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Melatonin Ameliorates Depressive-Like Behaviors in Ovariectomized Mice by Improving Tryptophan Metabolism via Inhibition of Gut Microbe Alistipes Inops.
Melatonin (N-acetyl-5-methoxytryptamine) is reported to improve mood disorders in perimenopausal women and gut microbiome composition is altered during menopausal period. The possible role of microbiome in the treatment effect of melatonin on menopausal depression remains unknown. Here, it is shown that melatonin treatment reverses the gut microbiota dysbiosis and depressive-like behaviors in ovariectomy (OVX) operated mice. This effect of melatonin is prevented by antibiotic cocktails (ABX) treatment. Transferring microbiota harvested from adolescent female mice to OVX-operated mice is sufficient to ameliorate depressive-like behaviors. Conversely, microbiota transplantation from OVX-operated mice or melatonin-treated OVX-operated mice to naïve recipient mice exhibits similar phenotypes to donors. The colonization of Alistipes Inops, which is abundant in OVX-operated mice, confers the recipient with depressive-like behaviors. Further investigation indicates that the expansion of Alistipes Inops induced by OVX leads to the degradation of intestinal tryptophan, which destroys systemic tryptophan availability. Melatonin supplementation restores systemic tryptophan metabolic disorders by suppressing the growth of Alistipes Inops, which ameliorates depressive-like behaviors. These results highlight the previously unrecognized role of Alistipes Inops in the modulation of OVX-induced behavioral disorders and suggest that the application of melatonin to inhibit Alistipes Inops may serve as a potential strategy for preventing menopausal depressive symptoms.
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The effects of Lactobacillus plantarum PS128 in patients with major depressive disorder: an eight-week double-blind, placebo-controlled study.
Major depressive disorder (MDD) is a complex mental disorder, potentially linked to the gut-microbiota-brain axis. Probiotics like Lactobacillus plantarum PS128 (PS128) may improve depressive symptoms by modulating the gut microbiota based on our previous open trial. We conducted an 8-week double-blind, placebo-controlled trial to investigate the impact of PS128 on depression severity, markers of inflammation and gut permeability, and the gut microbiota composition in 32 patients with MDD with stable antidepressant treatment but moderate symptom severity. Following the 8-week intervention, both the Hamilton Depression Rating Scale-17 score (HAMD), and Depression and Somatic Symptoms Scale (DSSS) showed a significant decrease in both groups (p<0.001). However, there was no significant difference in the change of depression severity between groups (p=0.203). Moreover, alterations in serum levels of high sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-α, and intestinal fatty acid binding protein, as well as changes in the gut microbiota composition, did not exhibit significant differences before and after intervention or between the groups. In comparison to the placebo group, our study did not find significant effects of PS128 on depressive symptoms, biomarkers of inflammation and gut permeability, and the overall gut microbiota composition. Nonetheless, we observed a potential impact of PS128 on the symbiosis of specific taxa. To comprehensively understand the psychophysiological effects of PS128 in patients with MDD, further research with a larger sample size is imperative.
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Multi-species probiotic supplement enhances vagal nerve function - results of a randomized controlled trial in patients with depression and healthy controls.
Major depression (MD) significantly impacts individual well-being and society. The vagus nerve plays a pivotal role in the gut-brain axis, facilitating bidirectional communication between these systems. Recent meta-analyses suggest potential antidepressant effects of probiotics, although their mechanisms remain unclear. This study aimed to assess the impact of a multi-species probiotic (OMNi-BiOTiC® STRESS Repair) on vagus nerve function in 43 MD patients and 43 healthy controls (HC). Participants received either probiotics or placebo twice daily. Serum and stool samples were collected at baseline, 7 days, 28 days, and 3 months. Vagus nerve (VN) function was evaluated using 24-hour electrocardiography (ECG) for heart rate variability (HRV), alongside stool microbiome analysis via 16S rRNA sequencing. After 3 months, MD patients receiving probiotics demonstrated significantly improved morning VN function compared to HC. MD participants who were in the probiotic group showed a significant increase in Christensellales, particularly Akkermansia muciniphila along with improved sleep parameters (use of sleep medication, sleep latency) as measured by the Pittsburgh Sleep Quality Inventory (PSI). This study highlights potential physiological benefits of probiotics in MD, potentially mediated through VN stimulation. Understanding these mechanisms could lead to novel therapeutic approaches for MD management.
