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Gut microbiome-gut brain axis-depression: interconnection.
OBJECTIVES: The relationship between the gut microbiome and mental health, particularly depression, has gained significant attention. This review explores the connection between microbial metabolites, dysbiosis, and depression. The gut microbiome, comprising diverse microorganisms, maintains physiological balance and influences health through the gut-brain axis, a communication pathway between the gut and the central nervous system. METHODS: Dysbiosis, an imbalance in the gut microbiome, disrupts this axis and worsens depressive symptoms. Factors like diet, antibiotics, and lifestyle can cause this imbalance, leading to changes in microbial composition, metabolism, and immune responses. This imbalance can induce inflammation, disrupt neurotransmitter regulation, and affect hormonal and epigenetic processes, all linked to depression. RESULTS: Microbial metabolites, such as short-chain fatty acids and neurotransmitters, are key to gut-brain communication, influencing immune regulation and mood. The altered production of these metabolites is associated with depression. While progress has been made in understanding the gut-brain axis, more research is needed to clarify causative relationships and develop new treatments. The emerging field of psychobiotics and microbiome-targeted therapies shows promise for innovative depression treatments by harnessing the gut microbiome's potential. CONCLUSIONS: Epigenetic mechanisms, including DNA methylation and histone modifications, are crucial in how the gut microbiota impacts mental health. Understanding these mechanisms offers new prospects for preventing and treating depression through the gut-brain axis.
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Gut microbiota and its metabolites in depression: from pathogenesis to treatment.
Major depressive disorder is one of the most disabling mental disorders worldwide. Increasing preclinical and clinical studies have highlighted that compositional and functional (e.g., metabolite) changes in gut microbiota, known as dysbiosis, are associated with the onset and progression of depression via regulating the gut-brain axis. However, the gut microbiota and their metabolites present a double-edged sword in depression. Dysbiosis is involved in the pathogenesis of depression while, at the same time, offering a novel therapeutic target. In this review, we describe the association between dysbiosis and depression, drug-microbiota interactions in antidepressant treatment, and the potential health benefits of microbial-targeted therapeutics in depression, including dietary interventions, fecal microbiota transplantation, probiotics, prebiotics, synbiotics, and postbiotics. With the emergence of microbial research, we describe a new direction for future research and clinical treatment of depression.
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The Gut Microbiome in Depression and Potential Benefit of Prebiotics, Probiotics and Synbiotics: A Systematic Review of Clinical Trials and Observational Studies.
An emerging body of literature demonstrates differences in the gut microbiome (GMB) of patients with major depressive disorder (MDD) compared to healthy controls (HC), as well as the potential benefits of prebiotic, probiotic, and synbiotic treatment. We conducted a systematic review of 24 observational studies (n = 2817), and 19 interventional trials (n = 1119). We assessed alpha diversity, beta diversity, and taxa abundance changes in patients with MDD relative to HC, as well as the effect of prebiotics, probiotics, and synbiotics on depressive symptoms in individuals with clinical or subclinical depression. We observed no significant differences in alpha diversity but a significant difference in beta diversity between patients with MDD and HC. There were fluctuations in the abundance of specific taxa in patients with MDD relative to HC. Probiotic and synbiotic, but not prebiotic, treatment showed a modest benefit in reducing depressive symptoms in patients with MDD over four to nine weeks. The GMB profiles of patients with MDD differ significantly from HC, but further studies are needed to elucidate the benefits of prebiotic, probiotic and synbiotic treatments relative to antidepressants and over longer follow-up before these therapies are implemented into clinical practice.
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Gut Microbiome, Diet and Depression: Literature Review of Microbiological, Nutritional and Neuroscientific Aspects.
PURPOSE OF REVIEW: This review explores the intricate relationships among the gut microbiota, dietary patterns, and mental health, focusing specifically on depression. It synthesizes insights from microbiological, nutritional, and neuroscientific perspectives to understand how the gut-brain axis influences mood and cognitive function. RECENT FINDINGS: Recent studies underscore the central role of gut microbiota in modulating neurological and psychological health via the gut-brain axis. Key findings highlight the importance of dietary components, including probiotics, prebiotics, and psychobiotics, in restoring microbial balance and enhancing mood regulation. Different dietary patterns exhibit a profound impact on gut microbiota composition, suggesting their potential as complementary strategies for mental health support. Furthermore, mechanisms like tryptophan metabolism, the HPA axis, and microbial metabolites such as SCFAs are implicated in linking diet and microbiota to depression. Clinical trials show promising effects of probiotics in alleviating depressive symptoms. This review illuminates the potential of diet-based interventions targeting the gut microbiota to mitigate depression and improve mental health. While the interplay between microbial diversity, diet, and brain function offers promising therapeutic avenues, further clinical research is needed to validate these findings and establish robust, individualized treatment strategies.
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The role of inflammation and the gut microbiome in depression and anxiety.
