The brain-gut axis dysfunctions and hypersensitivity to food antigens in the etiopathogenesis of schizophrenia
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I Klinika Psychiatrii, Psychoterapii i Wczesnej Interwencji UM w Lublinie
Zakład Neuropsychiatrii Klinicznej UM w Lublinie
Wojewódzki Podkarpacki Szpital Psychiatryczny w Żurawicy
Klinika Dermatologii, Wenerologii i Dermatologii Dziecięcej, Samodzielny Publiczny Szpital Kliniczny nr 1 w Lublinie
Katedra Psychologii Niepaństwowej Wyższej Szkoły Pedagogicznej w Białymstoku
Submission date: 2015-03-16
Acceptance date: 2015-06-08
Publication date: 2016-08-30
Corresponding author
Hanna Karakuła-Juchnowicz   

I Klinika Psychiatrii, Psychoterapii i Wczesnej Interwencji, Uniwersytet Medyczny w Lublinie, ul. Głuska 1, Lublin 20-439, Polska
Psychiatr Pol 2016;50(4):747-760
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.
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