The MRC 2001 Review of autism states that ‘to date, there have been two major studies’ (of autism - brain autopsies). ‘Each has reported some specific findings not yet replicated elsewhere, but areas of agreement include:

• brain weight is increased in an as yet uncertain proportion of individuals with ASDs ‘Autism Spectrum Disorders’;
• decreased Purkinje cell number is seen in the majority of (but not all) cases;
• developmental abnormalities of the inferior olive are a common observation.’

Brain weight
“A Pesticide Information Project of Cooperative Extension Offices in June 1996 identifies Chronic toxicity to (4-aminopyridine): ‘High dietary doses (2 to 3.25 mg/kg/day) caused increased brain weight. Brain appearance remained normal. However, since dietary intake is assumed to be negligible, and because significant repeated exposure is not expected to occur, epa (environmental protection agency) has not required long-term toxicity studies of 4-aminopyridine.’ Toxins from foods such as pyridine (i.e. coal-tar-derived food dye) and pesticides have been shown to result in increased brain size. ‘Poisonings are characterized by thirst, nausea, dizziness, weakness, and intense sweating, followed by impairment of normal mental functioning (toxic psychosis), lack of muscular coordination, tremors, labored breathing, and generalized seizures.’ Studies in autism have identified as many as 100% of the study group as having immune response to food dyes. No studies are available in relation to brain size and natural plant pesticide carcinogens or hapten-type substances which the immune system is known to react to such as some drugs.

Decreased Purkinje cell number
The brain of the developing fetus and infant could be affected by the selection of a pathogen and the research strongly indicates the pathogen would be a hapten-type. Lutein selection by the pre-immunocytes would result in the granule cell differences and could be anticipated because glutoredoxin required to protect cerebellar granule cells is produced in concert with immune-hormone signaling activity. The substantia nigra (melanin-containing cells) and dendrite relationship would be affected and the brain development would reflect the immune response. This may include changes to auditory processing mechanisms. This could result in purkinje cells, which ‘pull back’ climbing fibers as a result of granule cell loss and immune (cytokine release of free radicals) reactions contributing to altered sensory feedback. The results of purkinje neuron cell loss could contribute to findings of ‘ataxic gate’ and movement coordination disturbances found in autism. Bilateral synchronicity might be severely disturbed contributing to chaotic responses to incoming auditory, visual and other sensory stimuli for the autist. These factors can additionally be elucidated as resulting from immune system regulation of melanin and neuromelanin via the red nucleus and rubrospinal pathway as well as neuroimmune regulation via this pathway resulting from lost or disturbed serotonin-adrenal regulation potential. The impact of a toxic substance on the area of the brain most affected in the autist is described in the article: ‘Glial reaction to volkensin-induced selective degeneration of central neurons’: http://www.sciencedirect.com/

The MRC 2001 Review of autism includes: “The issue of immunological abnormalities in ASDs has been widely debated, but there is a lack of reports in the peer-reviewed literature. Studies of immunological function in children with ASDs have reported a wide array of abnormalities including decreased cellular responses, decreased serum C4b levels and increased humoral immune and autoantibody responses. A recently published abstract identified on PubMed (Medline) highlights a number of these changes: (This abstract) reported an excessive innate immune response and a disruption of the regulatory cytokines”
  Sometimes the reported differences are quite astounding: “The C4B null allele is known to be part of the extended or ancestral haplotype [B44-SC30-DR4], we investigated the incidence of [B44-SC30-DR4] in 21 autistic children and their parents. This extended haplotype was increased by almost six-fold in the autistic subjects as compared with healthy controls.”
  It is the function of the immune system to protect the host and each host is a unique human individual. The wide variation in the data indicating ‘excessive innate immune response’  as described by Jyonouchi and previously Warren, R. and Singh, V. strongly identify the likelihood that this innate response is to a hapten-type pathogen. In the event that the acting hapten (lutein) is used for scientific evaluation it is likely that convincing evidence will be forthcoming and that a wide degree of immune response will be recorded. The study of hapten-type immune response is still a new science. The immune system’s function, to protect the host, inevitably results in a wide degree of expression as unique as each member of the human population. The findings thus far obtained highlight this variety and could therefore be used as a strong argument for the immune system response as the primary candidate causal factor for autism.

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