The study of the gut microbiome has increasingly revealed an important role in modulating brain function and mental health. In this review, we underscore specific pathways and mechanisms by which the gut microbiome can promote the development of mental disorders such as depression and anxiety. First, we review the involvement of the stress response and immune system activation in the development of depression and anxiety. Then, we examine germ-free murine models used to uncover the role of the gut microbiome in developing and modulating pertinent activity in the brain and the immune system. We also document multiple pathways by which stress-induced inflammation harms brain function and ultimately affects mental health, and review how probiotic and prebiotic treatments have shown to be beneficial. Lastly, we provide an overview of gut microbiome-derived compounds (short-chain fatty acids, tryptophan catabolites, microbial pattern recognition) and related mechanisms (vagal nerve activity and fecal microbiota transplants) involved in mediating the influence of the gut microbiome to mental health. Overall, a picture of the gut microbiome playing a facilitating role between stress response, inflammation, and depression, and anxiety is emerging. Future research is needed to firmly establish the microbiome's causal role, to further elucidate the mechanisms by which gut microbes influence brain function and mental health, and to possibly develop treatments that improve mental health through microbiotic targets.
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Bifidobacterium breve CCFM1025 attenuates major depression disorder via regulating gut microbiome and tryptophan metabolism: A randomized clinical trial.
OBJECTIVE: Psychobiotics, as a novel class of probiotics mainly acting on the gut-brain axis, have shown promising prospects in treating psychiatric disorders. Bifidobacterium breve CCFM1025 was validated to have an antidepressant-like effect in mice. This study aims to assess its psychotropic potential in managing major depression disorder (MDD) and unravel the underlying mechanisms. METHODS: Clinical Trial Registration: https://www.chictr.org.cn/index.aspx (identifier: NO. ChiCTR2100046321). Patients (n = 45) diagnosed with MDD were randomly assigned to the Placebo (n = 25) and CCFM1025 (n = 20) groups. The freeze-dried CCFM1025 in a dose of viable bacteria of 1010 CFU was given to MDD patients daily for four weeks, while the placebo group was given maltodextrin. Changes from baseline in psychometric and gastrointestinal symptoms were evaluated using Hamilton Depression Rating scale-24 Items (HDRS-24), Montgomery-Asberg Depression Rating Scale (MADRS), Brief Psychiatric Rating Scale (BPRS), and Gastrointestinal Symptom Rating Scale (GSRS). Serum measures were also determined, i.e., cortisol, TNF-α, and IL-β. Serotonin turnover in the circulation, gut microbiome composition, and tryptophan metabolites were further investigated for clarifying the probiotics' mechanisms of action. RESULTS: CCFM1025 showed a better antidepressant-like effect than placebo, based on the HDRS-24 (placebo: M = 6.44, SD = 5.44; CCFM1025: M = 10.40, SD = 6.85; t(43) = 2.163, P = 0.036, d = 0.640) and MADRS (placebo: M = 4.92, SD = 7.15; CCFM1025: M = 9.60, SD = 7.37; t(43) = 2.152, P = 0.037, d = 0.645) evaluation. The factor analysis of BPRS and GSRS suggested that patients' emotional and gastrointestinal problems may be affected by the serotonergic system. Specifically, CCFM1025 could significantly and to a larger extend reduce the serum serotonin turnover compared with the placebo (placebo: M = -0.01, SD = 0.41; CCFM1025: M = 0.27, SD = 0.40; t(43) = 2.267, P = 0.029, d = 0.681). It may be due to changes in gut microbiome and gut tryptophan metabolism under the probiotic treatment, such as changes in alpha diversity, tryptophan, and indoles derivatives. CONCLUSION: B. breve CCFM1025 is a promising candidate psychobiotic strain that attenuates depression and associated gastrointestinal disorders. The mechanisms may be relevant to the changes in the gut microbiome and tryptophan metabolism. These findings support the future clinical applications of psychobiotics in the treatment of psychiatric disorders.
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The gut microbiota in anxiety and depression - A systematic review.
Growing evidence indicates the community of microorganisms throughout the gastrointestinal tract, (i.e., gut microbiota), is associated with anxiety and depressive disorders. We present the first systematic review of the gut microbiota in anxiety disorders, along with an update in depression. Consideration of shared underlying features is essential due to the high rates of comorbidity. Systematic searches, following PRISMA guidelines, identified 26 studies (two case-control comparisons of the gut microbiota in generalised anxiety disorder, 18 in depression, one incorporating both anxiety/depression, and five including symptom-only measures). Alpha and beta diversity findings were inconsistent; however, differences in bacterial taxa indicated disorders may be characterised by a higher abundance of proinflammatory species (e.g., Enterobacteriaceae and Desulfovibrio), and lower short-chain fatty acid producing-bacteria (e.g., Faecalibacterium). Several taxa, and their mechanisms of action, may relate to anxiety and depression pathophysiology via communication of peripheral inflammation to the brain. Although the gut microbiota remains a promising target for prevention and therapy, future research should assess confounders, particularly diet and psychotropic medications, and should examine microorganism function.
