22 Oct 2009, 10:40 am
22 Oct 2009, 12:11 pm
Here's another one: 
Quote:
Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia.
Ihara M, Makino F, Sawada H, Mezaki T, Mizutani K, Nakase H, Matsui M, Tomimoto H, Shimohama S.
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto.
OBJECTIVE: Gluten sensitivity is associated with multiple neurological abnormalities including gluten ataxia, motor neuron disease-like neuropathy, small fiber type neuropathy, cognitive impairment, and even parkinsonism. We investigated whether or not gluten sensitivity is involved in Japanese patients with idiopathic cerebellar ataxia with extracerebellar presentation. PATIENTS OR MATERIALS: Fourteen patients with idiopathic cerebellar ataxia with extracerebellar presentation (autonomic instability, parkinsonism, or pyramidal dysfunction in varying combinations) were screened for anti-gliadin antibodies (AGA) to analyze for the presence or absence of gluten sensitivity. Patients with typical MR findings of multiple system atrophy of the cerebellar type were excluded. As disease controls without cerebellar ataxia, 9 patients with Parkinson's disease and 18 patients with amyotrophic lateral sclerosis were screened for AGA. Forty-seven normal controls were also screened for AGA. RESULTS: We found a high prevalence of AGA in 5 (36%) of 14 cerebellar ataxia patients, but in only 1 (4%) of 27 disease controls without cerebellar ataxia (odds ratio, 14.4; 95% CI, 1.41147; p<0.05) and in only 1 (2%) of 47 normal controls (odds ratio, 25.6; 95% CI, 2.66246; p<0.001). Among the cerebellar ataxia patients, atypical features such as sensorimotor neuropathy and/or mild cognitive impairment were more prevalent in the AGA-positive group (60%) than in the AGA-negative group (0%). In one of the ataxic patients with AGA, a gluten-free diet had positive effects on neurological symptoms and nutritional status. CONCLUSION: Gluten sensitivity is involved in at least some of the unexplained neurological symptoms of Japanese patients with adult-onset, sporadic cerebellar ataxia.
Ihara M, Makino F, Sawada H, Mezaki T, Mizutani K, Nakase H, Matsui M, Tomimoto H, Shimohama S.
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto.
OBJECTIVE: Gluten sensitivity is associated with multiple neurological abnormalities including gluten ataxia, motor neuron disease-like neuropathy, small fiber type neuropathy, cognitive impairment, and even parkinsonism. We investigated whether or not gluten sensitivity is involved in Japanese patients with idiopathic cerebellar ataxia with extracerebellar presentation. PATIENTS OR MATERIALS: Fourteen patients with idiopathic cerebellar ataxia with extracerebellar presentation (autonomic instability, parkinsonism, or pyramidal dysfunction in varying combinations) were screened for anti-gliadin antibodies (AGA) to analyze for the presence or absence of gluten sensitivity. Patients with typical MR findings of multiple system atrophy of the cerebellar type were excluded. As disease controls without cerebellar ataxia, 9 patients with Parkinson's disease and 18 patients with amyotrophic lateral sclerosis were screened for AGA. Forty-seven normal controls were also screened for AGA. RESULTS: We found a high prevalence of AGA in 5 (36%) of 14 cerebellar ataxia patients, but in only 1 (4%) of 27 disease controls without cerebellar ataxia (odds ratio, 14.4; 95% CI, 1.41147; p<0.05) and in only 1 (2%) of 47 normal controls (odds ratio, 25.6; 95% CI, 2.66246; p<0.001). Among the cerebellar ataxia patients, atypical features such as sensorimotor neuropathy and/or mild cognitive impairment were more prevalent in the AGA-positive group (60%) than in the AGA-negative group (0%). In one of the ataxic patients with AGA, a gluten-free diet had positive effects on neurological symptoms and nutritional status. CONCLUSION: Gluten sensitivity is involved in at least some of the unexplained neurological symptoms of Japanese patients with adult-onset, sporadic cerebellar ataxia.
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29 Oct 2009, 11:35 am
Just bumping this because of a new thread asking about the effectiveness of gf and/or cf diets.
29 Oct 2009, 12:26 pm
CockneyRebel
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29 Oct 2009, 1:22 pm
29 Oct 2009, 1:54 pm
Blindspot149
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29 Oct 2009, 2:02 pm
31 Oct 2009, 8:45 am
31 Oct 2009, 8:57 am
31 Oct 2009, 9:31 am
31 Oct 2009, 9:56 am
31 Oct 2009, 10:37 am
However, while we're on the subject of "leaky guts" I recently came across some interesting new data on the effect of gliadin ( the part of gluten which triggers immune-system reactions ) on intestinal membrane cell-junctions, in "The Dark Side of Wheat" by Sayer Ji, available at:
http://www.greenmedinfo.com/content/dar ... e-sayer-ji
which states that gliadin actually causes an upregulation of zonulin in everyone, ( not just in the gluten-sensitive ); zonulin triggers increased intestinal permeability. The whole article is brilliant but I shall just quote a very small section:
Quote:
Wheat Gliadin Creates Intestinal Permeability
Gliadin upregulates the production of a protein known as zonulin, which modulates intestinal permeability. Over-expression of zonulin is involved in a number of autoimmune disorders, including celiac disease and Type 1 diabetes. Researchers have found that “gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules. A pathological response to wheat gluten is a normal or human, species specific response, and is not based entirely on genetic susceptibilities. Intestinal permeability is associated with wide range of disease states, including cardiovascular illness, liver disease and many autoimmune disorders.
