Background: There is growing interest in new factors contributing to the genesis of eating disorders (EDs). Research recently focused on the study of microbiota. Dysbiosis, associated with a specific genetic susceptibility, may contribute to the development of anorexia nervosa (AN), bulimia nervosa, or binge eating disorder, and several putative mechanisms have already been identified. Diet seems to have an impact not only on modification of the gut microbiota, facilitating dysbiosis, but also on its recovery in patients with EDs. Methods: This systematic review based on the PICO strategy searching into PubMed, EMBASE, PsychINFO, and Cochrane Library examined the literature on the role of altered microbiota in the pathogenesis and treatment of EDs. Results: Sixteen studies were included, mostly regarding AN. Alpha diversity and short-chain fatty acid (SCFA) levels were lower in patients with AN, and affective symptoms and ED psychopathology seem related to changes in gut microbiota. Microbiota-derived proteins stimulated the autoimmune system, altering neuroendocrine control of mood and satiety in EDs. Microbial richness increased in AN after weight regain on fecal microbiota transplantation. Conclusions: Microbiota homeostasis seems essential for a healthy communication network between gut and brain. Dysbiosis may promote intestinal inflammation, alter gut permeability, and trigger immune reactions in the hunger/satiety regulation center contributing to the pathophysiological development of EDs. A restored microbial balance may be a possible treatment target for EDs. A better and more in-depth characterization of gut microbiota and gut–brain crosstalk is required. Future studies may deepen the therapeutic and preventive role of microbiota in EDs.

Alterations of the immune system are known in eating disorders (EDs), however the importance of cytokine balance in this context has not been clarified. We compared cytokines and growth factors at opposite ends of BMI ranges, in 90 patients classified in relation to BMI, depressive and EDs comorbidities. Serum concentrations of interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF) were determined by a biochip analyzer (Randox Labs). Differences were calculated through ANOVA. Possible predictors of higher cytokine levels were evaluated through regression analysis. IL-1α, IL-10, EGF, and IFN-γ were altered individuals with anorexia nervosa (AN) and binge eating disorder (BED). Night-eating was associated with IL-8 and EGF levels, IL-10 concentrations with post-dinner eating and negatively with sweet-eating, long fasting with higher IFN-γ levels. IL-2 increase was not linked to EDs, but to the interaction of depression and BMI. Altogether, for the first time, IL-1α, IL-10, EGF, and IFN-γ were shown to differ between AN and HCs, and between AN and individuals with obesity with or without BED. Only IL-2 was influenced by depression. Dysfunctional eating behaviors predicted abnormal concentrations of IL-10, EGF, IL-8 and IFN-γ.

Food addiction (FA) has been associated with binge eating disorder (BED) and obesity at varying levels of severity and treatment outcomes. Despite much debate and scientific interest in FA, the mechanisms that underlie its co-occurrence with both conditions are not yet well understood. In order to understand this relationship, this study explores FA in a clinical sample of individuals with BED and obesity using network analysis (NA). A total of 303 patients (151 with BED and 152 with obesity) completed a battery of tests that investigated eating psychopathology, eating behaviours, emotional dysregulation, depression and FA. Two different NAs were conducted to investigate the interaction between these variables and FA. The BED and obesity groups were comparable in age (38 ± 14 vs. 42 ± 13 years), body mass index (38.8 ± 8.5 vs 42.4 ± 7.8), sex and demographics. According to the expected influence values, binge eating severity and depression were identified as the central nodes in both networks. In the BED group, binge eating severity was the central node and showed strong connections to both FA and grazing. In contrast, in the obesity group, depression was the central node, but its connections were weak, with only marginal associations to FA. These results suggest that FA represents an important and distinct construct of the two populations. In patients with BED, FA is intimately connected to other loss-of-control-related eating behaviours, such as binge eating and grazing. Conversely, in those with obesity, depression explains the relationship of FA with pathological eating behaviours. The presence of FA seems to be a distinguishing characteristic in the psychopathology of patients suffering from obesity with and without BED, and this could have implications for the prevention, treatment and management of these disorders.

Research has shown that a history of childhood adversities is common in patients with psychiatric disorders but few studies have investigated links between specific types of adversity and specific psychiatric disorders. We investigated the frequency of early childhood adversities in a sample consisting of 91 patients with diagnosis of schizophrenic spectrum disorders (SSD), 74 patients with bipolar disorder (BD), 83 patients with major depressive disorder (MDD) and 85 healthy controls and sought to identify adverse early childhood life events that predict the development of major psychiatric disorders. The Childhood Experiences of Care and Abuse questionnaire was used to collect data on traumatic experiences occurring before the age of 17 years and comprehensive demographic data were also collected. The data were analyzed with chi-squared tests, t-tests, post-hoc and logistic regression. Maternal absence/loss and economic difficulties in the early life were more prevalent in the BD group than other groups. Escape from home, cannabis abuse, psychological abuse, physical abuse and loneliness were more frequent in the SSD group than in other groups. Paternal absence, neglect of core needs, serious familial tension and absence of adult and peer confidants were all less common in the HC group than in the other groups. The regression model confirmed that different types of adversities play a crucial role in the development of the three investigated disorders. Our results support that SSD, BD and MDD are associated to different childhood adversities. This suggests that psychosocial interventions that reduce the incidence of these early life adversities might reduce the incidence of severe and disabling psychiatric disorders.

Patients with a generalized anxiety disorder (GAD) often report preeminent sleep disturbances. Recently, calcium homeostasis gained interest because of its role in the regulation of sleep–wake rhythms and anxiety symptoms. This cross-sectional study aimed at investigating the association between calcium homeostasis imbalance, anxiety, and quality of sleep in patients with GAD. A total of 211 patients were assessed using the Hamilton Rating Scale for Anxiety (HAM-A), Pittsburgh Sleep Quality Index questionnaire (PSQI) and Insomnia Severity Index (ISI) scales. Calcium, vitamin D, and parathyroid hormone (PTH) levels were evaluated in blood samples. A correlation and linear regression analysis were run to evaluate the association of HAM-A, PSQI, and ISI scores with peripheral markers of calcium homeostasis imbalance. Significant correlations emerged between HAM-A, PSQI, ISI, PTH, and vitamin D. The regression models showed that patients with GAD displaying low levels of vitamin D and higher levels of PTH exhibit a poor subjective quality of sleep and higher levels of anxiety, underpinning higher psychopathological burden. A strong relationship between peripheral biomarkers of calcium homeostasis imbalance, insomnia, poor sleep quality, and anxiety symptomatology was underlined. Future studies could shed light on the causal and temporal relationship between calcium metabolism imbalance, anxiety, and sleep.