A.U.I.T. has a long-term history of benefit. Used for over 15 years by several physicians in the U.S.and taught in immunology courses at Johns Hopkins, it is primarily being done in clinics outside the U.S. now by William Hitt, M.D., Ph.D., retired Professor of Immunology from Johns Hopkins and LSU for over 13 years. He is not in private practice & “semi-retired” in Tijuana, primarily working with the WHO in Addictions research & Immunogenetics. The mechanism of action in this particular type of therapy is similar to Hannemann’s Homeopathic law of cure…Like Cures Like. He is one of our clinical consulting colleagues and a friend…
AUIT has been found clinically effective in the treatment of the following conditions:
ATOPIC DISEASES (reaction occurs in a distant area from contact region) HAYFEVER, GASTROENTERITIS, DERMATITIS, ECZEMA, RASHES FOOD ALLERGY / INTOLERANCE STOMACH ACHES, RASHES, HEADACHES, DIARRHEA, I.B.S., CROHNS, ASTHMA, ARTHRITIS, ETC. CHEMICAL SENSITIVITIES & INTOLERANCE HEADACHES, MIGRAINES, RASHES, ASTHMA, CROHN’S, IRRITABLE BOWEL, ARTHRITIS, ETC. AUTOIMMUNE DISEASE LUPUS, M.S., PARKINSONS, ARTHRITIS, SCLERODERMA, RAYNAUD’S SYNDROME, PSORIASIS, DIABETES, IMMUNE SUPPRESSION CANCER, HIV & RELATED SYNDROMES, ETC.
HIV, HERPES, HEP, HPV, MYCOPLASMA INFECTIONS, ETC.
There is a multiplicity of complicated mechanisms involved. Indeed, urine contains many immunologically active substances, some antigen-specific, some antigen-independent. Both enhancer and suppressor substances are present. The term “immunomodulators” serves well to describe the mechanism of action with AUIT.
TYPE I Hypersensitivity
Many B-lymphocytes exhibit surface antibodies–IgG and IgM. These antibodies differ from circulating antibodies in 2 aspects: 1. They are smaller and in the case of IgM are monomers rather than pentamers. IgG is a suppressor, and IgM is an enhancer. IgG is controlled by two T-Cell suppressor factors (TSF & TSP2). When a B-Cell is stimulated–directed or indirectly–by the proper antigen, surface immunoglobulins multiply and polarize as switching occurs (surface Ig is replaced by specific Ig, which the B-Cell produces and, eventually is secreted by plasma cells), the B-Cell then sheds these surface Ig’s. They then circulate; some are metabolized, but a significant amount appear in the urine via glomerular filtration, where they are cross-linked and denatured (urea, proteases). When reinjected into the adipose tissue (fatty), they ABORT AN ALLERGENIC REACTION IN PROGRESS (i.e. asthma attack) and, as memory cells are produced by REPEATED INJECTIONS, (8-12 or more), a prolonged STATE OF NON-REACTIVITY (Tolerance) is produced. The mechanism of action is dual…One is the immediate stimulation of T-suppressor cells to produce TS1 and TS2. The second long-range action is the production of anti-idiotypes as well as suppressor factors to other antibody-dependent reactions, such as auto-immune disease or drug or transfusion or rejection responses.
TYPE II AND TYPE III (delated sensitivity)
So-called intolerances to foods, chemicals, etc. are mostly antigen-dependent BUT NOT ANTIBODY DEPENDENT(although antibodies are often produced, they become mostly “innocent bystanders”.) We’re dealing here with the cellular immune system. Phagocytic cells and lymphokines play a very important role. Neutrophils, in particular, are affected by these reactions. NEUTROPHILS NOT ONLYPHAGOCYTISE LARGE SUBSTANCES (PROTEINS), BUT ALSO ABSORB FOREIGN CHEMICAL SUBSTANCES (insecticides, pesticides, mycotoxins, etc.). Neutrophils are under autonomous and/or outside control. T-Cell, macrophages, and cytokines sensitize neutrophils to the point where they become hypersensitive to a given substance(s) and over-react and eventually suffer damage or destruction. AUIT suppresses these reactions by regulating #1, autonomous reactions of the neutrophils and #2, suppressing the production of cytokines.
