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The Canadian Network for Mood and Anxiety Treatments Task Force Recommendations for the Use of Probiotics, Prebiotics, Synbiotics, and Fecal Microbiota Transplants in Adults With Major Depressive Disorder: Recommandations du Groupe de travail du Réseau canadien pour le traitement des troubles de l'humeur et de l'anxiété (Canadian Network for Mood and Anxiety Treatments, CANMAT) concernant l'utilisation des probiotiques, des prébiotiques, des symbiotiques et de la transplantation de microbiote fécal chez les adultes atteints de trouble dépressif majeur.
BackgroundApproximately one-third of adults with major depressive disorder (MDD) experience limited response or intolerable side effects with existing pharmacotherapies. As such, innovative treatments targeting novel biological pathways are under investigation. One promising area of research is the gut microbiome and its influence on mood through the microbiota-gut-brain axis. Clinical studies have begun evaluating microbiome-targeted interventions such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) as potential treatments for MDD. The Canadian Network for Mood and Anxiety Treatments (CANMAT) convened a task force to evaluate the evidence for microbiome-targeted interventions in adults with MDD and to provide updated clinical recommendations.MethodsA systematic review of randomized controlled trials (RCTs) and meta-analyses was conducted, assessing interventions such as probiotics, prebiotics, synbiotics, and FMT in adults with MDD. The CANMAT methodology was used to determine levels of evidence and treatment line recommendations, which were presented in a question-and-answer format.ResultsTwenty-three RCTs and eight meta-analyses were included. Probiotics have been the most extensively studied and have demonstrated modest improvements in depressive symptoms, particularly when used in an adjunctive manner. However, recent high-quality trials yielded mixed results. Evidence for prebiotics and FMT was limited and inconclusive, while synbiotics were assessed in only one small RCT. Most interventions were well tolerated, with few serious adverse events.ConclusionsProbiotics may be cautiously considered as third-line adjunctive treatments for MDD, though findings remain inconsistent. There is currently insufficient evidence to recommend prebiotics, synbiotics, or FMT in clinical practice. Further large-scale, well-controlled trials are needed to clarify efficacy, safety, and optimal patient subgroups.
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The self-serving benefits of being a good host: A role for our micro-inhabitants in shaping opioids' function.
Opioids are highly efficacious in their ability to relieve pain, but they are liable for abuse, dependence, and addiction. Risk factors to develop opioid use disorders (OUD) include chronic stress, socio-environment, and preexisting major depressive disorders (MDD) and posttraumatic stress disorders (PTSD). Additionally, opioids reduce gut motility, induce loss of gut barrier function, and alter the composition of the trillions of microbes hosted in the gastrointestinal tract, known as the gut microbiota. The microbiota are significant contributors to the reciprocal communication between the central nervous system (CNS) and the gut, termed the gut-brain axis. They have strong influences on their host behaviors, including the ability to cope with stress, sociability, affect, mood, and anxiety. Thus, they are implicated in the etiology of MDD and PTSD. Here we review the latest studies demonstrating that intestinal flora can, directly and indirectly, by affecting sociability levels, responses to stress, and mental state, alter the responses to opioids. It suggests that microbiota can potentially be used to increase the resilience to develop analgesic tolerance and OUD.
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Investigation of the mechanism involved in high-fat diet-induced depressive behavior based on energy metabolism.
BACKGROUND: The specific mechanisms underlying high-fat diet (HFD) and depressive behaviors remain elusive. Meanwhile, the impact of calorie restriction (CR) on the development of depression has not been explored in-depth. Thus, we aimed to examine the pathways underlying how long-term HFD intake leads to depression, focusing on energy metabolism. METHODS: C57BL/6J mice were randomly divided into four groups-control (CK) group, CR group, HFD group, and chronic unpredictable mild stress (CUMS) group. Enzyme-linked immunosorbent assay, western blot, metabolomics and 16s rRNA gene sequencing analysis were undertaken to investigate the 5-hydroxytryptamine system, glucolipid metabolism, brain energy metabolism and gut microbiome. RESULTS: Mice with HFD- and CUMS-induced depressive-like symptoms exhibited a significant decrease in serotonergic activity in the hippocampus. The behaviors of CR mice did not differ significantly from CK mice. Fasting blood glucose levels, fatty acid contents, and reactive oxygen species (ROS) levels were all negatively affected in unrestricted HFD and CUMS mice, suggestive of energy metabolism disruption. Metabolomic analysis revealed that tricarboxylic acid cycle activity was inhibited in the HFD and CUMS groups but not in the CR group. Additionally, analysis of the gut microbiome revealed that [Ruminococcus] gnavus exhibited higher predictive potential for HFD-induced depression, while Allobaculum showed greater predictive potential for stress-induced depression. LIMITATIONS: Causal relationship between brain energy metabolism and gut microbiome unclear. CONCLUSION: An unrestricted HFD promotes dysbiosis of the gut microbiota, impairs energy metabolism in the brain, affects the serotonergic system, and ultimately induces depressive-like behaviors.
