http://groups.yahoo.com/group/Autism-Mercury/message/63344
Dr. Hugh H. Fudenberg Autism as an Autoimmune disease...
Interesting.
Classic infantile onset autism is an autoimmune disease
Clinical Research (abstracts) 37(2):556a (1998)
HH Fudenberg, NeuroImmuno Therapeutics Research Foundation, Spartanburg, S.C.; R Demirjian, Walnut Creek, CA; P Iversen, Los Angeles, CA.
40 infantile autistic patients were studied. They ranged from 6 years to 15 years of age at entry. None of the patients had fragile X-chromosome, 5-nucleotidase enzyme defect, pyruvate lactate defect or other enzyme defects, Landau-Kleffner Syndrome, nor the Coleman Syndrome (hypocalciuria and self-inflicted optic injury). Twenty-two were cases of classic infantile autism with onset at 12-18 months, often 1 day to 1 week after administration of live virus vaccine (e.g. Rubella, Hepatitis B); 18 had onset at less than 12 months or more than 20 months and lacked one or more of the clinical features associated with classic infantile autism (e.g. did not lose all speech, did not lose tactile or visual contact with parents and sibs, did not develop sleep depravation). This latter group is heterogenous, termed herein as "pseudo-autism". Of the 22 with classic autism, all had antibodies to myelin basic protein and to neuron axone filament proteins. Of the 22 with classic autism, 20 responded to dialyzable lymphocyte extract (DLyE) containing Transfer Factor (T.F.) derived from cells of household contact (parent or sib); no other therapeutic medications were administered during the T.F. administration. The responders lost at least 2 points in symptom severity score average; 10 became completely normal (5 points worst; 0 best) in that their clinical deficits were fully normalized and they were mainstreamed in school. Of the 12 remaining, 11 improved on T.F., some to other therapies. After cessation of T.F. therapy, 5 in the autistic group regressed, but they did not drop to baseline levels. Approximately 50% of the classic autistics and 80% of the pseudo autistics had food and/or respiratory hypersensitivity due to a deficiency of the enzymes phosphosulfotransferase and cytochrome P-450, respectively. Many had marked hypersensitivity to phenols. Only those who had repeated antibiotic therapy developed Candidiasis. The respiratory and gastro-intestinal hypersensitivities and the Candidiasis were treated and corrected prior to DLyE administration.
Many of the pseudo-autistics had clostridia in their stools (though they had neither fever nor diarrhea) and produced neurotoxins. Oral vancomycin followed by 60 billion lactobacillus organisms daily resulted in improvement for 2-3 weeks. The gene for classic autism has been localized to human chromosome-6, the site of human immune response genes and are linked to haplotypes containing the C4 null
allele.
