Autism Studies and Related Medical Conditions, January 2009 - TACA

Reichelt, K. L. and A. M. Knivsberg (2003). "Can the pathophysiology of autism be
explained by the nature of the discovered urine peptides?" Nutr Neurosci 6(1): 19-28.
Opioid peptides derived from food proteins (exorphins) have been found in urine
of autistic patients. Based on the work of several groups, we try to show that
exorphins and serotonin uptake stimulating factors may explain many of the
signs and symptoms seen in autistic disorders. The individual symptoms ought to
be explainable by the properties and behavioural effects of the found peptides.
The data presented form the basis of an autism model, where we suggest that
exorphins and serotonin uptake modulators are key mediators for the
development of autism. This may be due to a genetically based peptidase
deficiency in at least two or more peptidases and, or of peptidase regulating
proteins made manifest by a dietary overload of exorphin precursors such as by
increased gut uptake.
Sandler, R. H., S. M. Finegold, et al. (2000). "Short-term benefit from oral vancomycin
treatment of regressive-onset autism." J Child Neurol 15(7): 429-35.
In most cases symptoms of autism begin in early infancy. However, a subset of
children appears to develop normally until a clear deterioration is observed. Many
parents of children with "regressive"-onset autism have noted antecedent
antibiotic exposure followed by chronic diarrhea. We speculated that, in a
subgroup of children, disruption of indigenous gut flora might promote
colonization by one or more neurotoxin-producing bacteria, contributing, at least
in part, to their autistic symptomatology. To help test this hypothesis, 11 children
with regressive-onset autism were recruited for an intervention trial using a
minimally absorbed oral antibiotic. Entry criteria included antecedent broadspectrum
antimicrobial exposure followed by chronic persistent diarrhea,
deterioration of previously acquired skills, and then autistic features. Short-term
improvement was noted using multiple pre- and post-therapy evaluations. These
included coded, paired videotapes scored by a clinical psychologist blinded to
treatment status; these noted improvement in 8 of 10 children studied.
Unfortunately, these gains had largely waned at follow-up. Although the protocol
used is not suggested as useful therapy, these results indicate that a possible gut
flora-brain connection warrants further investigation, as it might lead to greater
pathophysiologic insight and meaningful prevention or treatment in a subset of
children with autism.
Schneider, C. K., R. D. Melmed, et al. (2006). "Oral human immunoglobulin for children
with autism and gastrointestinal dysfunction: a prospective, open-label study." J Autism
Dev Disord 36(8): 1053-64.
Immunoglobulin secretion onto mucosal surfaces is a major component of the
mucosal immune system. We hypothesized that chronic gastrointestinal (GI)
disturbances associated with autistic disorder (AD) may be due to an underlying
deficiency in mucosal immunity, and that orally administered immunoglobulin
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