A review on the relationship between gluten and schizophrenia: Is gluten the cause?

Ergün, Can; Urhan, Murat; Ayer, Ahmet

doi:10.1080/1028415x.2017.1313569

Cited by 23 publications

(15 citation statements)

References 102 publications

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“…Nevertheless, it should be underscored that zonulin levels are not only affected by the Hp-2 gene, but also by gliadin and other bacterial toxins, which may induce the release of zonulin and consequently displace the zonula occludens thereby opening the paracellular leak pathway which allows pathogens, bacterial antigens and other proteins to be translocated into the plasma [6]. In this respect, it is interesting to note that gluten sensitivity, antigliadin antibodies and celiac disease may play a role in schizophrenia [80][81][82] and that gut dysbiosis may occur in some patients with schizophrenia [83]. However, increased levels of pro-inflammatory cytokines, including IL-6, IFN-γ and TNF-α, cause gut barrier dysfunctions and disassemble TJs and AJs thereby upregulating the paracellular leak pathway [84][85][86][87] and c) lowered natural IgM which aggravates the effects of the first two paths.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia

Maes¹,

Sirivichayakul²,

Kanchanatawan³

et al. 2019

Preprint

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In 2001, the first author of this paper reported that schizophrenia is associated with an increased frequency of the haptoglobin (Hp)-2 gene. The precursor of Hp-2 is zonulin, a molecule that affects intercellular tight junction integrity. Recently, we reported increased plasma IgA/IgM responses to Gram-negative bacteria in deficit schizophrenia indicating leaky gut and gut dysbiosis. The current study was performed to examine the integrity of the paracellular (tight and adherens junctions) and transcellular (cytoskeletal proteins) pathways in deficit versus non-deficit schizophrenia. We measured IgM responses to zonulin, occludin, E-cadherin, talin, actin and vinculin in association with IgA responses to Gram-negative bacteria, CCL-11, IgA responses to tryptophan catabolites (TRYCATs), immune activation and IgM to malondialdehyde (MDA) and NO-cysteinyl in 78 schizophrenia patients and 40 controls. We found that the ratio of IgM to zonulin + occudin / talin + actin + viculin (PARA/TRANS) was significantly greater in deficit than in non-deficit schizophrenia and higher in schizophrenia than controls and was significantly associated with increased IgA responses to Gram-negative bacteria. IgM responses to zonulin were positively associated with schizophrenia (versus controls), while IgM to occludin was significantly associated with deficit schizophrenia (versus non-deficit schizophrenia and controls). A large part of the variance (90.8%) in negative and PHEM (psychosis, hostility, excitation and mannerism) symptoms was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, IgM to E-cadherin and malondialdehyde (MDA) and memory dysfunctions, while 53.3% of the variance in the latter was explained by PARA/TRANS ratio, IgA to Gram-negative bacteria, CCL-11, TRYCATs and immune activation. The results show an upregulated paracellular pathway with breakdown of the tight and ahherens junctions and increased bacterial translocation in deficit schizophrenia. These dysfunctions in the intestinal paracellular route together with lowered natural IgM, immune activation and production of CCL-11 and TRYCATs contribute to the phenomenology of deficit schizophrenia.

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Section: Discussionmentioning

confidence: 99%

Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia

Maes¹,

Sirivichayakul²,

Kanchanatawan³

et al. 2019

Preprint

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“…The objectives and outcome measures of the latter study [ 85 ] did not match the principal objective of the meta-analysis whereby the authors investigated the prevalence of autoimmune diseases (including CD) in patients with schizophrenia and not the other way around [ 85 ]. The association between CD and gluten-related disorders with schizophrenia has been under investigation for more than five decades but most studies evaluated the prevalence or risk of gluten-related disorders in patients already diagnosed with schizophrenia [ 86 ]. Current evidence suggests a two-fold increase in the prevalence of CD in schizophrenia patients [ 87 ] and an association between gluten ingestion and exacerbation of schizophrenia symptoms [ 88 ]; nonetheless, these findings are highly inconsistent across different clinical, immunological, and epidemiological studies [ 86 ] and have not been replicated in patients presenting with CD.…”

Section: Discussionmentioning

confidence: 99%

Psychiatric Comorbidity in Children and Adults with Gluten-Related Disorders: A Narrative Review

2018

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Gluten-related disorders are characterized by both intestinal and extraintestinal manifestations. Previous studies have suggested an association between gluten-related disorder and psychiatric comorbidities. The objective of our current review is to provide a comprehensive review of this association in children and adults. A systematic literature search using MEDLINE, Embase and PsycINFO from inception to 2018 using terms of ‘celiac disease’ or ‘gluten-sensitivity-related disorders’ combined with terms of ‘mental disorders’ was conducted. A total of 47 articles were included in our review, of which 28 studies were conducted in adults, 11 studies in children and eight studies included both children and adults. The majority of studies were conducted in celiac disease, two studies in non-celiac gluten sensitivity and none in wheat allergy. Enough evidence is currently available supporting the association of celiac disease with depression and, to a lesser extent, with eating disorders. Further investigation is warranted to evaluate the association suggested with other psychiatric disorders. In conclusion, routine surveillance of potential psychiatric manifestations in children and adults with gluten-related disorders should be carried out by the attending physician.

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“…Although, to our knowledge, this is the only study conducted to date, and further replication and extension of this study is required to elaborate on this finding, it has potential implications for people suffering from food allergies, because curcumin may influence allergenic responses to certain foods. Food allergies and sensitivities, particularly those associated with gluten, have been implicated in several diseases, including gastrointestinal disorders (103,104), rheumatic diseases (105), and even neurological and neuropsychiatric conditions such as depression (106), schizophrenia (107), autism (108,109), and dementia (110). However, the research is limited and often inconsistent.…”

Section: Antianaphylactic Effectsmentioning

confidence: 99%

The Problem of Curcumin and Its Bioavailability: Could Its Gastrointestinal Influence Contribute to Its Overall Health-Enhancing Effects?

Lopresti

2018

Advances in Nutrition

258

154

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Curcumin, from the spice turmeric, exhibits anti-inflammatory, antioxidant, anticancer, antiviral, and neurotrophic activity and therefore holds promise as a therapeutic agent to prevent and treat several disorders. However, a major barrier to curcumin's clinical efficacy is its poor bioavailability. Efforts have therefore been dedicated to developing curcumin formulations with greater bioavailability and systemic tissue distribution. However, it is proposed in this review that curcumin's potential as a therapeutic agent may not solely rely on its bioavailability, but rather its medicinal benefits may also arise from its positive influence on gastrointestinal health and function. In this review, in vitro, animal, and human studies investigating the effects of curcumin on intestinal microbiota, intestinal permeability, gut inflammation and oxidative stress, anaphylactic response, and bacterial, parasitic, and fungal infections are summarized. It is argued that positive changes in these areas can have wide-ranging influences on both intestinal and extraintestinal diseases, and therefore presents as a possible mechanism behind curcumin's therapeutic efficacy.

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A review on the relationship between gluten and schizophrenia: Is gluten the cause?

Cited by 23 publications

References 102 publications

Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia

Upregulation of the Intestinal Paracellular Pathway with Breakdown of Tight and Adherens Junctions in Deficit Schizophrenia

Psychiatric Comorbidity in Children and Adults with Gluten-Related Disorders: A Narrative Review

The Problem of Curcumin and Its Bioavailability: Could Its Gastrointestinal Influence Contribute to Its Overall Health-Enhancing Effects?

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