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Continuous Alterations in the Gut Microbial Landscape Associated With Suicidal Ideation in First-Episode Drug-naïve Major Depressive Disorder.
BACKGROUND: Major depressive disorder (MDD) has been closely associated with gut microbiota dysbiosis; however, the role of the gut microbiota in the progression from depression to suicidal ideation (SI) remains unclear. METHODS: We enrolled a well-characterized clinical cohort of first-episode, drug-naïve MDD patients, explicitly classified into those without SI (MDDNSI) and those with SI (MDDSI), and matched with healthy controls (HC) on demographic variables. A severity-ordered HC-MDDNSI-MDDSI framework was established to capture progressive microbial and functional shifts, and correlation analyses were used to evaluate their relationships with clinical symptoms and cognitive function. RESULTS: We identified a group of taxa showing clear severity-related trends, with the potential pathogenic species Bacteroides stercoris and Bacteroides eggerthii increasing across the clinical spectrum, while seven species, including Faecalibacillus intestinalis and Dialister massiliensis, showed a steady decrease. Functional annotation indicated that several major metabolic pathways, such as the bacterial secretion system, weakened progressively with disease severity and formed stable microbe-pathway modules together with pathways involved in energy metabolism and signal transduction. These differential taxa and pathways showed strong associations with clinical features, with Bacteroides stercoris positively correlated with SI, whereas Bifidobacterium pseudocatenulatum displayed a negative association. In addition, mediation analysis further showed that Bacteroides stercoris indirectly influenced SI through the bacterial secretion system pathway, suggesting a meaningful mediating role in SI. CONCLUSION: These results revealed progressive alterations in gut microbial composition and metabolic function associated with SI, indicating that gut dysbiosis serves as a potential biological marker for suicide risk in MDD.
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Behavioral phenotype, intestinal microbiome, and brain neuronal activity of male serotonin transporter knockout mice.
The serotonin transporter (5-HTT) plays a critical role in the regulation of serotonin neurotransmission. Mice genetically deficient in 5-HTT expression have been used to study the physiological functions of 5-HTT in the brain and have been proposed as a potential animal model for neuropsychiatric and neurodevelopmental disorders. Recent studies have provided evidence for a link between the gut-brain axis and mood disorders. However, the effects of 5-HTT deficiency on gut microbiota, brain function, and behavior remain to be fully characterized. Here we investigated the effects of 5-HTT deficiency on different types of behavior, the gut microbiome, and brain c-Fos expression as a marker of neuronal activation in response to the forced swim test for assessing depression-related behavior in male 5-HTT knockout mice. Behavioral analysis using a battery of 16 different tests showed that 5-HTT-/- mice exhibited markedly reduced locomotor activity, decreased pain sensitivity, reduced motor function, increased anxiety-like and depression-related behavior, altered social behavior in novel and familiar environments, normal working memory, enhanced spatial reference memory, and impaired fear memory compared to 5-HTT+/+ mice. 5-HTT+/- mice showed slightly reduced locomotor activity and impaired social behavior compared to 5-HTT+/+ mice. Analysis of 16S rRNA gene amplicons showed that 5-HTT-/- mice had altered gut microbiota abundances, such as a decrease in Allobaculum, Bifidobacterium, Clostridium sensu stricto, and Turicibacter, compared to 5-HTT+/+ mice. This study also showed that after exposure to the forced swim test, the number of c-Fos-positive cells was higher in the paraventricular thalamus and lateral hypothalamus and was lower in the prefrontal cortical regions, nucleus accumbens shell, dorsolateral septal nucleus, hippocampal regions, and ventromedial hypothalamus in 5-HTT-/- mice than in 5-HTT+/+ mice. These phenotypes of 5-HTT-/- mice partially recapitulate clinical observations in humans with major depressive disorder. The present findings indicate that 5-HTT-deficient mice serve as a good and valid animal model to study anxiety and depression with altered gut microbial composition and abnormal neuronal activity in the brain, highlighting the importance of 5-HTT in brain function and the mechanisms underlying the regulation of anxiety and depression.
