So, first up the "wow, that's a long title" study:
Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.
These results suggest that the autism Lymphoblastoid cells exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromis antioxidant defense and detoxification capacity under prooxidant conditionsOk, the antioxidant and detoxification processes might be be impaired in autism.
Next, the "Don't call me a fatty" study:
Plasma fatty acid profiles in autism: A case-control study.
Results showed that docosahexaenoic acid (DHA, 22:6n-3) was significantly decreased in phosphatidylethanolamine. Dimethyl acetals were significantly decreased in phosphatidylethanolamine and phosphatidylcholine as well. These results are consistent with the only other study to measure dimethyl acetals in children with autism, and suggest that the function of peroxisomes and the enzymes of the peroxisome involved with fatty acid metabolism may be affected in autism.So people with autism may have problems processing fatty acids. I know that isn't a good thing but don't ask me to explain it.
Finally we have the "I have 22 authors, how many do you have" study:
Therefore an immune hypothesis, involving also autoimmunity, is one possible pathogenetic mechanism in autismThere is more of that "mythical" immune system involvement. I have written about this before. It is a shame that with something as relatively easy to quantify as levels of immune cells that there has not been any wide spread study of this issue.
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