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Common mental disorders in irritable bowel syndrome: pathophysiology, management, and considerations for future randomised controlled trials.
The frequent co-occurrence of irritable bowel syndrome and the common mental disorders of anxiety and depression is well established. A range of biological and psychosocial disease mechanisms are common to both disorders, many of which contribute to a dysregulated gut-brain axis. Clinical and subthreshold psychological comorbidity adds to the functional impairment and disease burden in individuals with irritable bowel syndrome. Progress is being made with regard to understanding irritable bowel syndrome in the clinical setting from a biopsychosocial perspective. However, until now, most trials of irritable bowel syndrome treatment still consider the disease as a gut disorder in isolation, which leaves major gaps in knowledge about disease-disease interactions and treatment outcomes in irritable bowel syndrome. In this Viewpoint, we review the epidemiology, pathophysiology, and management of anxiety and depression in individuals with irritable bowel syndrome. We also provide methodological recommendations for future randomised controlled trials and outline guidance for research that better incorporates psychiatric comorbidity into its design, with a view to improve treatment outcomes for individuals with irritable bowel syndrome.
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Integrating metagenomics, lipidomics and proteomics to explore the effect and mechanism of ginsenoside Rb1 on atherosclerosis co-depression disease.
BACKGROUND: The comorbidity of atherosclerosis (AS) and depression presents a significant clinical challenge. Its pathogenesis entails complex abnormalities in inflammatory responses, lipid metabolism, and gut microbiota homeostasis. Ginsenoside Rb1 (GRb1)-a bioactive compound derived from the dried roots of Panax ginseng (Araliaceae)-demonstrates anti-inflammatory, antioxidant, lipid-lowering, and neuroprotective properties. However, GRb1's therapeutic potential and underlying mechanisms in AS co-depression remain inadequately characterized. PURPOSE: This study aims to elucidate the mechanism of GRb1 in AS co-depression disease, identify potential therapeutic targets, and thereby develop novel therapeutic strategies for this condition. METHODS: An AS co-depression comorbidity model was established using ApoE⁻/⁻ mice fed a high-fat diet and subjected to chronic restraint stress. To evaluate GRb1's therapeutic efficacy, we assessed serum lipid profiles, performed aortic Oil Red O staining, and conducted behavioral tests for depressive-like phenotypes. Furthermore, we employed an integrated multi-omics approach-combining metagenomics, targeted lipid metabolomics, and proteomics-to identify key alterations in gut microbiota, lipid metabolites, and proteins, with subsequent correlation analysis. Key differential proteins and associated pathways identified through multi-omics were validated using both in vivo (AS co-depression mouse model) and in vitro (HT22 cells) experiments. Finally, GRb1's effects on ferroptosis and specific signaling pathways (CD44/Gls2, ACSL4/LPCAT3/ALOX15, SLC7A11/GPX4) were examined via Western blotting, immunofluorescence, and transmission electron microscopy in both mouse tissues and HT22 cells. RESULTS: Proteobacteria, Helicobacter, and Helicobacter_typhlonius represent significant intestinal microbiota components. Their primary differential lipids include phosphatidylethanolamine (PE), phosphatidylcholine (PC), and lysophosphatidylcholine (LPC), while key differential proteins encompass CD44, Gls2, and Snrpf. Notably, a strong correlation exists among Helicobacter_typhlonius, PE, and CD44. GRb1 modulates PE metabolic dysregulation by reducing the relative abundance of Helicobacter_typhlonius, thereby inhibiting lipid peroxidation and ameliorating oxidative stress. Furthermore, GRb1 suppresses the CD44/Gls2 axis, ACSL4/LPCAT3/ALOX15 pathway, and activates the SLC7A11/GPX4-mediated ferroptosis pathway, thereby exerting its anti-AS co-depression effects through these multi-target mechanisms. CONCLUSION: GRb1 regulates the intestinal microbiota, abnormal lipid metabolism, modulates protein function, inhibits lipid peroxidation, improves oxidative stress, inhibits ferroptosis, regulates the CD44/Gls2, ACSL4/LPCAT3/ALOX15, SLC7A11/ GPX4 signaling pathways, and prevents the progression of AS co-depression disease.
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Gut microbiota is involved in the antidepressant effects of adipose-derived mesenchymal stem cells in chronic social defeat stress mouse model.