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The gut-microbiota-brain axis in a Spanish population in the aftermath of the COVID-19 pandemic: microbiota composition linked to anxiety, trauma, and depression profiles.
The prevalence of anxiety and depression soared following the COVID-19 pandemic. To effectively treat these conditions, a comprehensive understanding of all etiological factors is needed. This study investigated fecal microbial features associated with mental health outcomes (symptoms of anxiety, depression, or posttraumatic stress disorder (PTSD)) in a Spanish cohort in the aftermath of the COVID-19 pandemic. Microbial communities from stool samples were profiled in 198 individuals who completed validated, self-report questionnaires. 16S ribosomal RNA gene V3-4 amplicon sequencing was performed. Microbial diversity and community structure were analyzed, together with relative taxonomic abundance. In our cohort of N=198, 17.17% reported depressive symptoms, 37.37% state anxiety symptoms, 40.90% trait anxiety symptoms, and 8.08% PTSD symptoms, with high levels of comorbidity. Individuals with trait anxiety had lower Simpson's diversity. Fusicatenibacter saccharivorans was reduced in individuals with comorbid PTSD + depression + state and trait anxiety symptoms, whilst an expansion of Proteobacteria and depletion of Synergistetes phyla were noted in individuals with depressive symptoms. The relative abundance of Anaerostipes was positively correlated with childhood trauma, and higher levels of Turicibacter sanguinis and lower levels of Lentisphaerae were found in individuals who experienced life-threatening traumas. COVID-19 infection and vaccination influenced the overall microbial composition and were associated with distinct relative taxonomic abundance profiles. These findings will help lay the foundation for future studies to identify microbial role players in symptoms of anxiety, depression, and PTSD and provide future therapeutic targets to improve mental health outcomes.
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The dysbiosis of gut microbiota in major depressive disorder and comorbidity with overweight/obesity: unraveling biomarkers and metabolic pathways from a microbial perspective.
BACKGROUND: Major depressive disorder (MDD), a leading global public health concern, exhibits high comorbidity with overweight/obesity. While emerging evidence implicates shared gut microbial dysregulation in both conditions, the identification of specific microbial biomarkers and their interaction with metabolic pathways in comorbid MDD-obesity remains poorly characterized. Our study investigated gut microbiota signatures in patients with MDD, and evaluated their modulation by overweight/obesity comorbidity. METHOD: A total of 53 patients with MDD and 92 healthy controls (HCs) underwent 16 S rRNA gene sequencing. The KEGG function analysis was performed with potential differential microbiota. Correlation analysis related to bacterial taxa, biochemical parameters, and clinical indexes was aimed to indicate the specific metabolic dysregulation and gut microbiota imbalance in MDD, and whether these biomarkers were affected by the comorbidity of overweight/obesity. RESULTS: Sixty-three bacterial genera showed differential abundance between MDD and HCs. Notably, Succinivibrio, Megamonas, and Bifidobacterium demonstrate significant distinctions between overweight-MDD and normal weight-MDD. The significantly altered metabolic pathways between MDD and HC primarily involve the biosynthesis and metabolism of long-chain unsaturated fatty acids. Within the MDD group, BMI demonstrated pairwise negative correlations with Bifidobacterium and total bilirubin (TBIL), while positively associating with Fusobacterium and alanine transaminase (ALT). CONCLUSION: This study provides novel insights into the interplay between gut microbiota dysbiosis and metabolic perturbations in MDD. Despite intriguing associations between BMI and specific microbial taxa within the MDD group, the preliminary nature of these associations necessitates validation through larger cohorts, multi-omics approaches, and longitudinal designs.