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Soft Drink Consumption and Depression Mediated by Gut Microbiome Alterations.
IMPORTANCE: Soft drink consumption is linked to negative physical and mental health outcomes, but its association with major depressive disorder (MDD) and the underlying mechanisms remains unclear. OBJECTIVE: To examine the association between soft drink consumption and MDD diagnosis and severity and whether this association is mediated by changes in the gut microbiota, particularly Eggerthella and Hungatella abundance. DESIGN, SETTING, AND PARTICIPANTS: This multicenter cohort study was conducted in Germany using cross-sectional data from the Marburg-Münster Affective Cohort. Patients with MDD and healthy controls (aged 18-65 years) recruited from the general population and primary care between September 2014 and September 2018 were analyzed. Data analyses were conducted between May and December 2024. MAIN OUTCOMES AND MEASURES: Primary analyses included multivariable regression and analysis of variance (ANOVA) models examining the association between soft drink consumption and MDD diagnosis and symptom severity, controlling for site and education, and Eggerthella and Hungatella abundance, controlling for site, education, and library size. Mediation analyses tested whether microbiota abundance mediated the soft drink-MDD link. RESULTS: A total of 405 patients with MDD (275 female patients [67.9%]; mean [SD] age, 36.37 [13.33] years) and 527 healthy controls (345 female controls [65.5%]; mean [SD] age, 35.33 [13.13] years) were included. Soft drink consumption predicted MDD diagnosis (odds ratio [OR], 1.081; 95% CI, 1.008-1.159; P = .03) and symptom severity (P < .001; partial η2 [ηp2], 0.012; 95% CI, 0.004-0.035), with stronger effects in women (diagnosis: OR, 1.167; 95% CI, 1.054-1.292; P = .003; severity: P < .001; ηp2, 0.036; 95% CI, 0.011-0.062). In women, consumption was linked to increased Eggerthella (P = .007; ηp2, 0.017; 95% CI, 0.0002-0.068), but not Hungatella abundance. Mediation analyses confirmed that Eggerthella significantly mediated the soft drink-MDD association (diagnosis: P = .011; severity: P = .005), explaining 3.82% and 5.00% of the effect, respectively. CONCLUSIONS AND RELEVANCE: In this cohort study, it was found that soft drink consumption may contribute to MDD through gut microbiota alterations, notably involving Eggerthella. Public health strategies to reduce soft drink intake may help mitigate depression risk, especially among vulnerable populations; in addition, interventions for depression targeting the microbiome composition appear promising.
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Probiotics, Prebiotics and Postbiotics on Mitigation of Depression Symptoms: Modulation of the Brain-Gut-Microbiome Axis.
The brain-gut-microbiome axis is a bidirectional communication pathway between the gut microbiota and the central nervous system. The growing interest in the gut microbiota and mechanisms of its interaction with the brain has contributed to the considerable attention given to the potential use of probiotics, prebiotics and postbiotics in the prevention and treatment of depressive disorders. This review discusses the up-to-date findings in preclinical and clinical trials regarding the use of pro-, pre- and postbiotics in depressive disorders. Studies in rodent models of depression show that some of them inhibit inflammation, decrease corticosterone level and change the level of neurometabolites, which consequently lead to mitigation of the symptoms of depression. Moreover, certain clinical studies have indicated improvement in mood as well as changes in biochemical parameters in patients suffering from depressive disorders.
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Gut Microbiome Dysbiosis and Depression: a Comprehensive Review.
PURPOSE OF REVIEW: The human gut microbiome is involved in a bi-directional communication pathway with the central nervous system (CNS), termed the microbiota-gut-brain axis. The microbiota-gut-brain axis is believed to mediate or modulate various central processes through the vagus nerve. The microbiota-gut-brain axis is involved with the production of microbial metabolites and immune mediators which trigger changes in neurotransmission, neuroinflammation, and behavior. Little is understood about the utilization of microbiome manipulation to treat disease. RECENT FINDINGS: Though studies exploring the role of the microbiome in various disease processes have shown promise, mechanisms remain unclear and evidence-based treatments for most illnesses have not yet been developed. The animal studies reviewed in the present investigation include an array of basic science studies that clarify mechanisms by which the microbiome may affect mental health. More evidence is needed, particularly as it relates to translating this work to humans. The studies presented in this review demonstrate encouraging results in the treatment of depression. Limitations include small sample sizes and heterogeneous methodology. The exact mechanism by which the gut microbiota causes or alters neuropsychiatric disease states is not fully understood. In this review, we focus on recent studies investigating the relationship between gut microbiome dysbiosis and the pathogenesis of depression.