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Gut-brain axis and depression: focus on the amino acid and short-chain fatty acid metabolism.
Depression, a major psychiatric disorder with profound societal impact, remains incompletely understood in its etiology. Identifying novel pathogenic pathways is therefore essential. The gut microbiota ('second brain') critically regulates bidirectional gut-brain axis (GBA) communication with the central nervous system. Dysbiosis correlates strongly with depression, positioning microbiota restoration as a promising therapeutic strategy. Critically, gut microbial metabolic processes - particularly involving amino acids and short-chain fatty acids (SCFAs) - have emerged as key contributors to depression pathogenesis; however, depression-specific alterations in gut microbiota and their metabolic signatures are inadequately characterized, and the molecular mechanisms linking microbial metabolites to depression require further elucidation. This review synthesizes recent advances on GBA-mediated depression pathogenesis, with emphasis on gut dysbiosis-induced disruptions in amino acid and SCFA metabolism, and delineates their mechanistic links to depressive pathophysiology.
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Muribaculum intestinale alleviates depressive-like behaviors by inhibiting Th17 cell differentiation and M1 microglia polarization.
BACKGROUND: Gut microbiota dysbiosis has been implicated in the pathogenesis of depression. Our previous studies identified loganin as a potential antidepressant agent; however, its oral bioavailability is low. Whether loganin alleviates depression via modulation of the gut microbiota remains unclear. METHODS: Chronic unpredictable stress mice model was used to evaluate the antidepressant-like effects of loganin. To determine the role of gut microbiota, mice were treated with an antibiotic cocktail (ABX) to deplete microbiota. Fecal microbiota transplantation (FMT) from loganin-treated donors and Muribaculum intestinale (M. intestinale) were performed to assess microbial contributions. RESULTS: Loganin exerted antidepressant-like effects by modulating gut microbiota, as evidenced by reduced efficacy in ABX-treated mice and behavioral improvements in recipients of FMT from loganin-treated donors. Loganin modulated gut microbiota composition particularly increasing the abundance of Muribaculum, and increased short-chain fatty acids (SCFAs). M. intestinale alleviated depressive-like behaviors, prompted the butyrylation of RORγt, inhibited Th17 cells differentiation, and suppressed M1 microglia polarization. Importantly, overexpression of RORγt attenuated the behavioral benefits of M. intestinale. CONCLUSION: Loganin exerts antidepressant-like effects by enriching Muribaculum and SCFAs, thereby inhibiting Th17 cell differentiation and M1 microglia polarization. M. intestinale may represent a promising microbial-based therapeutic strategy for depression.
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A randomised controlled trial of the effects of Galacto-Oligosaccharides on the gut brain-axis of young females.
Galacto-oligosaccharides (GOS) are prebiotics that modulate gut microbiota and are implicated in the gut-brain axis (GBA), with preclinical models reporting effects on neurochemistry, brain function, and cognition. Here we report the results of a randomised, double-blind, placebo-controlled trial in 83 healthy females (17-25 years), who received GOS or placebo for 28 days. Assessments occurred at baseline, endline, and 28 days post-supplementation. The primary outcome was trait anxiety, secondary outcomes were brain-based levels of GABA and glutamate in the dorsolateral prefrontal cortex (dlPFC), anterior cingulate cortex, and inferior occipital gyrus (IOG) (measured with 1H-MRS), and gut microbiome composition. Tertiary outcomes included social anxiety, depression, emotion behaviour, reaction times, and nutritional intake. Analyses included intention-to-treat, per-protocol, and sensitivity approaches. Trait anxiety did not differ between groups at endline (p = 0.443), though trends favoured lower anxiety in the GOS group at follow-up (p = 0.069). GOS reduced GABA at trend significance in the IOG (p = 0.053) in the Intention to Treat (ITT) population and dlPFC (p = 0.088) in high-anxious participants, with effects persisting at follow-up. GOS transiently increased Bifidobacterium abundance (p = 0.001) but did not affect microbiome diversity. Tertiary outcomes showed no significant changes in social anxiety or depression but faster reaction rates in high-anxious participants for simple (p = 0.036) and choice tasks (p < 0.001). Nutritional intake was unaffected. While GOS supplementation did not significantly reduce trait anxiety, it produced neurochemical changes and transient modulations of the gut microbiome in Bifidobacterium abundance, indicating GOS-induced changes can be traced along the GBA.
