AUTHORS: F Torrente, P Ashwood, R Day, N Machado, RI Furlano, A Anthony, SE Davies, AJ Wakefield, MA Thompson, JA Walker-Smith and SH Murch
Centre for Paediatric Gastroenterology, with the Inflammatory Bowel Disease Study Group, Royal Free & University College Medical School, London, UK. The IBD Research Unit, St. Marks Hospital, Harrow, London, UK; Department of Medicine, Royal Free and University College Medical School, London, UK; Department of Histopathology, Royal Free and University College Medical School, London, UK
It remains unclear whether autism is a single disease or a condition occurring as an end result of various abnormalities. Fundamental uncertainty remains about the relative input of genetic predisposition and environmental exposures. Central to this uncertainty is the conflicting evidence concerning the incidence of autism. While there are several reports of rapid increase in incidence in Western countries - suggesting an important environmental component - others suggest that the increase is more apparent than real, and dependent on increased recognition , thus favoring a primarily genetic predisposition. Most research has focused on the genetics of autism, and several genes have been implicated in classic autism.
This study is based on children with a form of autism characterized by regression in the second year of life, after apparently normal early development. Most reports of immunological abnormalities in autistic children have been from this subgroup of affected children, and the authors cite the increasing body of evidence for abnormal immune regulation and autoimmunity in autism. The initial observation of unexpected bowel pathology in autistic children came from the same group, and centered on pathology in the colon (Lancet 1998; 351: 637-641, American Journal of Gastroenterology 2000;
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Contact: Frank Sissingh
molecularpsychiatry@mednet.ucla.edu
310-206-6739
Molecular Psychiatry
29-Apr-2002