fluid content. > This is prime territory for microbial growth, and since bacteria are a weaker species ecologically and in the molecular evolutionary process of microbes on earth, it would be normal for people exposed with cytotoxic and/or pathogenic microfungi colonization to have little or no body flora left to control their colonized growth patterns territorially, since nearly every living organism on earth falls prey to the decomposing processes of microfungi in the " Carbon Cycle. " The Ig testing process provides an excellent tool for confirming that this process is taking place and is out of control while an animal or human are still alive. > Additionally, high IgG levels confirm that inflammation is occurring at least within a 30- day period and if consistent testing is involved, currently in the living body. Inflammation is instigated by molecular agitation, leading to friction, and ultimately inflammation. Excreted mycotoxins are definitely a primary source of the inflammation process. Their cytotoxic chemicals (known intracellular poisons) are pathogenically dispensed when sensitized to their ecological niche, leading to only one scientifically observed conclusion, that human cells are increasingly being genetically challenged, deformed, and killed as long as the biochemistry of the human body is unable to successfully control or ultimately destroy their antigenic invaders. > As stated earlier herein, medical science is also aware through a process of " Molecular Mimicry " that microfungi, bacteria, and viruses are readily able and capable of initiating this process, as described through research conducted on the subject. > " What turns the T cells against the Self? Infection often precedes the onset of autoimmune disease, and so scientists have closely scrutinized the tactics that pathogens commonly employ to elude T cells. The answer appears to lie in molecular mimicry, an evolutionary adaptation whereby viruses and bacteria [as well as microfungi as decomposers] attempt to fool the body into granting them free access. Such mimicry works by showing the immune system stretches of amino acids that look like self. " > " An autoimmune response can begin even if the molecular mimicry is not quite exact. Research at the Scripps Research Institute demonstrated that hepatitis B virus polymerase shared a stretch of just six amino acids with a part of the myelin basic protein molecule that causes EAE in rabbits. " > > " When they immunized rabbits with this part of the virus, the animals developed inflammation in their brains. This research suggests that molecular mimicry between bacteria, or viruses [and microfungi], or bacteria, or viruses the self may be critical in initiating autoimmune responses. " (Source: Scientific American, September Issue, 1993, Pg. 109, L. Steinman, M.D., Ph.D., Article: " Autoimmune Disease " ) > > If such is the case, then there is another serious flawed complication with the normal blood testing process that medical doctors rely on currently for proper diagnosis of an " unknown cause, unknown cure " human ailment. If the immune system is not actively searching for specific microfungi because of molecular mimicry, then how is it that Ig blood serum testing is able to determine the levels of antibody to microbes, especially of a particular microfungi species. The answer lies in that Ig tests do not- serum samples are exposed to specific nutrients (media) that in effect " coax " specific microfungi species from the Ig to feed upon and are incubated to form microfungi colonies. The colonies are then counted. The forming of microfungi colonization actually clarifies the specific microfungi species, which are observed via high-powered microscopy. Microfungi can also be cultured from other sources, e.g., sputum, urine, bone marrow and specimens from infected tissues. Tissue invasion verification of microfungi type and level of disease process is presently the best confirmatory method available. > > > I hope that this will provide you with additional insight in to the strange world of immunoglobulins and generate more public interest in learning more about Immunology. > > God Bless and take care, > > Doug Haney > EnviroHealth Research & Consulting, Inc. > Email: _Haney52@... > > > > > > @...: happyru@...: Thu, 27 Dec 2007 23:39:41 +0000Subject: [] EUROPEAN RESPIRATORY REVIEW, 2007 > > > > > Since Mold won't go away, here's an idea ...Looks as if soon, there may be a medication that will just turn off the IgE - inflamatory stage, which is all well and good I would expect for anyone in an emergency situation....but, isn't a " REACTION " just that? You subject your body to something it isn't able to handle and WHAMO! It's the body's WARNING SYSTEM... So, I am... reading this right aren't I? They'll be developing a medication and soon you'll be able to inhale more of the bad stuff???? And shushhhh the body's SOS callhttp://err.ersjournals.com/cgi/content/full/16/104/61 > > > > > > > _________________________________________________________________ > Get the power of Windows + Web with the new Windows Live. > http://www.windowslive.com? ocid=TXT_TAGHM_Wave2_powerofwindows_122007 > > Quote Link to comment Share on other sites More sharing options...
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