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An exploratory analysis on the association between suicidal ideation and the microbiome in patients with or without major depressive disorder.
BACKGROUND: Scarce research has investigated associations between suicidal ideation and the gut microbiota. We aimed to explore variations in the gut microbiome associated with suicidal ideation and major depressive disorder (MDD). METHOD: A case-control study compared abundances of fecal microbiota and biomarkers of gut permeability among patients with MDD, with or without suicidal ideation, and healthy volunteers without depression. Information on demographic variables and assessments of suicidal ideation (Beck Suicidal Ideation Scale), depression (Hamilton Depression Scale, Patient Health Questionnaire, Hospital Anxiety and Depression Scale- Depression), as well as anxiety (Hospital Anxiety and Depression Scale- Anxiety), were obtained. Univariate and multivariate regression model was performed to explore the possible predictors of suicidal ideation. RESULTS: Among the 140 participants, significant differences in Beta diversity were found between MDD patients with (n = 43) or without suicidal ideation (n = 34), and healthy volunteers (n = 42) (all p < 0.001). The strain of g-Phascolarctobacterium was found to have significant positive associations with scores of BSSI and BSSI Part 1 (suicidal ideation), particularly in MDD patients with suicidal ideation, after controlling for demographic and mood covariates. Mediation analyses revealed that g-Phascolarctobacterium may be a partial mediator between depression and suicidal ideation; however, it is also possible that the association between g-Phascolarctobacterium and suicidal ideation was partially mediated by the level of depression. CONCLUSION: We found different compositions, diversities, and possible mediating of the gut microbiome associated with suicidal ideations. Potential mechanisms need further investigation to establish whether this reflects a biological process that might be the focus for intervention development. SYNOPSIS: Our objective was to investigate whether the diversities and abundances of the gut microbiome varied in people with or without suicidal ideation and with or without MDD after considering possible demographic and mood confounders.
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Multi-omics analysis reveals mechanisms of FMT in Enhancing antidepressant effects of SSRIs.
OBJECTIVE: This study explores the behavioral and molecular biological impacts of Fecal Microbiota Transplantation (FMT) on depressive mice unresponsive to treatment with Selective Serotonin Reuptake Inhibitors (SSRIs). METHODS: Healthy male C57BL/6 mice were used to establish a depression model through chronic restraint stress, treated with fluoxetine, and categorized into Response and Non-response groups. An FMT treatment was added to the Non-response group. Behavioral tests were conducted to assess symptoms of depression. The gut microbiome, plasma metabolites, and hippocampal tissue gene expression and function changes were analyzed using 16S rRNA gene sequencing, LC-MS, and RNA sequencing. RESULTS: FMT significantly improved the depressive symptoms in SSRIs-resistant mice. There was a partial restoration in the diversity and structure of the gut microbiota in the FMT group. Compared to the Non-response group, significant changes were noted in the metabolomic profiles of the FMT group, identifying various differential metabolites. Functional annotations indicated that these metabolites are involved in multiple metabolic pathways. In the Non-response group, certain gene expression levels were significantly restored. GO and KEGG enrichment analyses revealed that these differential genes mainly involve cytokine activity, receptor signaling regulation, and NOD-like receptor signaling pathways. Joint analysis suggested that FMT may exert its effects through an increase in the abundance of g__Paraprevotella, leading to decreased baicalin content and increased Tal2 expression. CONCLUSION: FMT has potential in improving depressive symptoms unresponsive to SSRIs treatment. Its mechanism may be related to the modulation of the gut microbiota and its metabolites, subsequently affecting gene expression.
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An Innovative Probiotic-Based Supplement to Mitigate Molecular Factors Connected to Depression and Anxiety: An In Vitro Study.
