Dariusz Juchnowicz

Processing speed is associated with differences in IQ and cognitive profiles between patients with schizophrenia and their healthy siblings

Abstract Background: Processing speed turns out to be the central area of research on cognition in schizophrenia. So far the relationship between this dimension and the IQ level of patients and their healthy siblings has not been investigated. Aim: To investigate the differences in cognitive speed in patients with schizophrenia and their healthy siblings, and to determine whether cognitive speed as a covariate affects differences in IQ and cognitive profiles between groups. Methods: Forty-seven inpatients diagnosed with schizophrenia according to DSM-IV (SCH) and their 36 healthy siblings (HSB) were tested with cognitive speed tasks according to Bartzokis et al. method and Wechsler Intelligence Scale. Additional control for the possible impact of antipsychotic drugs and selected demographic variables on the cognitive performance was taken into account. Results: The siblings scored significantly higher in the cognitive speed task (p < 0.01) than patients, the WAIS-R cognitive test profiles were also significantly different in two ways: between groups, and between single test results in each of the assessed groups. The interaction effect: ANOVA, F(10, 770) = 2.798, p = 0.002. Similarly, the Performance and Full Scale IQs were significantly different, at p < 0.01. After controlling for cognitive speed, all significant differences no longer exist: e.g. Full Scale IQ, p = 0.459. Conclusions: Significant differences in cognitive speed between patients and their healthy siblings generate the differences in the cognitive profile assessed with Wechsler Intelligence Scale. Some problems of cognitive speed diagnosis and further research on the cognitive schizophrenia endophenotype were discussed.

The brain-gut axis dysfunctions and hypersensitivity to food antigens in the etiopathogenesis of schizophrenia

Despite over 100-year history of research on schizophrenia, its etiology is still not fully understood, which might be due to the significant heterogeneity in terms of both its course, as well as the etiopathogenesis. One of the best-proven mediating mechanisms in the development of schizophrenia is the immuno-inflammatory response, the sources of which are believed to be the dysfunctions of brain-gut axis and pathological processes occurring in the intestines. This paper is a review of the literature on this subject which presents factors both involved in the functioning of brain-gut axis and important for the development of schizophrenia, i.e. 1. intestinal microbiome (intestinal microbiota), 2. permeable intestine (leaky gut syndrome), 3. hypersensitivity to food antigens, including gluten and casein of cows milk. Research results seem to be very promising and indicate the possibility of improved clinical outcomes in some patients with schizophrenia by modifying diet, use of probiotics, and the implementation of antibiotic therapy of specific treatment groups. However, further research is needed on links between the intestinal microbiome and intestinal function as factors mediating the activation of the immune system and the development and further course of schizophrenia.

The role of IgG hypersensitivity in the pathogenesis and therapy of depressive disorders

Depressive episodes are associated not only with changes in neurotransmission in the central nervous system, but also may lead to structural changes in the brain through neuroendocrine, inflammatory, and immunological mechanisms. The aim of this article is to present a new hypothesis connecting the inflammatory theory of depression with IgG food hypersensitivity and leaky gut syndrome. This new potential pathway that may mediate the pathogenesis of depression implies the existence of subsequent developmental stages. Overproduction of zonulin triggered, for example, by gliadin through activation of the epidermal growth factor receptor and protease-activated receptor causes loosening of the tight junction barrier and an increase in permeability of the gut wall (‘leaky gut’). This results in a process allowing larger molecules that would normally stay in the gut to cross into the bloodstream and in the induction of IgG-dependent food sensitivity. This condition causes an increased immune response and consequently induces the release of proinflammatory cytokines, which in turn may lead to the development of depressive symptoms. It seems advisable to assess the intestinal permeability using as a marker, for example, zonulin and specific IgG concentrations against selected nutritional components in patients with depression. In the case of increased IgG concentrations, the implementation of an elimination–rotation diet may prove to be an effective method of reducing inflammation. This new paradigm in the pathogenesis of depressive disorders linking leaky gut, IgG-dependent food sensitivity, inflammation, and depression is promising, but still needs further studies to confirm this theory.

