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Circulating Short-Chain Fatty Acid (SCFA) profiles as a biomarker of gut-brain axis dysfunction: A meta-analysis for the SCFA signature in major depression.
BACKGROUND: Major Depressive Disorder (MDD) is increasingly viewed through the lens of the neuroinflammatory hypothesis and gut-brain axis dysfunction. Short-Chain Fatty Acids (SCFAs), the primary metabolites produced by the gut microbiota, are vital signaling molecules that maintain intestinal barrier integrity, modulate peripheral immunity, and influence microglial function. While individual studies suggest altered SCFAs levels in MDD, a definitive, quantitative synthesis establishing a robust biomarker signature is currently lacking. This meta-analysis aimed to precisely characterize the signature of SCFAs (acetic, propionic, butyric, and isobutyric acid) in MDD patients compared to healthy controls. METHODS: We systematically searched major databases across PubMed, Embase, and Web of Science databases for studies quantifying SCFAs levels up to September 15, 2025. Studies examining SCFAs levels in depressed patients and depressive-like murine models, as well as studies investigating SCFAs interventions for depressive-like behavior, were selected for synthesis. Risk of bias was evaluated using the Newcastle-Ottawa Scale. The effect sizes were synthesized using a random-effects model and presented as standardized mean differences. RESULTS: Eight human and 52 murine studies were included in the meta-analyses. Depressed patients showed significantly lower concentrations in blood (plasma and serum) of propionic (SMD = -0.60, p-value = 0.007), butyric (SMD = -0.50, p-value = 0.006), isobutyric (SMD = -0.72, p-value = 0.020), valeric (SMD = -0.43, p-value = 0.040) and isovaleric acids (SMD = -0.75, p-value = 0.002). Secondary analysis of MDD patients confirmed consistent reductions. High heterogeneity was observed. In murine models, SCFAs depletion was frequently observed, while supplementation improved depressive-like behaviors. CONCLUSION: MDD is characterized by a significant, quantifiable deficit in the circulating SCFAs metabolome, which provides strong empirical validation for the gut-brain axis hypothesis in depression. We advocate for the investigation of SCFAs as novel, measurable peripheral biomarkers and targeted therapeutic agents (e.g., butyrate supplementation) for precision nutritional psychiatry.
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Gut Microbiota and Mood Disorders: How Bottom-Up Techniques Can Improve Mental Health.
The microbiome is dynamic and changes with early development, environmental factors such as diet and antibiotics, and in response to disease. Recently, its role in psychiatric disorders has gained interest. A new class of probiotics, psychobiotics, has emerged as a non-toxic intervention for psychiatric conditions. The relationship between gut microbial metabolism and mental health is gaining attention, with the gut microbiome playing a role in major depressive disorder. Understanding the microbiota offers new therapeutic opportunities for various medical conditions.
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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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Cross-sex cecal microbiota transfer alters depressive-like behaviours in mice.
Major depressive disorder (MDD) is a leading cause of non-fatal global disease burden, with females being two-fold more likely than males to be diagnosed with the disorder. Despite this sex-linked disparity of diagnosis, it is unclear what underlies the sex bias in MDD. Recent findings suggest a role for the gut in mediating affective disorders through the gut-brain-axis (GBA). However, few studies have included sex as a biological variable. For this study, cross-sex transfer of cecal microbiota was performed between male and female C57Bl/6 mice to elucidate the effects of sex and the gut microbiome on a standard battery of tests measuring depressive-like behaviours. Specifically, regardless of sex, recipients of male cecal content had a greater sucrose preference than controls and recipients of female cecum, although recipients of male cecal transfer also showed a trend towards increased passive coping on the force swim test. Conversely, in the splash test, recipients of female cecum displayed a decrease in grooming behaviour compared to both controls and recipients of male cecum, suggestive of an increase in depressive-like behaviour. These results support a role for female-specific gut microbes in contributing to female vulnerability to depression, particularly on self-care measures, while male-specific gut microbes may protect in part against an anhedonia-like phenotype, but increase passive coping.
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Differential Gut Microbiota Compositions Related With the Severity of Major Depressive Disorder.
OBJECTIVE: Increasing evidence shows a close relationship between gut microbiota and major depressive disorder (MDD), but the specific mechanisms remain unknown. This study was conducted to explore differential gut microbiota compositions related to the severity of MDD. METHODS: Healthy controls (HC) (n = 131) and MDD patients (n = 130) were included. MDD patients with Hamilton Depression Rating Scale (HDRS) score <25 and ≥25 were assigned into moderate (n = 72) and severe (n = 58) MDD groups, respectively. Univariate and multivariate analyses were used to analyze the gut microbiota compositions at the genus level. RESULTS: Thirty-six and 27 differential genera were identified in moderate and severe MDD patients, respectively. The differential genera in moderate and severe MDD patients mainly belonged to three (Firmicutes, Actinobacteriota, and Bacteroidota) and two phyla (Firmicutes and Bacteroidota), respectively. One specific covarying network from phylum Actinobacteriota was identified in moderate MDD patients. In addition, five genera (Collinsella, Eggerthella, Alistipes, Faecalibacterium, and Flavonifractor) from the shared differential genera by two MDD groups had a fair efficacy in diagnosing MDD from HC (AUC = 0.786). CONCLUSIONS: Our results were helpful for further exploring the role of gut microbiota in the pathogenesis of depression and developing objective diagnostic methods for MDD.
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Alterations of gut microbiota composition in post-finasteride patients: a pilot study.
