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Gut microbiome and daytime function in Chinese patients with major depressive disorder.
BACKGROUND: Major depressive disorder (MDD) is underscored by daytime dysfunction-associated features, including mood disturbances, impaired cognition, fatigue, and daytime sleepiness. Importantly, the gut-brain axis may represent a potential mechanistic link between MDD and daytime dysfunction. Therefore, this study aimed to explore the gut microbiome composition and daytime dysfunction in Chinese patients with MDD. METHODS: We enrolled 36 patients with MDD and 45 healthy controls (HCs) matched by age, sex, and body mass index (BMI). Daytime function including emotion, fatigue, and sleepiness were assessed using the Epworth Sleepiness Scale (ESS), Fatigue Severity Scale (FSS), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD). 16S rRNA sequencing was employed to characterize the gut microbiota in stool samples. RESULTS: The operational taxonomic units (OTUs) OTU255, OUT363 were positively correlated with HAMD and HAMA. OTU244, OTU542 and OTU221 were positively correlated with ESS, HAMD and HAMA. OTU725 and OTU80 were positively correlated with FSS, ESS, HAMD and HAMA, while OTU423 and OTU502 were negatively correlated with all above. Flavonifractor positively correlated with fatigue in patients with MDD and all individuals simultaneously. The correlation between gut microbiome and daytime function was different in MDD and HCs. CONCLUSIONS: We identified several OTUs associated with the severity of fatigue, depression, daytime sleepiness and anxiety in all individuals. Our results revealed the differences in microbiome found between patients with MDD and HCs. These findings provide insights into the potential microbiota changes that occur in MDD, and will enable the development of specific therapeutic strategies for targeting the various symptoms of depression.
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Gut microbiota in mental health and depression: role of pre/pro/synbiotics in their modulation.
The microbiome residing in the human gut performs a wide range of biological functions. Recently, it has been elucidated that a change in dietary habits is associated with alteration in the gut microflora which results in increased health risks and vulnerability towards various diseases. Falling in line with the same concept, depression has also been shown to increase its prevalence around the globe, especially in the western world. Various research studies have suggested that changes in the gut microbiome profile further result in decreased tolerance of stress. Although currently available medications help in relieving the symptoms of depressive disorders briefly, these drugs are not able to completely reverse the multifactorial pathology of depression. The discovery of the communication pathway between gut microbes and the brain, i.e. the Gut-Brain Axis, has led to new areas of research to find more effective and safer alternatives to current antidepressants. The use of probiotics and prebiotics has been suggested as being effective in various preclinical studies and clinical trials for depression. Therefore, in the present review, we address the new antidepressant mechanisms via gut microbe alterations and provide insight into how these can provide an alternative to antidepressant therapy without the side effects and risk of adverse drug reactions.
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Role of the gut microbiome in three major psychiatric disorders.
Major depressive disorder (MDD), bipolar disorder (BD) and schizophrenia-spectrum disorders (SSD) are heterogeneous psychiatric disorders, which place significant burden on patient's well-being and global health. Disruptions in the gut-microbiome may play a role in these psychiatric disorders. This review presents current data on composition of the human gastrointestinal microbiota, and its interaction mechanisms in the gut-brain axis in MDD, BD and SSD. Diversity metrics and microbial relative abundance differed across studies. More studies reported inconsistent findings (n = 7) or no differences (n = 8) than studies who reported lower α-diversity in these psychiatric disorders (n = 5). The most consistent findings across studies were higher relative abundances of the genera Streptococcus, Lactobacillus, and Eggerthella and lower relative abundance of the butyrate producing Faecalibacterium in patients with psychiatric disorders. All three increased genera were associated with higher symptom severity. Confounders, such as medication use and life style have not been accounted for. So far, the results of probiotics trials have been inconsistent. Most traditional and widely used probiotics (consisting of Bifidobacterium spp. and Lactobacillus spp.) are safe, however, they do not correct potential microbiota disbalances in these disorders. Findings on prebiotics and faecal microbiota transplantation (FMT) are too limited to draw definitive conclusions. Disease-specific pro/prebiotic treatment or even FMT could be auspicious interventions for prevention and therapy for psychiatric disorders and should be investigated in future trials.
