Abstract
Schizophrenia is a heterogeneous disorder without a fully elucidated etiology and mechanisms. One likely explanation for the development of schizophrenia is low-grade inflammation, possibly caused by processes in the gastrointestinal tract related to gluten sensitivity. The aims of this study were to: (1) compare levels of markers of gluten sensitivity, inflammation and gut permeability, and (2) determine associations between gluten sensitivity, inflammation, and intestinal permeability in patients with first-episode/chronic (FS/CS) schizophrenia and healthy individuals (HC). The total sample comprised 162 individuals (52 FS; 50 CS, and 60 HC). The examination included clinical variables, nutritional assessment, and serum concentrations of: high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), soluble CD14 (sCD14), anti-Saccharomyces cerevisiae antibody (ASCA), antigliadin antibodies (AGA) IgA/IgG, antibodies against tissue transglutaminase 2 (anti-tTG) IgA, anti-deamidated gliadin peptides (anti-DGP) IgG. A significant difference between groups was found in sCD14, ASCA, hs-CRP, IL-6 and AGA IgA levels. AGA IgG/IgA levels were higher in the FS (11.54%; 30.77%) and CS (26%; 20%) groups compared to HC. The association between intestinal permeability and inflammation in the schizophrenic patients only was noted. The risk for developing schizophrenia was odds ratio (OR) = 4.35 (95% confidence interval (CI 1.23–15.39) for AGA IgA and 3.08 (95% CI 1.19–7.99) for positive AGA IgG. Inflammation and food hypersensitivity reactions initiated by increased intestinal permeability may contribute to the pathophysiology of schizophrenia. The immune response to gluten in FS differs from that found in CS.
Highlights
Despite more than 100 years of research into schizophrenia, its etiology has still not been fully elucidated
The study sample consisted of 162 participants aged 18 to 65 years: 52 patients in the first episode of schizophrenia (FS group), 50 patients with chronic schizophrenia (CS group) and 60 healthy individuals as a control group (HC group)
The aim of our study was to find connections between markers of gluten sensitivity, inflammation and gut permeability in the first episode of schizophrenia (FS) and chronic schizophrenia (CS), and determine differences in immune responses to gluten between healthy individuals and patients suffering from schizophrenia
Summary
Despite more than 100 years of research into schizophrenia, its etiology has still not been fully elucidated. This is due to the heterogeneity of its etiopathogenesis and the clinical course [1]. In 2020, Roomruangwong et al proposed a model in which the key factor leading to the development of numerous neuroimmune disorders is the compensatory immune-regulatory reflex system (CIRS). According to these researchers, CIRS negatively regulates the immune–inflammatory response system, leading to a new homeostatic setpoint between both components and changes in immune response [9]
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