Your browser does not allow saving data (e.g. private mode): bookmarks will be lost when the tab closes.
Search PubMed
Keywords, author, journal, years — results from PubMed, abstracts with Russian translation, bookmarks in your browser.
Found: 3 214
Page 256 of 322-
Administration of galacto-oligosaccharide prebiotics in the Flinders Sensitive Line animal model of depression.
INTRODUCTION: Major depressive disorder is the leading source of disability globally and current pharmacological treatments are less than adequate. Animal models such as the Flinders Sensitive Line (FSL) rats are used to mimic aspects of the phenotype in the human disorder and to characterise candidate antidepressant agents. Communication between the gut microbiome and the brain may play an important role in psychiatric disorders such as depression. Interventions targeting the gut microbiota may serve as potential treatments for depression, and this drives increasing research into the effect of probiotics and prebiotics in neuropsychiatric disorders. Prebiotics, galacto-oligosaccharides and fructooligosaccharides that stimulate the activity of gut bacteria have been reported to have a positive impact, reducing anxiety and depressive-like phenotypes and stress-related physiology in mice and rats, as well as in humans. Bimuno, the commercially available beta-galacto-oligosaccharide, has been shown to increase gut microbiota diversity. AIM: Here, we aim to investigate the effect of Bimuno on rat anxiety-like and depressive-like behaviour and gut microbiota composition in the FSL model, a genetic model of depression, in comparison to their control, the Flinders Resistant Line (FRL) rats. METHODS: Sixty-four male rats aged 5-7 weeks, 32 FSL and 32 FRL rats, will be randomised to receive Bimuno or control (4 g/kg) daily for 4 weeks. Animals will be tested by an experimenter unaware of group allocation on the forced swim test to assessed depressive-like behaviour, the elevated plus maze to assess anxiety-like behaviour and the open field test to assess locomotion. Animals will be weighed and food and water intake, per kilogram of bodyweight, will be recorded. Faeces will be collected from each animal prior to the start of the experiment and on the final day to assess the bacterial diversity and relative abundance of bacterial genera in the gut. All outcomes and statistical analysis will be carried out blinded to group allocation, group assignments will be revealed after raw data have been uploaded to Open Science Framework. Two-way analysis of variance will be carried out to investigate the effect of treatment (control or prebiotic) and strain (FSL or FRL) on depressive-like and anxiety-like behaviours.
-
Depression in Individuals Coinfected with HIV and HCV Is Associated with Systematic Differences in the Gut Microbiome and Metabolome.
Depression is influenced by the structure, diversity, and composition of the gut microbiome. Although depression has been described previously in human immunodeficiency virus (HIV) and hepatitis C virus (HCV) monoinfections, and to a lesser extent in HIV-HCV coinfection, research on the interplay between depression and the gut microbiome in these disease states is limited. Here, we characterized the gut microbiome using 16S rRNA amplicon sequencing of fecal samples from 373 participants who underwent a comprehensive neuropsychiatric assessment and the gut metabolome on a subset of these participants using untargeted metabolomics with liquid chromatography-mass spectrometry. We observed that the gut microbiome and metabolome were distinct between HIV-positive and -negative individuals. HCV infection had a large association with the microbiome that was not confounded by drug use. Therefore, we classified the participants by HIV and HCV infection status (HIV-monoinfected, HIV-HCV coinfected, or uninfected). The three groups significantly differed in their gut microbiome (unweighted UniFrac distances) and metabolome (Bray-Curtis distances). Coinfected individuals also had lower alpha diversity. Within each of the three groups, we evaluated lifetime major depressive disorder (MDD) and current Beck Depression Inventory-II. We found that the gut microbiome differed between depression states only in coinfected individuals. Coinfected individuals with a lifetime history of MDD were enriched in primary and secondary bile acids, as well as taxa previously identified in people with MDD. Collectively, we observe persistent signatures associated with depression only in coinfected individuals, suggesting that HCV itself, or interactions between HCV and HIV, may drive HIV-related neuropsychiatric differences.IMPORTANCE The human gut microbiome influences depression. Differences between the microbiomes of HIV-infected and uninfected individuals have been described, but it is not known whether these are due to HIV itself, or to common HIV comorbidities such as HCV coinfection. Limited research has explored the influence of the microbiome on depression within these groups. Here, we characterized the microbial community and metabolome in the stools from 373 people, noting the presence of current or lifetime depression as well as their HIV and HCV infection status. Our findings provide additional evidence that individuals with HIV have different microbiomes which are further altered by HCV coinfection. In individuals coinfected with both HIV and HCV, we identified microbes and molecules that were associated with depression. These results suggest that the interplay of HIV and HCV and the gut microbiome may contribute to the HIV-associated neuropsychiatric problems.