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The interplay of gut microbiota, obesity, and depression: insights and interventions.
The gut microbiome, body weight, and related comorbidities are intricately linked through a complex interaction of microbial, genetic, environmental, and psychological factors. Alterations in gut microbiota can contribute to the development of weight disorders and depressive symptoms, with the potential for these relationships to be bidirectional. Effective management of these interconnected conditions often involves a combination of lifestyle modifications and psychological support. Medical interventions, including treatments for obesity, antidiabetic drugs, antidepressants, antibiotics, and probiotics, can have beneficial and detrimental effects on gut microbiota and mental health. Further research is needed to better understand their impact on gut microbiome and mental health in the context of obesity.
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Young Adults with Major Depression Show Altered Microbiome.
There is growing basic and clinical evidence that major depressive disorder (MDD) is associated with gut microbiome alterations, but clinical studies have tended not to adjust for confounding factors. And few studies on the gut microbiome focused on young adults with MDD. Here we performed a pilot study to compare the gut microbiome of young adults with MDD with healthy controls. Shotgun metagenomic sequencing was performed on stool samples obtained from 40 young adults with MDD and 42 healthy controls. After controlling for confounding factors including sex, age, BMI, alcohol or cigarette consumption, bowel movement quality, exercise or defecation frequency, we compared microbiome diversity between groups, identified differentially abundant taxa, and further compared functional differences through gut-brain and gut-metabolic module analysis. There were no significant differences in overall gut microbiome structure and function in young adults with MDD compared with controls. Abundance of Sutterellaceae and species belonging to Clostridium, Eubacterium, and Ruminococcus were significantly different between groups. The cysteine degradation I pathway was increased in MDD. After controlling for most confounding factors, this pilot study provides new evidence on the specific, often subtle gut dysbiosis affecting young adults with depression.
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Bupropion administration significantly impacts the gut microbiome, serum metabolites, and immune factors in chronic stress depression rats.
Emerging evidence suggests that the gut microbiota plays a crucial role in the pathogenesis of depression through the microbiota-gut-brain axis. Our previous research demonstrated that oral antidepressants were potent in regulating gut microbiome in depressive rats. Bupropion is a common antidepressant, but its regulatory mechanisms on the gut microbiota in the treatment of depression remain unclear. Here, we evaluated the potential mechanisms underlying the microbe-mediated behavioral effects of oral and injectable bupropion in chronic restraint stress (CRS)-induced depressive rat model through integrated microbiome, metabolome, and biochemical techniques. Oral bupropion modulated the gut microbiota composition in favor of beneficial bacteria such as Romboutsia and Muribaculum, while reducing potentially harmful bacteria, including Staphylococcus, Streptococcus, and Bacteroides. Metabolomic results revealed that oral bupropion improved the abnormal levels of acetic acid, butyric acid, tryptophan and its derivatives, nicotinamide, and biotin. Moreover, oral bupropion significantly reduced the percentage of CD4+ T lymphocytes and the levels of IL-1β and CXCL2. In comparison, injectable administration may not fully replicate the effects of oral administration on these alterations. Moreover, significant changes in the gut microbiota composition, particularly Muribaculum and Bacteroides, as well as tryptophan metabolites (L-tryptophan, 5-hydroxy-L-tryptophan, and indole-3-acetic acid), and immune indicators (CXCL2 levels and CD4+ T lymphocyte percentages), were correlated. Notably, bupropion administration may also selectively exert negative effects on the gut microbiota, metabolites, and immune factors. Collectively, this study presents the first comprehensive overview of changes in the gut microbiome, metabolome, and immune indicators after bupropion treatment, highlighting their role in mediating antidepressant effects.
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Beyond the Gut: Integrating Oral Microbiota into the Microbiota-Brain Axis in Depression.
