Inflammatory bowel disease (IBD) represents a group of disorders with no known cure. IBD is impacted by biopsychosocial factors. The burden, psychosocial difficulties, and gene-environment interaction involved in the manifestation of IBD necessitate a fuller understanding of factors which worsen or ameliorate IBD. Case complexity (CC) captures current and historical biopsychosocial risks for individuals with IBD and holds promise for understanding variation in treatment response and individuals' experiences with IBD. The present study aimed to understand the relative contributions of: 1) historical vs. current factors impacting CC in predicting global health; and 2) biological, psychological, social, family, and health system factors on global health. Within a longitudinal design, 8-17-year-old youth (N = 83) completed the self-report Pediatric Global Health 7 + 2 at diagnosis (baseline) and 4- and 12 months post-diagnosis. The p-IBD-INTERMED, a clinical-decision support tool, which standardizes inter-professional assessment of biopsychosocial risks contributing to CC was completed by the healthcare provider team at the same timepoints. CC was associated with global health at all time points (T1r = -0.27; T2r = -0.42; T3r = -0.50). Hierarchical regression revealed that across time the relative contribution of historical CC was surpassed by current CC when predicting global health (at T1 βHCC=-0.13;βCCC = -0.17; at T3 βHCC = -0.04; βCCC = -0.48). In this cohort, at 4- and 12-months post diagnosis, psychological factors were the only domain of current CC to significantly predict global health, accounting for 29.1 % and 24.1 % of its variance respectively. Findings suggest that the global health of patients with IBD is not fixed by early life experiences.

Inflammatory bowel disease (IBD) represents a prevalent group of disorders with no known cure. IBD is impacted by myriad biopsychosocial factors. The pervasive burden, pronounced psychosocial difficulties, and the potential gene-environment interaction involved in the manifestation of IBD necessitate a fuller understanding of factors which might worsen or ameliorate IBD. Case complexity (CC) captures current and historical biopsychosocial risks for individuals with IBD and holds promise for understanding variation in treatment response and individuals' experiences with this chronic illness.

We sought to understand the relative contributions of: 1) historical vs. current factors impacting CC in predicting global health (self-reported); and 2) biological, psychological, social, family, and health system factors on global health.

Within a longitudinal design, 8-17-year-old youth (N = 83) completed the self-report Pediatric Global Health 7 + 2 at diagnosis (baseline) and 4- and 12 months post-diagnosis. The p-IBD-INTERMED, an interview-based measure of CC, was completed by the healthcare provider team at the same timepoints.

CC was associated with global health at all time points (T1r = -0.27; T2r = -0.42; T3r = -0.50). Hierarchical regression revealed that across time points the relative contribution of historical CC was surpassed by current CC when predicting global health (at T1 βHCC= - 0.13;βCCC= - 0.17; at T3 βHCC= - 0.04;βCCC= - 0.48). In this cohort of newly diagnosed children that had good medical response by one-year post diagnosis, at 4- and 12-months post diagnosis, psychological factors were the only domain of current CC to significantly predict global health, accounting for 29.1 % and 24.1 % of its variance respectively.

Findings suggest that the global health of IBD patients is not fixed by early life experiences and shed light onto potential psychosocial treatment targets.

Major depressive disorder (MDD) is associated with gastrointestinal tract (GIT) disorders, while genetic correlation, pleiotropic loci and shared risk genes remain to be explored.

Leveraging genome-wide association study statistics for MDD (n = 170,756), peptic ulcer disease (PUD; n = 16,666), gastroesophageal reflux disease (GORD; n = 54,854), PUD and/or GORD and/or medications (PGM; n = 90,175), irritable bowel syndrome (IBS; n = 28,518), and inflammatory bowel disease (IBD; n = 7045), we determined global and local genetic correlations, identified pleiotropic loci, performed gene-level evaluations, and inferred causal associations using bidirectional Mendelian randomization.

We found global correlation of MDD with PUD (rg = 0.444, P = 3.135 × 10-24), GORD (rg = 0.459, P = 2.568 × 10-65), PGM (rg = 0.498, P = 6.094 × 10-114), IBS (rg = 0.621, P = 2.483 × 10-63), and IBD (rg = 0.171, P = 1.824 × 10-5). We identified 12 locally correlated regions between MDD and GIT disorders except for IBD, and one shared region (chr11:111985737-113,103,996) for PGM, GORD, and IBS. We found one pleiotropic locus for PUD, 12 for GORD, 30 for PGM, eight for IBS, and seven for IBD, and five shared loci (rs138786869, rs2284189, rs3130063, rs35789010, rs7568369) for GORD and PGM. We respectively observed 14 and 20 overlapping genes for MDD-GORD and MDD-PGM. We showed genetic liabilities to GORD, PGM, and IBS causally increase MDD risk, while all reverse causalities are significant.

Our work identifies genetic architectures shared between MDD and GIT disorders, contributes genetic insights to understand depression in the context of gut-brain interactions, and provides potential targets to treat gastrointestinal symptoms in depressive patients.

In patients with inflammatory bowel diseases (IBD), functional complaints frequently persist after the clearing of inflammation and are clinically difficult to distinguish from symptoms of inflammation. In recent years, the influence of bidirectional communication between the gut and brain on gut physiology, emotions, and behavior has been demonstrated.

What mechanisms underlie the development of functional gastrointestinal complaints in patients with irritable bowel syndrome (IBS) and IBD? What therapeutic approaches arise from this?

Narrative review.

The pathogenesis of IBS involves interactions between psychosocial factors, genetics, and microbiota as well as the central and peripheral nervous systems. The interplay between stress and visceral hypersensitivity is of central importance. Therapeutically, lifestyle changes with stress reduction and exercise alongside dietary, pharmacological, and psychotherapeutic options are useful.

The treatment of functional gastrointestinal disorders remains challenging, as pharmacological therapies are often ineffective and gut-directed psychotherapies are rarely available.

Background: Common mental disorders are an underdiagnosed comorbidity, which can significantly worsen the prognosis of the main disease and decrease the quality of life. We aimed to investigate the prevalence of depression and anxiety in a cohort of irritable bowel syndrome with diarrhea (IBS-D) and ulcerative colitis (UC) patients and to evaluate the risk factors for their occurrence. Materials and Methods: A total of 112 patients were evaluated. Multivariable analysis was used to determine associations between patient factors and common mental disorders, evaluated with PHQ-9 and GAD-7 questionnaires. Results: We found a significantly higher prevalence of moderate and severe anxiety among patients with IBS-D, when compared with the UC group (p < 0.01). Linear regression analysis revealed an inverse association between anti-TNF-alpha monoclonal antibodies treatment and a higher PHQ-9 score (p = 0.02). Multivariate analysis revealed that, in patients with UC, the presence of children has been associated with a higher GAD-7 score (p = 0.01), both individually and in combination with a higher duration of the disease. (p < 0.01). For IBS-D, a combination of active employment status and religious belief, active employment status and higher educational level, as well as religious belief and the presence of children correlated with higher GAD-7 scores (p = 0.03, p = 0.03 and p = 0.02, respectively). Conclusions: Infliximab used in the treatment for UC improved the parameters of depression. Patients with UC who have university education and a longer duration of the disease are at increased risk of developing depression and anxiety, especially if they have children in care. Regarding IBS-D patients who have an active work status, religious beliefs and caregivers are at increased risk of developing anxiety.