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The brain-gut-microbiota interplay in depression: A key to design innovative therapeutic approaches.
Depression is the most prevalent mental disorder in the world associated with huge socio-economic consequences. While depressive-related symptoms are well known, the molecular mechanisms underlying disease pathophysiology and progression remain largely unknown. The gut microbiota (GM) is emerging as a key regulator of the central nervous system homeostasis by exerting fundamental immune and metabolic functions. In turn, the brain influences the intestinal microbial composition through neuroendocrine signals, within the so-called gut microbiota-brain axis. The balance of this bidirectional crosstalk is important to ensure neurogenesis, preserve the integrity of the blood-brain barrier and avoid neuroinflammation. Conversely, dysbiosis and gut permeability negatively affect brain development, behavior, and cognition. Furthermore, although not fully defined yet, changes in the GM composition in depressed patients are reported to influence the pharmacokinetics of common antidepressants by affecting their absorption, metabolism, and activity. Similarly, neuropsychiatric drugs may shape in turn the GM with an impact on the efficacy and toxicity of the pharmacological intervention itself. Consequently, strategies aimed at re-establishing the correct homeostatic gut balance (i.e., prebiotics, probiotics, fecal microbiota transplantation, and dietary interventions) represent an innovative approach to improve the pharmacotherapy of depression. Among these, probiotics and the Mediterranean diet, alone or in combination with the standard of care, hold promise for clinical application. Therefore, the disclosure of the intricate network between GM and depression will give precious insights for innovative diagnostic and therapeutic approaches towards depression, with profound implications for drug development and clinical practice.
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Gut microbiome and major depressive disorder: insights from two-sample Mendelian randomization.
BACKGROUND: Existing evidence suggests that alterations in the gut microbiome are closely associated with major depressive disorder (MDD). We aimed to reveal the causal relationships between MDD and various microbial taxa in the gut. METHODS: We used the two-sample Mendelian randomization (TSMR) to explore the bidirectional causal effects between gut microbiota and MDD. The genome-wide association studies summary results of gut microbiota were obtained from two large consortia, the MibioGen consortium and the Dutch Microbiome Project, which we analyzed separately. RESULTS: Our TSMR analysis identified 10 gut bacterial taxa that were protective against MDD, including phylum Actinobacteria, order Clostridiales, and family Bifidobacteriaceae (OR: 0.96 ∼ 0.98). Ten taxa were associated with an increased risk of MDD, including phyla Firmicutes and Proteobacteria, class Actinobacteria, and genus Alistipes (OR: 1.01 ∼ 1.09). On the other hand, MDD may decrease the abundance of 12 taxa, including phyla Actinobacteria and Firmicutes, families Bifidobacteriaceae and Defluviitaleaceae (OR: 0.63 ∼ 0.88). MDD may increase the abundance of 8 taxa, including phylum Bacteroidetes, genera Parabacteroides, and Bacteroides (OR: 1.12 ∼ 1.43). CONCLUSIONS: Our study supports that there are mutual causal relationships between certain gut microbiota and the development of MDD suggesting that gut microbiota may be targeted in the treatment of MDD.
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Association between gut microbiota and perinatal depression and anxiety among a pregnancy cohort in Hunan, China.
