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The Relationship Between the Gut Microbiome-Immune System-Brain Axis and Major Depressive Disorder.
Major depressive disorder (MDD) is a prominent cause of disability worldwide. Current antidepressant drugs produce full remission in only about one-third of MDD patients and there are no biomarkers to guide physicians in selecting the best treatment for individuals. There is an urgency to learn more about the etiology of MDD and to identify new targets that will lead to improved therapy and hopefully aid in predicting and preventing MDD. There has been extensive interest in the roles of the immune system and the gut microbiome in MDD and in how these systems interact. Gut microbes can contribute to the nature of immune responses, and a chronic inflammatory state may lead to increased responsiveness to stress and to development of MDD. The gut microbiome-immune system-brain axis is bidirectional, is sensitive to stress and is important in development of stress-related disorders such as MDD. Communication between the gut and brain involves the enteric nervous system (ENS), the autonomic nervous system (ANS), neuroendocrine signaling systems and the immune system, and all of these can interact with the gut microbiota. Preclinical studies and preliminary clinical investigations have reported improved mood with administration of probiotics and prebiotics, but large, carefully controlled clinical trials are now necessary to evaluate their effectiveness in treating MDD. The roles that several gut microbe-derived molecules such as neurotransmitters, short chain fatty acids and tryptophan play in MDD are reviewed briefly. Challenges and potential future directions associated with studying this important axis as it relates to MDD are discussed.
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Fiber intake and fiber intervention in depression and anxiety: a systematic review and meta-analysis of observational studies and randomized controlled trials.
CONTEXT: Dietary fibers hold potential to influence depressive and anxiety outcomes by modulating the microbiota-gut-brain axis, which is increasingly recognized as an underlying factor in mental health maintenance. OBJECTIVE: Evidence for the effects of fibers on depressive and anxiety outcomes remains unclear. To this end, a systematic literature review and a meta-analysis were conducted that included observational studies and randomized controlled trials (RCTs). DATA SOURCES: The PubMed, Embase, CENTRAL, CINAHL, and PsychINFO databases were searched for eligible studies. DATA EXTRACTION: Study screening and risk-of-bias assessment were conducted by 2 independent reviewers. DATA ANALYSIS: Meta-analyses via random effects models were performed to examine the (1) association between fiber intake and depressive and anxiety outcomes in observational studies, and (2) effect of fiber intervention on depressive and anxiety outcomes compared with placebo in RCTs. A total of 181 405 participants were included in 23 observational studies. In cross-sectional studies, an inverse association was observed between fiber intake and depressive (Cohen's d effect size [d]: -0.11; 95% confidence interval [CI]: -0.16, -0.05) and anxiety (d = -0.25; 95%CI, -0.38, -0.12) outcomes. In longitudinal studies, there was an inverse association between fiber intake and depressive outcomes (d = -0.07; 95%CI, -0.11, -0.04). In total, 740 participants were included in 10 RCTs, all of whom used fiber supplements. Of note, only 1 RCT included individuals with a clinical diagnosis of depression. No difference was found between fiber supplementation and placebo for depressive (d = -0.47; 95%CI, -1.26, 0.31) or anxiety (d = -0.30; 95%CI, -0.67, 0.07) outcomes. CONCLUSION: Although observational data suggest a potential benefit for higher fiber intake for depressive and anxiety outcomes, evidence from current RCTs does not support fiber supplementation for improving depressive or anxiety outcomes. More research, including RCTs in clinical populations and using a broad range of fibers, is needed. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration no. CRD42021274898.
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Investigating the potential of fish oil as a nutraceutical in an animal model of early life stress.
