MEDICAL STUDIES
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Chronic Fatique Syndrome
EPILEPSY-Treatment with Transfer Factor
Herpes Treatment with Transfer Factor
Excerpts from "Natural Immune Booster" by William J. Hennen Ph.d.
"Autism is a condition characterized by insomnia, repetitive limb movements, diminished socialization, self-abuse, and a short attention span. Autism may have many causes. One of these is viral exposure with the strongest indication being congenital rubella. In these cases autism appears to be the outward manifestation of a see-saw battle between an ill equipped immune system and a vicious rubella attack as evidenced by cases of remission and relapse. It is not surprising then that autistic children have a depressed cellular immune system. In fact some autistic children exhibit no detectable immune response when challenged with rubella vaccine.
In a recent well-controlled study researchers reported some very encouraging results and raised some serious questions concerning vaccination of the very young. Of 22 true autistic children treated with Transfer Factor, 21 responded to Transfer Factor treatment. Ten of the children regained sufficient mental and emotional control to be able to enter mainstream schools. The disturbing finding of this study was that of the 22 truly autistic children studied, 15 developed autistic symptoms within a week of immunization with the measles, mumps, and rubella vaccine. Researchers propose that 'true autism is probably an adverse reaction to a live virus vaccine in a geneticlly predisposed individual' whose immune system is not yet mature."
INTRINSIC AND EXTRINSIC DETERMINANTS OF NEURONAL DEVELOPMENT: RELATION TO INFANTILE AUTISM. J.AUTISM DEV. DISORD 1982, 12(2), 115-45
VIRAL EXPOSURE AND AUTISM. DEYKIN EY, MACMAHON B. AM J EPIDEMIOL 1979 109(6) 628-38 (med studies continued bottom of page).
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DIALYSABLE LYMPHOCYTE EXTRACT (DLyE) IN INFANTILE ONSET AUTISM: A PILOT STUDY. FUDENBERG
40 infantile autistic patients were studied . They ranged from 6 years to 15 years of age at entry. 22 were cases of classical infantile autism; whereas 18 lacked one or more clinical defects associated with infantile autism ("pseudo-autism"). Of the 22 with classic autism, 21 responded to transfer factor treatment by gaining at least 2 points in symptoms severity score average (SSSA): and 10 became normal in that they were main-streamed in school and clinical characteristics were fully normalized. Of the 18 remaining, 4 responded to transfer factor, some to other therapies. After cessation of transfer factor therapy, 5 in the autistic group and 3 pseudo-autistic group regressed, but they did not drop as low as baseline levels.
PMID: 8993773 [PubMed - indexed for MEDLINE]
Fudenberg HH.
Neurolmmuno Therapeutic Research Foundation Spartanburg, S.C, USA.
Biotherapy 1996;9(1-30):143-7
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IMMUNOLOGICAL TREATMENTS FOR AUTISM
Several investigators, including ourselves, have reported significant changes in various immune responses in children with autism. These changes demonstrate dysregulation of the immune system (deficiency in some components of the immune system and excesses in others). In addition, certain genes in the major histocompatibility complex (that regulates immune responses) appear to be involved in autism. Based upon immunological abnormalities, various treatment modalities have been applied to children with autism. In this brief review, these immunological changes and various biological therapies are analyzed and summarized.
PMID: 11098887 [PubMed - indexed for MEDLINE]
Gupta S.
Division of Basic and Clinical Immunology, Medical Sciences I, University of California, Irvine 92697, USA. sgupta@uci.edu
J Autism Dev Disord. 2000 Oct; 30(5):475-9.
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AUTISM, AN EXTREME CHALLENGE TO INTEGRATIVE MEDICINE. PART 2: MEDICAL MANAGEMENT.
Autism and allied autistic spectrum disorder (ASD) present myriad behavioral, clinical, and biochemical abnormalities. Parental participation, advanced testing protocols, and eclectic treatment strategies have driven progress toward a cure. Behavioral modification and structured education are beneficial but insufficient.
Dietary restrictions, including removal of milk and other casein dairy products, wheat and other gluten sources, sugar, chocolate, preservatives, and food coloring are beneficial and prerequisite to benefit from other interventions. Individualized IgG or IgE testing can identify other troublesome foods but not non-immune mediated food sensitivities. Gastrointestinal improvement rests on controlling Candida and other parasites, and using probiotic bacteria and nutrients to correct dysbiosis and decrease gut permeability.
Detoxification of mercury and other heavy metals by DMSA/DMPS chelation can have marked benefit. Documented sulfoxidation-sulfation inadequacies call for sulfur- sulfhydryl repletion and other liver p450 support.