Gliadin upregulates the production of a protein known as zonulin, which modulates intestinal permeability. Over-expression of zonulin is involved in a number of autoimmune disorders, including celiac disease and Type 1 diabetes. Researchers have found that “gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules. A pathological response to wheat gluten is a normal or human, species specific response, and is not based entirely on genetic susceptibilities. Intestinal permeability is associated with wide range of disease states, including cardiovascular illness, liver disease and many autoimmune disorders.
Someone even better read on the subject
, much better in fact, on the forum where I posted this, replied that yes, this was true, ( gliadin has this effect on everyone's gut ) but that there were studies to show that the increase in zonulin production, ( which causes gut permeability ), is higher, and longer lasting, in people with celiac disease/gluten sensitivity: Quote:
Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.
Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A.
Mucosal Biology Research Center, Center for Celiac Research and Division of Pediatric Gastroenterology and Nutrition, University of Maryland, School of Medicine, Baltimore, MD 21201, USA.
OBJECTIVE: Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When exposed to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein interaction, and increased monolayer permeability. Pretreatment with the zonulin antagonist FZI/0 blocked these changes without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from celiac patients in remission expressed a sustained luminal zonulin release and increase in intestinal permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from non-celiac patients demonstrated a limited, transient zonulin release which was paralleled by an increase in intestinal permeability that never reached the level of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS: Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.
PMID: 16635908 http://www.ncbi.nlm.nih.gov/pubmed/1663 ... stractPlus
Drago S, El Asmar R, Di Pierro M, Grazia Clemente M, Tripathi A, Sapone A, Thakar M, Iacono G, Carroccio A, D'Agate C, Not T, Zampini L, Catassi C, Fasano A.
Mucosal Biology Research Center, Center for Celiac Research and Division of Pediatric Gastroenterology and Nutrition, University of Maryland, School of Medicine, Baltimore, MD 21201, USA.
OBJECTIVE: Little is known about the interaction of gliadin with intestinal epithelial cells and the mechanism(s) through which gliadin crosses the intestinal epithelial barrier. We investigated whether gliadin has any immediate effect on zonulin release and signaling. MATERIAL AND METHODS: Both ex vivo human small intestines and intestinal cell monolayers were exposed to gliadin, and zonulin release and changes in paracellular permeability were monitored in the presence and absence of zonulin antagonism. Zonulin binding, cytoskeletal rearrangement, and zonula occludens-1 (ZO-1) redistribution were evaluated by immunofluorescence microscopy. Tight junction occludin and ZO-1 gene expression was evaluated by real-time polymerase chain reaction (PCR). RESULTS: When exposed to gliadin, zonulin receptor-positive IEC6 and Caco2 cells released zonulin in the cell medium with subsequent zonulin binding to the cell surface, rearrangement of the cell cytoskeleton, loss of occludin-ZO1 protein-protein interaction, and increased monolayer permeability. Pretreatment with the zonulin antagonist FZI/0 blocked these changes without affecting zonulin release. When exposed to luminal gliadin, intestinal biopsies from celiac patients in remission expressed a sustained luminal zonulin release and increase in intestinal permeability that was blocked by FZI/0 pretreatment. Conversely, biopsies from non-celiac patients demonstrated a limited, transient zonulin release which was paralleled by an increase in intestinal permeability that never reached the level of permeability seen in celiac disease (CD) tissues. Chronic gliadin exposure caused down-regulation of both ZO-1 and occludin gene expression. CONCLUSIONS: Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules.
PMID: 16635908 http://www.ncbi.nlm.nih.gov/pubmed/1663 ... stractPlus
And here is link to further info on the subject:
http://jccglutenfree.googlepages.com/zonulin
Speculation:
In other words, as a huge study recently found a correlation between mothers with autoimmune diseases, ( particularly celiac ), and their having children on the autism spectrum, ( three times as likely to ) there is reason to think that the intestines of people on the spectrum may be more likely to react to gluten ( the gliadin in it ) in this way than the general population.
And so the theory that the brains of people on the spectrum are more exposed to food opioid peptides than the general population may turn out to be exact ... and Karl Reichelt's theory that gluten peculiarly affects the construction of the growing brain in many people on the spectrum may turn out to be solid.
Presumably your argument about mercury and the chain-reaction refers to the possibility that these immune-system reactions, ( such that gliadin causes more zonulin production and thus greater gut permeability ), rather than being innate/genetic etc, are epigenetic, triggered by vaccinations etc, which are challenges to the immune-system to which our bodies are simply not adapted.
I wonder if they would ever screen all babies for this gliadin-antibody/immune-system reaction ( which determines the strength of the zonulin/gut-"opening" response ), before allowing babies/infants to touch a crumb of wheat!
But even if gluten, and other factors in a complex chain reaction, turn out to be involved in creating autism, ( as the environment, epigenetically and otherwise, is responsible for creating all kinds of profound differences ), this does not mean that it would be possible, or even desirable, to "cure" it ...
[ Gluten and gliadin ( new protein molecules which emerged as the result of a mutation in goats grasses at the end of the last ice age, 15,000 years ago ) may after all be responsible for the beginnings of civilisation!
] ... now it's me going off-topic! 
.
31 Oct 2009, 11:54 am
31 Oct 2009, 12:01 pm
31 Oct 2009, 2:25 pm
01 Nov 2009, 11:34 am