RATIONALE: Growing evidence supports the role of microbiota in regulating gut-brain interactions and, thus, contributing to the pathogenesis of depression and the antidepressant actions. Adipose-derived mesenchymal stem cells (ADSCs), as important members of the stem cell family, were demonstrated to alleviate depression behaviors. However, the role of gut microbiota in ADSCs alleviating depression in chronic social defeat stress (CSDS) model is unknown. OBJECTIVES: To examine the effects of ADSCs on depression symptoms and detect the changes in the composition of gut microbiota. RESULTS: We found that ADSCs administration significantly ameliorated CSDS-induced depression behaviors, which was accompanied by alteration in the gut microbiota. The principal co-ordinates analysis (PCoA) results showed that there was a significant difference between the gut microbiota among the groups. Remarkably, receiver operating characteristic (ROC) curves revealed that order Micrococcales, order Rhizobiales and species Bacteroides acidifaciens are potentially important biomarkers for the antidepressant effects of ADSCs in CSDS model. CONCLUSIONS: ADSCs are effective in treating depression behaviors in CSDS model, which might be partly due to the regulation of abnormal composition of gut microbiota. Thus, ADSCs offer a promising therapeutic strategy for treating depression in patients.
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Butyrate Is Associated with the Antidepressant Effects of Weizmannia coagulans BC99: Functional Similarity of a Microbial Metabolite in the Microbiota-Gut-Brain Axis.
Butyrate, a short-chain fatty acid derived from the gut microbiota, has been linked to depression through correlational studies; however, whether it might act as a sufficient downstream mediator of the antidepressant effects of a probiotic remains poorly understood. To explore this, a chronic unpredictable mild stress (CUMS) rat model was established to evaluate the potential antidepressant effects of Weizmannia coagulans BC99. Behavioral assessments included the sucrose preference test (SPT), forced swim test (FST), tail suspension test (TST), and open field test (OFT). In addition, 16S rRNA sequencing, serum metabolomics, and short-chain fatty acid (SCFA) profiling were performed. Levels of inflammatory cytokines (IL-1β, IL-6, IL-4, and LPS) and brain-derived neurotrophic factor (BDNF) were measured in serum, hippocampus, and colon by ELISA. An independent sodium butyrate supplementation experiment was conducted to test functional sufficiency, and hippocampal BDNF/TrkB/CREB signaling was assessed by Western blotting. Treatment with BC99 was associated with alleviation of CUMS-induced depressive-like behaviors, increased butyrate levels, reduced neuroinflammation (IL-1β, IL-6, LPS, and IL-4), and restored hippocampal BDNF levels. BC99 also enriched butyrate-producing bacterial taxa (e.g., Lactobacillus, Bifidobacterium, Faecalibaculum) and normalized tryptophan and sphingolipid metabolism. Notably, sodium butyrate alone recapitulated several of the behavioral and anti-inflammatory effects observed with BC99 and, as shown by Western blot, partially restored hippocampal BDNF/TrkB/CREB signaling, which was impaired in CUMS rats. Together, these findings suggest that butyrate may be associated with the antidepressant effects of W. coagulans BC99, potentially acting through suppression of neuroinflammation and activation of the BDNF pathway. Our results support further investigation of butyrate-enhancing strategies as a nutritional approach for depression.
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Associations between psychological or biological stress indicators and gut microbiota in pregnant women - findings from a prospective longitudinal study.
BACKGROUND: The perinatal period has been linked with higher vulnerability to stress and symptoms of depression and anxiety, as well as with dynamic changes in the composition of maternal gut microbiota. While recent studies indicated significant associations between stress, depression, or anxiety, and alterations in gut microbiota in pregnant women, research in this avenue is still emerging, with existing studies often being limited by small sample sizes. METHOD: We conducted a prospective longitudinal study of 171 women, collecting gut microbiota samples in each trimester of pregnancy and in the early postpartum, questionnaire data (perceived stress via the Perceived Stress Scale, symptoms of depression via the Edinburgh Postnatal Depression Scale, and anxiety via the 6-item State-Trait Anxiety Inventory) twice in each trimester and twice in the early postpartum period, and blood samples for cortisol levels analysis in the first and third pregnancy trimesters. Gut microbiota samples were analyzed by amplicon sequencing of 16S rRNA gene. RESULTS: Perceived stress and symptoms of depression and anxiety showed moderate temporal changes and a high consistency at the individual level over the study period. Cortisol levels rose significantly from the first to the third trimester. There were significant temporal changes in microbiota composition between the first and second trimesters, and between the first and third trimesters. After controlling for false positive findings due to multiple testing, we found no significant associations between stress-related variables (perceived stress, cortisol levels, symptoms of depression and anxiety) and gut microbiota diversity, microbial community composition, or relative abundances of individual bacterial taxa. CONCLUSIONS: The present study results contradict previous research that indicated significant associations between emotions and gut microbiota in the perinatal period. Although we cannot provide an ultimate explanation for this discrepancy, we propose it can lie in insufficient control for false positives in the differential abundance analyses in most previous studies.