PURPOSE: Post-finasteride syndrome (PFS) has been reported in a subset of patients treated with finasteride (an inhibitor of the enzyme 5alpha-reductase) for androgenetic alopecia. These patients showed, despite the suspension of the treatment, a variety of persistent symptoms, like sexual dysfunction and cognitive and psychological disorders, including depression. A growing body of literature highlights the relevance of the gut microbiota-brain axis in human health and disease. For instance, alterations in gut microbiota composition have been reported in patients with major depressive disorder. Therefore, we have here analyzed the gut microbiota composition in PFS patients in comparison with a healthy cohort. METHODS: Fecal microbiota of 23 PFS patients was analyzed by 16S rRNA gene sequencing and compared with that reported in ten healthy male subjects. RESULTS: Sexual dysfunction, psychological and cognitive complaints, muscular problems, and physical alterations symptoms were reported in more than half of the PFS patients at the moment of sample collection. The quality sequence check revealed a low library depth for two fecal samples. Therefore, the gut microbiota analyses were conducted on 21 patients. The α-diversity was significantly lower in PFS group, showing a reduction of richness and diversity of gut microbiota structure. Moreover, when visualizing β-diversity, a clustering effect was found in the gut microbiota of a subset of PFS subjects, which was also characterized by a reduction in Faecalibacterium spp. and Ruminococcaceae UCG-005, while Alloprevotella and Odoribacter spp were increased compared to healthy control. CONCLUSION: Gut microbiota population is altered in PFS patients, suggesting that it might represent a diagnostic marker and a possible therapeutic target for this syndrome.
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Epigenetics of the molecular clock and bacterial diversity in bipolar disorder.
Objectives The gut microbiome harbors substantially more genetic material than our body cells and has an impact on a huge variety of physiological mechanisms including the production of neurotransmitters and the interaction with brain functions through the gut-brain-axis. Products of microbiota can affect methylation according to preclinical studies. The current investigation aimed at analyzing the correlation between gut microbiome diversity and the methylation of the clock gene ARNTL in individuals with Bipolar Disorder (BD). Methods Genomic DNA was isolated from fasting blood of study participants with BD (n = 32). The methylation analysis of the ARNTL CG site cg05733463 was performed by bisulfite treatment of genomic DNA with the Epitect kit, PCR and pyrosequencing. Additionally, DNA was extracted from stool samples and subjected to 16S rRNA sequencing. QIIME was used to analyze microbiome data. Results Methylation status of the ARNTL CpG position cg05733463 correlated significantly with bacterial diversity (Simpson index: r= -0.389, p = 0.0238) and evenness (Simpson evenness index: r= -0.358, p = 0.044). Furthermore, bacterial diversity differed significantly between euthymia and depression (F(1,30) = 4.695, p = 0.039). Discussion The results of our pilot study show that bacterial diversity differs between euthymia and depression. Interestingly, gut microbiome diversity and evenness correlate negatively with methylation of ARNTL, which is known to regulate monoamine oxidase A transcription. We propose that alterations in overall diversity of the gut microbiome represent an internal environmental factor that has an epigenetic impact on the clock gene ARNTL which is thought to be involved in BD pathogenesis.
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Dietary Tryptophan Allocation in Depression: Serotonin-Kynurenine Balance, Microbial Indole Pathways, and Inflammatory Phenotypes.
Depression is defined by clinical symptoms, but its biology varies considerably among patients. In this review, dietary tryptophan allocation describes the routes taken by tryptophan after intestinal absorption. Some is incorporated into proteins. Some enters serotonin and melatonin synthesis or the kynurenine pathway, while gut bacteria convert another fraction into indole compounds. Brain availability also depends on the circulating free pool and competition with other large neutral amino acids. This term does not imply a new biochemical pathway. It allows these known processes to be considered in relation to inflammation, metabolism, the gut microbiota, medication use, and current disease state. Recent meta-analyses indicate that peripheral tryptophan is lower in depression. They do not show a consistent increase in the kynurenine-to-tryptophan ratio, and findings from cerebrospinal fluid vary between studies. Human multiomics studies have associated microbial and metabolite profiles with cognition and response to treatment, although the evidence remains largely correlational. Changes in kynurenine, 3-hydroxykynurenine, and quinolinic acid are more apparent in inflammatory subgroups than in unselected samples. Modern evidence for L-tryptophan monotherapy is sparse. Trials of 5-hydroxytryptophan and interventions directed at the gut microbiota have also produced mixed results. Studies should characterize participants and sampling conditions more carefully. Diet and competition among amino acids need to be recorded. Albumin concentration, medication exposure, and disease state also affect interpretation. Considering these variables together may improve biomarker analyses and support trials in more biologically homogeneous groups. Dietary tryptophan allocation is proposed for these research purposes, not for clinical diagnosis or routine supplementation.
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"Gut-brain axis": Review of the role of the probiotics in anxiety and depressive disorders.
BACKGROUND: Depressive disorders are the leading cause of disability worldwide and together with anxiety contribute to a very high burden of disease. Therefore, improving their treatment is a significant medical research target: The role of probiotics is a topic of great interest for the current research in this field. OBJECTIVES: To explore the current literature about the impact of probiotics on anxious and depressive symptoms. METHODS: Scoping review following the PRISMA guidelines. RESULTS: The selection process yielded 23 studies. Probiotics positively affected depressive symptomatology and anxiety symptoms according to 53.83% and 43.75% of the selected studies, respectively. Among the studies assessing inflammatory biomarkers, 58.31% found they were decreased after administration of probiotics. CONCLUSION: The results emerging from the existing literature about probiotic supplementation for depression treatment are encouraging, but further research is needed considering the shortage of clinical trials on this topic and the heterogeneity of the samples analyzed.
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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.