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  • Jefferson Adams
    Jefferson Adams

    Gluten-sensitivity in Autism Different than Celiac Disease

    Reviewed and edited by a celiac disease expert.
    Gluten-sensitivity in Autism Different than Celiac Disease - Photo: CC--Bryce Edwards
    Caption: Photo: CC--Bryce Edwards

    Celiac.com 07/24/2013 - Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity.

    Photo: CC--Bryce EdwardsSo far, studies of the immune response to gluten in autistic individuals, along with its association with celiac disease have produced inconsistent data.



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    A team of researchers recently set out to assess immune reactivity to gluten in children diagnosed with autism according to strict criteria, and to evaluate the potential link between autism and celiac disease.

    The research team included Nga M. Lau, Peter H. R. Green, Annette K. Taylor, Dan Hellberg, Mary Ajamian, Caroline Z. Tan, Barry E. Kosofsky, Joseph J. Higgins, Anjali M. Rajadhyaksha, and Armin Alaedini.

    For their study, the team assessed 37 children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADI-R), 27 unaffected siblings, and 76 age-matched healthy controls.

    They then tested blood specimens for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). They then genotyped all children with positive antibody tests for celiac disease associated HLA-DQ2 and -DQ8 alleles.

    The team found that children with autism had substantially higher levels of IgG antibodies compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but were not statistically significant. Autistic children with gastrointestinal symptoms showed significantly greater IgG anti-gliadin antibody response, compared to those without them (p<0.01). All groups showed similar IgA response to gliadin across groups.

    Both study subjects and control subjects ahd similar levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2. The researchers found no association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8.

    Some children with autism do show a type of increased immune reactivity to gluten which appears to be different from celiac disease.

    The increased anti-gliadin antibody response and its association with GI symptoms suggests that these children may suffer from immunologic and/or intestinal permeability abnormalities.

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  • About Me

    Jefferson Adams

    Jefferson Adams is Celiac.com's senior writer and Digital Content Director. He earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,500 articles on celiac disease. His coursework includes studies in science, scientific methodology, biology, anatomy, medicine, logic, and advanced research. He previously served as SF Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.


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  • Related Articles

    Jefferson Adams
    Celiac.com 07/08/2009 - Kids whose moms have autoimmune diseases such as type 1 diabetes, rheumatoid arthritis and celiac disease face a risk of autism that is up to three times higher than that of the general population, according to a new study.
    Although earlier studies have documented a connection between autism and a maternal history of type 1 diabetes and rheumatoid arthritis, this is the first study to document a link between autism and celiac disease, according to the study's authors.
    A team of researchers led by Dr. William W. Eaton, chairman of the Department of Mental Health at the Bloomberg School of Public Health at Johns Hopkins University recently set out to review data related to autoimmune deficiency and autism.  
    Eaton's team collected data on 3,325 Danish children diagnosed with autism spectrum disorder, including 1,089 diagnosed with infantile autism. All of the children were born between 1993 and 2004, and their data was part of the Danish National Psychiatric Registry. Data on family members with autoimmune diseases came from the Danish National Hospital Register.
    The data showed that children whose mothers had autoimmune disease faced a higher risk of developing autism spectrum disorder than children of mothers who did not have these conditions. Moreover, children with a family history of type 1 diabetes faced an increased risk of infantile autism.
    Overall, the increased risk of autism in people with autoimmune diseases is not huge, Eaton said. "The increased risk for type 1 diabetes is a little less than two times, for rheumatoid arthritis it's about 1.5 times and for celiac disease it's more than three times," Eaton said. "That's enough to impress an epidemiologist, but not enough to make anybody in the general population start changing their behavior."
    Eaton added that this finding "reinforces the suggestion that autoimmune processes are connected somehow with the cause of autism and autism spectrum disorder, and...may point a flashlight to areas of the genome that connect to autism."
    The finding itself has no clinical significance, says Eaton, but could guide future efforts by researchers to determine the cause or causes of autism.
    One reason autoimmune diseases might have a role in autism lies in genetic history, Eaton said. Children who were underweight or premature at birth face a higher risk for autism, and both of these obstetric problems are associated with celiac disease, he added.
    There may be a significant overlap "in the genetics of some of the autoimmune diseases and autism," he said. "Autism is strongly inherited, but we don't have the faintest idea where...this finding is on the pathway of finding the cause of autism." Various environmental triggers may also affect the fetus, he said.
    Lead researcher, Dr. Hjordis O. Atladottir, from the Institute of Public Health at the University of Aarhus in Denmark calls the findings important because they support the theory that autism is somehow tied to problems with the immune system.

