#Źródło: Parnas J et al. EASE: examination of anomalous self-experience. Psychopathology, 2005, 38.5: 236-258.S. Użycie skali EASE w badaniach naukowych wymaga pisemnej zgody autora skali (Josef Parnas, e-mail: jpa@cfs.ku.dk) StreszczenieSkala 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 szczegó-łowe 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).Słowa kluczowe: schizofrenia, fenomenologia, zaburzenia Ja, Badanie Nieprawidłowego Doświadczania Siebie, EASE WstępTerminy i pojęcia wyjaśnione są w każdej pozycji Skali. Cele i opis populacji będącej przedmiotem badaniaSkala EASE skupia się na anomaliach subiektywnego doświadczenia, które wydają się odzwierciedlać zaburzenia samoświadomości.Skala ta zawiera opis fenomenologiczny, głównie o charakterze jakościowym i dąży do szczegółowego opisu zjawisk, które łączy zdeformowane w jakiś sposób poczucie perspektywy pierwszoosobowej, tj.: zaburzenie lub upośledzenie dotyczące poczucia bycia podmiotem, ośrodkiem, w którym automatycznie zbiegają się działa-nie, myśl i doświadczenie. Istnieje także możliwość oceny częstości i nasilenia tych doświadczeń.Skala ta opracowana została głównie dla zaburzeń ze spektrum schizofrenii, nie może jednak być stosowana jako jedyne narzędzie diagnostyczne (zaburzenia struktury Ja nie są wymieniane przez DSM-V czy ICD-10 jako kluczowe diagnostyczne lub nawet jako ważne cechy schizofrenii; derealizacja i depersonalizacja wspomniane są jako nieistotne cechy schizotypii). EASE nie obejmuje wszystkich możliwych nieprawidłowości doświadczenia siebie, skupia się jedynie na zaburzeniach stanów Ja (w przeciwieństwie do BSABS [1], nie są badane np. zaburzenia postrzegania).

Background Current treatment of major depressive disorder (MDD) often does not achieve full remission of symptoms. Therefore, new forms of treatment and/or adjunct therapy are needed. Evidence has confirmed the modulation of the gut–brain–microbiota axis as a promising approach in MDD patients. The overall purpose of the SANGUT study—a 12-week, randomized, double-blind, and placebo-controlled Study Evaluating the Effect of Probiotic Supplementation on the Mental Status, Inflammation, and Intestinal Barrier in Major Depressive Disorder Patients Using Gluten-free or Gluten-containing Diet — is to determine the effect of interventions focused on the gut-brain-microbiota axis in a group of MDD patients. Methods A total of 120 outpatients will be equally allocated into one of four groups: (1) probiotic supplementation+gluten-free diet group (PRO-GFD), (2) placebo supplementation+ gluten-free diet group (PLA-GFD), (3) probiotic supplementation+ gluten containing diet group (PRO-GD), and (4) placebo supplementation+gluten containing diet group (PLA-GD). PRO groups will receive a mixture of psychobiotics ( Lactobacillus helveticus R0052 and Bifidobacterium longum R0175), and GFD groups will follow a gluten-free diet. The intervention will last 12 weeks. The primary outcome measure is change in wellbeing, whereas the secondary outcome measures include physiological parameters. Discussion Microbiota and its metabolites have the potential to influence CNS function. Probiotics may restore the eubiosis within the gut while a gluten-free diet, via changes in the microbiota profile and modulation of intestinal permeability, may alter the activity of microbiota-gut-brain axis previously found to be associated with the pathophysiology of depression. It is also noteworthy that microbiota being able to digest gluten may play a role in formation of peptides with different immunogenic capacities. Thus, the combination of a gluten-free diet and probiotic supplementation may inhibit the immune-inflammatory cascade in MDD course and improve both psychiatric and gut barrier-associated traits. Trial registration NCT03877393 .

The coronavirus disease 2019 (COVID-19) pandemic has a significant impact on both physical and mental health. The aim of this cross-sectional study was to (1) evaluate depression, anxiety, and stress levels among students from Polish universities during the first weeks of the COVID-19 pandemic and (2) assess the risk factors of the higher intensity of emotional distress. We conducted an online survey using the Depression, Anxiety, and Stress Scale-21 (DASS-21) to assess well-being. The study included 2172 respondents (73% female, 27% male) with a mean age of 22.1 ± 2.2. Moderate to extremely severe scores of depression, anxiety, and stress were reported by 43.4%, 27.3%, and 41.0% of the respondents, respectively. Higher scores of DASS-21 were related to female sex (odds ratio (OR) = 3.01), studying sciences (OR = 2.04), co-residence with the roommates (OR = 1.25), suffering from a mental disorder (OR = 5.88), loneliness (OR = 293.30), the usage of psychiatric support before pandemic (OR = 8.06), poor economic situation (OR = 13.49), and the lower scores were found for being currently employed (OR = 0.4). This study highlights an urgent need for (1) crisis-oriented psychological and psychiatric support for students during the outbreak of the COVID-19 pandemic and (2) preparing appropriate psychological interventions to improve the mental health of students for a possible similar situation in the future.

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.

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 cow's 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.

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.

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.

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