BACKGROUND: Perinatal depression and anxiety pose significant risks to maternal health and may lead to suicide. The gut microbiota may play a crucial role in perinatal depression and anxiety. However, the relationship between the alterations in gut microbiota and perinatal depression and anxiety remains unclear. This study aimed to investigate the dynamic changes of gut microbiota over various perinatal stages and their associations with perinatal depression and anxiety symptoms, especially suicide ideation. METHODS: A total of 177 pregnant and 19 postpartum women were recruited in this study, with 48 of them participating longitudinally. Maternal depression and anxiety symptoms were assessed using the Edinburgh Postnatal Depression Scale (EPDS), 9-item Patient Health Questionnaire (PHQ-9), and 7-item Generalized Anxiety Disorder Scale (GAD-7). Fecal samples collected during the perinatal period were analyzed using 16S rRNA gene sequencing. RESULTS: Significant changes in microbial diversity and multi-taxonomic levels were observed during pregnancy. The random forest regression model showed significant associations of some gut microbial features with depression and anxiety symptoms. Several genera were significantly associated with gestation age and perinatal depression and anxiety, such as Akkermansia, Bifidobacterium and Streptococcus. In addition, Erysipelotrichaceae_UCG-003 and Eubacterium_hallii_group were positively associated with suicidal ideation. The glycine biosynthesis pathway might act as a mediator between Eubacterium_hallii_group and suicidal ideation (ab = 3.27, p < 0.05). CONCLUSION: The gut microbiota undergoes a programmed shift during pregnancy, which may play a critical role in perinatal depression and anxiety. Our findings underscore the impact of certain bacterial genera and metabolic pathways on perinatal mental health, which may help to develop new diagnostic tools and targeted interventions to reduce perinatal mental disorders and improve the outcomes for both mothers and infants.
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Dysbiosis of the oral-gut microbiome axis in a mouse model of depression.
This study aimed to characterize the alterations in both oral and gut microbiota in a mouse model of depression and to explore their potential role in the pathogenesis of major depressive disorder (MDD) through the oral-gut-brain axis. A depression model was established in male C57BL/6J mice using chronic social defeat stress (CSDS) paradigm. Depressive phenotypes were confirmed through social interaction, sucrose preference, open field, tail suspension, and forced swim tests. The microbial composition of oral and gut samples was analyzed using 16S rRNA sequencing, with Linear Discriminant Analysis Effect Size (LEfSe) employed to identify differentially abundant taxa and Spearman correlation analysis to examine microbiota-behavior relationships. CSDS successfully induced robust depression-like behaviors, including social avoidance, anhedonia, and behavioral despair. Beta-diversity analysis revealed significant separation in oral microbiota between CSDS and control groups. LEfSe analysis identified distinct microbial signatures: control mice were enriched in oral Streptococcus and gut commensals including Lachnospiraceae, Bacteroides and Oscillospiraceae, whereas CSDS mice showed expansion of oral Muribacter and Rodentibacter and gut Alloprevotella, Helicobacter and Colidextribacter. Correlation analyses demonstrated significant associations between specific microbial patterns and depression-like behaviors, with control-enriched taxa negatively correlating with behavioral deficits. Furthermore, significant cross-habitat microbial correlations were observed between oral and gut differential taxa. Our findings demonstrate that CSDS induces divergent microbial alterations in both oral and gut ecosystems, which are systematically associated with depression-like behaviors. These results provide compelling evidence for the involvement of the oral-gut-brain axis in depression pathophysiology and suggest that modulating these microbial ecosystems may represent a potential therapeutic strategy for MDD.
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The gut microbiome modulates gut-brain axis glycerophospholipid metabolism in a region-specific manner in a nonhuman primate model of depression.
Emerging research demonstrates that microbiota-gut-brain (MGB) axis changes are associated with depression onset, but the mechanisms underlying this observation remain largely unknown. The gut microbiome of nonhuman primates is highly similar to that of humans, and some subordinate monkeys naturally display depressive-like behaviors, making them an ideal model for studying these phenomena. Here, we characterized microbial composition and function, and gut-brain metabolic signatures, in female cynomolgus macaque (Macaca fascicularis) displaying naturally occurring depressive-like behaviors. We found that both microbial and metabolic signatures of depressive-like macaques were significantly different from those of controls. The depressive-like monkeys had characteristic disturbances of the phylum Firmicutes. In addition, the depressive-like macaques were characterized by changes in three microbial and four metabolic weighted gene correlation network analysis (WGCNA) clusters of the MGB axis, which were consistently enriched in fatty acyl, sphingolipid, and glycerophospholipid metabolism. These microbial and metabolic modules were significantly correlated with various depressive-like behaviors, thus reinforcing MGB axis perturbations as potential mediators of depression onset. These differential brain metabolites were mainly mapped into the hippocampal glycerophospholipid metabolism in a region-specific manner. Together, these findings provide new microbial and metabolic frameworks for understanding the MGB axis' role in depression, and suggesting that the gut microbiome may participate in the onset of depressive-like behaviors by modulating peripheral and central glycerophospholipid metabolism.