    PEDIATRICS



    Jefferson Adams
    Celiac.com 12/21/2012 - Over the past several years, researchers have made substantial progress in understanding the causes of autism, which now afflicts about 1 in 88 children. However, very little news of this progress seems to have spread into popular consciousness, much of which continues to focus on the possible role of vaccines.
    Recent discoveries indicates that one-third or more cases of autism look to be a kind of inflammatory disease, which begins well before birth.
    In the August 25th issue of the New York Times, Moises Velasquez-Manhoff has very interesting article in which he discusses the widening view among researchers that autism is, in fact, an inflammatory disease. The article is long and comprehensive, and cites numerous studies, findings and experiments.
    Inflammation is the body's natural response to certain kinds of threats. In a normal body, the immune system uses inflammation in a very precise, targeted way, before returning to a normal state.
    In autistic individuals, inflammatory signals become the dominant condition, and there is no balancing anti-inflammatory response. A state of chronic inflammation becomes normal. And the more skewed toward inflammation, the more acute the autistic symptoms.
    This inflammatory deregulation adversely impacts the brains of autistic individuals. Velasquez-Manhoff also cites a number of studies that trace these inflammatory effects back to the inflammatory responses of the mother during pregnancy.
    Among the studies cited in the article is a population-wide study from Denmark spanning two decades of births, which indicates that infection during pregnancy increases the risk of autism in the child. The study found that hospitalization for a viral infection, like the flu, during the first trimester of pregnancy triples the odds of autism. Bacterial infection, including of the urinary tract, during the second trimester increases chances by 40 percent.
    Another large Danish study, which included nearly 700,000 births over a decade, found that a mother’s rheumatoid arthritis, a degenerative disease of the joints, elevated a child’s risk of autism by 80 percent. Rates of autism in children of mothers with celiac disease were 350 percent higher than normal. Genetic studies had similar findings. Variations in genes associated with regulating the immune system also increase the risk of autism, especially when they occur in the mother.
    A mother’s diagnosis of asthma or allergies during the second trimester of pregnancy increases her child’s risk of autism. So does metabolic syndrome, a disorder associated with insulin resistance, obesity and, crucially, low-grade inflammation.
    Yet, viral and bacterials infections themselves do not seem the cause of the autism epidemic. The epidemiology doesn’t support that conclusion.
    A far more likely culprit is maternal immune dysregulation. Basically, the mother’s attempt to repel invaders, her inflammatory response, seems to be at fault. Research by Paul Patterson, an expert in neuroimmunity at Caltech, supports this idea. In his research, he introduces inflammation in pregnant mice artificially, without a live infection. This causes behavioral problems in the young. In this model, autism results from collateral damage. It’s an unintended consequence of self-defense during pregnancy.
    Since infantile autism was first described by Leo Kanner in 1943, diagnoses have risen tenfold. During that same period, viral and bacterial infections generally declined. However, overall rates of inflammatory diseases have risen sharply since then.
    As a group, these diseases include asthma, now estimated to affect 1 in 10 children, rates that have at least doubled since 1980, along with autoimmune disorders, which now afflict 1 in 20.
    Recently, William Parker at Duke University has chimed in. Some years back, he began comparing wild sewer rats with clean lab rats. The bodies of wild rats tightly controlled inflammation, but those of the lab rats did not. Parker found that the bodies of the wild rats contained high levels of parasites. Parasites are noted for limiting inflammation.
    One lesson from these rodent experiments is that fixing the maternal dysregulation will most likely prevent autism. That theory is supported by Swiss researchers, who created a lineage of mice with a genetically reinforced anti-inflammatory signal. They then inflamed the pregnant mice. The babies emerged fine, with no behavioral problems. This suggests that if inflammation is controlled during pregnancy, it won’t interfere with fetal brain development.
    Interestingly, asthma researchers are coming to similar conclusions: preventing inflammation in pregnant women will likely prevent asthma.
    Dr. Parker has introduced a more aggressive approach. He suggests that by using specially developed worms to restore “domesticated” parasites doctors can correct immune dysregulation.
    To determine if this is feasible, a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine. The trial is using a medicalized parasite called Trichuris suis, known as a whipworm, to treat autistic adults.
    The whipworm is native to pigs, and was first used medically to treat inflammatory bowel disease. It has shown anecdotal benefit in autistic children.
    The article suggests that the future of treating immune dysregulation, and thus preventing diseases like autism and asthma, may lie in reintroducing parasites into the human body. Stay tuned for more updates on this truly fascinating science.
    Read the full article by Moises Velasquez-Manhoff in the New York Times.