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The Role of Bacteria and Its Derived Metabolites in Chronic Pain and Depression: Recent Findings and Research Progress.
BACKGROUND: Chronic pain is frequently comorbid with depression in clinical practice. Recently, alterations in gut microbiota and metabolites derived therefrom have been found to potentially contribute to abnormal behaviors and cognitive dysfunction via the "microbiota-gut-brain" axis. METHODS: PubMed was searched and we selected relevant studies before October 1, 2019. The search keyword string included "pain OR chronic pain" AND "gut microbiota OR metabolites"; "depression OR depressive disorder" AND "gut microbiota OR metabolites". We also searched the reference lists of key articles manually. RESULTS: This review systematically summarized the recent evidence of gut microbiota and metabolites in chronic pain and depression in animal and human studies. The results showed the pathogenesis and therapeutics of chronic pain and depression might be partially due to gut microbiota dysbiosis. Importantly, bacteria-derived metabolites, including short-chain fatty acids, tryptophan-derived metabolites, and secondary bile acids, offer new insights into the potential linkage between key triggers in gut microbiota and potential mechanisms of depression. CONCLUSION: Studying gut microbiota and its metabolites has contributed to the understanding of comorbidity of chronic pain and depression. Consequently, modulating dietary structures or supplementation of specific bacteria may be an available strategy for treating chronic pain and depression.
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Gut Dysbiosis-Mediated Major Depressive Disorder: A Review of Pathogenic Mechanisms and Potential Therapeutic Strategies.
Major depressive disorder (MDD) is a mental illness with high mortality, suicide, and relapse rates that could become the leading cause of health problems worldwide by 2030. The microbiota-gut-brain axis involves bidirectional communication between the human gut microbiota and the central nervous system (CNS). The gut microbiome is a complex ecosystem of approximately 100 trillion microorganisms, including viruses, bacteria, and fungi. The gut microbiota has recently been recognized for its impact on various diseases and health concerns. Several factors influence the composition and structure of gut microbes, ultimately affecting human physiology, with the nervous system being particularly vulnerable. The gut-brain-microbiota axis influences several important brain functions through numerous pathways, including vagus nerve signaling, gut microbial synthesis of metabolites, and immune-related chemicals. These factors can influence neurotransmitter activity, neuroinflammation, behavior, and mental health. Despite increased interest, the possibility of modifying the gut microbiota as a therapeutic approach remains unclear. Although numerous studies suggest that microbiota play an important role in many illnesses, the precise mechanisms are yet to be elucidated, and there are currently no evidence-based, microbiota-focused treatments for these illnesses. Recent research indicates that gut dysbiosis (GD) causes increased intestinal permeability (leaky gut), initiates systemic inflammation, and contaminates the blood. Opportunistic microbial metabolites cross the blood-brain barrier, triggering a neuroinflammatory cascade and apoptotic pathways while affecting neurogenesis and neurotransmitters, ultimately resulting in the development of MDD and anxiety. This review examined the factors influencing normal gut microbiota and GD-mediated MDD, as well as possible therapeutic options. The study outlines its objectives and methodological approaches, including the screening and filtering of research on GD-induced depression. Furthermore, it explored the daily use of dietary supplements, revealing new paths for clinical and preclinical research.
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The use of diet for preventing and treating depression in young men: current evidence and existing challenges.
Emerging evidence suggests that diet therapy (nutrients, foods and dietary patterns) could be effective as a potential adjunctive treatment option for major depressive disorder. Numerous mechanisms have been proposed, including the role inflammation, oxidative stress, brain-derived neurotrophic factor, the gastrointestinal tract microbiome and tryptophan/serotonin metabolism. Despite known differences in depression characteristics and treatment responses between males and females, there are limited sex-specific studies examining the role of diet in young men specifically. This is important as young men are often reluctant to seek mental health support, so finding treatment strategies which appeal to this demographic is crucial. This brief report provides an overview of the most recent advances in the use of diet for preventing and treating depression in young men, highlighting existing challenges and opportunities for future research. We recommend that clinicians discuss the role of diet with depressed young men, so that diet may be used alongside current treatment options.