INTESTINAL MICROBIOTA – A KEY TO UNDERSTANDING THE PATHOPHYSIOLOGY OF ANOREXIA NERVOSA?

Anorexia nervosa (AN) is a psychiatric disorder related to very serious consequences for physical and mental health of patients. Due to a complex clinical picture, which consists of anumber of somatic and mental symptoms, AN remains a serious problem of modern medicine and encourages the search for possible causes of the illness and new, more effective therapies. The recent reports emphasize the role of the intestinal microbiota in regulation of body weight. In this light, the hypothesis that in AN patients there is a significant imbalance of the intestinal microbiota, which contributes to the pathogenesis of the illness, seems interesting. The results of the latest research suggest that abnormal composition of the intestinal microbiota may be an important factor supporting cachexia of AN patients. Detailed analyzes of the composition of the microbiota characteristic for anorexia nervosa could be useful in developing new methods for monitoring and treatment of this illness. This paper aims to present the current state of the art about the role of the intestinal microbiota in the pathogenesis, course and treatment of AN.

Review paper. Gluten-related disorders and schizophrenia - potential linking mechanisms, diagnostic and therapeutic challenge

Abstract More and more evidence confirms the theory that the intake of cereal products containing gluten may play an important role in the pathogenesis of many diseases. There are also premises indicating the relationship between the so-called gluten-related diseases and the development and course of mental disorders, including schizophrenia. The aim of this article is to review the literature on the potential relationship between the consumption of gluten and schizophrenia, considering the etiopathogenesis and the role of gluten-free diet in the treatment of schizophrenia. Methods: There were analysed available research papers in PubMed and Google Scholar with the key words: schizophrenia, gluten- related disorders, allergy to grain products, celiac disease, microbiota, immune system, exorphins and time span: 1960-2016 . Conclusions: Existing research results indicate a possible relationship between diet rich in grain products with high gluten content and the occurrence or exacerbation of schizophrenia symptoms. However, further studies are necessary to: 1) identify groups of patients for whom the consumption of cereal products (gluten) is associated with a particular risk of schizophrenia exacerbation, 2) determine the mechanisms relating the consumption of gluten with the mental state of schizophrenic patients, 3) get the possible benefits of implementing gluten-free diet in patients with schizophrenia.

The Food-Specific Serum IgG Reactivity in Major Depressive Disorder Patients, Irritable Bowel Syndrome Patients and Healthy Controls

There is an increasing amount of evidence which links the pathogenesis of irritable bowel syndrome (IBS) with food IgG hyperreactivity. Some authors have suggested that food IgG hyperreactivity could be also involved in the pathophysiology of major depressive disorder (MDD). The aim of this study was to compare levels of serum IgG against 39 selected food antigens between three groups of participants: patients with MDD (MDD group), patients with IBS (IBS group) and healthy controls (HC group). The study included 65 participants (22 in the MDD group, 22 in the IBS group and 21 in the HC group). Serum IgG levels were examined using enzyme-linked immunosorbent assay (ELISA). Medical records, clinical data and laboratory results were collected for the analysis. IgG food hyperreactivity (interpreted as an average of levels of IgG antibodies above 7.5 µg/mL) was detected in 28 (43%) participants, including 14 (64%) from the MDD group, ten (46%) from the IBS group and four (19%) from the HC group. We found differences between extreme IgG levels in MDD versus HC groups and in IBS versus HC groups. Patients with MDD had significantly higher serum levels of total IgG antibodies and IgG against celery, garlic and gluten compared with healthy controls. The MDD group also had higher serum IgG levels against gluten compared with the IBS group. Our results suggest dissimilarity in immune responses against food proteins between the examined groups, with the highest immunoreactivity in the MDD group. Further studies are needed to repeat and confirm these results in bigger cohorts and also examine clinical utility of IgG-based elimination diet in patients with MDD and IBS.