    Jefferson Adams
    Celiac.com 10/15/2013 - Most case reports suggest an association between autistic spectrum disorders (ASDs) and celiac disease (celiac disease) or positive celiac disease serologic test results, but larger studies are contradictory.
    A team of researchers recently set out to examine the association between ASDs and celiac disease according to small intestinal histopathologic findings.
    The research team included Jonas F. Ludvigsson; Abraham Reichenberg; Christina M. Hultman; and Joseph A. Murray. They are variously affiliated with the Department of Medicine, Clinical Epidemiology Unit, and the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, with the Department of Pediatrics at Orebro University Hospital, Orebro University in Orebro, Sweden, with the Division of Gastroenterology and Hepatology of the Department of Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, with the Department of Psychosis Studies at the Institute of Psychiatry at King’s College in London, United Kingdom, and with the Department of Psychiatry at the Mount Sinai School of Medicine in New York, New York.
    For their nationwide case-control study, the researchers used 28 Swedish biopsy registers to gather data on approximately 26,995 individuals with celiac disease, which they defined as the presence of villous atrophy, Marsh stage 3.
    They found 12,304 patients with inflammation (Marsh stages 1-2), 3719 patients with normal mucosa (Marsh stage 0), but positive celiac results for IgA/IgG gliadin, endomysium, or tissue transglutaminase. They then compared these results against and results for 213,208 age- and sex-matched control subjects. The team used conditional logistic regression to estimate odds ratios (ORs) for prior ASD diagnosis according to the Swedish National Patient Register and then conducted a second analysis, using Cox proportional hazards regression to estimate hazard ratios (HRs) for future ASDs in individuals undergoing small intestinal biopsy.
    They found that previous ASD was not associated with celiac disease (OR, 0.93; 95% CI, 0.51-1.68) or inflammation (OR 1.03; 95% CI, 0.40-2.64). However, they did finds that previous ASD was associated with a sharp higher risk of having normal mucosa but positive serologic test result for celiac disease (OR, 4.57; 95% CI, 1.58-13.22).
    Once the team restricted the data to individuals without no diagnosis for ASD at the time of biopsy, they found that celiac disease (HR, 1.39; 95% CI, 1.13-1.71) and inflammation (HR, 2.01; 95% CI, 1.29-3.13) were both connected with slightly higher risks of later ASDs, compared against the HR of 3.09 (95% CI, 1.99-4.80) for later ASDs in individuals with normal mucosa but positive celiac disease serologic test results.
    Even though this study showed no connection between previous ASD and celiac disease or inflammation, it did show that individuals with normal mucosa, but positive blood screens for celiac disease, have a much higher risk of ASD.
    Source:
    JAMA Psychiatry. Published online September 25, 2013. doi:10.1001/jamapsychiatry.2013.2048


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