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Lactobacillus reuteri strain 8008 attenuated the aggravation of depressive-like behavior induced by CUMS in high-fat diet-fed mice through regulating the gut microbiota.
Objective: Gut microbiota play a key role in the pathogenesis of obesity and depression. Probiotics are a preventive strategy for obesity and a novel treatment for depression symptoms. However, the ameliorative or therapeutic effect of potential probiotic candidate Lactobacillus reuteri (L. reuteri) on obesity and depression comorbidity still remains unclear. We investigated the effects of chronic unpredictable mild stress (CUMS) in high-fat diet-fed mice and the effects of Lactobacillus reuteri strain 8008 on various disease indicators of obesity and depression comorbidity disease. Methods: Forty male C57BL/6 mice were randomized into 2 groups: the normal control (NC) group (n = 10) and the high-fat diet (HFD) group (n = 30), being fed with normal diet (ND) or high-fat diet (HFD) for 8 weeks, respectively. Then the obese mice fed with HFD were randomly allocated into 3 sub-groups: the HFD group (n = 10); the HFD + CUMS group (n = 10); the HFD + CUMS + L.r group (n = 10). The latter 2 subgroups underwent CUMS for 4 weeks to build the obesity and depression comorbidity mice model. During the duration of treatment, mice were gavaged with 0.5 mL PBS solution or L. reuteri (2 × 109 CFU/mL) once a day, respectively. The body weight, food intake, organ weight, behavioral indicators, histology, blood lipids, levels of inflammatory cytokines and tight junction proteins and abundance of colonic contents bacteria were measured. Results: The obesity and depression comorbidity mice model was successfully established after HFD feeding and chronic stress. The comorbid mice demonstrated inflammatory responses increase in liver and adipose tissues, worsened damage to the intestinal barrier as well as gut microbiota disorder. Gavaged with L. reuteri attenuated depressive-like behavior, improved blood lipids and insulin resistance, reduced inflammation in liver and adipose tissues, improved intestinal tight junctions as well as the microbiome dysbiosis in obesity and depression comorbidity mice. Conclusion: Lactobacillus reuteri strain 8008 could alleviate depressive-like behaviors and related indicators of obesity disorders by regulating the gut microbiota in obesity and depression comorbid mice.
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Dynamic Human Gut Microbiome and Immune Shifts During an Immersive Psychosocial Therapeutic Program.
BACKGROUND: Depression is a leading cause of disability worldwide yet its underlying factors, particularly microbial associations, are poorly understood. METHODS: We examined the longitudinal interplay between the microbiome and immune system in the context of depression during an immersive psychosocial intervention. 142 multi-omics samples were collected from 52 well-characterized participants before, during, and three months after a nine-day inquiry-based stress reduction program. RESULTS: We found that depression was associated with both an increased presence of putatively pathogenic bacteria and reduced microbial beta-diversity. Following the intervention, we observed reductions in neuroinflammatory cytokines and improvements in several mental health indicators. Interestingly, participants with a Prevotella-dominant microbiome showed milder symptoms when depressed, along with a more resilient microbiome and more favorable inflammatory cytokine profile, including reduced levels of CXCL-1. CONCLUSIONS: Our findings reveal a protective link between the Prevotella-dominant microbiome and depression, associated with a less inflammatory environment and moderated symptoms. These insights, coupled with observed improvements in neuroinflammatory markers and mental health from the intervention, highlight potential avenues for microbiome-targeted therapies in depression management.
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In the Mouth or in the Gut? Innovation Through Implementing Oral and Gastrointestinal Health Science in Chronic Pain Management.