INTERFERON: The mode of action against viral infections is due to the antiviral effect of the interferons, Interferon Gamma (IFNg) is the most active one in this respect. Cells have IFN receptors on their surfaces. When IFNg attaches to them, it is internalized. Interferon-gamma then acts as an anti-replicator. Interferons also inhibit mitosis (division) of infected cells. INF receptors once internalized, DO NOT REPRODUCE. Usually, about 40% of receptors are left on the cell surface. INTERLUKINS: Another immunomodulator closely related to these activities is Interleukin-1 (IL-1). IL1 has to be renewed by the proper stimulant in order to cause its effects. Therefore, the clinical observation that AUIT controls but does not kill (cure) infected cells, is supported by immunological facts.
Much has been said in the past by critics of AUIT–who, by the way, have no personal experience with this type of therapy–regarding the danger of producing glomerula basement membrane disease (Goodpasture’s disease). In some experimental models using animals, such a disease has been produced using the injection of urine, often in previously sensitized animals. However, in close to a million injections of urine in humans in both Texas and So. Calif. clinics, not a single case of Goodpasture’s disease, marked proteinuria or hematuria (all patients undergo a urinalysis prior to the injection of the urine) has been observed. Furthermore, in 5 cases of long-term (more than 1 year) of AUIT, no glomerular basement membrane antigen was found in the blood. The objection to the presence of the CBM antigen in the urine of many normal individuals can easily be overcome by the removal of this antigen by filtration. The antigen has an MW of 80,000 daltons, which is the limit of glomerular filtration.
Removing all substances heavier than MW 60,000 daltons would leave all the immunomodulators and remove the CBM antigen. The other criticism of AUIT is that the urine does not possess immunologically active substances. This statement is so patently false, that only someone alarmingly ignorant of even the basic facts of immunology can render it. It is suggested that in order to elevate AUIT to an “up-do-date” incontrovertible therapeutic modality, the following studies must be undertaken: 1. A double-blind, randomized, placebo, controlled study in cases of atopic disease 2. Measurement of IL, production of IL2, Receptor numbers, Interferon production before and after AUIT 3. Publication in journals and dissemination of the findings to the Medical and Lay communities…especially as it refers to AIDS.
Auto-urine Therapy; 1984, Martin Krebs, M.D. Auto-urine Vaccine therapy for acute Hemorrhagic Nephritis, 1934, R. Tiberi, M.D. Urine Therapy, Prof. Lish. J. Plesch, M.D., 1947 English Medical Journal,l The Effects of Human Urine on Tubercule Bacilli, 1951, Sweden Bacterial Effects of URE, Tulane School of Medicine, 1961 Antibacterial Effects of Human Urine, 1968, Dr. Donald Kaye, Cornell Univ. Med. College Neutralizing Antibody to Polioviruses in Normal Urine, 1962, Lesner, Remington, Maxwell, Finland, Harvard Med. Serv. AntiNeoplaston in Cancer Therapy, Stanislaw R. Burzynski The Use of Injected and Subligual Urine in Allergy Therapy, 1981, Nancy Dunne, M.D. Immuno-Tollerance, Physicians Handbook, 1982 edition Autoimmuno-therapy Against Human Allergenic Disease, a physiological self-defense factor, 1983, C.W.M. Wilson, & A. Lend, M.D. Bactericidal Properties of Urine for Neisseric Gonurrhuae, 1987, Robert Noble, M.D. & M.Darekh, M.S., Univ. Kentucky The Role of Lymphokines in Allergy & Immune Diseases, DeWeck, A.L., Immun.Pract., 357:15 ; Sept. 1985 Specific Immunologic Unresponsiveness, Linscott, W.D.; Basic & Clinical Immunol. 3rd Ed; Lange Med. Pub., Palto Alto, CA, 1981 Proceedings of the 3rd Int’l. Lymphokine Workship; Oppenheimer, J.; Academic Press, 1983 Interlukins & Interferons in Basic & Clinical Immunology, G.H. Edition; Ruscotti, F.W.; Faltyner, C.R., Appleton & Lange, Los Altos, CA 1987