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Posted by Margaret on September 02, 2000 at 18:25:53:

Dr. Vijendra Singh

Dr. Vijendra Singh, a neuroimmunologist, is working on the developmental aspect of the immune
system and nervous system and itís relationships to autism. He firmly believes that up to 80% (and
possibly all) cases of autism are caused by an abnormal immune reaction, commonly known as
autoimmunity. Specifically, he is exploring the role of autoimmune factors (for example, viruses,
autoantibodies, T cells, cytokines, ect.) because they serve as the prime targets of therapy with
immune modulating drugs, he said.

Dr. Singh thinks that autism is a complex disorder of a very complicated interaction between the
nervous system and the immune system. He postulated a "Neuroautoimmunity Model of Autism"
which he recently discussed at two recent meetings: First, the Biomedical Treatments for Autism
and PDD Conference held in Orlando, Florida (May, 1999); and secondly, the Neuro-Immune
Dysfunction Syndromes (NIDS) Conference held in Bethesda, Maryland (June, 1999). Briefly, he
hypothesized that an autoimmune reaction to brain structures, in particular myelin sheath, plays a
critical role in causing neurological impairments of patients with autism. He thinks that an immune
damage to developing myelin (after a natural infection or vaccination) causes "nicks" or small
changes in the myelin sheath, which ultimately leads to life-long problems of higher mental functions
such as the skills for learning, memory, communication, social interaction, etc.

Dr. Singh believes that autoimmunity has a strong prospect for treating patients with autism. He
said that the lessons learned from other autoimmune diseases should also apply to autism. Because
of autoimmunity involvement, he emphasizes the need to focus on immune therapies and urge
doctors to pay attention to this line of research. Consequently, he says, there is a strong potential
for restoring brain functions in autistic patients, including children as well as adults. With this goal in
mind, Dr. Singh is committed to finding a cause and cure for autism.

For further information, please contact him directly:
Dr. Vijendra Singh, Ph.D.
Biotechnology Center
Department of Biology
Utah State University
4700 Old Main Hill
Logan, UT 84322-4700
E-mail: [email protected]

Sydney M. Finegold, M.D.

The following hypothesis, based on the work of Ellen Bolte, is at the heart of the research that is
being done at the Wadsworth Anaerobic Bacteriology Laboratory, West Los Angeles, CA.
Hypothesis: A bacterial toxin, genetically related to the clostridial neurotoxins, causes the
behavioral abnormalities associated with autism (via severe disruption of neurotransmitter release)
in a narrowly defined subset of children.

Many autistic children have severe gastrointestinal problems. Chronic diarrhea or loose stools is
commonly reported from parents of autistic children. The research team at the Wadsworth
Laboratory speculate that broad-spectrum antibiotics (frequently used to treat ear infections) may
cause significant disruption of the protective intestinal tract flora and that this disruption may allow
for colonization by one or more neurotoxin-producing bacteria. The neurotoxin produced in the
intestinal tract then ascends to the central nervous system and creates an on-going state of
neurotransmitter disruption.

In an initial study, eleven children were treated with a minimally absorbed oral antibiotic. Nine of
the eleven children showed improvement during therapy. One child had no change and the other
possibly became worse. Pre-treatment stools were found to have numerous unidentifiable
Clostridium species. No Clostridium were found in the stools from the "on-therapy" specimens of
the children that benefitted from the treatment. Interestingly, the "on-therapy" stool specimen from
the child who appeared to deteriorate during treatment contained multiple Clostridium species.
The improvements in these children was short term and did not continue after treatment was
terminated. However, the fact that there was improvement in such a short time period, shows that
it is highly probable that a bacterial infection causes or worsens at least some (if not all) of the
autistic symptoms in these children.

The research team is working to identify the specific offending organism(s) involved, which causes
the autistic symptoms. Upon isolation of the organism(s), the team will then be able to determine
an effective treatment for the elimination of this "bug" from the gut. This work looks extremely
promising. The BHARE Foundation feels it is simply a matter of time before this research yields
discoveries that will directly benefit our children.

Sydney M. Finegold, M.D.
Professor of Medicine, Professor of Microbiology & Immunology
Infectious Diseases Section
VA Medical Center West Los Angeles
UCLA School of Medicine

Andrew Wakefield, FRCS

Andrew Wakefield, leads a team of eight medical and scientific researchers, investigating a
meta-hypothesis; that a complex relationship between a genetic predisposition, and early
environmental exposures results in immune derangement and metabolic dysfunction. This primary
sequence of events takes place in the gut which then triggers an autistic disorder.

Andrew Wakefield's particular interest is in children who develop normally and then manifest an
autistic disorder combined with gastrointestinal symptoms. A few years ago such cases were very
rare. More recently there is evidence of a significant increase in their prevalence. Wakefield and
colleagues have dubbed this syndrome 'autistic enterocolitis'. Examples of three current
programmes receiving assistance from the BHARE Foundation are mentioned below.

Histopathologist Dr Andrew Anthony, is investigating the gut pathology of autistic enterocolitis,
and assessing possible non-invasive tests of specific features of the gut disorder seen in autistic
enterocolitis. At present most children referred to Andrew Wakefield's colleagues require
ileo-colonoscopy, an invasive procedure for which there is a lengthy wait. Children with autistic
enterocolitis display a remarkable uniformity in their endoscopic and histological symptoms. At
present 98% of affected children show a distinctive pattern of swollen lymph glands at the end of
the small bowel and 88% have inflammation of the large bowel.

Immunologist Dr Paul Ashwood, is investigating specific immunologic features of autistic
enterocolitis. These concern the apparent dysregulation of certain helper T cells, thus impairing
their ability to stimulate a full cytotoxic response from particular classes of cytolytic T cells.
Epidemiologist Dr Scott Montgomery, is engaged in population-based studies to confirm the
reported temporal trends in the epidemiology of autism. These studies will be used to explore
explanations for the apparent increase in the incidence of autistic spectrum disorders and the
reported changes in phenotype, such as an increase in the number of children with regressive
autism. The work will include an investigation of the role of potential risk factors for autism,
specifically the combination of environmental exposures resulting in disease among susceptible
individuals. Identification of markers of susceptibility in both parents and the children themselves
will also assist in defining the 'at-risk' group for specific exposures. Other current and planned
investigations, include studies in virology, molecular biology, genetics and two trials of potential

For further information please contact Andrew Wakefield directly, at the address below or by
e-mail via [email protected] (Robert Sawyer handles all general enquiries and research
funding for Andrew Wakefield and his research team).

Andrew Wakefield, FRCS
Reader in the Department of Histopathology and Medicine
Reader in Experimental Gastroenterology
Director, Inflammatory Bowel Disease Study Group
Royal Free and University College Medical School
Rowland Hill Street, London NW3 2PF


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