-
Novel insights into gut microbiota alterations in major depressive disorder with suicidal ideation: a metagenomic analysis.
INTRODUCTION: Suicidal ideation in major depressive disorder (MDD) is common, yet its biological mechanisms and biomarkers remain unclear. The gut microbiota, a key component of the gut-brain axis, has been implicated, but current evidence is limited. METHODS: We analyzed fecal samples from 141 participants, including 52 healthy controls (HCs) and 89 first-episode, drug-naïve MDD patients, further classified into suicidal ideation (SI, n = 57) and non-suicidal ideation (NSI, n = 32) groups using the Beck Scale for Suicide Ideation (BSSI). Shotgun metagenomic sequencing with HUMAnN3-based taxonomic and functional profiling was performed. Microbial diversity, differential abundance, and partial correlation analyses with suicidal ideation severity were conducted to identify key microbial taxa associated with suicidal ideation. For functional difference analysis, MaAsLin2 was employed across four levels: KEGG Orthology (KO), KEGG pathways, CAZy, and MetaCyc pathways. Mediation analysis was used to assess potential mediating effects between suicidal ideation and key microbial taxa after adjustment for age, sex, education, and BMI. RESULTS: No significant differences were observed in overall microbial diversity. Bacteroides cellulosilyticus was enriched in HCs and showed a significant negative association with suicidal ideation severity. Functionally, compared with the NSI group, patients with suicidal ideation exhibited reduced microbial capacities related to peptidoglycan biosynthesis. Mediation analysis further indicated that B. cellulosilyticus may modulate suicidal ideation through pathways involved in carbohydrate transport and metabolism, vitamin K2 biosynthesis, and DNA repair. CONCLUSION: Bacteroides cellulosilyticus may act as a potentially protective microbial species, negatively regulating suicidal ideation, possibly by enhancing carbohydrate metabolism and short-chain fatty acid production. Notably, this species has received limited attention in the context of psychiatric disorders, highlighting its potential as a novel microbial target. These findings provide new microbiome-based insights into suicidal ideation in MDD.
-
Hypomagnesemia: A Clinical and Nutritional Update.
PURPOSE OF REVIEW: Hypomagnesemia, defined as low serum/plasma magnesium concentration, is a highly prevalent yet underrecognized electrolyte disorder with extensive clinical, metabolic, and nutritional implications. This review provides an updated synthesis of magnesium physiology, dietary determinants, homeostatic regulation, diagnostic challenges, and therapeutic strategies, with particular emphasis on recent meta-analyses and large-scale epidemiological evidence linking hypomagnesemia to multisystem disease. RECENT FINDINGS: Accumulating evidence has shown consistent associations between low serum or dietary magnesium and increased risk of cardiometabolic disorders (hypertension, type 2 diabetes mellitus, metabolic syndrome, and cardiovascular disease), neuropsychiatric conditions (migraine, depression, cognitive impairment, and dementia), osteoporosis, immune dysregulation, and adverse outcomes in hospitalized, critically ill, and chronic kidney disease patients. Mechanistic studies have clarified the roles of TRPM6/7 channels, tight junction claudins, and basolateral magnesium transporters in intestinal and renal magnesium handling, elucidating pathways underlying both inherited and acquired deficiencies. Research has also highlighted the contribution of modern dietary patterns, food processing, mineral-depleted drinking water, medication use (notably proton pump inhibitors, diuretics and chemotherapeutic agents), and gut microbiome alterations to widespread subclinical deficiency. Meta-analyses of RCTs indicate that magnesium supplementation confers modest but clinically relevant improvements in blood pressure, glycemic control, inflammatory markers, endothelial function, migraine frequency, and depressive symptoms, particularly in individuals with baseline hypomagnesemia. However, serum magnesium remains an insensitive biomarker of total body magnesium status, and consensus on optimal diagnostic thresholds and replacement strategies is lacking. Magnesium deficiency contributes to a wide spectrum of multisystem disorders, and is driven by dietary insufficiency, gastrointestinal and renal losses, medication use, chronic disease, and altered microbiome function. Meta-analytic evidence supports its role as a modifiable risk factor across cardiovascular, metabolic, neurological, skeletal, and immune disorders. Dietary modification, optimized supplementation, and correction of underlying causes of deficiency remain central to management. Future research should focus on improved diagnostic tools, personalized dosing approaches and long-term outcomes of magnesium repletion. Enhancing clinical awareness and integrating magnesium evaluation into routine care may reduce the growing burden of hypomagnesemia.
