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The role of gut microbiota in adolescent depression: Insights from adverse childhood experiences.
BACKGROUND: Depression has become a leading global mental health disorder, with a rising prevalence of 15-20 % among adolescents. Emerging evidence suggests that adolescent depression may constitute a distinct subtype, differing clinically and neurobiologically from adult presentations. The gut microbiota's role in psychiatric disorders has garnered increasing attention, as dysbiosis may modulate behavior and mood via the microbiota-gut-brain axis, potentially contributing to depressive pathogenesis. METHODS: This study included 60 depressed and 64 healthy adolescents (aged 11-18). Fecal samples were immediately flash-frozen in liquid nitrogen after collection, stored at -80 °C within 30 min, and processed within 6 months to minimize DNA degradation. And microbial DNA was extracted using the HiPure Stool DNA Mini Kit. The V3-V4 hypervariable regions of the 16S rRNA gene were amplified via PCR with primers 341F (5'-CCTAYGGGRBGCASCAG-3') and 805R (5'-GACTACHVGGGTATCTAATCC-3'), followed by Illumina NovaSeq 6000 sequencing. PCR cycle optimization was performed via gradient testing (20-30 cycles), confirming 25 cycles as optimal to prevent chimera formation while maintaining amplicon yield. Bioinformatics pipelines included QIIME2 for quality filtering, DADA2 for ASV inference, and PICRUSt2 for functional prediction. Statistical analyses included t-tests, mediation analysis, and Linear discriminant analysis Effect Size (LEfSe). RESULTS: Fifty percent of depressed adolescents originated from single-parent or grandparent-led households and exhibited reduced resilience scores alongside elevated adverse childhood experiences (ACEs). Gut microbiota analysis revealed significant compositional and functional dysbiosis in depressed youth, marked by depletion of beneficial taxa (e.g., Bifidobacterium, Faecalibacterium) and butyrate-producing species, alongside enrichment of pro-inflammatory genera (e.g., Escherichia-Shigella). Mediation analyses implicated ACEs as a potential driver of these microbial alterations. CONCLUSIONS: This study reveals distinct gut microbiota profiles in adolescents with depression compared to healthy controls, offering mechanistic insights into how ACEs and microbial dysbiosis may contribute to depressive etiology.
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Fermented foods, the gut and mental health: a mechanistic overview with implications for depression and anxiety.
Mental disorders including depression and anxiety are often comorbid with gut problems, suggesting a bidirectional relationship between mental health and gut function. Several mechanisms might explain this comorbidity, such as inflammation and immune activation; intestinal permeability; perturbations in the hypothalamic-pituitary-adrenal axis; neurotransmitter/neuropeptide dysregulation; dietary deficiencies; and disturbed gut microbiome composition. The potential of modulating the microbiome-gut-brain axis, and subsequently mental health, through the use of functional foods, is an emerging and novel topic of interest. Fermented foods are considered functional foods due to their putative health benefits. The process of microbial fermentation converts food substrates into more nutritionally and functionally rich products, resulting in functional microorganisms (probiotics), substrates that enhance proliferation of beneficial bacteria in the gut (prebiotics), and bioactive components (biogenics). These functional ingredients act biologically in the gastrointestinal tract and have the ability to modify the gut microbiota, influence translocation of endotoxins and subsequent immune activation, and promote host nutrition. This narrative review explores the theoretical potential of the functional components present in fermented foods to alter gut physiology and to impact the biological mechanisms thought to underpin depression and anxiety. Pre-clinical studies indicate the benefits of fermented foods in relieving perturbed gut function and for animal models of depression and anxiety. However, in humans, the literature relating to the relevance of fermented food for treating or preventing depression and anxiety is sparse, heterogeneous and has significant limitations. This review identifies a critical research gap for further evaluation of fermented foods in the management of depression anxiety in humans.
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Gut microbiota alterations and signatures across subthreshold depression and major depressive disorders in adolescents.
BACKGROUND: Adolescent depression, including subthreshold depression (SD) and major depressive disorder (MDD), is a growing public health concern, yet objective signatures remain lacking. Accumulating evidence implicates gut microbiota alterations in depression. Our study aimed to characterize gut microbiota alterations among healthy controls (HCs), SD, and MDD, and to identify microbial signatures with potential discriminative value in adolescents. METHODS: We profiled gut microbiota from 411 adolescents, including 117 HCs, 87 with SD, and 117 with MDD in the discovery set, along with an independent validation cohort of 45 HCs and 45 MDD patients. 16S rRNA sequencing was used to assess compositional and predicted functional differences. Random forest (RF) models and Linear discriminant analysis Effect Size (LEfSe) were applied to identify microbial signatures associated with depressive states. RESULTS: Adolescents with MDD exhibited significantly reduced microbial diversity compared with HCs and SD, accompanied by compositional differences, with modest effect sizes observed for beta-diversity. Using LEfSe and RF modeling, twelve microbial features were identified that showed discriminative capacity across depressive states. Among these, Turicibacter (amplicon sequence variant, ASV792) and Clostridiaceae (ASV6392) emerged as the most consistently discriminative features, both showing a stepwise decrease across groups. The rsulting multi-ASV panel demonstrated reproducible classification performance, achieving area under the curve (AUC) values of 0.89 for MDD vs. HCs and 0.83 for MDD vs. SD. PICRUSt2-based functional prediction suggested differences in amino acid- and carbohydrate metabolsm-related pathways in MDD. CONCLUSIONS: Our observational study demonstrates distinct gut microbiota profiles across different levels of depressive symptom severity in adolescents. The identified microbial features provide a research framework for future studies examining microbiome-associated patterns in adolescent depression.