Chronic disease is generally known to affect dogs' quality of life (QoL) as well as being associated with increased strain on their owners. Gastrointestinal (GI) disease is a common problem in companion animal practice, yet little is known about the QoL of dogs with chronic enteropathy (CE) and how their owners and veterinarians assess it.

The aim of this study was to explore: (i) how dog owners and veterinarians observed and evaluated QoL for dogs with chronic GI disease, (ii) how having a dog with CE affected the owner's QoL, and (iii) characteristics of the communication and relationship between the dog owner and veterinarian. Twenty owners of dogs with CE and 20 companion animal veterinarians were included in this qualitative, interview-based, exploratory study.

Owners evaluated QoL based on their dog's apparent emotional state, the presence of clinical signs, or restrictions in their daily life. In their assessments, veterinarians looked at the presence or absence of normal behavior, but also at disease severity and the emotional state of the dog. The majority of owners experienced many concerns and burdens that impacted their own QoL, including daily logistical challenges, implementing therapeutic regimens such as diet restriction, administering multiple daily medications, and the strain of nursing responsibilities on the owner-dog relationship. Dog owners generally felt that communication with their veterinarians was good, while veterinarians found the communication laborious and time-consuming.

In general, owners and veterinarians were aligned in their QoL assessments, and the majority of veterinarians relied heavily on the owners' input and observations. However, assessments were not done in a standardized fashion among either group. Logistical challenges of having a dog with a chronic GI disease often lead to lifestyle changes for the owners, including altering working hours and cancelling holidays or other social arrangements. Having a dog with CE therefore affected the owners' QoL even when the dogs were clinically stable. Providing owners with written material about the condition in addition to medical and feeding regimen instructions may help the owner, improve compliance, and decrease the non-billable hours the veterinarian must spend communicating with the owner about their dog's CE.

Emerging evidence suggests that patients with inflammatory bowel diseases (IBDs) are predisposed to psychosocial disturbances, such as depression and anxiety. Regrettably, clinical antidepressants exhibit unsatisfactory therapeutic efficacy in IBD-associated psychosocial disturbances, primarily attributed to the inherent intestinal disorders and intricate bidirectional relationship between the gut and the brain. Herein, we report a metal-polyphenol-based antidepressant to alleviate mental disorders in dextran sulfate sodium-induced experimental acute colitis mice via modulating the microbiota-gut-brain axis. The antidepressant, termed CSMTC, comprises a core of melittin-encapsulated natural antioxidant enzymes (i.e., catalase and superoxide dismutase) and a protective shell composed of tannic acid-cerium ion network. Upon oral administration to colitis mice, CSMTC can effectively restore colonic redox balance, reinforce the intestinal barrier, modulate gut microbiota composition, maintain the blood-brain barrier integrity, and regulate systemic immune responses. Notably, behavioral test results reveal that CSMTC significantly alleviates the colitis-associated mental disorder (e.g., depression-like behavior) via the microbiota-gut-brain axis by reducing neuroinflammation, enhancing hippocampal neural plasticity, modulating hippocampal immune responses, and restoring neurotransmitter homeostasis. This work may have implications for the development of new nanodrugs for treating inflammation-associated complications.

Pharmacological treatment of psychiatric disorders remains challenging in clinical, pharmacological, and scientific practice. Even if many different substances are established for treating different psychiatric conditions, subgroups of patients show only small or no response to the treatment. The neuroinflammatory hypothesis of the genesis of psychiatric disorders might explain underlying mechanisms in these non-responders. For that reason, recent research focus on neuroinflammatory processes and oxidative stress as possible causes of psychiatric disorders. G-protein coupled receptors (GPCRs) form the biggest superfamily of membrane-bound receptors and are already well known as pharmacological targets in various diseases. The G-protein coupled receptor 55 (GPR55), a receptor considered part of the endocannabinoid system, reveals promising modulation of neuroinflammatory and oxidative processes. Different agonists and antagonists reduce pro-inflammatory cytokine release, enhance the synthesis of anti-inflammatory mediators, and protect cells from oxidative damage. For this reason, GPR55 ligands might be promising compounds in treating subgroups of patients suffering from psychiatric disorders related to neuroinflammation or oxidative stress. New approaches in drug design might lead to new compounds targeting different pathomechanisms of those disorders in just one molecule.

Ghrelin is a hormone consisting of 28 amino acids. Growth hormone secretagogue receptor (GHSR) is a receptor for ghrelin, which is expressed in the brain, pituitary gland, and adrenal glands, especially in the hypothalamus. The binding of ghrelin to the receptor 1a subtype mediates most of the biological effects of ghrelin. Ghrelin has a close relationship with the onset of psychosis. Ghrelin can affect the onset of psychosis by regulating neurotransmitters such as dopamine, γ-aminobutyric acid (GABA), and 5-hydroxytryptamine (5-HT) through the hypothalamus-pituitary-adrenal (HPA) axis, brain-gut axis, the mesolimbic dopamine system, and other ways. Ghrelin activates neuropeptide Y (NPY) in the hypothalamic arcuate nucleus (ARC) through the GHSR. Ghrelin binds to neurons in the ventral tegmental area (VTA), where it promotes the activity of dopamine neurons in the nucleus accumbens (NAcs) in a GHSR-dependent way, increasing dopamine levels and the reward system. This article summarized the recent research progress of ghrelin in depression, anxiety, schizophrenia, anorexia nervosa (AN), and bulimia nervosa (BN), and emphasized its potential application for psychiatric disorders treatment.

To investigate the prevalence and risk factors of psychological symptoms and quality of life (QoL) in early patients with inflammatory bowel disease (IBD).

From September 2021 to May 2022, a unified questionnaire was developed to collect clinical data from early patients with IBD from 42 tertiary care hospitals. The influencing factors of psychological symptoms and poor QoL are screened by logistic regression analysis for constructing model in predicting poor QoL. The consistency index, receiver operating characteristic (ROC) curve, area under the ROC curve (AUC), net reclassification improvement (NRI), integrated discrimination improvement (IDI), calibration curve, and decision curve analysis (DCA) were used to evaluate the performance of the model.

A total of 939 early patients with IBD were surveyed, Among them, 20.3% exhibited anxiety, 21.7% had depression, 57.3% experienced sleep disturbance, and 41.9% reported poor QoL. The factors influencing psychological symptoms varied between ulcerative colitis (UC) and Crohn's disease (CD) patients. The QoL was primarily affected by disease activity, income level and depression. The AUC value of the model in the training group was 0.781 (95% CI: 0.748-0.814). The calibration diagram of the model closely matched the ideal curve. Compared to other prediction models, our model showed superior predictive capability, with NRI and IDI values of 0.324 (95%CI:0.196-0.4513) and 0.026 (95%CI:0.014-0.038), respectively. DCA indicated that the nomogram model could provide clinical benefits.

Early patients with IBD exhibit a high prevalence of psychological symptoms and poor QoL. The nomogram prediction model we constructed demonstrates high accuracy and performance in predicting QoL in early patients with IBD.