-
The Gut-Brain Axis and Mental Health: How Diet Shapes Our Cognitive and Emotional Well-Being.
The gut-brain axis (GBA) connects the gastrointestinal (GI) system and the central nervous system (CNS) in a two-way communication system that greatly impacts mental health and overall well-being. Dietary choices significantly influence the gut microbiome, thereby affecting emotional, cognitive, and neurological health. This review explores how specific dietary patterns, including high-fiber, plant-based, and Mediterranean diets (MD), enhance microbial diversity, decrease inflammation, and enhance gut-brain communication. It highlights the importance of probiotics, prebiotics, omega-3 fatty acids, and antioxidants in controlling gut microbiota, enhancing intestinal barrier function, and reducing systemic inflammation associated with anxiety, depression, and cognitive decline. The article covers practical methods for integrating dietary adjustments into personalized mental health treatment, while also addressing challenges such as individual microbiome variability and the need for long-term research. This review underscores the possibility of using nutritional interventions as a non-invasive and easily accessible way to promote mental health and resilience based on existing evidence. The methodology involved a comprehensive examination of existing literature exploring the GBA and its influence on mental health. We searched relevant databases, including PubMed and Google Scholar, using keywords such as "gut-brain axis," "microbiome," "diet," and "mental health." Peer-reviewed articles were selected based on their relevance to the relationship between dietary interventions and mental health outcomes, with a focus on studies exploring cognitive and emotional well-being.
-
How does Quorum Sensing of Intestinal Bacteria Affect Our Health and Mental Status?
The human gut is host to almost 3000 microbial species, of which 90% are bacteria. Quorum sensing (QS) molecules generated by intestinal bacteria are important in establishing species- and strain-level structures within the gut microbiome but are also used to communicate with the host. Although we do not know which QS molecules have the most direct interaction with intestinal and sensory neurons, it is clear they affect our physiological and mental health. Signals produced by bacteria are diverse and include autoinducers (AIs), homoserine lactones (HSLs), quinolines, peptides, toxins and proteases. These signaling molecules activate specific receptors in the bacterial cell wall and trigger sensors in the cytoplasm that regulate gene expressions. A better understanding of the gene structures encoding the production of QS molecules is of importance when selecting strains with neurogenerative and other probiotic properties. Furthermore, QS molecules may be used as biomarkers in the diagnosis of inflammable bowel disease (IBD), irritable bowel syndrome (IBS) and colorectal cancer (CRC). In the future, it should be possible to use QS biomarkers to diagnose neurological and psychiatric diseases such as anxiety and depression, major depressive disorder (MDD), schizophrenia, bipolar disorder, autism and obsessive-compulsive disorder (OCD).
-
The development of an ingestible biosensor for the characterization of gut metabolites related to major depressive disorder: hypothesis and theory.
The diagnostic process for psychiatric conditions is guided by the Diagnostic and Statistical Manual of Mental Disorders (DSM) in North America. Revisions of the DSM over the years have led to lowered diagnostic thresholds across the board, incurring increased rates of both misdiagnosis and over-diagnosis. Coupled with stigma, this ambiguity and lack of consistency exacerbates the challenges that clinicians and scientists face in the clinical assessment and research of mood disorders such as Major Depressive Disorder (MDD). While current efforts to characterize MDD have largely focused on qualitative approaches, the broad variations in physiological traits, such as those found in the gut, suggest the immense potential of using biomarkers to provide a quantitative and objective assessment. Here, we propose the development of a probiotic Escherichia coli (E. coli) multi-input ingestible biosensor for the characterization of key gut metabolites implicated in MDD. DNA writing with CRISPR based editors allows for the molecular recording of signals while riboflavin detection acts as a means to establish temporal and spatial specificity for the large intestine. We test the feasibility of this approach through kinetic modeling of the system which demonstrates targeted sensing and robust recording of metabolites within the large intestine in a time- and dose- dependent manner. Additionally, a post-hoc normalization model successfully controlled for confounding factors such as individual variation in riboflavin concentrations, producing a linear relationship between actual and predicted metabolite concentrations. We also highlight indole, butyrate, tetrahydrofolate, hydrogen peroxide, and tetrathionate as key gut metabolites that have the potential to direct our proposed biosensor specifically for MDD. Ultimately, our proposed biosensor has the potential to allow for a greater understanding of disease pathophysiology, assessment, and treatment response for many mood disorders.