Background: Early life stress is a key predisposing factor for depression and anxiety disorders. Selective serotonin re-uptake inhibitors (SSRI) are frequently used as the first line of pharmacology treatment for depression but have several negative qualities, i.e. a delay or absence of effectiveness and negative side-effects. Therefore, there is a growing need for new nutraceutical-based strategies to blunt the effects of adverse-life events.Objectives: This study aimed to use the maternal separation model in rats to test the efficacy of fish oil dietary supplementation, on its own and in conjunction with the SSRI anti-depressant fluoxetine, as a treatment for depressive and anxiety-like symptoms associated with early life stress.Methods: Behavioural tests (open field test, elevated plus maze test and forced swim test) and biochemical markers (corticosterone, BDNF, brain fatty acids and short chain fatty acids) were used to analyse the effects of the dietary treatments. Gut microbial communities and relating metabolites (SCFA) were analysed to investigate possible changes in the microbiota-gut-brain axis.Results: Maternally separated rats showed depressive-like behaviours in the forced swim and open field tests. These behaviours were prevented significantly by fluoxetine administration and in part by fish oil supplementation. Associated biochemical changes reported include altered brain fatty acids, significantly lower plasma corticosterone levels (AUC) and reduced brain stem serotonin turnover, compared to untreated, maternally separated (MS) rats. Untreated MS animals had significantly lower ratios of SCFA producers such as Caldicoprobacteraceae, Streptococcaceae, Rothia, Lachnospiraceae_NC2004_group, and Ruminococcus_2, along with significantly reduced levels of total SCFA compared to non-separated animals. Compared to untreated MS animals, animals fed fish oil had significantly higher Bacteroidetes and Prevotellaceae and reduced levels of butyrate, while fluoxetine treatment resulted in significantly higher levels of Neochlamydia, Lachnoclostridium, Acetitomaculum and Stenotrophomonas and, acetate and propionate.Conclusion: Despite the limitations in extrapolating from animal behavioural data and the notable differences in pharmacokinetics between rodents and humans, the results of this study provide a further advancement into the understanding of some of the complex systems within which nutraceuticals and pharmaceuticals effect the microbiota-gut-brain axis.
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Gut microbiome: A potential indicator for predicting treatment outcomes in major depressive disorder.
The therapeutic outcomes in major depressive disorder (MDD), one of the most common and heterogeneous mental illnesses, are affected by factors that remain unclear and often yield unsatisfactory results. Herein, we characterized the composition and metabolic function of the gut microbiota of patients with MDD during antidepressant treatment, based on 16S rRNA sequencing and metabolomics. The microbial signatures at baseline differed significantly between responder and non-responder groups. The gut microbiota of the non-responder group was mainly characterized by increased relative abundances of the phylum Actinobacteria, families Christensenellaceae and Eggerthellaceae, and genera Adlercreutzia and Christensenellaceae R7 group compared to that of the responder group. Additionally, the gut microbiota composition of the responder and non-responder groups differed significantly before and after treatment, especially at the genus level. Moreover, 20 differential metabolites between the responder and non-responder groups were identified that were mainly involved in lipid metabolism (cholestane steroids and steroid esters). Eggerthellaceae and Adlercreutzia displayed strong co-occurrence relationships with certain metabolites, suggesting alternations in the gut microbiome, and associated metabolites may be potential mediators of successful antidepressant treatment. Overall, our study demonstrates that alterations in gut microbiota composition and metabolic function might be relevant to the response to antidepressants, thereby providing insight into mechanisms responsible for their efficacy.
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Interrelationships between diet quality and health-related quality of life in Irish adults living with cystic fibrosis.
PURPOSE: In the Cystic Fibrosis (CF) modulator era, focus for many has shifted from growth and survival to prevention of diet-related chronic diseases. In doing so, diet quality should be prioritised. However, factors influencing diet quality in CF have yet to be examined. This study aims to explore relationships between health-related quality of life (HRQoL), demographic and clinical characteristics, and diet quality in adults living with CF. METHODS: Cross-sectional study of Irish adults with CF. Dietary intake was assessed using three-day food diaries and analysed using the Healthy Eating Index-2020 (HEI-2020) and Diet Quality Index-International (DQI-I), both scored 0–100, with higher scores indicating better diet quality. Patient-reported outcome measure questionnaires collected HRQoL data and symptom status. Data was statistically analysed in SPSS®. RESULTS: Among N = 73 participants (female: 56.2%, age: 35.1 ± 10.3 years), 79.4% were taking CFTR modulators. Mean predicted percentage forced expiratory volume (FEV1%) was 78.7 ± 24.9%, and median body mass index was 23.9 (4.2) kg/m2. Mean HEI-2020 and DQI-I scores were 59.3 ± 12.4 and 51.2 ± 9.8, respectively. Anxiety/depression symptoms were reported by 43.1% of participants, and 30.6% reported the presence of pain/discomfort. Bloating in stomach was reported in 68.1% of participants, with 43.1% reporting moderate to severe symptoms. FEV1% and digestive symptoms were independently positive significant predictors of HEI-2020 scores (R2adj = 0.166, n = 67, p = 0.004). CONCLUSION: In the modulator era, suboptimal vitality, anxiety / depression, and gut symptoms remain prevalent among adults living with CF. Future dietary interventions should aim to improve diet quality and consider incorporating dietary patterns that positively influence the gut microbiome.