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Vitamin D and Depression in Women: A Mini-review.
Affective-related disorders, including depression, are constantly rising, complicating people's personal lifestyle increasing disqualification and hospital care. Because of the high intensity of urbanization, our lifestyle and food have altered dramatically in the last twenty years. These food modifications have been associated with scores of depression and other affective-related disorders in urbanized countries with high economic levels. Nutrients imbalance is considered as one of the critical causes enabling the pathophysiological mechanisms for the development of psychiatric disorders. The application of additional nutritional interventions for treatment of mood deteriorations can be beneficial for both the prophylaxis and therapy of affective-related disorders. This paper will review recent research on the relation of Vitamin D levels and the epidemiology of depression in women. In this paper, we will provide an overview of the results of a variety of different studies taking into account research which both suggests and refutes an association. Based on these findings we will propose important directions for future research in relation to this topic.
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Bridging Mind and Gut: The Molecular Mechanisms of microRNA, Microbiota, and Cytokine Interactions in Depression.
Depression is a complex psychiatric disorder that arises from various underlying biological mechanisms. In this review, the role of microRNAs (miRNAs) in modulating gut microbiotacytokine communication and their potential to unravel the pathophysiology of depression and develop novel therapeutic strategies are discussed. MiRNAs are small non-coding RNA molecules that have emerged as key regulators in the bidirectional signaling of the gut-brain axis by modulating gene expression and fine-tuning an intricate dialogue between the microbiota, immune system, and central nervous system. Results show how gut microbiota can shape miRNA expression in brain regions involved in mood regulation; conversely, evidence is accumulating, elucidating how miRNA perturbations can shape microbial ecology. Gut bacteria-derived short-chain fatty acids (SCFAs) fuel this nexus by exerting effects on neurogenesis, neurotransmitter synthesis, neuroinflammation, affective behavior alterations, and depressive-like phenotypes. Pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β are also known to be associated with depressive symptoms related to altered expression patterns of specific miRNAs across these disorders. This review exposes the novel potential biomarkers and therapeutic targets/strategies to develop innovative methods in the diagnosis and treatment of depression by exploring bidirectional relations among miRNAs, gut microbiota, and cytokines. The knowledge of these molecular networks and pathways has provided the opportunity for designing new-generation therapeutics such as phytobiotics, probiotics, psychobiotics, diet therapies, and nanomedicine based on miRNAs from a future perspective, which will revolutionize the management of mental disorders.
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KETO-MOOD: Ketogenic Diet for Microbiome Optimization and Overcoming Depression - A Protocol for a Randomized Controlled Trial.
INTRODUCTION: Major depressive disorder (MDD) significantly impacts millions worldwide, with limited success in achieving remission for many patients, leading to high disease burden and increased suicide risk. Psychotherapy and antidepressants, although effective, do not provide relief for all, prompting the search for alternative treatments. Ketogenic diets have demonstrated positive effects on brain health. Our study aims to investigate the efficacy of the ketogenic diet in alleviating MDD symptoms, filling a critical gap in psychiatric treatment options and offering a novel dietary approach with potential to mitigate disease burden and enhance mental well-being. METHODS: This phase 2 randomized controlled trial will evaluate the efficacy of a 10-week program of dietitian counseling and ketogenic meal provision versus an intervention with similar dietetic contact promoting a healthy, insulin-lowering, non-ketogenic diet. The primary outcome is the change in the Patient Health Questionnaire nine-item depression score. Secondary outcomes include cognitive and affective mindfulness, self-efficacy, sleep, cognitive function, work and social adjustment, and various immunological, metabolic, and microbiome markers at weeks 6 and 10. CONCLUSION: This study addresses a critical gap in depression treatment by exploring the ketogenic diet's potential as a metabolic mood enhancing intervention. Given the global impact of depression and limitations of current therapies, this research is valuable for exploring previously underappreciated neuroprotective and metabolic mechanisms and clinical benefits.