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The unique role of fluoxetine in alleviating depression and anxiety by regulating gut microbiota and the expression of vagus nerve-mediated serotonin and melanocortin-4 receptors.
Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) widely used for depression, but its potential effects on gut microbiota regulation and vagus nerve-mediated serotonin receptor expression have not been well studied. We investigated changes in the gut microbiome regulated by fluoxetine and vagus nerve-mediated expression of several serotonin (5-HT) receptor types associated with anxiety and depression. Oral administration of fluoxetine alleviated lipopolysaccharide (LPS)-induced depressive and anxiety behaviors, increased 5-HT1A, 2 C, and melanocortin 4 (MC4) receptor expression, and the composition of Lactobacillus in mice's gut microbiome. In contrast, in the vagotomized group, fluoxetine did not modulate behaviors and receptor expression. Increased Lactobacillus composition was found to correlate significantly with behavioral test results. The importance of Lactobacillus growth to the efficacy of fluoxetine was confirmed by the effectiveness of fluoxetine, which was reduced by co-administering antibiotics. To determine the additional impact of the gut microbiome, we isolated Limosilactobacillus reuteri and Ligilactobacillus murinus, which were increased in the fluoxetine-treated group and administrated. The results showed that administration of each strain improved anxious or depressive behavior, as did fluoxetine, and vagotomy eliminated these effects. These results suggest that fluoxetine administration increases the proportion of Lactobacillus in the gut, which modulates 5-HT1A, 2 C, and MC4 receptor expression through the enteric nervous system and improves depression.
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[Major depression and liver disease: the role of microbiome and inflammation].
Depression and liver disease are closely associated. Every third patient with liver cirrhosis or hepatitis shows depressive symptoms. On the other hand, every third patient with depressive disorder develops an alcohol disorder at some point during his / her life. A crucial link between depression and hepatic disease seems to be inflammatory processes in which the microbiome and increased intestinal permeability of the intestine play a pivotal role. Depression as well as liver disease, alcohol consumption, stress, and aging processes disturb the delicate balance of intestinal microbiota resulting in increased intestinal permeability. Therefore, bacteria or their metabolites such as the endotoxine lipopolysaccharide are able to reach the blood circulation resulting in inflammation in the liver as well as in the brain via a cytokine cascade, which in turn can lead to liver changes, depression, obesity, and metabolic syndrome. Therefore, liver values, blood glucose levels, and metabolic parameters should be closely monitored in patients with depressive disorders, and in the case of patients with hepatic diseases, increased attention should be given to depressive symptoms, diabetes and obesity.
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Reduced anti-inflammatory gut microbiota are associated with depression and anhedonia.
INTRODUCTION: Characterise gut microbiota distributions of participants with co-occurring depression and anxiety, in those with only depression or with anxiety, and determine if gut bacteria differentially correlates with distinct clinical presentations. METHODS: Participants (10 healthy controls [mean age: 33, 60% female] and 60 psychiatric subjects; major depressive disorder (comorbid with anxiety), n = 38 [mean age: 39.2, 82% female], anxiety only, n = 8 [mean age: 40.0, 100% female], depression only without anxiety, n = 14 [mean age: 41.9, 79% female]) were characterized by psychiatric assessments. Quantitative PCR and 16S rRNA sequencing were used to characterize the gut microbiota in stool samples. RESULTS: Altered microbiota correlated with pre-defined clinical presentation, with Bacteroides (p = 0.011) and the Clostridium leptum subgroup (p = 0.023) significantly different between clinical categories. Cluster analysis of the total sample using weighted UniFrac β-diversity of the gut microbiota identified two different clusters defined by differences in bacterial distribution. Cluster 2 had higher Bacteroides (p = 0.006), and much reduced presence of Clostridales (p<0.001) compared to Cluster 1. Bifidobacterium (p = 0.0173) was also reduced in Cluster 2 compared to Cluster 1. When evaluated for clinical charateristics, anhedonia scores in Cluster 2 were higher than in Cluster 1. LIMITATIONS: The sample is smaller and predominately female. CONCLUSIONS: Reduced or absent Clostridia was consistently seen in those with depression, independent of the presence of anxiety. Conversely, reduced Bacteroides may be more associated with the presence of anxiety, independent of the presence of depression. These differences suggest that gut microbiota distribution could help clarify the underlying pathology of comorbid clinical presentation.
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Probiotic treatment improves post-traumatic stress disorder outcomes in mice.