The gut-brain axis is a bidirectional relationship between the microbiota and the brain; genes related to the brain and gut synaptic formation are similar. Research on the causal effects of gut microbiota on human behavior, brain development, and function, as well as the underlying molecular processes, has emerged in recent decades. Probiotics have been shown in several trials to help reduce anxiety and depressive symptoms. Because of this, probiotic combinations have been tested in in vitro models to see whether they might modulate the gut and alleviate depression and anxiety. Therefore, we sought to determine whether a novel formulation might affect the pathways controlling anxiety and depression states and alter gut barrier activities in a 3D model without having harmful side effects. Our findings indicate that B. bifidum novaBBF7 10 mg/mL, B. longum novaBLG2 5 mg/mL, and L. paracasei TJB8 10 mg/mL may influence the intestinal barrier and enhance the synthesis of short-chain fatty acids. Additionally, the probiotics studied did not cause neuronal damage and, in combination, exert a protective effect against the condition of anxiety and depression triggered by L-Glutamate. All these findings show that probiotics can affect gut function to alter the pathways underlying anxiety and depression.
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Metabolomic signature of exposure and response to citalopram/escitalopram in depressed outpatients.
Metabolomics provides valuable tools for the study of drug effects, unraveling the mechanism of action and variation in response due to treatment. In this study we used electrochemistry-based targeted metabolomics to gain insights into the mechanisms of action of escitalopram/citalopram focusing on a set of 31 metabolites from neurotransmitter-related pathways. Overall, 290 unipolar patients with major depressive disorder were profiled at baseline, after 4 and 8 weeks of drug treatment. The 17-item Hamilton Depression Rating Scale (HRSD17) scores gauged depressive symptom severity. More significant metabolic changes were found after 8 weeks than 4 weeks post baseline. Within the tryptophan pathway, we noted significant reductions in serotonin (5HT) and increases in indoles that are known to be influenced by human gut microbial cometabolism. 5HT, 5-hydroxyindoleacetate (5HIAA), and the ratio of 5HIAA/5HT showed significant correlations to temporal changes in HRSD17 scores. In the tyrosine pathway, changes were observed in the end products of the catecholamines, 3-methoxy-4-hydroxyphenylethyleneglycol and vinylmandelic acid. Furthermore, two phenolic acids, 4-hydroxyphenylacetic acid and 4-hydroxybenzoic acid, produced through noncanconical pathways, were increased with drug exposure. In the purine pathway, significant reductions in hypoxanthine and xanthine levels were observed. Examination of metabolite interactions through differential partial correlation networks revealed changes in guanosine-homogentisic acid and methionine-tyrosine interactions associated with HRSD17. Genetic association studies using the ratios of these interacting pairs of metabolites highlighted two genetic loci harboring genes previously linked to depression, neurotransmission, or neurodegeneration. Overall, exposure to escitalopram/citalopram results in shifts in metabolism through noncanonical pathways, which suggest possible roles for the gut microbiome, oxidative stress, and inflammation-related mechanisms.
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Breakfast skipping is linked to a higher risk of major depressive disorder and the role of gut microbes: a mendelian randomization study.
BACKGROUND: Observational studies have indicated that breakfast skipping and gut microbiome dysbiosis are associated with a higher risk of major depressive disorder (MDD). However, it remains unknown whether the alteration of gut microbes is implicated in the associations between breakfast skipping and MDD. METHODS: Leveraging genome-wide association studies (GWAS) on breakfast skipping, gut microbes, and MDD, we conducted a two-step Mendelian randomization (MR) study to determine the causal associations between breakfast skipping (N = 193,860) and MDD (N = 1,815,091), and evaluate the role of gut microbes (N = 18,340). Genetic variants with a P-value less than 5E-08 were selected as instrumental variables (IVs). The false discovery rate (FDR) method was employed to correct the P-values for multiple tests in gut microbes. RESULTS: Breakfast skipping was associated with an increased risk of MDD (odds ratio [OR] = 1.36, 95%CI = 1.12-1.65, P = 0.002), but no effect of MDD on breakfast skipping was observed (β per doubling odds of MDD =-0.001, 95%CI=-0.024 to 0.023, P = 0.957). After adjusting for multiple comparisons, the MR analysis provided little evidence for an association between breakfast skipping and the abundance of any gut microbes (PFDR>0.05). Among the 21 gut microbes with IVs available, only the abundance of Class Actinobacteria was causally associated with a reduced risk of MDD (OR = 0.85, 95%CI = 0.75-0.97, PFDR=0.015). CONCLUSIONS: Our findings demonstrated that breakfast skipping was associated with an increased risk of MDD, but provided little evidence supporting the role of the abundance of gut microbes in it. Further efforts with a large sample size are warranted to clarify the findings.