White adipose tissue (WAT) and the gut are involved in the development of neuroinflammation when an organism detects any kind of injury, thereby triggering metainflammation. In fact, the autonomous nervous system innervates both tissues, although the complex role played by the integrated sympathetic, parasympathetic, and enteric nervous system functions have not been fully elucidated. Our aims were to investigate the participation of inflamed WAT and the gut in neuroinflammation. Firstly, we conducted an analysis into how inflamed peripheral WAT plays a key role in the triggering of metainflammation. Indeed, this included the impact of the development of local insulin resistance and its metabolic consequences, a serious hypothalamic dysfunction that promotes neurodegeneration. Then, we analyzed the gut-brain axis dysfunction involved in neuroinflammation by examining cell interactions, soluble factors, the sensing of microbes, and the role of dysbiosis-related mechanisms (intestinal microbiota and mucosal barriers) affecting brain functions. Finally, we targeted the physiological crosstalk between cells of the brain-WAT-gut axis that restores normal tissue homeostasis after injury. We concluded the following: because any injury can result not only in overall insulin resistance and dysbiosis, which in turn can impact upon the brain, but that a high-risk of the development of neuroinflammation-induced neurodegenerative disorder can also be triggered. Thus, it is imperative to avoid early metainflammation by applying appropriate preventive (e.g., lifestyle and diet) or pharmacological treatments to cope with allostasis and thus promote health homeostasis.

Prior research has suggested a correlation between gallstones and depressive symptoms, yet the specifics of this relationship remain unclear. This study aims to explore the association between gallstones and depressive symptoms among adults.

Initially, we conducted a cross-sectional study using data from the National Health and Nutrition Examination Survey (NHANES) 2017 - March 2020. After propensity score matching (PSM) for participants with gallstones and those without gallstones, multivariate logistic regression analysis was used to explore the potential association between gallstones and depressive symptoms. This was followed by Mendelian randomization (MR) analysis to further elucidate the causal relationship between them. Using the genome-wide association study database, we extracted instrumental variables and performed bidirectional univariate and multivariate MR analyses.

In the cross-sectional study of NHANES 2017 - March 2020, 835 pairs of participants with comparable characteristics, both with and without gallstones, were identified after PSM. The multivariate adjusted logistic regression analyses revealed a significant association between gallstones and depressive symptoms [fully adjusted model: OR=1.821 (95% CI, 1.181-2.808), P=0.007]. Subsequent MR analyses further clarified the causal relationship, indicating that genetically determined gallstones significantly increase the risk of developing depressive symptoms [forward univariate MR analysis: OR=1.04 (95% CI, 1.01-1.06), P=0.002; multivariate MR analysis: OR=1.03 (95% CI, 1.01-1.05), P=0.009], with no evidence of reverse causation [inverse univariate MR analysis: OR=1.28 (95% CI, 0.90-1.83), P=0.17].

Gallstones are a risk factor for depressive symptoms among adults. Hence, we recommend timely depression screening for patients diagnosed with gallstones, facilitating early detection and effective treatment of depressive symptoms, thus alleviating its impact on both individuals and society.

Ulcerative colitis (UC) is a common inflammatory bowel disease with a complex origin in clinical settings. It is frequently accompanied by negative emotional responses, including anxiety and depression. Enteric glial cells (EGCs) are important components of the gut-brain axis and are involved in the development of the enteric nervous system (ENS), intestinal neuroimmune, and regulation of intestinal motor functions. Since there is limited research encompassing the regulatory function of EGCs in anxiety- and depression-like behaviors induced by UC, this study aims to reveal their regulatory role in such behaviors and associated intestinal inflammation. This study applied morphological, molecular biological, and behavioral methods to observe the morphological and functional changes of EGCs in UC mice. The results indicated a significant activation of EGCs in the ENS of dextran sodium sulfate -induced UC mice. This activation was evidenced by morphological alterations, such as elongation or terminal swelling of processes. Besides EGCs activation, UC mice exhibited significantly elevated expression levels of pro-inflammatory cytokines in the peripheral blood, accompanied by anxiety- and depression-like behaviors. The inhibition of EGCs activity within the ENS can ameliorate the anxiety- and depression-like behaviors caused by UC. Our data suggest that UC and its resulting behaviors may be related to the activation of EGCs within the ENS. Moreover, the modulation of intestinal inflammation through inhibition of EGCs activation emerges as a promising clinical approach for alleviating UC-induced anxiety- and depression-like behaviors.

Patients diagnosed with inflammatory bowel disease (IBD) exhibit a notable prevalence of psychiatric disorders, such as anxiety and depression. Nevertheless, the etiology of psychiatric disorders associated with IBD remains uncertain, and an efficacious treatment approach has yet to be established. Herein, an oral hydrogel strategy (SP@Rh-gel) is proposed for co-delivery of Spirulina platensis and rhein to treat IBD and IBD-associated anxiety and depression by modulating the microbiota-gut-brain axis. SP@Rh-gel improves the solubility, release characteristics and intestinal retention capacity of the drug, leading to a significant improvement in the oral therapeutic efficacy. Oral administration of SP@Rh-gel can reduce intestinal inflammation and rebalance the disrupted intestinal microbial community. Furthermore, SP@Rh-gel maintains intestinal barrier integrity and reduces the release of pro-inflammatory factors and their entry into the hippocampus through the blood-brain barrier, thereby inhibiting neuroinflammation and maintaining neuroplasticity. SP@Rh-gel significantly alleviates the colitis symptoms, as well as anxiety- and depression-like behaviors, in a chronic colitis mouse model. This study demonstrates the significant involvement of the microbiota-gut-brain axis in the development of IBD with psychiatric disorders and proposes a safe, simple, and highly efficient therapeutic approach for managing IBD and comorbid psychiatric disorders.

Psychological distress, especially depression, associated with perianal fistulizing Crohn's disease (PFCD) is widespread and refractory. However, there is a surprising paucity of studies to date that have sought to identify the prevalence and risk factors of depression associated with PFCD.

To estimate the prevalence of depressive symptoms and investigate the depression-related risk factors in patients with PFCD.

The study was conducted in the form of survey and clinical data collection via questionnaire and specialized medical staff. Depressive symptoms, life quality, and fatigue severity of patients with PFCD were assessed by Patient Health Questionnaire-9, Inflammatory Bowel Disease Patient Quality of Life Questionnaire (IBDQ), and Inflammatory Bowel Disease (IBD) Fatigue Patient Self-assessment Scale. The basic demographic information, overall disease features, perianal clinical information, and laboratory inflammation indicators were also gathered. Multivariate regression analysis was ultimately used to ascertain the risk factors of depression associated with PFCD.

A total of 123 patients with PFCD were involved, and 56.91% were suffering from depression. According to multivariate logistic regression analysis, Perianal Disease Activity Index (PDAI) score [odds ratio (OR) = 0.69, 95% confidence interval (CI): 0.50 to 0.95], IBDQ score (OR = 0.93, 95%CI: 0.88 to 0.97), modified Van Assche index (OR = 1.24, 95%CI: 1.01 to 1.53), and IBD Fatigue score (OR = 1.72, 95%CI: 1.23 to 2.42) were independent risk factors of depression-related prevalence among patients with PFCD (P < 0.05). Multiple linear regression analysis revealed that the increasing perianal modified Van Assche index (β value = 0.166, 95%CI: 0.02 to 0.31) and decreasing IBDQ score (β value = -0.116, 95%CI: -0.14 to -0.09) were independently associated with the severity of depression (P < 0.05).