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Effects of obesity on depression: A role for inflammation and the gut microbiota.
Depression is a mental disorder associated with environmental, genetic and psychological factors. Recent studies indicate that chronic neuro-inflammation may affect brain physiology and alter mood and behavior. Consumption of a high-fat diet leads to obesity and chronic systemic inflammation. The gut microbiota mediates many effects of a high-fat diet on human physiology and may also influence the mood and behavior of the host. We review here recent studies suggesting the existence of a link between obesity, the gut microbiota and depression, focusing on the mechanisms underlying the effects of a high-fat diet on chronic inflammation and brain physiology. This body of research suggests that modulating the composition of the gut microbiota using prebiotics and probiotics may produce beneficial effects on anxiety and depression.
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Healthy Eating Index-2020 and post-stroke depression (PSD): cross-sectional analysis of NHANES data.
BACKGROUND: Post-stroke depression (PSD) is a common complication after stroke and contributes to poor functional recovery and reduced quality of life. Dietary quality has been associated with depression in the general population, but evidence in individuals with stroke remains limited. This study examined the cross-sectional association between the Healthy Eating Index-2020 (HEI-2020) and PSD. METHODS: This study included 962 adults with a history of stroke from seven cycles of the National Health and Nutrition Examination Survey from 2005 to 2018. Depressive symptoms were assessed using the Patient Health Questionnaire-9, with a score ≥ 10 indicating probable depression. Dietary quality was evaluated using HEI-2020 and categorized into tertiles. Multivariate logistic regression, restricted cubic spline analysis, and mediation analysis were used to assess associations and the statistical indirect association of the Dietary Index for Gut Microbiota (DI-GM). RESULTS: After multivariate adjustment, each one-point increase in HEI-2020 score was associated with 2% lower odds of probable depression (PHQ-9-defined) (OR = 0.98). Compared with the low dietary quality group, the high dietary quality group had 59% lower odds (OR = 0.41). The dose-response relationship was nonlinear, with a significant inverse association observed only when HEI-2020 scores exceeded 57. This exploratory threshold may serve as a reference for future prospective studies but requires validation before clinical application. Furthermore, a significant interaction with race or ethnicity was identified (P for interaction = 0.033). DI-GM showed a significant indirect association (P = 0.04), but the direct and indirect components were in opposite directions, indicating an inconsistent mediation pattern. Given that DI-GM is a dietary proxy, these findings reflect statistical associations with a dietary pattern, not biological mediation. Future studies with direct microbiome measurements are needed to verify gut-brain axis involvement in PSD. CONCLUSIONS: In this cross-sectional study, HEI-2020 was inversely associated with PSD, with nonlinear and race-specific patterns. DI-GM showed a significant but inconsistent indirect association, suggesting a suppressive rather than mediating role. Findings are associational, not causal.
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Behavior, hormone, and gut microbiota change by YYNS intervention in an OVX mouse model.
OBJECT: Perimenopause depression disorder (PDD) is a very common problem in clinical practice and is characterized by depression and autonomic nervous symptoms, including hot flashes, palpitation, and night sweating. In addition, the comorbidity of menopause depression has long been an integral component of the estradiol (E2) shortage. Previous studies have suggested that the mechanisms underlying this comorbidity involved overlap of endocrine and cerebellar networks. Emerging evidence has shown that the endocrine-brain-gut-microbiota axis plays a key role in the regulation of affective disorders. Yangyin-ningshen formula (YYNS) is a traditional Chinese decoction tailored by Yijintang for menopausal depression intervention. Thus, we hypothesized that the YYNS may be involved in the menopause depression alleviation through the endocrine-brain-gut-microbiota axis. METHODS: To verify this, we constructed a bilateral ovariectomy (OVX) mouse model to simulate menopausal-related depression. Subsequently, behavioral tests including the open field test (OFT) and the forced swimming test (FST) were conducted to examine the depression state post-OVX. With YYNS or E2 intervention, enzyme-linked immunosorbent assay (ELISA) was used to determine the serum sex hormones level. 16S rRNA gene sequencing and liquid chromatography-mass spectrometry (LC-MS) were used to analyze the microbiome of the colon samples collected from mice in the sham surgery group (CSH), the OVX model group (CMD), the OVX with E2 hormone intervention group (CHM), and the OVX with YYNS intervention group (CYYNS). One week after OVX, CMD, CHM, and CYYNS showed depression in OFT, FST. Three weeks post-OVX, CHM and CYYNS showed a notable relief of depression; CMD shaped the OTUs shrinkage; and OTUs were raised in the sham, CHM, and CYYNS group. The CMD group showed that the abundance of Actinobiota decreased but that of Bacteriodia increased. The relative abundance of the genus varied in each group. Moreover, functional correlation of changes in sex hormone and gut microbes between different groups showed that the PRL level was negatively correlated with Odoribacter. T level was positively correlated with Lachnospiraceae NK4A136 group and Odoribacter abundance (p < 0.05). CONCLUSION: Our results not only offer novel insights into the sex hormones and depression with OVX mice but also build an important basis for E2 or YYNS therapeutic efficacy on PDD, which provide for future research on this etiology through the endocrine-brain-gut-microbiota network.