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Prenatal antidepressant exposures and gastrointestinal complaints in childhood: A gut-brain axis connection?
Selective serotonin/norepinephrine reuptake inhibitors (collectively, SRIs) are the most commonly prescribed antidepressant agents for the treatment of depression in pregnancy. SRIs affect maternal and placental serotonin signaling, which might impact fetal brain development. Alterations in serotonin signaling might also impact the developing gut-brain axis (GBA) via alterations in the fetal enteric nervous system (ENS). Emerging evidence suggests that gestational SRI exposure may be associated with offspring gastrointestinal problems. However, prospective human studies of the effects of fetal SRI exposure on the ENS and function are absent in the literature. In this paper we present data demonstrating significant associations between prenatal SRI exposure and children's gastrointestinal (GI) problems in two well-characterized, prospective cohorts of preschool and later childhood individuals. The results support the hypothesis that prenatal SRI exposure can increase the risk for childhood GI difficulties. Further research is warranted on the potential SRI-induced changes to the child gut including the role of the microbiome and the GBA in the development of GI problems.
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Metagenomics reveals unique gut mycobiome biomarkers in major depressive disorder - a non-invasive method.
BACKGROUND: An increasing amount of evidence suggests a potential link between alterations in the intestinal microbiota and the onset of various psychiatric disorders, including depression. Nevertheless, the precise nature of the link between depression and the intestinal microbiota remains largely unknown. A significant proportion of previous research has concentrated on the study of gut bacterial communities, with relatively little attention paid to the link between gut mycobiome and depression. METHODS: In this research, we analyzed the composition and differences of intestinal fungal communities between major depressive disorder (MDD) and healthy controls. Subsequently, we constructed a machine learning model using support vector machine-recursive feature elimination to search for potential fungal markers for MDD. RESULTS: Our findings indicated that the composition and beta diversity of intestinal fungal communities were significantly changed in MDD compared to the healthy controls. A total of 22 specific fungal community markers were screened out by machine learning, and the predictive model had promising performance in the prediction of MDD (area under the curve, AUC = 1.000). Additionally, the intestinal fungal communities demonstrated satisfactory performance in the validation cohort, with an AUC of 0.884 (95% CI: 0.7871-0.9476) in the Russian validation cohort, which consisted of 36 patients with MDD and 36 healthy individuals. The AUC for the Wuhan validation cohort was 0.838 (95% CI: 0.7403-0.9102), which included 40 patients with MDD and 42 healthy individuals. CONCLUSION: To summarize, our research revealed the characterization of intestinal fungal communities in MDD and developed a prediction model based on specific intestinal fungal communities. Although MDD has well-established diagnostic criteria, the strategy based on the model of gut fungal communities may offer predictive biomarkers for MDD.
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Gut microbial biomarkers for major depressive disorder: a cross-sectional study.