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Abnormal Gut Microbiota is Associated with Depressive-like Behavior in the Rat Model of Autoimmune Prostatitis.
Many patients with chronic prostatitis (CP)/chronic pelvic pain syndrome (CPPS) also experience depression, although the pathogenesis was unclear. Some studies have shown that gut microbiota disorder might be related to both prostatitis and depression. Therefore, we investigated the alteration of the gut microbiota in autoimmune CP/CPPS complicated with depression in a rat model. The rat model of autoimmune CP with comorbid depressive-like behavior was constructed by experimental autoimmune prostatitis (EAP) and chronic unpredictable mild stress (CUMS). Then, enzyme linked immunosorbent assay (ELISA) was performed to determine the concentration of inflammatory cytokines. The depression-like behaviors in rats were also detected using the open field test (OFT), forced swimming test (FST), and sucrose preference test (SPT). The composition of the gut microbiota and the microbial profile in rats were measured by bioinformatics analysis of the 16S rRNA gene sequence. The level of interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNF-α), and depression-like behavior in rats showed that the CP/CPPS complicated with depression model was established successfully. The results of the 16S rRNA sequence analysis showed disordered abundance, uniformity, and composition of gut microbiota in EAP + CUMS rats. Over 60 gut microbial metabolic pathways were predicted to be disordered among the four groups of rats. Additionally, metabolomics profiling indicated significant differences in EAP + CUMS rats compared to other groups, including reduced PWY-922, PWY-5198 and PWY-7159, and increased PWY0-321 and PWY-6629, which were predicted to be altered by Lactobacillus, Shigella, Blautia, Clostridiales, Comamonadaceae and Rhodospirillales. Our results have shown that gut microbiota disorders are associated with depressive-like behavior in experimental prostatitis. Our findings concerning gut microbiota provide new insights in understanding prostatitis-associated depression.
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Banxia Xiexin decoction alleviates AS co-depression disease by regulating the gut microbiome-lipid metabolic axis.
ETHNOPHARMACOLOGICAL RELEVANCE: Banxia Xiexin decoction (BXD) is a classic Chinese herbal formulation consisting of 7 herbs including Pinelliae Rhizoma, Scutellariae Radix, Zingiberis Rhizoma, Ginseng Radix, Glycyrrhizae Radix, Coptidis Rhizoma, and Jujubae Fructus, which can exert effects on lowering lipids and alleviating depressive mood disorders via affecting gastrointestinal tract. AIM OF THE STUDY: The pathogenesis of atherosclerosis (AS) co-depression disease has not been well studied, and the current clinical treatment strategies are not satisfactory. As a result, it is critical to find novel methods of treatment. Based on the hypothesis that the gut microbiome may promote the development of AS co-depression disease by regulating host lipid metabolism, this study sought to evaluate the effectiveness and action mechanism of BXD in regulation of the gut microbiome via an intervention in AS co-depression mice. MATERIALS AND METHODS: To determine the primary constituents of BXD, UPLC-Q/TOF-MS analysis was carried out. Sixteen C56BL/6 mice were fed normal chow as a control group; 64 ApoE-/- mice were randomized into four groups (model group and three treatment groups) and fed high-fat chow combined with daily bind stimulation for sixteen weeks to develop the AS co-depression mouse model and were administered saline or low, medium or high concentrations of BXD during the experimental modeling period. The antidepressant efficacy of BXD was examined by weighing, a sucrose preference test, an open field test, and a tail suspension experiment. The effectiveness of BXD as an anti-AS treatment was evaluated by means of biochemical indices, the HE staining method, and the Oil red O staining method. The impacts of BXD on the gut microbiome structure and brain (hippocampus and prefrontal cortex tissue) lipids in mice with the AS co-depression model