Depressive symptoms in PFCD patients have significantly high prevalence. PDAI score, modified Van Assche index, quality of life, and fatigue severity were the main independent risk factors.

The impact of antidepressants on Inflammatory bowel diseases (IBD) has been extensively studied. However, the biological effects and molecular mechanisms of antidepressants in alleviating colitis remain unclear.

We systematically assessed how antidepressants (fluoxetine, fluvoxamine and venlafaxine) affected IBD and chose fluoxetine, the most effective one, for mechanism studies. We treated the C56BL/6 mice of the IBD model with fluoxetine and their controls. We initially assessed the severity of intestinal inflammation in mice by body weight loss, disease Activity Index scores and the length of the colon. The H&E staining and immunohistochemical staining of MUC2 of colon sections were performed to observe the pathological changes. RT-qPCR and western blot were conducted to assess the expression level of the barrier and inflammation-associated genes. Then, single-cell RNA sequencing was performed on mouse intestinal mucosa. Seurat was used to visualize the data. Uniform Manifold Approximation and Projection (UMAP) was used to perform the dimensionality reduction. Cell Chat package was used to perform cell-cell communication analysis. Monocle was used to conduct developmental pseudotime analysis. Last, RT-qPCR, western blot and immunofluorescence staining were conducted to test the phenomenon discovered by single-cell RNA sequencing in vitro.

We found that fluoxetine treatment significantly alleviated colon inflammation. Notably, single-cell RNA sequencing analysis revealed that fluoxetine affected the distribution of different cell clusters, cell-cell communication and KEGG pathway enrichment. Under the treatment of fluoxetine, enterocytes, Goblet cells and stem cells became the dominating cells. The pseudotime analysis showed that there was a trend for M1 macrophages to differentiate into M2 macrophages. Lastly, we tested this phenomenon in vitro, which exhibited anti-inflammatory effects on enterocytes.

Fluoxetine exhibited anti-inflammatory effects on intestinal mucosa via remodeling of the intestinal cells and macrophages, which reveals that fluoxetine is a promising therapeutic drug for the treatment of IBD and psychiatric comorbidities.

Inflammatory bowel diseases [IBD] are chronic and pervasive conditions of the gastrointestinal tract with a rising incidence in paediatric and young adult populations. Evidence suggests that psychological disorders might be associated with relapse of disease activity. This study aims to evaluate the efficacy of short-term psychodynamic psychotherapy [STPP] in addition to standard medical therapy [SMT] in maintaining clinical remission in adolescents and young adults [AYA] with quiescent IBD, compared with SMT alone.

A two-arm, single-centre, randomised, controlled trial was conducted in 60 IBD AYA in clinical remission. Patients were randomised to receive an 8-week STPP + SMT [n = 30] or SMT alone [n = 30]. The primary outcome was the steroid-free remission rate at 52 weeks after treatment. Secondary outcomes included the overall hospitalisation rate within 52 weeks after treatment, and medication adherence obtained from patient's electronic medical records.

Intention-to-treat analysis showed significant improvement in maintaining disease remission rates in the 8-week STPP + SMT group compared with the control one. The proportion of patients maintaining steroid-free remission at 52 weeks was higher in patients in STTP group [93.1%] compared with patients randomised to control group [64.3%; p = 0.01]. There were no significant differences in secondary outcomes, except for depression reduction in STPP + SMT group.

An 8-week STPP intervention in addition to SMT effectively increases the steroid-free remission rates in AYA with quiescent IBD. Results do not support effects for other secondary outcomes, except for depression reduction.

Inflammatory bowel disease (IBD), a common term for Crohn's disease and ulcerative colitis, is a chronic, relapse-remitting condition of the gastrointestinal tract that is increasing worldwide. Psychiatric comorbidities, including depression and anxiety, are more prevalent in IBD patients than in healthy individuals. Evidence suggests that varying levels of neuroinflammation might underlie these states in IBD patients. Within this context, microglia are the crucial non-neural cells in the brain responsible for innate immune responses following inflammatory insults. Alterations in microglia's functions, such as secretory profile, phagocytic activity, and synaptic pruning, might play significant roles in mediating psychiatric manifestations of IBD. In this review, we discuss the role played by microglia in IBD-associated comorbidities.

Patients with inflammatory bowel disease (IBD), including ulcerative colitis (UC), show an increased incidence of anxiety and depression; however, the association between UC-associated psychiatric disorders and the gut microbiota is unclear. This study aimed to examine whether gut microbiota from patients with UC can alter colonic gene expression, leading to anxiety- and depression-like behavior in mice receiving fecal microbiota transplantation (FMT). RNA sequencing transcriptome analyses revealed a difference in colonic gene expression between mice receiving FMT from patients with UC (UC-FMT mice) and those receiving FMT from healthy controls (HC-FMT mice). Gene ontology analysis revealed the downregulation of neuropeptide signaling pathways, including neuropeptide Y (NPY) expression, in the colons of UC-FMT mice. The protein levels of NPY also decreased in the colon and plasma of UC-FMT mice compared to those in HC-FMT mice. The oral administration of Enterococcus mundtii (EM), a bacterium isolated from the feces of patients with UC, reduced NPY expression in the colons of mice and induced intestinal inflammation, anxiety, and depression-like behavior. Reduced NPY protein levels were also observed in the plasma and hippocampus of EM-treated mice. Intraperitoneal administration of NPY significantly alleviated anxiety- and depressive-like behaviors induced by EM in mice. Capsular polysaccharide in EM was associated with EM-induced NPY downregulation in the colon. Analysis of Gene Expression Omnibus datasets showed markedly reduced NPY expression in the inflamed colons of patients with UC compared with that in the colons of healthy controls. In summary, EM-induced reduction in the colonic expression of NPY may be associated with a decrease in hippocampal NPY and anxiety- and depression-like behavior in mice.

The prevalence of depression is higher in patients with inflammatory bowel disease (IBD) than in the general population. Women are more significantly affected by depression among those with IBD and in the general population. This review presents evidence on sex-based differences in depression pathogenesis and the effect of depression on various factors associated with IBD that affect women's lives, including sexual dysfunction, body image dissatisfaction, fertility, and overall quality of life. We also discuss sex-specific effects on IBD treatment, disease activity, and health care costs. Interestingly, women with IBD tend to seek and are more receptive to depression-related information. Given the underdiagnosis and undertreated nature of depression in individuals with IBD, effective screening and an optimal integrative treatment approach with relevant sex-specific needs are discussed. Evidence regarding the efficacy of psychotherapy, antidepressant pharmacotherapy, and IBD-specific therapy for depression is discussed. This review summarizes evidence of the effect of depression on both personal and professional aspects of the daily lives of women with IBD, which extends beyond negative moods. It applies this information to screening and integrative treatment, resulting in a holistic approach to this multidimensional problem. We also discuss how depression affects males with IBD differently from females. Finally, we discuss the need for gender-based studies on depression in individuals with IBD.