BACKGROUND: Alterations in the gut microbiota have been associated with a variety of psychiatric disorders, including major depressive disorder (MDD). However, the relationship between MDD and gut microbial communities remains incompletely understood. Most previous studies have primarily focused on gut bacteria, with relatively limited attention to other microbial components. METHODS: In this study, we analyzed gut microbial profiles from 36 patients with MDD and 36 healthy controls using metagenomic sequencing data. The MaAsLin2 algorithm was applied to identify potential microbial biomarkers associated with MDD. RESULTS: A total of 6 bacterial biomarkers and 7 viral biomarkers were identified. The models based on these features demonstrated strong predictive performance, with area under the curve (AUC) values of 0.891 for bacteria and 0.878 for viruses. Notably, the combined bacterial-viral model achieved an AUC of 0.946. These findings were further evaluated through external testing in two unrelated research cohorts. In the Shanxi cohort, the AUC values were 0.825 (bacteria), 0.803 (viruses), and 0.972 (combined model). In the Wuhan cohort, the AUC values were 0.683 (bacteria), 0.693 (viruses), and 0.784 (combined model). CONCLUSION: In summary, our results highlight the potential of gut bacterial and viral biomarkers as candidate biomarkers and potential auxiliary tools for MDD assessment and suggest that integrating multi-domain microbial features may improve prediction accuracy.
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Investigating the bacterial profiles of Lactobacillus, Bifidobacterium, Actinobacteria, Fusobacterium, Firmicutes, and Bacteroides in stool samples from patients with severe depression and healthy individuals.
Depression is a multifaceted mental health disorder with complex etiology and significant global burden. Recent research indicates that the gut microbiota plays a role in the pathophysiology of depression, highlighting the potential role of specific bacterial species in influencing mood and cognitive function. In this study, we aimed to investigate the presence, copy numbers, and Ct values of selected bacterial species in stool samples from depressed patients (n=50) compared to control subjects (n=50). Our findings revealed significant differences in the abundance of Fusobacterium spp., Bifidobacterium spp., Lactobacillus spp., Bacteroidetes phylum, Firmicutes phylum, and Actinobacteria spp. between the two groups. Dysregulation of the gut microbiota, characterized by decreased presence of beneficial bacteria (e.g., Bifidobacterium spp., Lactobacillus spp.) and altered abundance of potentially pathogenic bacteria (e.g., Fusobacterium spp.), may contribute to the development or exacerbation of depression. These findings support the emerging concept of the gut-brain axis and its role in mental health. However, further research is needed to better understand the underlying mechanisms and explore the therapeutic potential of microbiota-targeted interventions for depression. Understanding the intricate interplay between the gut microbiota and depression could pave the way for novel treatment strategies and personalized approaches in mental health care.
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Abnormal gut microbiota and bile acids in patients with first-episode major depressive disorder and correlation analysis.
AIM: Gut microbiota and its metabolite bile acids may play a significant role in the occurrence and development of major depressive disorder (MDD). Therefore, this study analyzes gut microbiota and bile acids, as well as their correlation in patients. METHODS: Thirty-one patients with MDD and 29 healthy controls (HCs) were enrolled in this study. We collected their both blood and feces. Plasma bile acid content was determined by liquid chromatography-mass spectrometry and gut microbiota was detected by 16SrRNA gene sequencing and subsequently analyzed. We also analyzed the correlation between different gut microbiota, bile acids, and Hamilton Depression (HAMD) score. RESULTS: The α-diversity analysis found that Simpson and Pielou evenness index was much higher in HCs than in the patients with MDD. The β-diversity of the two groups were differences by nonmetric multidimensional scaling analysis. Linear discriminant analysis effect size analysis identified 16 different strains. Bile acids detection showed that 23-nordeoxycholic acid in patients with MDD was significantly higher than in HCs, whereas taurolithocholic acid (TLCA), glycolithocholic acid (GLCA), and lithocholic acid 3-sulfate were significantly lower. Spearman correlation analysis showed that Turicibacteraceae, Turicibacterales, and Turicibacter were positively related with TLCA, GLCA, glycodeoxycholic acid (GDCA), and taurodeoxycholic acid, and were negatively correlated with HAMD score. At the same time, TLCA, GLCA, and GDCA were negatively correlated with HAMD score. CONCLUSIONS: Gut microbiota and bile acids metabolism are disturbances in MDD, and there exists a correlation between gut microbiota and bile acids metabolism. Moreover, their interaction may be related to the pathophysiological mechanism of MDD.