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Microbiota-Gut-Brain Axis and Antidepressant Treatment.
In the treatment of depressive disorders, conventional antidepressant therapy has been the mainstay of clinical management, along with well-established nonpharmacological interventions such as various kinds of psychotherapy. Over the last 2 decades, there has been considerable interest in the role of the gastrointestinal system and its microbiota on brain function, behavior, and mental health. Components of what is referred to as the microbiota-gut-brain axis have been uncovered, and further research has elicited functional capabilities such as "gut-brain modules." Some studies have found associations with compositional alterations of gut microbiota in patients with depressive disorders and individuals experiencing symptoms of depression. Regarding the pathogenesis and neurobiology of depression itself, there appears to be a multifactorial contribution, in addition to the theories involving deficits in catecholaminergic and monoamine neurotransmission. Interestingly, there is evidence to suggest that antidepressants may play a role in modulating the gut microbiota, thereby possibly having an impact on the microbiota-gut-brain axis in this manner. The development of prebiotics, probiotics, and synbiotics has led to studies investigating not only their impact on the microbiota but also their therapeutic value in mental health. These psychobiotics have the potential to be used as therapeutic adjuncts in the treatment of depression. Regarding future directions, and in an attempt to further understand the role of the microbiota-gut-brain axis in depression, more studies such as those involving fecal microbiota transplantation will be required. In addition to recent findings, it is also suggested that more research will have to be undertaken to elicit whether specific strains of gut organisms are linked to depression. In terms of further investigation of the therapeutic potential of prebiotics, probiotics, and synbiotics as adjuncts to antidepressant treatment, we also expect there to be more research targeting specific microorganisms, as well as a strong focus on the effects of specific prebiotic fibers from an individualized (personalized) point of view.
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Gut microbes and depression: Still waiting for Godot.
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How Microbes Affect Depression: Underlying Mechanisms via the Gut-Brain Axis and the Modulating Role of Probiotics.
Accumulating evidence suggests that the gut microbiome influences the brain functions and psychological state of its host via the gut-brain axis, and gut dysbiosis has been linked to several mental illnesses, including major depressive disorder (MDD). Animal experiments have shown that a depletion of the gut microbiota leads to behavioral changes, and is associated with pathological changes, including abnormal stress response and impaired adult neurogenesis. Short-chain fatty acids such as butyrate are known to contribute to the up-regulation of brain-derived neurotrophic factor (BDNF), and gut dysbiosis causes decreased levels of BDNF, which could affect neuronal development and synaptic plasticity. Increased gut permeability causes an influx of gut microbial components such as lipopolysaccharides, and the resultant systemic inflammation may lead to neuroinflammation in the central nervous system. In light of the fact that gut microbial factors contribute to the initiation and exacerbation of depressive symptoms, this review summarizes the current understanding of the molecular mechanisms involved in MDD onset, and discusses the therapeutic potential of probiotics, including butyrate-producing bacteria, which can mediate the microbiota-gut-brain axis.
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Modulating depression through the gut-brain axis: the role of gut microbiota in therapeutic interventions.
Depression is a multifactorial mental disorder increasingly linked to gut microbiota through the microbiota-gut-brain axis (MGBA). This review aims to explore how alterations in gut microbial composition influence depressive symptoms via neurochemical, immunological, and neuroendocrine pathways. Key mechanisms include microbial modulation of serotonin, dopamine, and GABA levels; systemic inflammation; hypothalamic-pituitary-adrenal (HPA) axis dysregulation; and vagus nerve signaling. Emerging evidence suggests that gut microbiota may also influence the efficacy of selective serotonin reuptake inhibitors (SSRIs), potentially via vagal pathways. Additionally, a distinct microbial signature has been observed in individuals with depression, with therapeutic probiotics targeting this dysbiosis showing beneficial effects. This review further evaluates the therapeutic potential of probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary interventions in managing depression. We highlight the need for microbiota-based biomarkers and personalized interventions in future clinical applications. Overall, this review underscores the therapeutic relevance of targeting the gut-brain axis in depression treatment.
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Causal relationships between gut microbiota and depression/anxiety disorders: A 2-sample Mendelian randomization study.
