Autism Studies and Related Medical Conditions, January 2009 - TACA

Nested case-control study. SETTING: UK General Practice Research Database.
SUBJECTS: Children born after 1 January 1988 and registered with the General
Practice Research Database within 6 months of birth. OUTCOME MEASURES:
Chronic inflammation of the gastrointestinal tract, coeliac disease, food
intolerance, and recurrent gastrointestinal symptoms recorded by the general
practitioner. RESULTS: 9 of 96 (9%) children with a diagnosis of autism (cases)
and 41 of 449 (9%) children without autism (matched controls) had a history of
gastrointestinal disorders before the index date (the date of first recorded
diagnosis of autism in the cases and the same date for controls). The estimated
odds ratio for a history of gastrointestinal disorders among children with autism
compared with children without autism was 1.0 (95% confidence interval 0.5 to
2.2). CONCLUSIONS: No evidence was found that children with autism were
more likely than children without autism to have had defined gastrointestinal
disorders at any time before their diagnosis of autism.
Black, D., H. Prempeh, et al. (1998). "Autism, inflammatory bowel disease, and MMR
vaccine." Lancet 351(9106): 905-6; author reply 908-9.
Bolte, E. R. (1998). "Autism and Clostridium tetani." Med Hypotheses 51(2): 133-44.
Autism is a severe developmental disability believed to have multiple etiologies.
This paper outlines the possibility of a subacute, chronic tetanus infection of the
intestinal tract as the underlying cause for symptoms of autism observed in some
individuals. A significant percentage of individuals with autism have a history of
extensive antibiotic use. Oral antibiotics significantly disrupt protective intestinal
microbiota, creating a favorable environment for colonization by opportunistic
pathogens. Clostridium tetani is an ubiquitous anaerobic bacillus that produces a
potent neurotoxin. Intestinal colonization by C. tetani, and subsequent
neurotoxin release, have been demonstrated in laboratory animals which were
fed vegetative cells. The vagus nerve is capable of transporting tetanus
neurotoxin (TeNT) and provides a route of ascent from the intestinal tract to the
CNS. This route bypasses TeNT's normal preferential binding sites in the spinal
cord, and therefore the symptoms of a typical tetanus infection are not evident.
Once in the brain, TeNT disrupts the release of neurotransmitters by the
proteolytic cleavage of synaptobrevin, a synaptic vesicle membrane protein. This
inhibition of neurotransmitter release would explain a wide variety of behavioral
deficits apparent in autism. Lab animals injected in the brain with TeNT have
exhibited many of these behaviors. Some children with autism have also shown a
significant reduction in stereotyped behaviors when treated with antimicrobials
effective against intestinal clostridia. When viewed as sequelae to a subacute,
chronic tetanus infection, many of the puzzling abnormalities of autism have a
logical basis. A review of atypical tetanus cases, and strategies to test the validity
of this paper's hypothesis, are included.
Autism Studies & Related Medical Conditions – TACA © Page 14