To investigate the frequency of psychiatric disorders before and after onset of paediatric-onset immune-mediated inflammatory diseases (pIMID).

In a nationwide study from 1996 to 2018, we investigated psychiatric disorders in patients with paediatric-onset inflammatory bowel diseases, autoimmune liver diseases and rheumatic diseases, using Danish national healthcare and population registers. Each case was matched with up to 10 controls from the background population. The cumulative incidence for psychiatric disorders prior to pIMID onset in patients was compared with controls. Cox proportional regression was used to estimate adjusted HRs (aHR) with a 95% CI between cases and controls after the index date.

We included 11 208 cases (57% female) and 98 387 controls. The median age at disease onset was 12.5 years (IQR 8-15) and follow-up time 9.8 years (IQR 5-15). We found an association between psychiatric disorders before index date and a diagnosis of subsequent pIMID (OR 1.3, 95% CI 1.2 to 1.4). Notably, after index date, cases also had an increased risk (aHR 1.6, 95% CI 1.5 to 1.7) of psychiatric disorders compared with controls. This risk was increased for all groups of psychiatric disorders. Female patients had an increased risk of suicide attempt after index date (aHR 1.4, 95% CI 1.1 to 1.8).

Patients with pIMID are at increased risk for a broad spectrum of psychiatric disorders both before and after onset of pIMID. The results support the need for awareness of psychiatric morbidity in this young patient group and the need for coordinated healthcare for those with comorbid states.

Oral administration of chitooligosaccharides (COS) has been reported to alleviate colitis in mice. However, the mechanism of action of COS with specific polymerization degree on gut inflammation and metabolism remains unclear. This study aimed to investigate the effects of chitobiose (COS2), chitotetraose (COS4), and chitohexaose (COS6) on colitis, and to elucidate their underlying mechanisms. COS2, COS4, and COS6 were able to significantly alleviate colonic injury and inflammation levels. COS6 has the best anti-inflammatory effect. Furthermore, COS6 could down-regulate the level of indoleamine-2,3-dioxygenase1 (IDO1) and restore the levels of indole, indoleacetic-3-acid (IAA), and indole-3-carbaldehyde (I3A) in the cecum of chronic colitis mice (p < 0.05), thereby regulating tryptophan metabolism. In the aromatic hydrocarbon receptor-IL-22 (AHR-IL-22) pathway, although there were differences between chronic colitis and acute colitis mice, COS intervention could restore the AHR-IL-22 pathway to normal, promote the expression of MUC2, and repair the intestinal mucosal barrier. In conclusion, the results of this study suggested that COS had a good inhibitory effect on IDO1 under inflammation and the changes of AHR and IL-22 levels at different stages of disease development. This provides new insights into the potential use of COS as a functional food for improving intestinal inflammation and metabolism.

This study aims to assess the relative of social support and psychological distress in disease activity among patients with Crohn's disease (CD) in China, and explore whether sex moderates the relationship between disease activity and social support and psychological distress in CD.

Our study has a cross-sectional design.

This was a single-centre study, which was conducted in Wuhan, China.

A total of 184 patients with CD at Union Hospital, Tongji Medical College, Huazhong University of Science and Technology were enrolled in this study; of these,162 patients were included in the final analysis.

The main study outcome was the CD patients' clinical and questionnaire data. The association of disease activity, social support and psychological distress with patients with CD was also evaluated based on the collected data.

A total of 162 patients with CD were enrolled. Compared with patients with CD in remission (CD-R), the patients with CD in activity (CD-A) had higher C reactive protein (CRP) (p=0.001), anaemia (p<0.001) and relapse rates in the last year (p<0.001). Independent samples t-tests indicated that the CD-A group reported lower Social Support Rating Scale scores and higher Symptom Checklist-90 scores than the CD-R group. Moreover, men with CD had lower somatisation (p=0.030) and anxiety (p=0.050) scores than women. In binary logistic regression models, the subjective support (beta=0.903, p=0.013), the clinical factors of CRP (beta=1.038, p=0.001) and psychological distress factors of anxiety (beta=1.443, p=0.008) and other (beta=1.235, p=0.042) were disease activity predictors.

The findings highlight the importance of the psychological distress and social support factors that may play a role in CD patients' health. Interventions to address these issues should be part of management in CD.

Many patients with inflammatory bowel disease (IBD) have persistent symptoms and disease activity despite the best available medical or surgical treatments. These patients are commonly referred to as having difficult-to-treat IBD and need additional therapeutic strategies. However, the absence of standard definitions has impeded clinical research efforts and comparisons of data. Under the guidance of the endpoints cluster of the International Organization for the Study of Inflammatory Bowel Disease, we held a consensus meeting to propose a common operative definition for difficult-to-treat IBD. 16 participants from 12 countries voted on 20 statements covering various elements of difficult-to-treat IBD, such as failure of medical and surgical treatments, disease phenotypes, and specific complaints from patients. "Agreement" was defined as at least 75% consensus. The group agreed that difficult-to-treat IBD is defined by the failure of biologics and advanced small molecules with at least two different mechanisms of action, or postoperative recurrence of Crohn's disease after two surgical resections in adults, or one in children. In addition, chronic antibiotic-refractory pouchitis, complex perianal disease, and comorbid psychosocial complications that impair disease management also qualified as difficult-to-treat IBD. Adoption of these criteria could serve to standardise reporting, guide enrolment in clinical trials, and help identify candidates for enhanced treatment strategies.

The association and interaction between the central nervous system (CNS) and enteric nervous system (ENS) is well established. Essentially ENS is the second brain, as we call it. We tried to understand the structure and function, to throw light on the functional aspect of neurons, and address various disease manifestations. We summarized how various neurological disorders influence the gut via the enteric nervous system and/or bring anatomical or physiological changes in the enteric nervous system or the gut and vice versa. It is known that stress has an effect on Gastrointestinal (GI) motility and causes mucosal erosions. In our literature review, we found that stress can also affect sensory perception in the central nervous system. Interestingly, we found that mutations in the neurohormone, serotonin (5-HT), would result in dysfunctional organ development and further affect mood and behavior. We focused on the developmental aspects of neurons and cognition and their relation to nutritional absorption via the gastrointestinal tract, the development of neurodegenerative disorders in relation to the alteration in gut microbiota, and contrariwise associations between CNS disorders and ENS. This paper further summarizes the synergetic relation between gastrointestinal and neuropsychological manifestations and emphasizes the need to include behavioral therapies in management plans.

Gender differences were identified in the frequency and clinical presentations of inflammatory bowel disease (IBD) and depressive and anxiety disorders, which are more common in IBD patients than in the general population. The present manuscript provides a critical overview of gender differences in the frequency and clinical course of mood and anxiety disorders in IBD patients, with the aim of helping clinicians provide individualized management for patients. All of the included studies found that IBD patients reported a higher frequency of depressive and anxiety disorders than the general population. These findings should encourage healthcare providers to employ validated tools to monitor the mental health of their IBD patients, such as the Patient Health Questionnaire (PHQ-9). In addition, most studies confirm that women with IBD are more likely than men to develop affective disorders and show that up to 65% of women with IBD have depressive and anxiety disorders. Women with IBD require close mental health monitoring and ultimately a multidisciplinary approach involving mental health professionals. Drug treatment in women should be individualized and medications that may affect mental health (e.g., corticosteroids) should be thoroughly reconsidered. Further data are needed to ensure individualized treatment for IBD patients in a framework of precision medicine.