Depression, a major contributor to years lived with disability (YLD), affects nearly 300 million people worldwide. In the aftermath of the COVID-19 pandemic, cases of major depressive disorder (MDD) or clinical depression have risen by 28% particularly among women and young adults. Characterized by persistent low mood, cognitive impairment, suicidal ideation, sleep disturbances, appetite changes, and fatigue, depression continues to impose a profound public health burden, compounded by the limited efficacy of current treatments and the lack of reliable diagnostic or predictive biomarkers. While the gut microbiota has been extensively implicated in depression's pathophysiology, emerging evidence indicates that the oral microbiome which ranks second only to the gut in microbial diversity also plays a significant role in neuropsychiatric health. Oral microbial dysbiosis may contribute to depression through immune, inflammatory, and neuroactive pathways, positioning the oral microbiome as both a potential non-invasive biomarker and a novel therapeutic target. Incorporating oral microbial profiling into clinical research could not only refine our understanding of depression's underlying mechanisms but also facilitate the development of microbiome-based strategies in precision psychiatry. This growing recognition highlights the importance of expanding research beyond the gut-brain axis to encompass the oral-brain axis as an integral component in the quest for effective diagnostics and interventions.
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Role of gut microbiota in depression: Understanding molecular pathways, recent research, and future direction.
Gut microbiota, also known as the "second brain" in humans because of the regulatory role it has on the central nervous system via neuronal, chemical and immune pathways. It has been proven that there exists a bidirectional communication between the gut and the brain. Increasing evidence supports that this crosstalk is linked to the etiology and treatment of depression. Reports suggest that the gut microbiota control the host epigenetic machinery in depression and gut dysbiosis causes negative epigenetic modifications via mechanisms like histone acetylation, DNA methylation and non-coding RNA mediated gene inhibition. The gut microbiome can be a promising approach for the management of depression. The diet and dietary metabolites like kynurenine, tryptophan, and propionic acid also greatly influence the microbiome composition and thereby, the physiological activities. This review gives a bird-eye view on the pathological updates and currently used treatment approaches targeting the gut microbiota in depression.
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Relationship between the gut microbiome and brain function.
It has become increasingly evident in recent years that the gut microbiome and the brain communicate in a bidirectional manner, with each possibly affecting the other's functions. Substantial research has aimed to understand the mechanisms of this interaction and to outline strategies for preventing or treating nervous system-related disturbances. This review explores the evidence demonstrating how the gut microbiome may affect brain function in adults, thereby having an impact on stress, anxiety, depression, and cognition. In vitro, in vivo, and human studies reporting an association between a change in the gut microbiome and functional changes in the brain are highlighted, as are studies outlining the mechanisms by which the brain affects the microbiome and the gastrointestinal tract. Possible modes of action to explain how the gut microbiome and the brain functionally affect each other are proposed. Supplemental probiotics to combat brain-related dysfunction offer a promising approach, provided future research elucidates their mode of action and possible side effects. Further studies are warranted to establish how pre- and probiotic interventions may help to balance brain function in healthy and diseased individuals.
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Intestinal Barrier, Immunity and Microbiome: Partners in the Depression Crime.
Depression is a highly prevalent disorder and a leading cause of disability worldwide. It has a major impact on the affected individual and on society as a whole. Regrettably, current available treatments for this condition are insufficient in many patients. In recent years, the gut microbiome has emerged as a promising alternative target for treating and preventing depressive disorders. However, the microbes that form this ecosystem do not act alone but are part of a complicated network connecting the gut and the brain that influences our mood. Host cells that are in intimate contact with gut microbes, such as the epithelial cells forming the gut barrier and the immune cells in their vicinity, play a key role in the process. These cells continuously shape immune responses to maintain healthy communication between gut microbes and the host. In this article, we review how the interplay among epithelial cells, the immune system, and gut microbes mediates gut-brain communication to influence mood. We also discuss how advances in our knowledge of the mechanisms underlying the gut-brain axis could contribute to addressing depression. SIGNIFICANCE STATEMENT: This review does not aim to systematically describe intestinal microbes that might be beneficial or detrimental for depression. We have adopted a novel point of view by focusing on potential mechanisms underlying the crosstalk between gut microbes and their intestinal environment to control mood. These pathways could be targeted by well defined and individually tailored dietary interventions, microbes, or microbial metabolites to ameliorate depression and decrease its important social and economic impact.