-
Mental Health Symptom Reduction Using Digital Therapeutics Care Informed by Genomic SNPs and Gut Microbiome Signatures.
Neuropsychiatric diseases and obesity are major components of morbidity and health care costs, with genetic, lifestyle, and gut microbiome factors linked to their etiology. Dietary and weight-loss interventions can help improve mental health, but there is conflicting evidence regarding their efficacy; and moreover, there is substantial interindividual heterogeneity that needs to be understood. We aimed to identify genetic and gut microbiome factors that explain interindividual differences in mental health improvement after a dietary and lifestyle intervention for weight loss. We recruited 369 individuals participating in Digbi Health’s personalized digital therapeutics care program and evaluated the association of 23 genetic scores, the abundance of 178 gut microbial genera, and 42 bacterial pathways with mental health. We studied the presence/absence of anxiety or depression, or sleep problems at baseline and improvement on anxiety, depression, and insomnia after losing at least 2% body weight. Participants lost on average 5.4% body weight and >95% reported improving mental health symptom intensity. There were statistically significant correlations between: (a) genetic scores with anxiety or depression at baseline, gut microbial functions with sleep problems at baseline, and (b) genetic scores and gut microbial taxa and functions with anxiety, depression, and insomnia improvement. Our results are concordant with previous findings, including the association between anxiety or depression at baseline with genetic scores for alcohol use disorder and major depressive disorder. As well, our results uncovered new associations in line with previous epidemiological literature. As evident from previous literature, we also observed associations of gut microbial signatures with mental health including short-chain fatty acids and bacterial neurotoxic metabolites specifically with depression. Our results also show that microbiome and genetic factors explain self-reported mental health status and improvement better than demographic variables independently. The genetic and microbiome factors identified in this study provide the basis for designing and personalizing dietary interventions to improve mental health.
-
A psychology of the human brain-gut-microbiome axis.
In recent years, we have seen increasing research within neuroscience and biopsychology on the interactions between the brain, the gastrointestinal tract, the bacteria within the gastrointestinal tract, and the bidirectional relationship between these systems: the brain-gut-microbiome axis. Although research has demonstrated that the gut microbiota can impact upon cognition and a variety of stress-related behaviours, including those relevant to anxiety and depression, we still do not know how this occurs. A deeper understanding of how psychological development as well as social and cultural factors impact upon the brain-gut-microbiome axis will contextualise the role of the axis in humans and inform psychological interventions that improve health within the brain-gut-microbiome axis. Interventions ostensibly aimed at ameliorating disorders in one part of the brain-gut-microbiome axis (e.g., psychotherapy for depression) may nonetheless impact upon other parts of the axis (e.g., microbiome composition and function), and functional gastrointestinal disorders such as irritable bowel syndrome represent a disorder of the axis, rather than an isolated problem either of psychology or of gastrointestinal function. The discipline of psychology needs to be cognisant of these interactions and can help to inform the future research agenda in this emerging field of research. In this review, we outline the role psychology has to play in understanding the brain-gut-microbiome axis, with a focus on human psychology and the use of research in laboratory animals to model human psychology.
-
The importance of the gut microbiome and its signals for a healthy nervous system and the multifaceted mechanisms of neuropsychiatric disorders.
Increasing evidence links the gut microbiome and the nervous system in health and disease. This narrative review discusses current views on the interaction between the gut microbiota, the intestinal epithelium, and the brain, and provides an overview of the communication routes and signals of the bidirectional interactions between gut microbiota and the brain, including circulatory, immunological, neuroanatomical, and neuroendocrine pathways. Similarities and differences in healthy gut microbiota in humans and mice exist that are relevant for the translational gap between non-human model systems and patients. There is an increasing spectrum of metabolites and neurotransmitters that are released and/or modulated by the gut microbiota in both homeostatic and pathological conditions. Dysbiotic disruptions occur as consequences of critical illnesses such as cancer, cardiovascular and chronic kidney disease but also neurological, mental, and pain disorders, as well as ischemic and traumatic brain injury. Changes in the gut microbiota (dysbiosis) and a concomitant imbalance in the release of mediators may be cause or consequence of diseases of the central nervous system and are increasingly emerging as critical links to the disruption of healthy physiological function, alterations in nutrition intake, exposure to hypoxic conditions and others, observed in brain disorders. Despite the generally accepted importance of the gut microbiome, the bidirectional communication routes between brain and gut are not fully understood. Elucidating these routes and signaling pathways in more detail offers novel mechanistic insight into the pathophysiology and multifaceted aspects of brain disorders.