Recent scientific advances point towards an important role for oral and gastrointestinal health in people with chronic pain. Poor oral health (e.g., periodontitis, tooth loss) is observed in subgroups of the chronic pain population, including abdominal pain, low back pain, fibromyalgia, and rheumatoid arthritis. In addition to poor oral health, studies have also revealed altered intestinal microbiota compositions in various types of chronic pain, including people with chronic low back pain, knee osteoarthritis, visceral pain, fibromyalgia, tinnitus, and migraine. While overweight/obesity contributes to the likelihood of gut dysbiosis, normal-weight individuals with chronic pain also more often present with poor gut health. Both gastrointestinal and oral health problems (e.g., periodontitis, tooth loss) are increasingly recognized across multiple chronic pain conditions, including abdominal pain, low back pain, fibromyalgia, and rheumatoid arthritis. This perspective paper provides an overview of the requirements for integrating oral and gastrointestinal health in chronic pain management. First and foremost, oral and gastrointestinal health issues need to be recognized as common chronic pain comorbidities that require tailored treatment. Next to recognition of the issue, individuals seeking care for chronic pain need to be screened routinely for these oral and gastrointestinal comorbidities. In terms of management, the following options are suggested: (1) providing oral and gastrointestinal health science education; (2) considering the possible interplay between the gut microbiome and drug treatment (including polypharmacy); (3) expanding the importance of dietary interventions; and (4) considering the potential interplay with other lifestyle factors (e.g., chronic insomnia, overweight/obesity, depression and anxiety). To inform the implementation of these suggestions, longitudinal cohort studies investigating the role of oral and gastrointestinal health in people with chronic pain, as well as studies exploring possible (modifiable) factors that affect the oral and/or gut microbiome, are needed. This includes the bidirectional interplay between the gut microbiome and drugs commonly prescribed to patients with chronic pain. Likewise, adequately powered and controlled clinical trials evaluating the effectiveness of possible treatments for oral and/or gastrointestinal comorbidities in people with chronic pain represent another research priority. Such randomized clinical trials can not only examine the possible causal link between poor oral/gut health and treatment outcomes, but also inform the development of new, innovative ways to improve care for people with chronic pain.
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An Overview and Proposed Research Framework for Studying Co-Occurring Mental- and Physical-Health Dysfunction.
Mental- and physical-health conditions co-occur at a rate much higher than chance. Of patients who have a mental-health condition, more than half also have a physical disease, and these cases are associated with increased human suffering and societal cost. Comorbidity research to date has focused on co-occurring mental- and physical-health disorders separately, and relatively little research has examined the co-occurrence of mental- and physical-health dysfunction. In addition, even less is known about why mental- and physical-health dysfunction co-occurs or how to treat these cases. Thus, the aims of this article are to highlight the need for research at the intersection of physical- and mental-health dysfunction and to provide guidance on how to research cases of comorbidity. Toward these ends, we begin by presenting a selective overview of the possible role of biological processes in the co-occurrence of physical- and mental-health dysfunction using specific illustrative examples. Specifically, we outline how biological processes within the immune system and gastrointestinal system could underlie depression, irritable bowel syndrome, and their co-occurrence. We then advance and discuss a proposed research framework, including methodological and analytic guidance, that researchers could use when studying the phenomenon of co-occurring physical- and mental-health dysfunction.
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Probiotics as Modulators of Adult Neurogenesis and Synaptic Plasticity: New Perspectives in the Pathophysiology and Treatment of Affective Disorders.
Affective disorders, such as major depressive disorder and anxiety disorders, represent a major global health burden, with current treatments proving inadequate for a substantial proportion of patients. Emerging research highlights the microbiota-gut-brain (MGB) axis as a crucial bidirectional communication system influencing brain function and neuroplasticity through neural, endocrine, immune, and metabolic pathways. This narrative review examines probiotics-live beneficial microorganisms-as modulators of adult neurogenesis and synaptic plasticity, two processes fundamentally implicated in the pathophysiology of affective disorders. Preclinical evidence demonstrates that specific strains, particularly from the Lactobacillus and Bifidobacterium genera, promote hippocampal neurogenesis and synaptic function through epigenetic regulation via short-chain fatty acids (SCFAs), notably butyrate-mediated histone deacetylase inhibition, modulation of neuroinflammatory pathways, regulation of neurotransmitter receptor expression across glutamatergic, GABAergic, and monoaminergic systems, and production of neuroactive peptides. Clinical evidence from randomized controlled trials and recent meta-analyses indicates that probiotic supplementation produces significant reductions in depressive and anxiety symptoms, with effects correlating to changes in gut microbiota composition and peripheral neuroplasticity biomarkers, particularly brain-derived neurotrophic factor (BDNF). However, significant methodological limitations persist, including small sample sizes, lack of standardization in probiotic strains and dosages, inconsistent outcome measures, and considerable interindividual variability. While the mechanistic and clinical evidence is biologically plausible and directionally promising, it is not yet sufficient to support definitive therapeutic recommendations. Future research must prioritize adequately powered clinical trials with standardized consortia, comprehensive multi-omics biomarker panels, and precision psychobiotic strategies guided by microbiome-defined patient stratification.
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A Review of Inflammatory Bowel Disease: A Model of Microbial, Immune and Neuropsychological Integration.
