The gluten/schizophrenia connection has been tossed around since the 1970's. It is still controversial. Yet, some with schizophrenia (statistics say around 10-20%) may be miraculously helped by a simple dietary change. It is important to realize that many people have problems with gluten who do not test positive for Celiac Disease. Gluten can cause different types of problems. Casein sensitivity may be involved as well, for some.
Gluten Intolerance Linked to Schizophrenia
MEDSCAPE (must register, but it's free)
Schizophrenia Linked to Variety of Autoimmune Disorders March 2006
Brain Allergies by Williaim Philpott~ the author suggests any food or chemical to which one is sensitive can potentially cause schizophrenia, among other mental illness. Gluten happens to top the list of problem foods.
Thus, identifying people in schizophrenia who may benefit from a gluten-free diet remains possible by blood test only.
Gluten sensitivity and relationship to psychiatric symptoms in people with schizophrenia.
PMID:25311778 Oct 2014
Several risk factors for the development of schizophrenia can be linked through a common pathway in the intestinal tract. It is now increasingly recognized that bidirectional communication exists between the brain and the gut that uses neural, hormonal, and immunological routes. An increased incidence of gastrointestinal (GI) barrier dysfunction, food antigen sensitivity, inflammation, and the metabolic syndrome is seen in schizophrenia. These findings may be influenced by the composition of the gut microbiota. A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet. Antimicrobials and probiotics have therapeutic potential for reducing the metabolic dysfunction and immune dysregulation seen in patients with schizophrenia.
Schizophrenia and the gut-brain axis.
PMID:25240858 Sep 2014
Our results indicate a higher prevalence of tTG6 antibodies in SZ that may represent a biomarker useful to identify SZ patients who would benefit from a gluten-free diet.
Increased prevalence of transglutaminase 6 antibodies in sera from schizophrenia patients.
RESULTS: Individuals with recent-onset psychosis had increased levels of
IgG (odds ratio [OR] 5.50; 95% confidence interval [CI] 2.65-11.42) and
IgA (OR 2.75; 95% CI 1.31-5.75) antibodies to gliadin compared with
control subjects. Individuals with multi-episode schizophrenia also had
significantly increased levels of IgG antibodies to gliadin (OR 6.19;
95% CI 2.70-14.16). IgG antibodies to deamidated gliadin and IgA
antibodies to tissue transglutaminase were not elevated in either
psychiatric group, and fewer than 1% of individuals in each of the
groups had levels of these antibodies predictive of celiac disease.
There were no significant differences in the distribution of the HLA
DQ2/8 alleles among the groups. CONCLUSIONS: Individuals with
recent-onset psychosis and with multi-episode schizophrenia who have
increased antibodies to gliadin may share some immunologic features of
celiac disease, but their immune response to gliadin differs from that
of celiac disease.
Markers of Gluten Sensitivity and Celiac Disease in Recent-Onset Psychosis and Multi-Episode Schizophrenia.
Biol Psychiatry. 2010 May 13. [Epub ahead of print]
PMID: 20471632 May 2010
A link between celiac disease and schizophrenia has been postulated for several years, based primarily on reports of elevated levels of antibody to gliadin in patients. We sought to examine the proposed connection between schizophrenia and celiac disease by characterizing the molecular specificity and mechanism of the anti-gliadin immune response in a subset of individuals with schizophrenia. Blood samples from individuals with schizophrenia and elevated anti-gliadin antibody titer were examined for celiac disease-associated biomarkers, including antibodies to transglutaminase 2 (TG2) enzyme and deamidated gliadin peptides, as well as the HLA-DQ2 and -DQ8 MHC genes. The anti-gliadin antibody response was further characterized through examination of reactivity towards chromatographically separated gluten proteins. Target proteins of interest were identified by peptide mass mapping. In contrast to celiac disease patients, an association between the anti-gliadin immune response and anti-TG2 antibody or HLA-DQ2 and -DQ8 markers was not found in individuals with schizophrenia. In addition, the majority of individuals with schizophrenia and anti-gliadin antibody did not exhibit antibody reactivity to deamidated gliadin peptides. Further characterization of the antibody specificity revealed preferential reactivity towards different gluten proteins in the schizophrenia and celiac disease groups. These findings indicate that the anti-gliadin immune response in schizophrenia has a different antigenic specificity from that in celiac disease and is independent of the action of transglutaminase enzyme and HLA-DQ2/DQ8. Meanwhile, the presence of elevated levels of antibodies to specific gluten proteins points to shared immunologic abnormalities in a subset of schizophrenia patients. Further characterization and understanding of the immune response to gluten in schizophrenia may provide novel insights into the etiopathogenesis of specific disease phenotypes.
Novel immune response to gluten in individuals with schizophrenia.
PMID: 19748229 Sept 2009
Among schizophrenia patients, 23.1% had moderate to high levels of IgA-AGA compared with 3.1% of the comparison group (chi(2) = 1885, df = 2, P < .001.) Moderate to high levels of tTG antibodies were present in 5.4% of schizophrenia patients vs 0.80% of the comparison group (chi(2) = 392.0, df = 2, P < .001). Adjustments for sex, age, and race had trivial effects on the differences. Regression analyses failed to predict PANSS scores from AGA and tTG antibodies. Persons with schizophrenia have higher than expected titers of antibodies related to CD and gluten sensitivity.
