Interaction between the gastrointestinal tract (GI) and brain functions has recently become a topic of growing interest in psychiatric research. These multidirectional interactions take place in the so-called gut-brain axis or more precisely, the microbiota-gut-brain axis. The GI tract is the largest immune organ in the human body and is also the largest surface of contact with the external environment. Its functions and permeability are highly influenced by psychological stress, which are often a precipitating factor in the first episode, reoccurrence and/or deterioration of symptoms of psychiatric disorders. In recent literature there is growing evidence that increased intestinal permeability with subsequent immune activation has a major role in the pathophysiology of various psychiatric disorders. Numerous parameters measured in this context seem to be aftermaths of those mechanisms, yet at the same time they may be contributing factors for immune mediated psychopathology. For example, immune activation related to gut-derived bacterial lipopolysaccharides (LPS) or various food antigens and exorphins were reported in major depression, schizophrenia, bipolar disorder, alcoholism and autism. In this review the authors will summarize the evidence and roles of such parameters and their assessment in major psychiatric disorders.

BMI (body mass index) can be misleading regarding the level of adiposity in a normal-weight individual. Recently, a bioelectrical impedance analysis (BIA) method was developed that can measure body composition variables. The main objectives of this study were to use BIA to compare the body composition variables between chronic non-diabetic schizophrenic patients with normal weight and healthy individuals. The secondary objective was to compare the nutritional pattern of schizophrenia patients with that of matched healthy subjects, and to identify possible relationships between the content of different components of their diet and visceral adiposity. The subjects were 52 normal-weight patients (33 males and 19 females) diagnosed with schizophrenia based on the DSM-IV and 45 (23 males and 22 females) BMI- matched controls. The patients had been receiving atypical or typical antipsychotic agents for at least one year before enrollment into the study but continuously for 3 months preceding the study and were psychiatrically stable. Body fat (kg), percent (%) body fat, fat-free mass, VAT (visceral adipose tissue) and SAT (subcutaneous adipose tissue) were measured using the bioelectrical impedance analysis (BIA) method. Daily food rations (DFR) were quantitatively evaluated by a 24-h dietary recall method covering 3 days preceding the examination. In normal-weight patients schizophrenia was significantly linked with higher VAT, VAT/SAT ratio and lower fat- free mass. Men had over 5 times and women over 2 times as much VAT as BMI matched groups. In women with schizophrenia and in their controls, the amount of magnesium, niacin and vitamin B6 in their diet inversely correlated with VAT, while in men lower zinc and vitamin C intake was related to higher visceral adiposity. Our study has shown that normal-weight patients with chronic schizophrenia have higher levels of visceral fat (VAT) than controls but similar volume of subcutaneous adipose tissue (SAT). Although no clear conclusion can be made regarding cause-and-effect relationships between the dietary content of food served to our patients and visceral obesity, we suggest that schizophrenia diet should be further investigated as a possible factor related to this type of obesity.