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Gut microbial metabolites in depression: understanding the biochemical mechanisms.
Gastrointestinal and central function are intrinsically connected by the gut microbiota, an ecosystem that has co-evolved with the host to expand its biotransformational capabilities and interact with host physiological processes by means of its metabolic products. Abnormalities in this microbiota-gut-brain axis have emerged as a key component in the pathophysiology of depression, leading to more research attempting to understand the neuroactive potential of the products of gut microbial metabolism. This review explores the potential for the gut microbiota to contribute to depression and focuses on the role that microbially-derived molecules - neurotransmitters, short-chain fatty acids, indoles, bile acids, choline metabolites, lactate and vitamins - play in the context of emotional behavior. The future of gut-brain axis research lies is moving away from association, towards the mechanisms underlying the relationship between the gut bacteria and depressive behavior. We propose that direct and indirect mechanisms exist through which gut microbial metabolites affect depressive behavior: these include (i) direct stimulation of central receptors, (ii) peripheral stimulation of neural, endocrine, and immune mediators, and (iii) epigenetic regulation of histone acetylation and DNA methylation. Elucidating these mechanisms is essential to expand our understanding of the etiology of depression, and to develop new strategies to harness the beneficial psychotropic effects of these molecules. Overall, the review highlights the potential for dietary interventions to represent such novel therapeutic strategies for major depressive disorder.
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Anxiolytic- and antidepressant-like effects of Bacillus coagulans Unique IS-2 mediate via reshaping of microbiome gut-brain axis in rats.
BACKGROUND: Due to the rising cases of treatment-refractory affective disorders, the discovery of newer therapeutic approaches is needed. In recent times, probiotics have garnered notable attention in managing stress-related disorders. Herein, we examined the effect of Bacillus coagulans Unique IS-2® probiotic on anxiety- and depression-like phenotypes employing maternal separation (MS) and chronic-unpredictable mild stress (CUMS) model in rats. METHODS: Both male and female Sprague-Dawley rats were subjected to MS + CUMS. Probiotic treatment was provided for 6 weeks via drinking water. Anxiety- and depression-like phenotypes were assessed using sucrose-preference test (SPT), forced-swimming test (FST), elevated-plus maze test (EPM), and open-field test (OFT). Blood, brain, intestine, and fecal samples were obtained for biochemical and molecular studies. RESULTS: Stress-exposed rats drank less sucrose solution, showed increased passivity, and explored less in open-arms in SPT, FST, and EPM, respectively. These stress-generated neurobehavioral aberrations were alleviated by 6-week of Bacillus coagulans Unique IS-2 treatment. The overall locomotor activity in OFT remained unchanged. The decreased levels of BDNF and serotonin and increased levels of C-reactive protein, TNF-α, IL-1β, and dopamine, in the hippocampus and/or frontal cortex of stress-exposed rats were reversed following probiotic treatment. Administration of probiotic also restored the systemic levels of L-tryptophan, L-kynurenine, kynurenic-acid, and 3-hydroxyanthranilic acid, villi/crypt ratio, goblet-cell count, Firmicutes to Bacteroides ratio, and levels of acetate, propionate, and butyrate in fecal samples. These results indicate remodeling of the microbiome gut-brain axis in Bacillus coagulans Unique IS-2 recipient rats. However, protein levels of doublecortin, GFAP, and zona occludens in the hippocampus and occludin-immunoreactivity in the intestine remained unchanged. No prominent sex-specific changes were noted. CONCLUSION: Anxiolytic- and antidepressant-like effects of Bacillus coagulans Unique IS-2 in MS + CUMS rat model may be mediated via reshaping the microbiome gut-brain axis.
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Vitamin B12 and Affective Disorders: A Focus on the Gut-Brain Axis.