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Gut microbiota dysbiosis drives depression-like behavior in adolescent rats via lysine-regulated mTOR autophagy pathway.
The prevalence of major depressive disorder (MDD) is increasing globally, particularly among adolescents. Although gut-brain axis dysfunction has been implicated in adolescent depression, the mechanisms by which gut microbiota dysbiosis drives depressive behaviors and potential antidepressant targets remain unclear. In this study, fecal microbiota transplantation (FMT) was performed from either healthy controls (HCs) or adolescents with MDD into antibiotic-treated adolescent rats. FMT from MDD adolescents induced depressive-like behaviors in recipient rats. Metagenomic sequencing revealed that FMT from MDD adolescents led to alterations in gut microbiota in recipient rats. While qPCR, Western blotting, immunofluorescence, and transmission electron microscopy (TEM) confirmed that these rats exhibited prefrontal cortex (PFC) autophagy hyperactivation, evidenced by a reduction in SQSTM1/p62 levels, an elevation in the LC3-II/LC3-I ratio, upregulated Beclin1, and increased numbers of autolysosomes. Similar autophagy-related transcriptional changes were observed in peripheral blood from MDD adolescents. Furthermore, ELISA showed reduced plasma lysine levels in MDD adolescents and decreased lysine concentrations in the PFC of FMT-MDD rats. The antidepressant effect of lysine and its interaction with autophagy were explored in a chronic unpredictable mild stress (CUMS) rat model with or without rapamycin (the autophagy activator, RAPA). Lysine supplementation alleviated depressive-like behaviors and suppressed PFC autophagy hyperactivation, while these effects were abolished by RAPA co-treatment. These findings reveal lysine deficiency as a metabolic bridge between gut microbiota imbalance and neuronal autophagy dysregulation, suggesting a gut microbiota-lysine-autophagy axis as an innovative mechanism and therapeutic focus for adolescent depression.
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Advances in the gut microbiome and mood disorders.
PURPOSE OF REVIEW: The gut microbiome is in constant bidirectional communication with the brain through the microbiota-gut-brain-axis. Mood disorders are among the most common psychiatric disorders and include major depressive disorder and bipolar disorder. The gut microbiome is altered in individuals with mood disorders and has a role in its inflammatory pathophysiology. In this article, we performed a narrative review of clinical studies, randomized controlled trials and meta-analyses addressing advances in gut microbiome research in mood disorders and included articles that were published between 2021 and 2022. RECENT FINDINGS: Studies highlight transdiagnostic alterations of microbiota in mood disorders, with reductions of butyrate-producing bacteria. Participants with major depressive disorder showed altered beta-diversity, while participants with bipolar disorder showed reduced alpha-diversity. Both disorders exhibit alterations in the metabolome. Early pilot studies addressed the possibility of using the gut microbiome for the prediction of treatment response and the blood microbiome for the diagnosis of psychiatric disorders. Findings from clinical trials support the use of probiotics as an add-on therapy for major depressive disorder. The second published case report in the literature reported a favourable outcome of a patient with bipolar disorder after faecal microbiota transplantation. SUMMARY: Gut microbiome modulations allow new treatment strategies including the use of psychobiotics for the treatment and prevention of mood disorders. Well designed clinical trials aiming for personalized medicine are needed to investigate the efficacy and safety of psychobiotic interventions.