The causality of the association between depression and gastrointestinal diseases is undetermined. We conducted Mendelian randomization (MR) analyses to systematically explore the associations of depression with 24 gastrointestinal diseases. Independent genetic variants associated with depression at the genome-wide significance level were selected as instrumental variables. Genetic associations with 24 gastrointestinal diseases were obtained from the UK Biobank study, the FinnGen study, and large consortia. Multivariable MR analysis was conducted to explore the mediation effects of body mass index, cigarette smoking, and type 2 diabetes. After multiple-testing corrections, genetic liability to depression was associated with an increased risk of irritable bowel syndrome, non-alcohol fatty liver disease, alcoholic liver disease, gastroesophageal reflux, chronic pancreatitis, duodenal ulcer, chronic gastritis, gastric ulcer, diverticular disease, cholelithiasis, acute pancreatitis, and ulcerative colitis. For the causal effect of genetic liability to depression on non-alcoholic fatty liver disease, a substantial proportion was mediated by body mass index. Genetic predisposition to smoking initiation mediated half of effect of depression on acute pancreatitis. This MR study suggests that depression may play a causal role in many gastrointestinal diseases.

Background and aims: Inflammatory bowel diseases (IBD) are chronic disorders associated with a reduced quality of life, and patients often also suffer from psychiatric comorbidities. Overall, both mood and cognitive disorders are prevalent in chronic organic diseases, especially in the case of a strong immune component, such as rheumatoid arthritis, multiple sclerosis, and cancer. Divergent data regarding the true incidence and prevalence of mental disorders in patients with IBD are available. We aimed to review the current evidence on the topic and the burden of mental illness in IBD patients, the role of the brain-gut axis in their co-existence, and its implication in an integrated clinical management. Methods: PubMed was searched to identify relevant studies investigating the gut-brain interactions and the incidence and prevalence of psychiatric disorders, especially of depression, anxiety, and cognitive dysfunction in the IBD population. Results: Among IBD patients, there is a high prevalence of psychiatric comorbidities, especially of anxiety and depression. Approximately 20-30% of IBD patients are affected by mood disorders and/or present with anxiety symptoms. Furthermore, it has been observed that the prevalence of mental illnesses increases in patients with active intestinal disease. Psychiatric comorbidities continue to be under-diagnosed in IBD patients and remain an unresolved issue in the management of these patients. Conclusions: Psychiatric illnesses co-occurring in IBD patients deserve acknowledgment from IBD specialists. These comorbidities highly impact the management of IBD patients and should be studied as an adjunctive therapeutic target.

To explore the gender differences in the psychological symptoms, sleep quality, and quality of life of patients with inflammatory bowel disease (IBD).

A unified questionnaire was developed to collect clinical data on the psychology and quality of life of IBD patients from 42 hospitals in 22 provinces in China from September 2021 to May 2022. The general clinical characteristics, psychological symptoms, sleep quality, and quality of life of IBD patients of different genders were analyzed via a descriptive statistical analysis. A multivariate logistic regression analysis was conducted, and independent influencing factors were screened to construct a nomogram to predict the quality of life. The consistency index (C-index), receiver operating characteristic (ROC) curve, area under the ROC curve (AUC), and calibration curve were used to evaluate the discrimination and accuracy of the nomogram model. Decision curve analysis (DCA) was used to evaluate the clinical utility.

A total of 2478 IBD patients (1371 patients with ulcerative colitis (UC) and 1107 patients with Crohn's disease (CD)) were investigated, including 1547 males (62.4%) and 931 females (37.6%). The proportion of anxiety in females was significantly higher than in males (IBD: 30.5% vs. 22.4%, p < 0.001; UC: 32.4% vs. 25.1%, p = 0.003; CD: 26.8% vs. 19.9%, p = 0.013), and there were differences in the severity of anxiety between the genders (IBD: p < 0.001; UC: p < 0.001; CD: p = 0.050). The proportion of depression in females was higher than in males (IBD: 33.1% vs. 27.7%, p = 0.005; UC: 34.4% vs. 28.9%, p = 0.031; CD: 30.6% vs. 26.6%, p = 0.184), and there were differences in the severity of depression between the genders (IBD: p = 0.004; UC: p = 0.022; CD: p = 0.312). The proportion suffering from sleep disturbances among females was slightly higher than among males (IBD: 63.2% vs. 58.4%, p = 0.018; UC: 63.4% vs. 58.1%, p = 0.047; CD: 62.7% vs. 58.6%, p = 0.210), and the proportion of females with a poor quality of life was higher than that of males (IBD: 41.8% vs. 35.2%, p = 0.001; UC: 45.1% vs. 39.8%, p = 0.049; CD: 35.4% vs. 30.8%, p = 0.141). The AUC values of the female and male nomogram prediction models for predicting poor quality of life were 0.770 (95% CI: 0.7391-0.7998) and 0.771 (95% CI: 0.7466-0.7952), respectively. The calibration diagrams of the two models showed that the calibration curves fitted well with the ideal curve, and the DCA that showed nomogram models could bring clinical benefits.

There were significant gender differences in the psychological symptoms, sleep quality, and quality of life of IBD patients, suggesting that females need more psychological support. In addition, a nomogram model with high accuracy and performance was constructed to predict the quality of life of IBD patients of different genders, which is helpful for the timely clinical formulation of personalized intervention plans that can improve the prognosis of patients and save medical costs.

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is defined as chronic inflammation in the gastrointestinal tract. Notably, more than 20% of people with IBD experience depressive symptoms. Understanding the immunological mechanism of chronic intestinal inflammation on cognitive behavior has become a key research focus. Previous studies have shown that a dysregulated immune response contributes to chronic inflammation and depressive symptoms. The tolerant phenotype exhibited by immune cells regulates the course of chronic inflammation in distinct ways. In addition, neuroglia, such as microglia and astrocytes specific to the brain, are also influenced by deregulated inflammation to mediate the development of depressive symptoms. The kynurenine pathway (KP), a significant tryptophan metabolic pathway, transforms tryptophan into a series of KP metabolites that modulate chronic inflammation and depressive symptoms. In particular, indoleamine 2,3-dioxygenase 1 (IDO1), a rate-limiting enzyme in the KP, is activated by chronic inflammation and leads to the production of kynurenine. In addition, disruption of the brain-gut axis induced by IBD allows kynurenine to cross the blood-brain barrier (BBB) and form a series of neuroactive kynurenine metabolites in glial cells. Among them, quinolinic acid continuously accumulates in the brain, indicating depression. Thus, KP metabolites are critical for driving the comorbidity of IBD and depressive symptoms. In this review, the pathological mechanism of KP metabolite-mediated chronic intestinal inflammation and depressive symptoms by regulating the immune response is summarized according to the latest reports.

Symptoms of common mental disorders, such as anxiety or depression, are associated with adverse clinical outcomes in inflammatory bowel disease (IBD). We report trajectories of these symptoms in IBD, patient characteristics associated with different trajectories, and effects on healthcare utilization and prognosis.

