Celiac Disease (CD) is an immunological disease that affects about 1 percent of the population. It results from an autoimmune response to gluten, a protein found in barley, wheat and rye. It is characterized by villous atrophy, crypt hyperplasia and increased intraepithelial lymphocytes. It has a genetic basis and results from possession of haplotyes HLA-DQ2 or HLA DQ8.
Gluten sensitivity (GS) has been identified as a distinct disease that is 6x as prevalent as that of CD. Those who are gluten sensitive lack villous atrophy or antibodies, both of which are present in celiac disease. Instead, they test positive for gliadin. In both diseases, extraintestinal symptoms, including neuropsychiatric symptoms, can result. Unfortunately, it oftentimes goes unacknowledged, unrecognized, and untreated. While those with gluten sensitivity lack villous atrophy and antibodies tTG or EMA, they can nonetheless test positive to antibodies to gliadin. Only half of those with gluten sensitivity will test positive for the aforementioned haplotypes.
The neurological effects of celiac are well-known and have been observed for 40 years. Interestingly enough, gluten-sensitive patients not only exhibit psychiatric problems as well, but these psychiatric problems may actually be a primary, rather than secondary, symptom of the disease. Gluten sensitivity may therefore be readily confused with psychiatric problems, and may remain untreated. Over 20 percent of those with celiac disease may develop psychiatric or neurological problem.
Approximately 57 of those with neurological dysfunction test positive, furthermore, for anti-gliadin antibodies. Neurological and psychiatric complications are very frequently observed with gluten-mediated immune responses in general. Numerous articles have been published on the psychiatric and neurological complications of both disorders. These disorders include ataxia, seizure disorders, cerebellar degeneration, schizophrenia, neuropathy, depression, anxiety disorders, ADHD, migraine, multiple sclerosis, autism, myasthenia gravis, white matter lesions and myopathy.
The most well-known neurological symptom of gluten sensitivity is ataxia. It results from positive anti-gliadin antibodies, resulting in changes in the cerebellum. This can result in gait ataxia, dysarthria and upper and lower limb atasia. In one study, 41 percent of 143 patients with sporadic idiopathic ataxia had anti-gliadin antibodies, compared with only 12 percent of control subjects. Cerebellar atrophy and Bergmann astrocytosis have been found in post-mortem examinations of gluten-sensitive individuals. In one study, those with neuropathy and gluten-free ataxia improved significantly after switching to a gluten-free diet.
Epilepsy is frequently found in both gluten-sensitivity and celiac disease, with up to 6 percent of those with epilepsy suffering from celiac disease. Such individuals experience blurred vision and seeing colored dots. Neurologically, bilateral cortical calcification is observed, with hypodense areas in the white matter around their calcifications. In one study, reduction in these areas resulted from a gluten-free diet. Seizure activity was also better managed and was experienced less frequently.
Those with celiac disease were found to be significantly more predisposed to state anxiety relative to controls. A year on a gluten-free diet led to significant improvement. Those with celiac disease are also much more likely to experience social phobia and panic disorder. Major depressive disorder, adjustment disorders and dysthmia were likewise found to be much more common in individuals with celiac disease relative to controls. This was not the case, however, with bipolar disorder. An elderly population exhibiting gluten sensitivity was found to be over twice as likely to have depression relative to those without gluten sensitivity.
Some studies have correlated gluten intolerance with ADHD. Those with celiac disease were found to be more likely to exhibit ADHD symptoms relative to the general population. A 6 month gluten-free diet was found to improve ADHD symptoms in almost 75 percent of the patients. Autism spectrum disorders (ASD) were likewise found to be highly associated with gluten intolerance. One study found a correlation between ASDs in children with a maternal history of both celiac disease and rheumatoid arthritis. Another correlated it with both diseases, as well as IBS. Individuals with ASD, along with their family members, tend to have abnormal intestinal permeability, which improves with gluten-free diets.
Schizophrenia is more correlated with gluten intolerance than any other psychiatric disorder. This has been noted as early as the 1950s, and was further fund on a study of those with celiac disease and schizophrenia in the 1960s. Another study published in the late 1960s found that schizophrenia was lower in countries with low grain consumption. Milk-free and cereal-free diets have also been found to improve the symptoms of schizophrenia. Patients on this diet were likewise found to have been moved more quickly to a non-locked ward than those without the diet. They were also discharged twice as quickly, and recovery was found to be hindered with the administration of a diet with gluten.
In the late 1990s, a case study was produced which described a schizophrenic women who exhibited negative symptoms, as well as hallucinations. She exhibited hpoperfusion in the left frontal cortex on SPECT scan and fronto-temporal abnormalities on an EEG scan. A gluten-free diet produced significant improvement, leading to the remission of hypoperfusion as well as psychiatric symptoms. She was eventually able to discontinue antipsychotic medication and remained symptom-free for a year. Another study detailed 14 subjects on a locked research ward who were put on a gluten-free diet, and then put back on a diet with gluten.
Significant improvement were reported by blinded assessors on 30 of the 39 psychopathology and social avoidance measures, as well as participation measures. During a blinded study, 16 were put on a gluten-free diet. Two exhibited improved functioning, and one of these two exhibited major regression after being put back on a diet with gluten in it. Those with schizophrenia, in one study, were found to have significantly higher amounts of anti-gliadin antibodies. Another study found abnormally high levels of IgA and lgG antibodies to gliadin in those with recent-onset psychosis, relative to controls and schizophrenics with multi-episodes which were not of recent onset. This study’s results were replicated, with 27 percent of patients with schizophrenia exhibiting anti-gliadin antibodies relative to 18 percent of controls.