Celiac Disease, Gluten Sensitivity and Autism

AusticBoy Is there a relationship between celiac disease and autism? Many people believe there might be. This is in part because many children with autism have intestinal symptoms that are similar to those of celiac disease. Another reason is that some parents who have tried gluten-free diets for their autistic children report both an improvement in autistic symptoms and behavior as well as improvements in the gastrointestinal symptoms.

Studies so far have not proved that autistic children are more likely to have celiac disease, or that the autistic children with intestinal complains have celiac disease. But researchers continue to examine the possibility of a relationship. There is some evidence that the intestines of children with autism may be leakier than normal, which is also the case in celiac disease.

A recently published study has yielded more information about what all this might mean. Researchers looked at140 children, 37 who had autism, 27 who were siblings of the autistic children and of similar ages who were not autistic, and 76 who were healthy children.

The autistic children were part of the Autism Genetic Research Exchange (AGRE) in the United States. These children met two different sets of diagnostic criteria for autism. Blood samples as well as histories and information about symptoms were provided for these children, their unaffected siblings, and the matched healthy children who came from both the United States and Sweden.

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The blood of all the participants was examined for the presence of a number of antibodies. In order to understand the results, antibodies in general and the antibodies involved in celiac disease have to be understood. The numbers of affected individuals with certain antibodies were checked for statistical significance. This information can seem scientific and dry. But it does lead to some possible conclusions.

The body makes antibodies, also called immunoglobulins, in reaction to what it perceives as a threat, such as an infection. When the threat comes in through the mouth and intestinal tract, the body makes what is called IgA (Immunoglobulin A). When it comes into the bloodstream, like many viruses, the body makes two different kinds of immunoglobulins, first IgM, and later IgG.
Sometimes the body gets confused, as in autoimmune diseases, and makes various forms of immunoglobulins to something that is not a danger. If the body is reacting in an allergic manner, to foods, pollen, or pet dander, it makes IgE.

In celiac disease, pieces of gliadin, which are parts of gluten, get across the intestinal barrier and the intestine makes IgA in response. The IgA antibodies are made to gliadin which has been partly broken down and is called deamidated gliadin. IgA antibodies to tissue transglutaminase, which is found in the intestine, are also made in CD. This is sometimes called TG2.

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The main blood tests for celiac disease currently measure IgA against deamidated gliadin and tissue transglutaminase. About 5% of people with celiac disease do not make any IgA at all. In these cases, IgG antibodies can be measured to both deamidated gliadin and tissue transglutaminase. This is not as reliable.

The body can also make IgG antibodies to gliadin. This is not what happens in celiac disease, but it does mean that a person with these antibodies is reacting to a part of the gluten protein as if it were a danger. This is also different than an allergy, in which case IgE would be made.

In the study, all the participants had levels measured of antibodies to gliadin, both IgA and IgG. Both IgG and IgA levels of antibodies to deamidated gluten and transglutaminase were also measured.

All participants were checked using the currently accepted best tests for celiac disease antibodies. These are measurements of IgA and IgG antibodies to deamidated gliadin, as well as IgA antibodies to transglutaminase (TG2). None of the research subjects was positive for IgA antibody to TG2.  None of the autistic children had IgA to deamidated gliadin, while 1of the siblings (out of 27) and 1 healthy control (out of 76) were found to have IgA to deamidated gliadin. This was not statistically significant.

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Out of the 37 autistic children, two had levels considered positive for IgG antibody to deamidated gluten.  Three siblings and no healthy controls had values above the manufacturer’s assigned cutoff for IgG antibody to deamidated gliadin. This was again not statistically significant.

However, the children with autism were more likely to have IgG antibodies to (whole) gliadin. 24.2% of the autistic children, none on a gluten-free diet, had anti-gliadin IgG antibodies, compared with 7.4% of their healthy siblings, and 5.3% of the controls. IgA antibody levels to gliadin were similar among all the groups.

Dr. Anna Kaplan

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