Accumulating evidence highlights the role of Vitamin B12 (VitB12) in the pathophysiology of affective disorders. However, its influence on brain function and the underlying mechanisms remain incompletely understood. In humans, VitB12 is obtained solely from dietary sources, primarily animal-based foods. VitB12 deficiency leads to the accumulation of homocysteine, a known contributor to emotional and behavioral dysregulation. VitB12 plays a critical role in maintaining neuron stability, synapsis plasticity, and regulating neuroinflammation by modulating key bioactive factors. These processes help to alleviate hippocampal damage, mitigate blood-brain barrier disruption, reduce oxidative stress, and enhance both structural and functional connectivity-collectively contributing to resilience against affective disorders. VitB12 from both diet and microbial sources is essential to gut homeostasis. Within the gut lumen, it stabilizes gut microbial communities, promotes short-chain fatty acid (SCFA) production, and supports neurotransmitter metabolism (e.g., serotonin and dopamine) via its role in S-adenosyl-l-methionine biosynthesis. Crucially, VitB12, gut microbiota, SCFAs, intestinal mucosa, and vagal nerve signaling interact synergistically within the gut-brain axis (GBA) to maintain gut microenvironment stability, protect the gut-blood barrier, and suppress neuroinflammatory cascades, eventually reducing the susceptibility to affective disorders. This review synthesizes current evidence on the involvement of VitB12 in the GBA, its association with mood regulation, and its potential as a nutritional adjunct in managing affective disorders. By elucidating this integrative mechanism, we provide new insights into targeting the GBA to improve clinical outcomes in affective disorders.
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From the Gut to the Mind: Elucidating the Microbiome-chronobiology Axis in the Context of Depressive Illness.
INTRODUCTION: Depression is a highly prevalent mood disorder and is often comorbid with gastrointestinal dysfunction and circadian disturbances. Many studies suggest that gut microbiota (GM) dysbiosis and circadian rhythm disruption may contribute to depressive pathophysiology; however, the mechanistic interactions between these systems remain incompletely defined. Deciphering these interactions may provide insights into prospective therapeutic targets or biomarkers for depression, although further mechanistic studies are needed to validate these findings. METHODS: The PubMed, Web of Science, Embase, and the Cochrane Library for articles published between January 2000 and December 2024 served as the basis of this review for analyzing, which covers original research, meta-analyses, high-impact reviews published in English, and excluding conference abstracts, case reports, and studies focusing solely on animal models without potential translational implications. After independently screening all retrieved articles and resolving discrepancies, a narrative synthesis approach was adopted to integrate data on mechanistic pathways, clinical associations, and translational potential. RESULTS: In this review, we focused on the dynamic interaction network between the GM and circadian rhythms, considering a new pathway by which they participate in the occurrence and development of depressive symptoms through bidirectional regulation: significant abnormalities in the GM structure of depressed patients are specifically associated with disruption of the circadian rhythm, and this association is dysbiosis-misalignment. DISCUSSION: Deciphering the molecular mechanisms of the regulatory loop may provide valuable information that can help screen specific therapeutic targets and biomarkers for depression, which may promote the transformation of depression diagnosis and treatment models from symptomatic treatment to precision-targeted intervention. CONCLUSION: Studies have confirmed dysbiosis-misalignment between the GM and circadian rhythms: dysbiosis can reshape the regulatory system underlying circadian rhythm, and disruption of the circadian rhythm in turn exacerbates dysbiosis. This interaction imbalance may drive the pathophysiological processes of depression. In this review, we highlighted that a comprehensive assessment of the interaction mechanism of the microbiome-chronobiology axis may help overcome the current bottleneck in treating depression and may provide a theoretical basis for developing novel intervention strategies with both timeliness and targeting.
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Microbes and Monoamines: Potential Neuropsychiatric Consequences of Dysbiosis.
From an evolutionary perspective, the genes of enteric microbes transmitted reliably across generations are nearly as much a part of the human organism as our own genes. Disruption of the microbiome leading to extinction of key 'heirloom' taxa can deprive individuals of metabolic pathways that have been present in their ancestors for millennia. Some of these pathways support essential synthesis and toxin clearance processes, including the generation of blood-brain barrier-crossing metabolic products crucial for normal brain function. Here, we discuss three such pathways: endogenous benzodiazepine synthesis, production of queuine/queuosine, and excretion of dietary mercury. Among them, these pathways have the potential to impact systems relevant to a wide range of neurodevelopmental and psychiatric conditions including autism, depression, anxiety, and schizophrenia.