Prevalence of Celiac Disease and Gluten Sensitivity in the United States Clinical Antipsychotic Trials of Intervention Effectiveness Study Population.
PMID: 19494248 June 2009
ABSTRACT: We report the unexpected resolution of longstanding schizophrenic symptoms after starting a low-carbohydrate ketogenic diet. After a review of the literature, possible reasons for this include the metabolic consequences from the elimination of gluten from the diet, and the modulation of the disease of schizophrenia at the cellular level.
While more research is needed to confirm the association between gluten intake and
schizophrenia and whether dietary change can ameliorate schizophrenic symptoms, health care
providers could consider screening patients with schizophrenia for celiac disease and/or augment
the medical regimen with a gluten-free or low-carbohydrate, ketogenic diet.
Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and
review of the literature
PMID: 19245705 Feb 2009
PMID:17327937 Feb 2007
Growing evidence suggests that autoantibodies to neuronal or endothelial targets in psychiatric disorders exist and may be pathogenic. This review describes and discusses the possible role of autoantibodies related to the psychiatric manifestations in autoimmune diseases, autoantibodies related to the psychiatric disorders present in post-streptococcal diseases, celiac disease, chronic fatigue syndrome and substance abuse, and autoantibodies related to schizophrenia and autism, disorders now considered of autoimmune origin.
Autoantibodies associated with psychiatric disorders.
PMID: 16719797 May 2006
The gluten connection: the association between schizophrenia and celiac disease.
PMID: 16423158 Feb 2006
Discussion and conclusions. - 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. [It is frustrating to me that this study focused only on celiac disease (anti-endomysial or anti-tTG) and not gluten sensitivity as indicated by antigliadin antibodies. jcc]
"Bread madness" revisited: screening for specific celiac antibodies among schizophrenia patients.
PMID: 15276666 Aug 2004
A history of coeliac disease is a risk factor for schizophrenia, as shown in this epidemiological study.
Coeliac disease and schizophrenia: population based case control study with linkage of Danish national registers.
PMID: 14976100 Feb 2004
There are several case reports of coexistence of coeliac sprue and depression, schizophrenia and anxiety. Coeliac disease should be taken into consideration in patients with psychiatric disorders, particularly if they are not responsive to psychopharmacological therapy, because withdrawal of gluten from the diet usually results in disappearance of symptoms.
Psychiatric symptoms and coeliac disease.
PMID: 12298186 Aug 2002
This is the first case in which, in an undiagnosed and untreated coeliac patient with psychiatric manifestations, the (99mTc)HMPAO SPECT demonstrated a dysfunction of frontal cortex disappearing after a gluten-free diet.
Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet.
PMID: 9408073 Nov 1997
Dohan has proposed that schizophrenia is a genetic disposition which interacts with an overload of dietary proteins such as casein and gluten or gliadin.
Could schizophrenia be reasonably explained by Dohan's hypothesis on genetic interaction with a dietary peptide overload?
PMID: 8938813 Oct 1996
IgA antibody levels in serum were examined in two groups of schizophrenic patients. All were diagnosed according to DSM-III-R criteria. One group of 36 males and 12 females were compared to historical controls. The other group consisted of 13 males off drugs for at least 3 months; these were compared with age- and sex-matched controls. An increase in specific IgA antibodies was found. More schizophrenics than controls showed IgA antibody levels above the upper normal limit to gliadin, beta-lactoglobulin, and casein
Specific IgA antibody increases in schizophrenia.
PMID: 7772650 Mar 1995
This model is supported by a variety of evidence, including a significant effect of gluten or its absence on relapsed schizophrenic patients, the high correlation of changes in first admission rates for schizophrenia with changes in grain consumption rates, and the rarity of cases of schizophrenia where grains and milk are rare.
Genetic hypothesis of idiopathic schizophrenia: its exorphin connection.
PMID: 2851166 1988
Two patients improved during the gluten-free period and relapsed when the gluten diet was reintroduced.
A double-blind gluten-free/gluten-load controlled trial in a secure ward population.
PMID: 3524724 April 1986
Schizophrenic psychosis disappearing after patient is given gluten-free diet
PMID: 6700311 Feb 1984
Four aspects of clinical evidence for an association between gluten and schizophrenia are examined. The scientific evidence for the role of gluten is set out. Finally, reference is made to other dietary approaches.
Diet (gluten) and schizophrenia.
PMID: 6989901 April 1980
Schizophrenics maintained on a cereal grain-free and milk-free diet and receiving optimal treatment with neuropleptics showed an interruption or reversal of their therapeutic progress during a period of "blind" wheat gluten challenge. The exacerbation of the disease process was not due to variations in neuroleptic doses. After termination of the gluten challenge, the course of improvement was reinstated. The observed effects seemed to be due to a primary schizophrenia-promoting effect of wheat gluten.
Wheat gluten as a pathogenic factor in schizophrenia.
PMID: 1246624 Jan 1976