Evidence shows that the composition of the gut microbiota (GM) is associated with depression and anxiety disorders. However, the causal relationship between them remains controversial. To investigate the potential causal relationship between the GM and depression/anxiety disorders and to identify specific bacterial taxa, we conducted a 2-sample Mendelian randomization (MR) analysis on the gut microbiome implicated in depression and anxiety disorders. We incorporated summary data from genome-wide association studies (GWAS) of the microbiome derived from 7738 individuals in the Dutch Microbiome Project and 18,340 individuals in the MiBioGen consortium as our exposure variable. Concurrently, the GWAS of depression and anxiety disorders was employed as our outcome variable. The principal estimates were procured using the inverse-variance weighted test complemented by 4 robust methods: MR Egger, weighted median, simple mode, and weighted mode. In addition, we performed comprehensive sensitivity and directionality analyses. The results showed that 5 bacterial taxa were positively correlated with depression, 6 were negatively correlated; 5 were positively correlated with anxiety disorders, and 11 were negatively correlated. This study provides new insights into the connection between the GM and the pathogenesis of depression and anxiety disorders and offers new perspectives for the diagnosis and treatment of these disorders.
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Distinguishing bipolar depression, bipolar mania, and major depressive disorder by gut microbial characteristics.
BACKGROUND: Gut microbial disturbance has been widely confirmed in mood disorders. However, little is known about whether gut microbial characteristics can distinguish major depressive disorder (MDD), bipolar depression (BP-D), and bipolar mania (BP-M). METHODS: This was a prospective case-control study. The composition of gut microbiota was profiled using 16S ribosomal RNA (rRNA) gene sequencing of fecal samples and compared between healthy controls (HC; n = 46), MDD (n = 51), BP-D (n = 44), and patients with BP-M (n = 45). RESULTS: Gut microbial compositions were remarkably changed in the patients with MDD, BP-D, and BP-M. Compared to HC, distinct gut microbiome signatures were found in MDD, BP-D, and BP-M, and some gut microbial changes were overlapping between the three mood disorders. Furthermore, we identified a signature of 7 operational taxonomic units (OUT; Prevotellaceae-related OUT22, Prevotellaceae-related OUT31, Prevotellaceae-related OTU770, Ruminococcaceae-related OUT70, Bacteroidaceae-related OTU1536, Propionibacteriaceae-related OTU97, Acidaminococcaceae-related OTU34) that can distinguish patients with MDD from those with BP-D, BP-M, or HC, with area under the curve (AUC) values ranging from 0.910 to 0.996. CONCLUSION: Our results provide the clinical rationale for the discriminative diagnosis of MDD, BP-D, and BP-M by characteristic gut microbial features.
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Bulimia Nervosa and Depression, from the Brain to the Gut Microbiota and Back.
Bulimia nervosa (BN) is a condition marked by a typical cyclical behavioural activity, characterized by restrictions, binges and vomiting, as well as a disturbance of the emotional value of food. Food stimuli acquire excessive relevance, giving rise to a succession of states of excitement and anxiety. The depressive condition accompanies very often BN. Most people with BN also experience one or more anxiety disorders. The aim of the review is to identify a link at a central and peripheral level that connects an eating disorder with a mood state. Altered nervous mechanisms are involved in BN. Among the cerebral areas, the insula is functionally compromised in BN. The insula is also implicated in depressive states. The insula is the primary gustatory cortex, where gustatory sensory information such as taste discrimination and higher cognitive functions such as food anticipation and reward are processed. The insula is anatomically connected to a wide range of cortical, limbic and paralimbic structures, and functionally implicated in high-order cognition, emotional responses, and empathic processes. The insula plays a crucial role in empathy, or in the ability to share the emotional states of others, and in particular negative emotions. In fact, the insular cortex is also activated in conditions of anxiety and depression. One of the pathophysiological factors that influences bulimia and depression is the composition of gut microbiota, as there is a strong association between the microbial signature and the brain function. Gut dysbiosis condition may contribute to the development of eating disorders, including BN. Dysbiosis may promote intestinal inflammation, alter gut permeability, and trigger immune reactions in the hunger/satiety regulation center contributing to the pathophysiological development of eating disorders. From this emerges the importance of adequate probiotic integration as a preventive and/or therapeutic tool in these pathologies.
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Just a gut feeling: Faecal microbiota transplant for treatment of depression - A mini-review.