We collected demographic, symptom, psychological, and quality-of-life data, with questionnaires at 3-month intervals, over 12 months of follow-up. We collected healthcare utilization and IBD outcomes through notes review. We compared characteristics of those with persistently normal or improving anxiety or depression scores with those with persistently abnormal or worsening scores and the number of flares, glucocorticosteroid prescriptions, escalations of therapy, hospitalizations, or intestinal resections due to IBD activity.

Among 771 and 777 patients, respectively, worsening or persistently abnormal anxiety or depression scores were associated with increased antidepressant (28.6% vs 12.3% anxiety, 35.8% vs 10.1% depression, P < 0.001) and opiate use (19.0% vs 7.8% anxiety, P = 0.001 and 34.0% vs 7.4% depression, P < 0.001), compared with those with persistently normal or improving scores. These individuals were also more likely to have been diagnosed with IBD in the last 12 months (16.3% vs 5.0% anxiety, P = 0.001, and 15.1% vs 5.5% depression, P = 0.006), to have clinically active disease at baseline (57.1% vs 26.6% anxiety and 71.7% vs 29.1% depression, P < 0.001) and lower quality-of-life scores ( P < 0.001). Individuals with worsening or persistently abnormal trajectories of anxiety or depression required significantly more outpatient appointments, radiological investigations, and endoscopic procedures for IBD-related symptoms.

In this 12-month follow-up study, patients with IBD with worsening or persistently high anxiety or depression scores were higher utilizers of health care but were not at an increased risk of future adverse disease outcomes.

Crohn's disease (CD) has been related to an increased prevalence of psychiatric disorders and suicide risk (SR). However, the nature of their relationship still deserves clarification. The aim of this study is to assess the prevalence of major depressive disorder (MDD) in patients with CD, and to investigate the relationship between MDD and CD outcomes.

A cross-sectional study involving CD patients was performed. CD activity was evaluated by the Harvey-Bradshaw index and CD phenotype by the Montreal classification. The presence of MDD was assessed by the Patient Health Questionnaire score-9 (PHQ-9). Sociodemographic data and other characteristics were retrieved from electronic medical records.

283 patients with CD were included. The prevalence of MDD was 41.7%. Females had a risk of MDD 5.3 times greater than males. CD disease duration was inversely correlated with MDD severity. Individuals with active CD were more likely to have MDD (OR = 796.0; 95% CI 133.7‒4738.8) than individuals with CD remission. MDD was more prevalent in inflammatory behavior (45.5%) and there were no statistical differences regarding the disease location. 19.8% of the sample scored positive for SR.

The present results support data showing an increased prevalence of MDD in individuals with CD. Additionally, it indicates that MDD in CD might be related to the activity of CD. Prospective studies are warranted to confirm these results and to address whether MDD leads to CD activity, CD activity leads to MDD or both ways are existent.

Mental health disorders are common in inflammatory bowel disease (IBD) and affect patients' quality of life, impacting on disease outcomes and health care-related costs.

Even if psychological issues in IBD patients are highly burdened in terms of quality of life, psychiatric comorbidities still receive less attention into routine care than the physical symptoms of the disease. The present review provides an overview of recent literature, focusing on the association between perceived stress and IBD outcomes. For this purpose, the epidemiology of more common psychological comorbidities in IBD and their potential effect on the onset and disease course have been examined. Moreover, therapeutic interventions in the management of these patients have also been evaluated.

Screening of patients at high risk of psychological issues is currently an unmet, clinical need in the management of IBD. Under-diagnosed and under-treated mental health disorders in IBD patients may impact outcomes, leading to increased disability and health-care utilization and associated costs. A patient-tailored, integrated model of care in the management of IBD is required to optimize disease outcomes and improve patients' quality of life.

Neurological involvement and psychiatric manifestations have been documented in clinical cases of inflammatory bowel disease (IBD); however, the presence of a causal relationship remains elusive. The objective of this study is to investigate the modifications occurring in the cerebral cortex as a result of IBD.

A compendium of data extracted from a genome-wide association study (GWAS) involving a maximum of 133,380 European subjects. A series of Mendelian random analyses were applied to exclude heterogeneity and pleiotropy, ensuring the stability of the results.

Neither IBDs nor inflammatory cytokines (IL-6/IL-6Rα) were found to have a significant causality with surface area (SA) and thickness (TH) at the global level. At the regional functional brain level, Crohn's disease (CD) significantly decreased the TH of pars orbitalis (β=-0.003mm, Se=0.001mm, p_ivw =4.85×10^-4). IL-6 was observed to reduce the SA of middle temporal (β=-28.575mm², Se=6.482mm², p_ivw=1.04×10^-5) and increase the TH of fusiform (β=0.008mm, Se=0.002mm, p_ivw=8.86×10^-5) and pars opercularis (β=0.009mm, Se=0.002mm, p_ivw=2.34×10^-4). Furthermore, a causal relationship between IL-6Rα and an increase in the SA of superior frontal (β=21.132mm², Se=5.806mm², p_ivw=2.73×10^-4) and the TH of supramarginal (β=0.003mm, Se=0.0002mm, p_ivw=7.86×10^-37). All results passed sensitivity analysis and no heterogeneity and pleiotropy were detected.

The correlation between IBD and changes in cerebral cortical structures implies the existence of a gut-brain axis at the organismal level. It is recommended that clinical patients with IBD prioritize long-term management of inflammation, as changes at the organismal level can lead to functional pathologies. Magnetic resonance imaging (MRI) may be considered as an additional screening option for IBD.

Inflammatory bowel diseases [IBD], which are associated with a high disease burden, are also reported to be accompanied by a high prevalence of psychiatric disorders. However, the literature on IBD and psychiatric disorders has not been reviewed.

This systematic review followed the PRISMA guidelines, and its protocol was registered at PROSPERO [ID: CRD42020214359]. PubMed, Embase and PsycINFO were consulted for the literature search. Studies reporting on diagnosed psychiatric disorders in IBD were included. Pooled prevalence rates were calculated using random effects meta-analyses. Study quality was assessed using the Newcastle-Ottawa Scale [NOS].

Sixty-nine studies were identified with an average cohort size of 60 114 patients. Pooled prevalence rates were: mood disorders, 10% (95% confidence interval [CI] = 7%; 15%); anxiety disorders, 12% [95% CI = 8%; 18%]; substance misuse, 3% [95% CI = 1%; 7%]; psychotic disorders, 2% [95% CI = 1%; 4%]; behavioural disorders, 1% [95% CI = 0%; 3%]; personality disorders, 3% [95% CI = 1%; 10%]; developmental disorders, 1% [95% CI = 0%; 3%]; and behavioural and emotional disorders with onset usually during childhood, 1% [95% CI = 1%; 3%]. All analyses had high statistical heterogeneity [I2 > 99%]. Seven studies reported an increased risk of suicide in IBD patients compared to controls.

The prevalence of psychiatric comorbidities was high [11-82%] in patients with IBD and was higher than in the background population. Addressing mental health problems in patients with IBD can improve their adherence to treatment and the somatic disease course and, consequently, reduce morbidity and mortality.

