Eur Psychiatry. 2004 Aug;19(5):311-4. Celiac.com 09/12/2004 - Israeli researchers conducted a study designed to determine whether or not an association exists between celiac disease and schizophrenia. Past studies have indicated that such a connection may exist. The researchers screened 50 consecutive patients over 18 years old who were diagnosed with schizophrenia and their matched controls for celiac-specific anti-endomysial IgA antibodies. All patients also completed a detailed questionnaire. There were no significant differences between the groups in gender, Body Mass Index (BMI) or country of birth, and the mean age of the study group was significantly higher than the controls. All tests for anti-endomysial antibodies in both groups were negative, and the researchers concluded that "In contrast to previous reports, we found no evidence for celiac disease in patients with chronic schizophrenia as manifested by the presence of serum IgA anti-endomysial antibodies. It is unlikely that there is an association between gluten sensitivity and schizophrenia"
Celiac.com Comments on this Study:
This was a relatively small study that did not include other celiac disease screening methods, such as IgG (antigliadin antibody), tTG (tissue Transglutaminase), or intestinal biopsies. A recent study has shown that only 77% of those with total and 33% of those with partial villous atrophy actually have positive blood tests for celiac disease, so many cases of celiac disease may be missed by using only blood tests to screen for it. Further, about 4% of celiacs are anti-endomysial IgA deficient, so anyone in this subclass would have been missed in the study. Given such a small number of people in the study--50--if even one celiac were missed it would greatly affect the outcome of the study. Both groups should have been given much more comprehensive celiac disease screening to ensure that no cases of celiac disease were missed.
In the article by Dr. Hadjivassiliou titled Gluten Sensitivity as a Neurological Illness he says:
The introduction of more celiac disease specific serological markers such as anti-endomysium and more recently transglutaminase antibodies may have helped in diagnosing celiac disease but their sensitivity as markers of other manifestations of gluten sensitivity (where the bowel is not affected) is low. This certainly reflects our experience with patients with gluten sensitivity who present with neurological dysfunction. Endomysium and transglutaminase antibodies are only positive in the majority but not in all patients who have an enteropathy. Patients with an enteropathy represent only a third of patients with neurological manifestations and gluten sensitivity. Antigliadin antibodies unlike endomysium and transglutaminase antibodies are not autoantibodies. They are antibodies against the protein responsible for gluten sensitivity.
Only one third of the patients with neurological disorders associated with gluten sensitivity have villous atrophy on duodenal biopsy. Even some with biochemical markers of malabsorption such as low serum vitamin B12, low red cell folate, or vitamin D concentrations had normal conventional duodenal histology. These cases may illustrate the patchy nature of bowel involvement in coeliac disease and the inaccurate interpretation of duodenal biopsies by inexperienced histopathologists. Preliminary data based on staining of the subpopulation of T cells in the small bowel epithelium suggests that these patients have potential celiac disease. There are, however, patients where the immunological disorder is primarily directed at the nervous system with little or no damage to the gut. Our practice is to offer a gluten-free diet to these patients unless the HLA genotype is not consistent with susceptibility to gluten intolerance (that is, other than HLA DQ2, DQ8, or DQ1). All patients are followed up and any clinical response is documented.