BACKGROUND: The microbiota-gut-brain axis (MGBA) allows bidirectional crosstalk between the brain and gut microbiota (GM) and is believed to contribute to regulating mood/cognition/behaviour/metabolism/health and homeostasis. Manipulation of GM through faecal microbiota transplant (FMT) is a new, exciting and promising treatment for major depressive disorder (MDD). AIMS: This mini-review examines current research into GM and FMT as a therapy for depression. METHODS: Original research articles published in Medline/Cochrane Library/PubMed/EMBASE/PsycINFO databases/National Institute of Health website Clinicaltrials.gov/controlled-trials.com were searched. Full articles included in reference lists were evaluated. We summarise current data on GM and depression and discuss communication through the MGBA and the interaction of antidepressants and GM through this. We review compositions of dysbiosis in depressed cohorts, focusing on future directions in the treatment of MDD. RESULTS: Studies have demonstrated significant gut dysbiosis in depressed patients compared to healthy cohorts, with overgrowth of pro-inflammatory microbiota, reduction in anti-inflammatory species and reduced overall stability and taxonomic richness. FMT allows the introduction of healthy microbiota into the gastrointestinal tract, facilitating the restoration of eubiosis. CONCLUSION: The GM plays an integral role in human health and disease through its communication with the rest of the body via the MGBA. FMT may provide a means to transfer the healthy phenotype into the recipient and this concept in humans is attracting enormous attention as a prospective treatment for psychopathologies, such as MDD, in the future. It may be possible to manipulate the GM in a number of ways, but further research is needed to determine the exact likelihood and profiles involved in the development and amelioration of MDD in humans, as well as the long-term effects and potential risks of this procedure.
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A systematic review on gut microbiota consortium in the management of depression: Preclinical and clinical evidence.
Major depressive disorder (MDD) is a disturbing mental condition affecting millions of people globally. The gut microbiota has garnered a major attention in the neurobiology and treatments of brain disorders, including depression. In this systematic review, we emphasized how prebiotics, probiotics, synbiotics, and postbiotics treatments manage depression. We registered this review on the Open Science Framework platform (Registration number: osf.io/bu674). As per PRISMA guidelines, we obtained 224 preclinical and clinical studies from five electronic databases (PubMed, Medline, EMBASE, Cochrane Library, and Web of Science) for the period of December 2008 to February 2025. Pan-probiotic approaches showed superior mood-elevating effects compared to a single-strain intervention. The mechanistic investigations of these studies unveiled complex neuroendocrine alterations, including the increase in serotonergic neurotransmission, anti-inflammatory responses, brain-derived neurotrophic factor expression, microbial diversity, and normalization of cortisol. Lactobacillus and Bifidobacterium genera exhibited the most consistent antidepressant-like effects at 1-10 billion colony-forming units (CFU) administered for 8-10 weeks. The probiotic and prebiotic interventions also demonstrated beneficial effects across the diverse clinical subpopulations, including patients with comorbid gastrointestinal disorders, heart complications, metabolic disorders, and postpartum depression. While these findings underscore the potential of microbiota-targeted therapeutics in depression, large-scale and long-term clinical trials are needed to identify a precise probiotic strain and treatment regimen.
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Interaction of the gut microbiota and brain functional connectivity in late-life depression.
BACKGROUND: Increasing evidence suggests an important role of the gut microbiome in the pathogenesis of mental disorders, including depression, along the microbiota-gut-brain axis. We sought to explore the interactions between gut microbe composition and neural circuits in late-life depression (LLD). METHODS: We performed fecal 16S ribosomal RNA (rRNA) sequencing and resting-state functional magnetic resonance imaging in a case-control cohort of older adults with LLD and healthy controls to characterize the association between gut microbiota and brain functional connectivity (FC). We used the Hamilton Depression Rating Scale (HAMD) to assess depressive symptoms. RESULTS: We included 32 adults with LLD and 16 healthy controls. At the genus level, the relative abundance of Enterobacter, Akkermansiaceae, Hemophilus, Burkholderia, and Rothia was significantly higher among patients with LDD than controls. Reduced FC within mood regulation circuits was mainly found in the frontal cortex (e.g., the right superior and inferior frontal gyrus, right lateral occipital cortex, left middle frontal gyrus, and left caudate) among patients with MDD. Group-characterized gut microbes among controls and patients showed opposite correlations with seed-based FC, which may account for the aberrant emotion regulation among patients with LDD. The abundance of Enterobacter (dominant genus among patients with LLD) was positively correlated with both HAMD scores (r = 0.49, p = 0.0004) and group-characterized FC (r = -0.37, p < 0.05), while Odoribacter (dominant genus among controls) was negatively correlated with both HAMD scores (r = -0.30, p = 0.04) and group-characterized FC. LIMITATIONS: The study's cross-sectional design and small sample size limit causal inferences; larger longitudinal studies are required for detailed subgroup analyses. CONCLUSION: We identified significant correlations between LDD-characterized gut microbes and brain FC, as well as depression severity, which may contribute to the pathophysiology of depression development among patients with LLD. Specific microbes were linked to altered brain connectivity, suggesting potential targets for treating LLD.