Major depressive disorder is a prominent psychiatric illness in the United States. It has been found to be higher among patients with inflammatory bowel disease. However, few studies have focused on depression among minority populations with inflammatory bowel disease. Our study determined the prevalence of depression in minority patients with inflammatory bowel disease at our safety-net hospital, which serves a predominantly African American patient population.

We conducted a single centre retrospective cohort study at a large, urban outpatient centre. We retrieved the electronic medical records of patients with inflammatory bowel disease who were seen in the gastroenterology clinic from December 2018-December 2019. Data on the severity of depression within the minority population, using the nine-question Patient Health Questionnaire, was obtained. The effects of age, sex, inflammatory bowel disease diagnosis, and comorbidities were analysed. A p-value <0.05 was considered statistically significant.

A total of IBD patients were included in the study, of which 46.7% were female and 53.3% were male. Mean age was 44 years. With regard to race, 88.4% were African American, 5.3% Asian, 2.1% Hispanic, 1.1% American Indian/Alaskan Native, and 3.2% multiracial. A total of 71.6% had Crohn's disease and 28.4% had ulcerative colitis. Overall prevalence of major depressive disorder was 25.3%; 45.8% had minimal, 8.3% mild, 33.3% moderate, and 12.5% severe depression. A total of 34.7% of patients were never screened for depression, and 13.8% had other psychiatric conditions. There was a difference in depression rates based on psychiatric conditions (p = 0.00), but no difference based on sex (p = 0.37), IBD subtype (p = 0.34), or medical conditions (p = 0.84).

Rates of depression among minority patients, predominantly African American, with inflammatory bowel disease were higher than previously reported for all patients with inflammatory bowel disease. Over 40% experienced moderate to severe depression. There was a low screening rate for depression. This data will be used to improve depression screening, especially among minorities.

Inflammatory bowel disease (IBD), which includes Crohn's disease and ulcerative colitis, is a chronic, relapsing immune-mediated disease with a varying and sometimes severe disease course. IBD is often diagnosed in early adulthood and can lead to a substantial decline in quality of life. It has been suggested that patients with IBD are at increased risk of depression and anxiety, but it is still unclear to what extent these diseases co-occur and in what sequence they arise. This Review summarizes the literature on the degree of co-occurrence of IBD with depression and anxiety and the temporal relationship between these diseases. We also discuss the effect of psychological stress on the onset and course of IBD. In addition, we outline the possible mechanisms underlying the co-occurrence of IBD and depression and anxiety, which include changes in brain signalling and morphology, increases in peripheral and intracerebral pro-inflammatory cytokines, impairment of the nitric oxide pathway, changes in vagal nerve signalling, gut dysbiosis and genetics. Finally, we examine the possible effects of treatment of depression and anxiety on the risk and course of IBD, the influence of psychological interventions on IBD, and the effects of IBD treatment on psychiatric comorbidity.

Cerebral hemodynamic dysfunction and hypoperfusion have been found to underlie vascular depression, but whether the gut-brain axis is involved remains unknown. In this study, a rat model of bilateral common carotid artery occlusion (BCCAO) was adopted to mimic chronic cerebral hypoperfusion. A reduced sucrose preference ratio, increased immobility time in the tail suspension test and forced swim test, and compromised gut homeostasis were found. A promoted conversion of tryptophan (Trp) into kynurenine (Kyn) instead of 5-hydroxytryptamine (5-HT) was observed in the hippocampus and gut of BCCAO rats. Meanwhile, 16S ribosomal RNA gene sequencing suggested a compromised profile of the gut SCFA-producing microbiome, with a decreased serum level of SCFAs revealed by targeted metabolomics analysis. With SCFA supplementation, BCCAO rats exhibited ameliorated depressive-like behaviors and improved gut dysbiosis, compared with the salt-matched BCCAO group. Enzyme-linked immunosorbent assays and quantitative RT-PCR suggested that SCFA supplementation suppressed the conversion of Trp to Kyn and rescued the reduction in 5-HT levels in the hippocampus and gut. In addition to inhibiting the upregulation of inflammatory cytokines, SCFA supplementation ameliorated the activated oxidative stress and reduced the number of microglia and the expression of its proinflammatory markers in the hippocampus post BCCAO. In conclusion, our data suggested the participation of the gut-brain axis in vascular depression, shedding light on the neuroprotective potential of treatment with gut-derived SCFAs.

The role of the brain-gut axis is of increasing interest in IBD, as the link between common mental disorders and GI inflammation may be bidirectional. We performed a systematic review examining these issues.

We searched EMBASE Classic and EMBASE, Medline, and APA PsychInfo (to 11 July 2021) for longitudinal follow-up studies examining effect of symptoms of anxiety or depression on subsequent adverse outcomes in IBD, or effect of active IBD on subsequent development of symptoms of anxiety or depression. We pooled relative risks (RRs) and HRs with 95% CIs for adverse outcomes (flare, escalation of therapy, hospitalisation, emergency department attendance, surgery or a composite of any of these) according to presence of symptoms of anxiety or depression at baseline, or RRs and HRs with 95% CIs for new onset of symptoms of anxiety or depression according to presence of active IBD at baseline.

We included 12 separate studies, recruiting 9192 patients. All 12 studies examined brain-to-gut effects. Anxiety at baseline was associated with significantly higher risks of escalation of therapy (RR=1.68; 95% CI 1.18 to 2.40), hospitalisation (RR=1.72; 95% CI 1.01 to 2.95), emergency department attendance (RR=1.30; 95% CI 1.21 to 1.39), or a composite of any adverse outcome. Depression at baseline was associated with higher risks of flare (RR=1.60; 95% CI 1.21 to 2.12), escalation of therapy (RR=1.41; 95% CI 1.08 to 1.84), hospitalisation (RR=1.35; 95% CI 1.17 to 1.57), emergency department attendance (RR=1.38; 95% CI 1.22 to 1.56), surgery (RR=1.63; 95% CI 1.19 to 2.22) or a composite of any of these. Three studies examined gut-to-brain effects. Active disease at baseline was associated with future development of anxiety or depression (RR=2.24; 95% CI 1.25 to 4.01 and RR=1.49; 95% CI 1.11 to 1.98, respectively).

Bidirectional effects of the brain-gut axis are present in IBD and may influence both the natural history of the disease and psychological health.

Inflammatory bowel disease (IBD) is a globally rising chronic intestinal disease that affects individuals in many parts of the world. Immunosuppressive medications such as corticosteroids are used to manage flare-ups and to induce remission in IBD. Corticosteroids are said to cause several systemic symptoms, but they are also associated with drug-induced neuropsychiatric disorders. This article examines the existing data on psychiatric and cognitive effects associated with corticosteroid therapy in relation to IBD. Many studies have found that corticosteroids appear to cause mood disturbances such as mania, hypomania, depression, and cognitive problems in the first few weeks of therapy, but these effects are dose-dependent and often mild. The purpose of this literature review is to shed light on the impact corticosteroids can have on individuals' mental health, which will aid physicians in the future when treating patients with IBD. Healthcare professionals should advise patients of this risk and assess the need for intervention. While there is evidence that corticosteroids can elicit neuropsychiatric symptoms, more data on people with IBD who are on corticosteroid therapy is needed to determine the prevalence of glucocorticoid-induced mood changes in this population.