Objective: Inflammatory bowel diseases (IBDs) are complex chronic inflammatory disorders of the gastro-intestinal (GI) tract with uncertain etiology. IBDs comprise two idiopathic disorders: Crohn's disease (CD) and ulcerative colitis (UC). The aetiology, severity and progression of such disorders are still poorly understood but thought to be influenced by multiple factors (including genetic, environmental, immunological, physiological, psychological factors and gut microbiome) and their interactions. The overarching aim of this review is to evaluate the extent and nature of the interrelationship between these factors with the disease course. A broader conceptual and longitudinal framework of possible neuro-visceral integration, core microbiome analysis and immune modulation assessment may be useful in accurately documenting and characterizing the nature and temporal continuity of crosstalk between these factors and the role of their interaction (s) in IBD disease activity. Characterization of these interactions holds the promise of identifying novel diagnostic, interventions, and therapeutic strategies. Material and Methods: A search of published literature was conducted by exploring PubMed, EMBASE, MEDLINE, Medline Plus, CDSR library databases. Following search terms relating to key question were set for the search included: "Inflammatory bowel diseases," "gut microbiota," "psychological distress and IBD," "autonomic reactivity and IBD," "immune modulation," "chronic inflammation," "gut inflammation," "enteric nervous system," "gut nervous system," "Crohn's disease," "Ulcerative colitis", "depression and IBD", "anxiety and IBD", "quality of life in IBD patients," "relapse in IBDs," "remission in IBDs," "IBD disease activity," "brain-gut-axis," "microbial signature in IBD," "validated questionnaires in IBD," "IBD activity indices," "IBD aetiology," "IBDs and stress," "epidemiology of IBDs", "autonomic nervous system and gut inflammation", "IBD and environment," "genetics of IBDs," "pathways of immune response in IBDs," "sleep disturbances in IBD," "hypothalamic-pituitary-adrenal axis (HPA)," "sympatho-adrenal axis," "CNS and its control of gut function" "mucosal immune response," "commensal and pathogenic bacteria in the gut," "innate and adaptive immunity." Studies evaluating any possible associations between gut microbiome, psychological state, immune modulation, and autonomic function with IBDs were identified. Commonly cited published literatures with high quality research methodology/results and additional articles from bibliographies of recovered papers were examined and included where relevant. Results: Although there is a substantial literature identifying major contributing factors with IBD, there has been little attempt to integrate some factors over time and assess their interplay and relationship with IBD disease activity. Such contributing factors include genetic and environmental factors, gut microbiota composition and function, physiological factors, psychological state and gut immune response. Interdependences are evident across psychological and biological factors and IBD disease activity. Although from the available evidence, it is implausible that a single explanatory model could elucidate the interplay between such factors and the disease course as well as the sequence of the effect during the pathophysiology of IBD. Conclusion: Longitudinal monitoring of IBD patients and integrating data related to the contributing/risk factors including psychological state, physiological conditions, inflammatory/immune modulations, and microbiome composition/function, could help to explain how major factors associate and interrelate leading to exacerbation of symptoms and disease activity. Identifying the temporal trajectory of biological and psychosocial disturbances may also help to assess their effects and interdependence on individuals' disease status. Moreover, this allows greater insight into understanding the temporal progressions of subclinical events as potential ground for disease severity in IBD. Furthermore, understanding the interaction between these risk factors may help better interventions in controlling the disease, reducing the costs related to disease management, further implications for clinical practice and research approaches in addition to improving patients' mental health and quality of life.
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The Role of the Microbiota-Gut-Brain Axis in Perinatal Depression: Novel Insights for Treatment.
Perinatal depression, a prevalent mood disorder complicating pregnancy and childbirth, poses significant threats to maternal health and neonatal development. While psychotherapy and antidepressants constitute current standard treatments, their clinical application faces substantial limitations during pregnancy and lactation, including safety concerns, treatment resistance, and poor adherence rates. These therapeutic constraints have spurred growing interest in novel gut-brain axis (GBA)-targeted interventions. Emerging evidence suggests that the gut microbiota communicates with the brain through a complex network of neural, immune, and endocrine pathways, playing a critical role in regulating mood, behavior, and cognitive functions. Interventions such as probiotics and fecal microbiota transplantation (FMT) are increasingly explored for their potential to restore microbial balance and alleviate depressive symptoms. This review aims to systematically examine the role of the GBA in the context of perinatal depression, offering novel insights to inform clinical treatment strategies. Furthermore, it evaluates the promise and limitations of microbiota-targeted interventions while discussing future directions for personalized microbiome therapeutics.
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Visceral Pain and Psychiatric Disorders.