GPR120: Mechanism of action, role and potential for medical applications

G protein-coupled receptors (GPCRs) constitute a family of transmembrane proteins that mediate many cellular processes. GPR120/FFAR4, a receptor from this family that is activated by fatty acids, has received considerable attention recently. This paper presents a literature review concerning the role of GPR120 and its mechanism of action in animal and human studies as well as the potential use of GPR120 for the treatment of chronic diseases. Two electronic databases - Medline and Google Scholar - were searched for available studies addressing the review topic that were written in English and published from 2000 to June 2017. The following key terms were used in the search: GPR120, FFA4, GPR120 agonist, PUFAs, EPA, DHA, adipocyte, obesity, hyperlipidemia, inflammation, cancer, diabetes, insulin resistance, taste, atherogenesis, hepatis, central nervous system. In humans, GPR120 expression is expressed in macrophages, eosinophils, and adipose tissue, in cells of the tongue, liver, lungs, small and large intestine, gastric mucosa, and pancreas, in the central nervous system and placental microvilli. Medium- and long-chain fatty acids act as ligands for the receptor. Through the internalization of beta-arrestin-2 complex and the inhibition of NF-κB, GPR120 mediates the activation of the cells anti-inflammatory mechanisms. The receptor is also involved in the maturation of adipocytes, the modulation of insulin signalling pathways, the regulation of glucose metabolism, and the secretion of intestinal hormones. GPR120 is a promising target for the treatment of numerous diseases, whose pathophysiology is associated with low-grade inflammation. As a result of intensive searches, a likely group of synthetic agonists of the receptor was determined with potential therapeutic applications in conditions such as obesity, impaired carbohydrate metabolism, inflammatory bowel diseases, cancer, mental disorders.

EASE: Examination of Anomalous Self-Experience

Streszczenie Skala EASE jest listą objawów do częściowo ustrukturalizowanego fenomenologicznego badania subiektywnych lub empirycznych nieprawidłowości (anomalii), które można uznać za zaburzenia podstawowej, „minimalnej” samoświadomości. EASE opracowana została na podstawie samoopisów otrzymanych od pacjentów chorujących na zaburzenia ze spektrum schizofrenii. Skala ma duże znaczenie dla opisu, diagnozy oraz diagnozy różnicowej zaburzeń ze spektrum schizofrenii. Prezentowana wersja zawiera istotne szczegółowe kwestie dotyczące zbierania wywiadu oraz opisy objawów psychopatologicznych (Podręcznik), arkusz wyników (Aneks A), listę pozostałych pozycji Skali stosowanych w czasie wywiadu (Aneks B) oraz porównawczą listę pozycji EASE/BSABS (Bonner Skala für die Beurteilung von Basissymptomen, Bońska Skala do Oceny Objawów Podstawowych) (Aneks C).

Omega-3 fatty acids in schizophrenia Part II: Clinical applications

Abstract Ω-3 unsaturated fatty acids are compounds belonging to the group of essential fatty acids (EFAs). The history of the discovery of EFAs dates back to the 1930s of the twentieth century, however, growing interest in ω-3 EFAs in the context of mental health has been observed since the year 2000. In view of their multidirectional action, these compounds are a promising form of adjunctive therapy of many illnesses, including psychiatric disorders. The present article aims to review the literature on the clinical applicability of ω-3 EFAs in treating schizophrenia. We present the results of preclinical studies in this area and the mechanisms of ω-3 EFAs action discussed by the authors. The randomized controlled trials (RCTs) evaluating the possibility of using ω-3 EFAs in schizophrenia are characterized in detail. The results of the tests are not clear, which may result from the methodological diversity of interventions made. Ω-3 EFAs seem to be a promising form of adjunctive therapy of schizophrenia. Further research is needed, which will allow for defining groups of patients in which intervention will bring the expected results.