Post-traumatic stress disorder (PTSD) is a mental disorder resulting from traumatic events which are characterized primarily by anxiety and depressive disorder. In this study, we determine the role of gut bacteria in PTSD. PTSD-like symptoms were produced by single prolonged stress (SPS). SPS animals showed increased levels of anxiety as measured by the elevated plus maze test, while depressive behaviour was confirmed using sucrose preference, force swim, and tail suspension tests. Gut dysbiosis was confirmed in PTSD animals by next-generation sequencing of 16 s RNA of faecal samples, while these animals also showed increased intestinal permeability and altered intestinal ultrastructure. Probiotic treatment increases beneficial microbiota, improves intestinal health and reduces PTSD-associated anxiety and depression. We also found a decrease in cortical BDNF levels in PTSD animals, which was reversed after probiotic administration. Here, we establish the link between gut dysbiosis and PTSD and show that probiotic treatment may improve the outcome of PTSD like symptoms in mice.
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Strain-level structure of gut microbiome showed potential association with cognitive function in major depressive disorder: A pilot study.
BACKGROUND: Although the association between gut microbiota and the pathogenesis of major depressive disorder (MDD) has been well studied, it is unclear whether gut microbiota affects cognitive function in patients with MDD. In this study, we explored the association between gut microbiota and cognitive function in MDD and its possible mechanisms. METHODS: We enrolled 57 patients with MDD and 30 healthy controls (HCs) and used 16S rRNA gene sequencing analysis and shotgun metagenomic sequencing analysis to determine gut microbial composition. RESULTS: The richness and diversity of gut microbiota in patients with MDD were the same as those in HCs, but there were differences in the abundance of Bifidobacterium and Blautia. Compared with HCs, two strains (bin_32 and bin_55) were significantly increased, and one strain (bin_31) was significantly decreased in patients with MDD based on the strain-level meta-analysis. Time to complete the Stroop-C had significant negative correlations with bin_31 and bin_32. Bin_55 had significant negative correlations with time to complete the Stroop-C, time to complete the Stroop-CW, and repeated animal words in 60 s but significant positive correlations with correct answers in 120 s on the Stroop-CW. LIMITATIONS: This study only tested the cognitive function of MDD in a small sample, which may have caused some bias. CONCLUSIONS: Based on our strain-level analysis, we found that gut microbiota may be associated with the pathogenesis of MDD and may have potential effects on cognitive function.
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From isoniazid to psychobiotics: the gut microbiome as a new antidepressant target.
An awareness of the importance of the gut-brain axis in psychiatric disorders such as depression is increasing. The gut microbiome is a key component of this axis. Gut bacteria can communicate with the brain through a variety of pathways including the hypothalamic-pituitary-adrenal axis, immune modulation, tryptophan metabolism and the production of various neuroactive compounds. Patients with depression, and other mood and anxiety disorders, show distinct compositional changes in their gut bacteria profile, raising the question about a possible aetiological role for the microbiome in these disorders. Evidence is emerging that the gut microbiome may represent a new potential antidepressant target and the term 'psychobiotic' has been coined to describe bacteria which confer mental health benefits. Gut bacteria are easily accessible and can be altered in a variety of ways including through the use of probiotics, prebiotics and dietary change. Psychobiotics containing various Lactobacillus and Bifidobacterium species have demonstrated the ability to improve mood, reduce anxiety and enhance cognitive function in both healthy populations and patient groups. This article provides an overview of the identification and development of antidepressant psychobiotics, from the preclinical evidence in the laboratory to the more recent encouraging results from human trials.
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Microbial metabolites in the gut-brain axis: their impact on depression pathophysiology and treatment.
Gut microbiota influences major depressive disorder (MDD) via the microbiota-gut-brain axis through various metabolites, but a systematic understanding of their neuroregulatory mechanisms is lacking. This review categorizes gut microbial metabolites according to their metabolic origin and physiological function, clarifies their roles in depression-related neurobiological processes, and explores their therapeutic potential. Following PRISMA-ScR guidelines, a scoping review screened 1,249 records from five databases (2020-2025), including 23 studies on tryptophan metabolism, short-chain fatty acids (SCFAs), gamma-aminobutyric acid (GABA), and other metabolites that regulate depression-related neurobiological pathways; tryptophan metabolism affects serotonin/kynurenine pathways, causing neuroinflammation and neurotransmitter imbalance; SCFAs(primarily butyrate, less so propionate) modulate gene expression, neuroinflammation, and microglial function as histone deacetylase (HDAC) inhibitors; GABA-producing bacteria influence synaptic plasticity and suppress hypothalamic-pituitary-adrenal (HPA) axis hyperactivity; and other metabolites (e.g., homovanillic acid and β-hydroxybutyrate) have neuroprotective effects and affect neurotransmitter dynamics. Notably, this review advances the field via an integrative cross-pathway perspective, a critical appraisal of evidence strength across animal/human studies, and translational implications. Microbiome-modifying interventions (like probiotics, prebiotics, and dietary changes), are promising in animal models for correcting metabolite dysregulation and alleviating depressive symptoms.