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The Gut Microbiota Metabolite Butyrate Modulates Acute Stress-Induced Ferroptosis in the Prefrontal Cortex via the Gut-Brain Axis.
Stress has been implicated in the onset of mental disorders such as depression, with the prefrontal cortex (PFC) playing a crucial role. However, the underlying mechanisms remain to be fully elucidated. Metabolites secreted by intestinal flora can enter the bloodstream and exert regulatory effects on the body. Consequently, this study aims to investigate the molecular mechanisms by which gut flora influences ferroptosis in PFC neurons, thereby affecting depression-like behavioral changes in mice subjected to acute stress. Initially, we established a mouse model of acute restraint stress (3-day duration) and verified that stress-induced ferroptosis of PFC neurons contributed to depression-like behavioral alterations in mice, as evidenced by morphological, behavioral, and molecular biology assessments. Subsequently, through fecal microbiota transplantation (FMT) experiments, we established a significant correlation between gut microbiota and ferroptosis of PFC neurons in acute stress-exposed mice. 16S rDNA sequencing identified butyric acid-producing bacteria, specifically g_Butyricimonas and its primary metabolite, butyric acid, as critical regulators of ferroptosis in PFC neurons in acutely stressed mice. Furthermore, the intervention of butyrate demonstrated its potential to ameliorate damage to the intestinal and blood-brain barriers in these mice. This intervention also mitigated depression-like behaviors induced by ferroptosis of PFC neurons by alleviating systemic inflammatory responses. The findings of this study indicate that acute stress-induced ferroptosis of PFC neurons plays a critical role in depression-like behavioral changes in mice. Additionally, the gut microbiota metabolite butyrate can modulate ferroptosis and depression-like behavioral changes through the gut-brain axis.
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Gut Microbiota and Its Metabolites: The Emerging Bridge Between Coronary Artery Disease and Anxiety and Depression?
The increasing studies indicated that cardiovascular diseases, such as coronary artery disease (CAD), usually induce and exacerbate psychological problems, including anxiety and depression. These psychological issues are admitted as independent risk factors of heart disease as well. The interaction between CAD and anxiety and depression deteriorates the development and prognosis of CAD, which severely threatens the quality of life of patients. Although the existing mechanisms revealed the pathological relationship between CAD and anxiety and depression, there are few studies investigating the correlation between CAD and anxiety and depression from the aspect of gut microbiota (GM) and its metabolites. Therefore, in this review, we summarized whether GM and its metabolites are the emergent bridge between CAD and anxiety and depression. The results showed that there are four kinds of jointly up-regulated bacteria (i.e., Staphylococcus, Escherichia coli, Helicobacter pylori, and Shigella) and five kinds of jointly down-regulated bacteria (i.e., Prevotella, Lactobacillus, Faecalibacterium prausnitzii, Collinsella, and Bifidobacterium) in CAD as well as anxiety and depression. In addition, in CAD and anxiety and depression, the dysbiosis of the former four kinds of bacterium frequently leads to the outburst of inflammatory response, and the dysbiosis of the latter five kinds of bacterium is usually related to the metabolic abnormality of short-chain fatty acids, bile acids, and branched-chain amino acids. Therefore, we believe that GM and its metabolites act as the emergent bridge between CAD and anxiety and depression. The findings of this review provide novel insights and approaches for the clinical treatment of patients with both CAD and anxiety and depression.