Many nutrient supplements are beneficial and well tolerated, including dimethylglycine (DMG) and a combination of pyridoxine (vitamin B6) and magnesium, both of which benefit roughly half of ASD cases, Vitamins A, B3, C, and folic acid; the minerals calcium and zinc; cod liver oil; and digestive enzymes, all offer benefit. Secretin, a triggering factor for digestion, is presently under investigation.
Immune therapies (pentoxifyllin, intravenous immunogloblin, Transfer Factor, and colostrum) benefit selected cases. Long-chain omega-3 fatty acids offer great promise.
Current pharmaceuticals fail to benefit the primary symptoms and can have marked adverse effects. Individualized, in-depth clinical and laboratory assessments and integrative parent-physician-scientist cooperation are the keys to successful ASD management.
Kidd PM.
PMID: 12495373 [PubMed - Indexex for MEDLINE]
Altern Med Rev 2002 Dec; 7(6): 472-99
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IMMUNOLOGICAL FINDINGS IN AUTISM
The immunopathogenesis of autism is presented schematically in Fig. 1 Two main immune dysfunctions in autism are immune regulation involving pro-inflammatory cytokines and autoimmunity. Mercury and an infectious agents like the measles virus are currently two main candidate environmental triggers for immune dysfunction. Genetically immune dysfunction in autism involves the MHC region, as this is an immunologic gene cluster whose gene products are Class I, II, and III molecules. Class I and II molecules are associated with antigen presentation. The antigen in virus infection initiated by the virus particle itself while the cytokine production and inflammatory mediators are due to the response to the putative antigen in question. The cell-mediated immunity is impaired as evidenced by low numbers of CD4 cells and a concomitant T-cell polarity with an imbalance of Th1/Th2 subsets toward Th2.
Impaired humoral immunity on the other hand is evidenced by decreased IgA causing poor gut protection. Studies showing elevated brain specific antibodies in autism support an autoimmune mechanism. Viruses may initiate the process but the subsequent activation of cytokines is the damaging factor associated with measles virus have been demonstrated in autistic subjects. Environmental exposure to mercury is believed to harm human health possibly through modulation of immune homeostasis. A mercury link with the immune system has been postulated due to the involvement of postnatal exposure to thimerosal, a preservative added in the MMR vaccines. The occupational hazard exposure to mercury causes edema in astrocytes and, at the molecular level, the CD95/Fas apoptotic signaling pathway is disrupted by Hg2+. Inflammatory mediators in autism usually involve activation of astrocytes and microglial cells.
Pro-inflammatory chemokines (MCP- and TARC), and an anti-inflammatory and modulatory cytokine, TGF-beta1, are consistently elevated in autistic brains. In measles virus infection, it has been postulated that there is immune suppression by inhibiting T-cell proliferation and maturation and down regulation MHC class II expression. Cytokine alteration of TNF-alpha is increased in autistic populations. Toll-like-receptors are also involved in autistic development. High NO levels are associated with autism. Maternal antibodies may trigger autism as a mechanism of autoimmunity . MMR vaccination may increase risk for autism via an autoimmune mechanism in autism. MMR antibodies are significantly higher in autistic children as compared to normal children, supporting a role of MMR in autism.
Autoantibodies (IgG isotope) to neuronaxon filament protein (NAFP) and glial fibrillary acidic protein (GFAP are significantly increased in autistic patients (Singh et al., 1997). Increase in Th2 may explain the increased autoimmunity, such as the findings of antibodies to MBP and neuronal axonal filaments in the brain . There is further evidence that there are other participants in the autoimmune phenomenon. (Kozlovskaia et al., 2000). The possibility of its involvment in autism cannot be ruled out. Further investigations at immunological, cellular, molecular and genetic levels will allow researchers to continue to unravel the immunopathogenic mechanisms associated with autistic processes in the developing brain. This may open new avenues for prevention and/or cure of this devasting neurodevelopmental disorder.
PMID: 16512356 [PubMed - indexed for MEDLINE] Cohly HH, Panja A.
Department of Biology, Jackson State University, Mississippi 39217, USA
Int Rev Neurobiol. 2005;71:317-41.
Medical Studies Continued:
FOLLOW-UP REPORT IN CONGENITAL RUBELLA. CHESS S. AUTISM CHILD SCHIZOPR 1977, 7 (1) 69-81
BEHAVIORAL CONSEQUENCES OF CONGENITAL RUBELLA. CHESS S. FERNANDEZ P, KORN S. J PEDIATT, 1978, 93940, 699-703.
DEPRESSED LYMPHOCYTE RESPONSIVENESS IN AUTISTIC CHILDREN. STUBBS EG. CRAWFORD ML. J AUTISM CHILD SCHIZOPHR 1977, 7(1), 49-55.