The high comorbidity existing between visceral pain and psychiatric disorders such as depression and anxiety is well documented and it is gaining increasing interest among scientists. When visceral pain and psychiatric disorders are comorbid, they present a more debilitating condition than each disorder alone, impacting significantly on the quality of life of these patients. Despite several groups having shown that an overlapping pathophysiology exists between visceral pain and stress-related disorders the link between them is not clear yet. Moreover, it still remains to be elucidated if psychiatric conditions predispose the individual to develop visceral hypersensitivity or vice versa. The brain-gut-microbiome axis is the bidirectional communication between the CNS and the gastrointestinal tract. Alterations at different levels of this axis have been implicated in both visceral hypersensitivity and psychiatric disorders. Here we give an overview of what it is known about comorbid visceral pain and psychiatric disorders and provide evidence of potential overlapping pathophysiological mechanisms involved. Preclinical models of comorbid visceral pain and stress-related disorders are also discussed.
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Global trends and risk factors in gastric cancer: a comprehensive analysis of the Global Burden of Disease Study 2021 and multi-omics data.
Background: Gastric cancer (GC) remains a significant global health challenge. This study aimed to comprehensively analyze GC epidemiology and risk factors to inform prevention and intervention strategies. Methods: We analyzed the Global Burden of Disease Study 2021 data, conducted 16 different machine learning (ML) models of NHANES data, performed Mendelian randomization (MR) studies on disease phenotypes, dietary preferences, microbiome, blood-based markers, and integrated differential gene expression and expression quantitative trait loci (eQTL) data from multiple cohorts to identify factors associated with GC risk. Results: Global age-standardized disability-adjusted life year rates (ASDR) for GC declined from 886.24 to 358.42 per 100,000 population between 1990 and 2030, with significant regional disparities. Despite this decline, total disability-adjusted life years show a concerning upward trend from 2015, rising from approximately 22.9 million to a projected 24.3 million by 2030. The slope index of inequality shifted from 87 in 1990 to -184 in 2021, indicating a reversal in GC burden distribution, with higher ASDR now associated with lower socio-demographic index countries. The ML models analysis identified higher levels of clinical characteristics such as phosphorus, calcium, eosinophils percent, and triglycerides, as well as lower levels of iron and monocyte percent, may be associated with an increased risk of GC. MR analyses revealed causal associations between GC risk and disease phenotypes such as Helicobacter pylori infection, chronic gastritis, obesity, depression, and dietary preferences such as dairy and processed meats. Gut microbiome analysis showed associations with microbiome such as Phascolarctobacterium and Ruminococcaceae species. Blood-based markers analysis identified protective and risk effects for cortisol, glutamate, nicotinamide, Natural Killer %lymphocyte, CD4-CD8- T cell Absolute Count, Phosphatidylcholine (16:0_18:1), and Interleukin-1-alpha. Integrated genomic analysis identified 10 genes significantly associated with GC risk, with strong evidence for colocalization in genes such as CCR6 and PILRB. Conclusions: This systematic analysis reveals complex global trends in GC burden and identifies novel clinical, disease phenotypes, dietary preferences, microbial, blood-based, and genetic risk factors. These findings provide potential targets for improved risk stratification, prevention, and intervention strategies to reduce the global burden of GC.
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Microbiome-Metabolomics Reveals the Bidirectional Associations Between Aging and Depression.
UNLABELLED: Aging increases the susceptibility to depression, and depression accelerates the aging process of body. However, it is needed to be studied deeply that the connotations of the correlation between aging and depression. By integrally applying metabolome and microbiome techniques, the study aimed to explore underlying mechanisms of bidirectional associations between aging and depression. Aging rat model and depression rat model were carried out. Classical behaviors were measured to assess the impacts of aging and depression on rats. On top of this, potential changes in the organism are revealed to elucidate the bi-directional associations between aging and depression based on the 16S rRNA sequencing of gut flora and 1H-NMR of gut metabolites, respectively. Depression weakened the ability of autonomous activities, spatial memory, and gastrointestinal functions of rats, which are also closely related to aging. Vice versa, aging also weakens the autonomous activities of rats, which frequently appears in depression. Secondly, valine, propionate, etc. are potential fecal metabolites that are commonly shared by aging and depression, and these metabolites are closely related to changes in gut microbiota composition. Lastly, both aging and depression decreased the ratio of Firmicutes to Bacteroidetes. Spearman's analysis found that a variety of metabolites, including proline, strongly correlated with Lactobacillus and Corynebacterium, suggesting that these bacterial species play a significant role in the metabolic changes observed in both aging and depression. Meanwhile, differential metabolites and gut microbiota were strongly associated with the number of rearings and gastrointestinal movement of rats, suggesting that potential associations between aging and depression remarkably occur at multiple levels. Exploring the bidirectional association of aging and depression from the perspectives of metabolome and microbiome will not only deepen our understanding of aging and depression, but also provide novel ideas for clinically treating the co-existence and co-occurrence of aging with depression. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12088-025-01538-0.