were examined by 16S rDNA sequencing combined with lipidomics analysis. RESULTS: The main components of BXD include baicalin, berberine, ginsenoside Rb1, and 18 other substances. BXD could improve depression-like behavioral characteristics and AS-related indices in AS co-depression mice; BXD could regulate the abundance of some flora (phylum level: reduced abundance of Proteobacteria and Deferribacteres; genus level: reduced abundance of Clostridium_IV, Helicobacter, and Pseudoflavonifractor, Acetatifactor, Oscillibacter, which were significantly different). The lipidomics analysis showed that the differential lipids between the model and gavaged high-dose BXD (BXH) groups were enriched in glycerophospholipid metabolism, and lysophosphatidylcholine (LPC(20:3)(rep)(rep)) in the hippocampus and LPC(20:4)(rep) in the prefrontal cortex both showed downregulation in BXH. The correlation analysis illustrated that the screened differential lipids were mainly linked to Deferribacteres and Actinobacteria. CONCLUSION: BXD may exert an anti-AS co-depression therapeutic effect by modulating the abundance of some flora and thus intervening in peripheral lipid and brain lipid metabolism (via downregulation of LPC levels).
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Alteration of Gut Microbiome and Correlated Lipid Metabolism in Post-Stroke Depression.
BACKGROUND: The pathogenesis of post-stroke depression (PSD) remains largely unknown. There is growing evidence indicating that gut microbiota participates in the development of brain diseases through the gut-brain axis. Here, we aim to determine whether and how microbial composition and function altered among control, stroke and PSD rats. MATERIALS AND METHODS: After the PSD rat model was successfully established, gut microbiome combined with fecal metabolome approach were performed to identify potentially PSD-related gut microbes and their functional metabolites. Then, correlations between behavior indices and altered gut microbes, as well as correlations between altered gut microbial operational taxonomic units (OTUs) with differential metabolites in PSD rats were explored. Enrichment analysis was also conducted to uncover the crucial metabolic pathways related to PSD. RESULTS: Although there were some alterations in the microbiome and metabolism of the control and stroke rats, we found that the microbial and metabolic phenotypes of PSD rats were significantly different. The microbial composition of PSD showed a decreased species richness indices, characterized by 22 depleted OTUs mainly belonging to phylum Firmicutes, genus Blautia and Streptococcus. In addition, PSD was associated with disturbances of fecal metabolomics, among them Glutamate, Maleic acid, 5-Methyluridine, Gallocatechin, 1,5-Anhydroglucitol, L-Kynurenine, Daidzein, Cyanoalanine, Acetyl Alanine and 5-Methoxytryptamine were significantly related to disturbed gut microbiome (P ≤ 0.01). Disordered fecal metabolomics in PSD rats mainly assigned to lipid, amino acid, carbohydrate and nucleotide metabolism. The steroid biosynthesis was particularly enriched in PSD. CONCLUSIONS: Our findings suggest that gut microbiome may participate in the development of PSD, the mechanism may be related to the regulation of lipid metabolism.
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The gut microbiota in neuropsychiatric disorders.
The purpose of this review is to summarize current knowledge about the gut microbiota in neuropsychiatric disorders. It is estimated that the human gut is colonized by up to 1018 microorganisms, mostly anaerobic bacteria. The gut microbiome is responsible for multiple functions, e.g. tightness of the intestine barrier, digestion and absorption. The correlation between gut dysbiosis and development of psychiatric, autoimmune and allergic diseases as well as bidirectional communication between brain and gut microflora have been shown. Recent findings suggest that specific bacteria can be involved in the development of clinical conditions, such as Autism Spectrum Disorders, depression and schizophrenia, and microbiota may be a target for therapeutic intervention providing novel treatment strategies.