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Quite by coincidence, the BBC lately carried an interesting article about new vaccines probably coming from some evaluation on the UK synchrotron, the Diamond Light Source (see here – click on the interactive video) which quite neatly sums up the hows and whys of vaccination. But of maybe equal significance was the observation that “The evaluation of ASD mothers with brain-reactive antibodies additionally revealed an elevated prevalence of autoimmune diseases, particularly rheumatoid arthritis and systemic lupus erythematosus”. Insofar as the other parameters on antibodies to deamidated gliadin and tTG, there was little difference to write home about. That being mentioned, anti-goblet (the mucus producing cells) and anti-Paneth (essential defender cells of the gut) cell antibodies have also been reported in cases. Selective deamidation by tissue transglutaminase strongly enhances gliadin-particular T cell reactivity. They looked at antibodies to tissue transglutaminase (tTG). Antibodies against food antigens in patients with autistic spectrum disorders (ASDs). The query of ‘treating’ congenital CMV infection also arises, and what effect this may need on the presentation of autism or autistic traits.
Retrospective diagnosis of congenital cytomegalovirus infection in youngsters with autism spectrum disorder but no different main neurologic deficit. Based on a ultimate comparison of 256 youngsters diagnosed with an autism spectrum disorder (ASD) with an asymptomatic control group of 752 children (all born between 1994 -1999), vaccination histories have been examined and publicity to “whole antibody-stimulating proteins and polysaccharides from vaccines was decided by summing the antigen content material of every vaccine acquired”. The study produced odds ratios (ORs) for ASD ‘outcomes’ during the first 2-years and located no proof for any increased danger of autism primarily based on antigen publicity. Thimerosal publicity and the position of sulfation chemistry and thiol availability in autism. The paper by Momeni and colleagues describing the basics of a blood-based biomarker for autism additionally grabbed my running a blog attention given the give attention to the use of metabolomics. A speculative however interesting paper revealed by T. Andrew Clayton on gut bacteria and amino acids in relation to autism caught my eye and continued the interest in all things gut microbiota.
The authors report that levels of IgG anti-gliadin antibody had been elevated in the autism group compared to siblings and controls. This discovering accords with other research suggesting that coeliac disease is probably not over-represented in cases of autism (bearing in thoughts this does not mean autism is somehow protective against coeliac illness). I’ll come back to this finding shortly. As per the Grauniad (sorry, Guardian) write-up of her ebook “Cahalan is rarely in any doubt concerning the extent of her luck: the luck to find a delicate doctor who listened to her, and took her case on its own deserves”. For those more involved within the adult presentation of the situation, the book ‘Brain on Fire’ by Susannah Cahalan might be a superb place to begin. A couple of selection quotes from the authors: “The findings indicate that the observed anti-gliadin immune response in patients with autism is more likely to contain a mechanism that is distinct from celiac illness, with out the requirement for TG2 activity or antigen presentation via DQ2/DQ8 MHC molecules”.
I am unable to pretend to know why schizophrenia analysis took the lead; maybe one thing to do with Dohan and his unique discussions on food plan and schizophrenia or that schizophrenia analysis has some very talented folks like Emily Severance and colleagues (see here and here and here) taking an curiosity. I do know some folks still look on things like ‘leaky gut’ as being the stuff of tree-huggers, but the proof is rising for some effect in instances of autism (see right here) with the promise of extra investigations to come back (see right here for the Paul Patterson mouse work and right here for a video from everyone’s favorite autism – intestine specialist researcher, Alessio Fasano). Protean by the best way, means readily assuming completely different types or characters (yes, I had to look it up). If you’d like some more information about the whole coeliac disease process, you can do worse than have a take a look at my current submit on what we expect we find out about it (see right here). And the whole thought, which simply occurred to converge on the date of the Winter Solstice, was a little far-fetched?
If you’re a bit of bit sick and tired of poo and micro organism, there was this submit on maternal fever and offspring autism threat (Cost once once more) or if you like, some necessary knowledge on parental pre-diagnostic experiences of their youngsters. Whilst I am fairly buoyed by seeing that this space is beginning to get some analysis interest, I’m containing my pleasure for now. The implication right here is that whilst not being coeliac disease – certainly the lack of any significant HLA-DQ2/DQ8 haplotype findings within the autism group is testomony to that – gluten peptides would possibly nonetheless be acting on some instances of autism. So what might have been the problem/s? Although not wholly related, I’ll refer you again to some fascinating work down on tTG with autism in mind from some time again (see here). That and point out of these other words bacterial translocation which seem to go hand-in-hand with leaky intestine, (think Sutterella and autism for instance).
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